THE UNITED REPUBLIC OF TANZANIA
STANDARD TREATMENT GUIDELINES AND 
NATIONAL ESSENTIAL MEDICINES LIST FOR 
TANZANIA MAINLAND
MINISTRY OF HEALTH, COMMUNITY DEVELOPMENT, 
GENDER, ELDERLY AND CHILDREN
SIXTH EDITION 2021

THE UNITED REPUBLIC OF TANZANIA
STANDARD TREATMENT GUIDELINES AND 
NATIONAL ESSENTIAL MEDICINES LIST FOR 
TANZANIA MAINLAND
SIXTH EDITION 2021
MINISTRY OF HEALTH, COMMUNITY DEVELOPMENT, 
GENDER, ELDERLY AND CHILDREN


i
FOREWORD 
The Government is committed to ensure adequate availability and accessibility of safe, efficacious 
and affordable essential medicines at all times to all Tanzanians. To realize this objective, the 
development and implementation of Standard Treatment Guidelines (STG) and National Essential 
Medicines List (NEMLIT) is an important step in the health care system for quality diagnosis, 
treatment and prevention of diseases as well as procurement and supply of essential medicnes.  
The 2017 edition of STG/NEMLIT has been updated to reflect new therapeutic options and changing 
therapeutic needs, the need to ensure drug quality, safety issues, medicines for emerging diseases, 
medicines to meet changing resistance pattern and to reconsider levels of care. A new chapter 
“approach to patients with emergency conditions” has been added to guide clinicians in the 
management of patients with emergency conditions and provide initial resuscitation and 
stabilization. In addition, under notifiable diseases, guidance for the management of COVID-19 has 
been addressed.  
The list of medicines has been selected with due regard to disease prevalence and public health 
relevance, evidence of clinical efficacy and safety, comparative costs, availability and treatment 
facilities. The review considered the ongoing expansion of services in primary health facilities; 
hence, levels of some medicines have been lowered to be available at that level. Inparticular, 
special attention has been paid to medicines used to manage non-communicable diseases, such as 
diabetes and cardiovascular diseases. Also, this new version of STG/NEMLIT adopted the World 
Health Organization classification of antibiotics into Access, Watch, Reserve (AWaRe) groups, 
aiming to improve the rational use of antimicrobial agents and minimize the burden of antimicrobial 
resistance.  
The Standard Treatment Guidelines comprise statements to assist practitioners in making decisions 
about appropriate treatment for specific clinical conditions. Hence, this is a key tool, which should be 
used to effectively promote access to essential medicines, to achieve maximum therapeutic benefit 
and optimize patient outcomes. Further, the document will guide the procurement and supply of 
medicines at the Medical Stores Department (MSD)prescribing and dispensing of medicines in 
public health facilities as well as the reimbursements of medicines at the National Health Insurance 
Fund (NHIF).  
I therefore urge all responsible institutions and experts to adhere to STG/NEMLIT and to ensure 
availability of essential medicines at all times, in adequate amounts, in appropriate dosage forms, 
with assured quality and adequate information, and at a price the individual and the community can 
afford. Comments and suggestions that may help us to improve a next edition of STG/NEMLIT are 
welcome and much appreciated. I am confident that health care workers and responsible institutions 
will find this document very useful. 
Hon. Dr. Dorothy O. Gwajima (MP) 
MINISTER FOR HEALTH, COMMUNITY DEVELOPMENT, GENDER, ERLDERLY AND 
CHILDREN 

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ACKNOWLEDGEMENTS 
This document was developed through a co-creation process that engaged a broad range of 
stakeholders. This participatory approach permits ownership of the Standard Treatment Guidelines 
and Essential Medicines List of Tanzania (STG/NEMLIT)and facilitatesits successful implementation. 
The development process was initiated in December 2019 by identifying key stakeholders. 
Thereafter, all key stakeholders, including all hospitals were asked to provide their inputs on 
essential medicines to be added or deleted based on scientific evidence. In addition, stakeholders 
were asked to recommend stratification forlevels of use for specific medicines. I highly appreciate 
support fromMuhimbili National Hospital, Bugando and Mbeya Zonal Referral hospitals as well as 
Bukoba, Katavi, Njombe and Sekou Toure Regional Referral Hospitals who provided inputs. Your 
comments were valuable and were incorporated in this STG/NEMLIT edition. 
Further, the Ministry in collaboration with Health Promotion and System Strengthening (HPSS) 
project conducted a surveyfor the collection of recommendations regardingthe review of 
STG/NEMLIT in 26 health facilities in six regions of Dodoma, Singida, Manyara, Morogoro, Pwani 
and Dar es Salaam.  I thank all health care workers who provided recommendations for 
STG/NEMLIT improvements; your contributions were consolidated and used to enrich this 
document. 
In a further step, Lead Reviewers for individual chapters were nominated. We thank all Professional 
Associations who participated in the review through their professional peer reviewersrendering the 
process fully participatory. I acknowledge the Association of Physicians of Tanzania (APHYTA), 
Association of Gynecologists and Obstetricians of Tanzania (AGOTA), Association of 
Pulmonologists-Chest Tanzania, Emergency Medicine Association of Tanzania (EMAT), Nephrology 
Society of Tanzania (NESOT), Pediatric Association of Tanzania (PAT), Pharmaceutical Society of 
Tanzania (PST), Tanzania Association for Respiratory Diseases (TARD), Tanzania Cardiac Society 
(TCS), Tanzania Dental Association (TDA), Tanzania Diabetes Association (TDA), Tanzania Ear 
Nose & Throat Society (TENTS), Tanzania Gastroenterology and Endoscopy Society (TGES), 
Tanzania Oncology Society (TOS), Tanzania Ophthalmology Society (TOS), Tanzania Orthopedic 
Association (TOA), Tanzania Society for Dermatovenereology (TASOD) and Tanzania Surgical 
Associations (TSA). I also acknowledge the Holistic Approach to Unravel Antibacterial Resistance in 
East Africa (HATUA-MR/S004785/1)-Tanzania for their preliminary results of patients with urinary 
tract infections (UTI) which provided insight of the susceptibility patterns of common isolates causing 
UTI in Tanzania, which was useful to update the relevant chapter. I trust that in the future review you 
will continue providing technical support. 
I sincerely thank the National Medicines and Therapeutic Committee (NMTC), all Lead Reviewers 
and the NMTC Secretariat who made this a reality. Their names are annexed. Finally, I would like to 
gratefully acknowledgethe financial support provided by the USAID Medicines, Technologies and 
Pharmaceutical Services (MTaPS) program implemented by Management Science for Health, the 
Swiss Agency for Development and Cooperation (SDC) through the Health Promotion and System 
Strengthening (HPSS) project, the Global Fund for AIDS, TB and Malaria (GFATM) and the National 
Health Insurance (NHIF). 
Prof. Abel N. Makubi 
PERMANENT SECRETARY (HEALTH) 

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TABLE OF CONTENTS 
FOREWORD ............................................................................................................................ i 
ACKNOWLEDGEMENTS ....................................................................................................... ii 
PART I ..................................................................................................................................... 1 
THE NATIONAL ESSENTIAL MEDICINES LIST (NEMLIT) .................................................. 1 
PART II .................................................................................................................................. 30 
THE STANDARD TREATMENT GUIDELINE (STG) ............................................................ 30 
CHAPTER ONE ..................................................................................................................... 31 
APPROACH TO PATIENTS WITH EMERGENCY CONDITIONS ....................................... 31 
1.1 The Concept of Emergency Care and Resuscitation ................................................. 31 
1.2 Cardiac Arrest and Cardiopulmonary Resuscitation ................................................. 32 
1.3 Approach to Stridor ....................................................................................................... 33 
1.4 Approach to Upper Gastrointestinal Bleeding ............................................................ 34 
1.5 Approach to Seizure and Status Epilepticus .............................................................. 35 
1.6 Approach to Altered Mental Status .............................................................................. 36 
1.7 Approach to Difficult in Breathing ............................................................................... 36 
1.8 Anaphylaxis .................................................................................................................... 37 
1.9 Cardiac Tamponade ...................................................................................................... 38 
1.10 Pulmonary Edema ....................................................................................................... 38 
1.11 Approach to Shock ...................................................................................................... 39 
1.12 
Sepsis and Septic Shock ..................................................................................... 41 
1.13 
Approach to Pain ................................................................................................. 43 
1.13.1 Approach to chest pain ............................................................................................ 43 
1.13.2 Approach to Abdominal Pain .................................................................................. 44 
1.13. 3 Headache .................................................................................................................. 45 
1.13.4 Other Pains ................................................................................................................ 46 

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1.14 
Approach to Fever (Pyrexia) ............................................................................... 46 
1.15 
Cough .................................................................................................................... 47 
1.16 
. Approach to the Trauma Patient ....................................................................... 48 
1.17 
Approach to Dehydrated Patient ........................................................................ 48 
1.18 
Hyponatremia ....................................................................................................... 50 
1.19 
Hypokalaemia ....................................................................................................... 51 
1.20 
Triage Overview ................................................................................................... 52 
CHAPTER TWO .................................................................................................................... 55 
ANAESTHESIA ..................................................................................................................... 55 
2.1   General Anaesthesia ................................................................................................... 55 
2.2   Local Anaesthesia ....................................................................................................... 57 
2.3 Sedation .......................................................................................................................... 58 
2.4 Anaesthesia in Special Conditions .............................................................................. 59 
2.4.1 Surgery in Diabetic Patient ........................................................................................ 59 
2.4.2 Surgery in Hypertensive Patient ............................................................................... 60 
2.4.3 Surgery in Asthmatic Patient ..................................................................................... 60 
2.4.4 Surgery in Sickle Cell Patient .................................................................................... 61 
CHAPTER THREE ................................................................................................................ 62 
HAEMATOLOGY AND BLOOD TRANSFUSION ................................................................. 62 
3.1 Anaemia .......................................................................................................................... 62 
3.1.1 Iron Deficiency Anaemia ............................................................................................ 62 
3.1.2 Megaloblastic Anemia ................................................................................................ 63 
3.1.3 Haemolytic Anaemia ................................................................................................... 64 
3.1.4   Sickle Cell Disease (SCD) ........................................................................................ 64 
3.1.4 G6PD Deficiency ......................................................................................................... 68 
3.1.5   Aplastic Anaemia (Bone Marrow Failure) ............................................................... 68 
3.1.6 Myelodysplastic syndrome (MDS) ............................................................................ 69 
3.2    Bleeding Disorders ..................................................................................................... 69 

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3.2.1 Hereditary Bleeding Disorders .................................................................................. 69 
3.2.3Acquired Bleeding Disorders/Platelet Disorders ...................................................... 71 
3.3 Coagulation Disorders .................................................................................................. 72 
3.3.1 Deep Vein Thrombosis (DVT) .................................................................................... 72 
3.3.2 Pulmonary Embolism (PE) ......................................................................................... 73 
3.4 Blood Transfusion ......................................................................................................... 73 
CHAPTER FOUR .................................................................................................................. 77 
NOTIFIABLE DISEASES ...................................................................................................... 77 
4.1 Bacterial Infections ........................................................................................................ 77 
4. 1.1 Cholera ....................................................................................................................... 77 
4.1.2 Anthrax ........................................................................................................................ 80 
4.1.3 Plague .......................................................................................................................... 82 
4.1.4Bacterial Cerebro-Spinal Meningitis .......................................................................... 84 
4.1.6 Tick-Borne Relapsing Fever (TBRF) ......................................................................... 87 
4.2 Viral Infections ............................................................................................................... 88 
4.2.1 Viral Haemorrhaghic Fevers (VHF) ........................................................................... 88 
4.2.2 Measles (Rubeola) ...................................................................................................... 98 
4.2.3 Rabies .......................................................................................................................... 99 
4.2.4   Zika Virus Disease .................................................................................................. 101 
4.2.5 COVID-19 ................................................................................................................... 103 
CHAPTER FIVE .................................................................................................................. 109 
MALARIA ............................................................................................................................ 109 
5.1 Asymptomatic Malaria Case ....................................................................................... 109 
5.2 Symptomatic Malaria Case ......................................................................................... 109 
5.2.1    Uncomplicated Malaria .......................................................................................... 109 
5.2.2    Severe Malaria ........................................................................................................ 111 
5.3 Management of Malaria in Special Groups ............................................................... 114 
5.3.1    Malaria in Pregnancy (MIP) ................................................................................... 114 

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5.3.2 Management of Malaria in Neonates ....................................................................... 115 
5.3.3 Management of Malaria in HIV and AIDS patients ................................................. 116 
CHAPTER SIX ..................................................................................................................... 117 
HIVAND AIDS ..................................................................................................................... 117 
6.1 Treatment of HIV and AIDS in Adults and Adolescents ........................................... 117 
6.1.1 First-Line Regimens for Adults and Adolescents ................................................. 117 
6.1.2 ART in women of childbearing potential or pregnant women .............................. 117 
6.1.3 Prevention of Mother to Child Transmission ......................................................... 118 
6.1.4 Second-line ART in Adults and Adolescents ......................................................... 119 
6.1.5 Third-line Antiretroviral Therapy ............................................................................. 119 
6.2 Changing Antiretroviral Therapy ................................................................................ 120 
6.2.1 Drug Specific Adverse Events-Toxicities ............................................................... 120 
6.2.2 Changing ART due to Treatment Failure ................................................................ 123 
6.3 Monitoring Patients on Antiretroviral Therapy ......................................................... 123 
6.4 Immune Reconstitution Inflammatory Syndrome (IRIS) .......................................... 124 
6.5   Antiretroviral Therapy in Children and Adolescents Living with HIV ................... 125 
6.6. Changing ART in Children Under 15 Years .............................................................. 128 
6.7   HIV Prevention ........................................................................................................... 132 
6.7.1 Post Exposure Prophylaxis (PEP) ........................................................................... 132 
6.7.2 Pre-Exposure Prophylaxis (PrEP) ........................................................................... 133 
CHAPTER SEVEN .............................................................................................................. 135 
TUBERCULOSIS AND LEPROSY ..................................................................................... 135 
7.1General Management of Tuberculosis ........................................................................ 135 
7.1.1 Drug Resistance Tuberculosis (DR-TB) ................................................................. 136 
7.1.2 Treatment of Tuberculosis in Special Cases ......................................................... 138 
Treatment of TB/HIV co-infected patients ....................................................................... 138 
7.2 General Treatment of Leprosy .................................................................................... 139 
7.2.1 Treatment of Leprosy in Special Cases .................................................................. 139 

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CHAPTER EIGHT ............................................................................................................... 141 
NERVOUS SYSTEM DISEASE CONDITIONS ................................................................... 141 
8.1 Infections of the Nervous System .............................................................................. 141 
8.1.1 Bacterial infections ................................................................................................... 141 
8.1.2 Fungal Infections ...................................................................................................... 144 
8.1.3 Protozoa infections .................................................................................................. 145 
8.1.4 Helminthic infections ............................................................................................... 146 
8.1.5 Viral infections .......................................................................................................... 147 
8.2 Initial Management of Stroke ...................................................................................... 148 
8.2.1 Management of acute hemorrhagic stroke ............................................................ 148 
8.2.2 Initial Management of Acute Subarachnoid Hemorrhage from Ruptured Cerebral 
Aneurysm ........................................................................................................................... 149 
8.2.3 Initial management of Acute Ischemic Stroke ....................................................... 150 
8.3 Management of Epilepsy ............................................................................................. 153 
8.4. Parkinson’s disease ................................................................................................... 155 
8.5 Congenital Pediatric Nervous System Diseases ...................................................... 155 
8.5.1 Pediatric Hydrocephalus .......................................................................................... 155 
8.5.2 Management of Pediatric CSF shunt infections .................................................... 156 
8.5.3 Congenital Spina Bifida ........................................................................................... 157 
8.6 Cranial Nerve Disorders .............................................................................................. 157 
8.6.1 Trigeminal Neuralgia ................................................................................................ 157 
8.6.2 Bell’s palsy ................................................................................................................ 158 
8.7 Spinal Cord and Peripheral Nerve Disorders ............................................................ 158 
8.7.1 Acute Transverse Myelitis (TM) ............................................................................... 158 
8.7.2 Guillan Barre syndrome ........................................................................................... 159 
8.7.3 Peripheral neuropathy .............................................................................................. 160 
CHAPTER NINE .................................................................................................................. 162 
RESPIRATORY DISEASE CONDITIONS .......................................................................... 162 
9.1 Acute Respiratory Infections (ARI) ............................................................................ 162 

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9.1.1 Pneumonia ................................................................................................................ 162 
9.2 Obstructive Lung Diseases ........................................................................................ 166 
9.2.1 Asthma ....................................................................................................................... 166 
9.2.2 Chronic Asthma in Adults ........................................................................................ 168 
9.3 Bronchitis ..................................................................................................................... 170 
9.3.1 Acute Bronchitis ....................................................................................................... 170 
9.3.2 Chronic Bronchitis ................................................................................................... 171 
9.4 Emphysema .................................................................................................................. 172 
9.5 COPD Exacerbation ..................................................................................................... 173 
9.6 Other Respiratory Infections ...................................................................................... 173 
9.6.1 Acute Laryngo-tracheobronchitis ........................................................................... 173 
9.6.2 Laryngeal Diphtheria ................................................................................................ 174 
9.6.3 Whooping Cough ...................................................................................................... 174 
9.6.4 Bronchiectasis .......................................................................................................... 175 
9.6.5 Lung Abscess ........................................................................................................... 176 
9.6.6 Aspergilosis .............................................................................................................. 176 
9.6.7 Pneumocystis Pneumonia (PCP) ............................................................................ 177 
9.6.8 Silicosis ..................................................................................................................... 177 
9.6.11 Obstructive sleep apnea syndrome (OSA ............................................................ 178 
9.6.12 Cor Pulmonale ........................................................................................................ 179 
9.6.13 Pleural effusion ....................................................................................................... 180 
9.6.14 Respiratory Failure ................................................................................................. 182 
10.1.1 Amoebiasis .............................................................................................................. 183 
10.1.2 Amoebic Liver Abscess ......................................................................................... 183 
10.1.3. Giardiasis ............................................................................................................... 183 
10.1.4 Ascariasis ................................................................................................................ 184 
10.1.5 Ancylostomiasis ..................................................................................................... 184 
10.1.6 Strongyloidiasis ...................................................................................................... 185 

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10.1.7 Taeniasis ................................................................................................................. 185 
10.1.8 Echinococcosis ...................................................................................................... 186 
10.1.9 Schistosomiasis ..................................................................................................... 186 
10.1.10 Typhoid and Paratyphoid ..................................................................................... 187 
10.1.11 Shigellosis ............................................................................................................. 187 
10.2. Disorders of Gastrointestinal Tract ........................................................................ 188 
10.2.1 Peptic Ulcer Disease .............................................................................................. 188 
10.2.2 Ulcer Related Conditions ....................................................................................... 190 
10.2.3 Gastrointestinal (GI) Bleeding ............................................................................... 191 
10.3 Diseases of the Intestine ........................................................................................... 194 
10.3.1 Inflammatory Bowel Diseases ............................................................................... 194 
10.3.2 Pseudomembranous Colitis .................................................................................. 195 
10.3.3 Radiation Proctitis .................................................................................................. 196 
10.3.4 Irritable Bowel Syndrome ...................................................................................... 197 
10.3.5 Diverticulosis .......................................................................................................... 197 
10.3.6 Diverticulitis ............................................................................................................ 197 
10.3.7 Polyps and Adenomas ........................................................................................... 198 
10.3.8 Hemorrhoids ........................................................................................................... 199 
10.3.9 Anal Fissures .......................................................................................................... 199 
10.3.10 Fistula in ano ......................................................................................................... 200 
10.3.11 Appendicitis .......................................................................................................... 200 
10.4 Pancreatitis ................................................................................................................ 201 
10.4.1 Acute Pancreatitis .................................................................................................. 201 
10.4.2 Chronic Pancreatitis ............................................................................................... 201 
10.4   Disorders of The Liver and Biliary Tract ............................................................... 202 
10.4.1 Hepatitis ................................................................................................................... 202 
10.4.2 Portal Hypertension ................................................................................................ 209 
10.4.3 Biliary Tract Diseases ............................................................................................ 212 

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CHAPTER ELEVEN ............................................................................................................ 217 
OBSTETRICS, GYNECOLOGY AND CONTRACEPTION ................................................. 217 
11.1 Bleeding in Pregnancy .............................................................................................. 217 
11.1.1 Abortion ................................................................................................................... 217 
11.2 Ectopic Pregnancy .................................................................................................... 222 
11.2.1 Un-ruptured ectopic pregnancy ............................................................................ 222 
11.2.2 Ruptured ectopic pregnancy ................................................................................. 222 
11.3 Antepartum Hemorrhage .......................................................................................... 223 
11.3.1 Placenta Praevia ..................................................................................................... 223 
11.3.2. Placental Abruption ............................................................................................... 223 
11.4 Obstructed Labour .................................................................................................... 224 
11.5 Postpartum Hemorrhage (PPH) ................................................................................ 225 
11.6 Prelabour Rupture of Membranes (PROM) .............................................................. 226 
11.7 Antenatal Care ........................................................................................................... 227 
11.7.1 Anaemia in Pregnancy ........................................................................................... 227 
11.7.2 Hypertensive Disorders in Pregnancy .................................................................. 228 
11.7.3 Pre-eclampsia ......................................................................................................... 228 
11.7.4 HELLP syndrome .................................................................................................... 229 
11.7.5 Eclampsia ................................................................................................................ 230 
11.7.6 Antiphospholipid Syndrome (APS) in Pregnancy ............................................... 231 
11.7.7 Deep Vein Thrombosis in Pregnancy ................................................................... 232 
11.7.8 Pulmonary Embolism in Pregnancy ..................................................................... 232 
11.7.9 Vomiting in Pregnancy and Hyperemesis Gravidarum ....................................... 233 
11.7.10 Heartburn in Pregnancy ....................................................................................... 234 
11.7.11 Other Medical Disorders in Pregnancy ............................................................... 234 
11.7.12 Stimulation of labour and Myometrial Relaxation ............................................. 234 
11.7.13 Rhesus Incompatibility ........................................................................................ 236 
11.8 Postpartum care ........................................................................................................ 236 

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11.8.1 Mastitis .................................................................................................................... 236 
11.8.2 Puerperal Sepsis ..................................................................................................... 237 
11.8.4 Dysmenorrhea ......................................................................................................... 239 
11.8.5 Endometriosis ......................................................................................................... 240 
11.9 Contraception ............................................................................................................ 240 
11.9.1 Short term Contraceptive Methods ....................................................................... 240 
11.9.2 Long term methods ................................................................................................ 241 
11.9.3 Permanent (surgical) contraceptive methods ...................................................... 242 
11.8.4 Infertility ................................................................................................................... 242 
CHAPTER TWELVE ........................................................................................................... 244 
SEXUALLY TRANSMITTED INFECTIONS ........................................................................ 244 
12.1 STIs/RTIs Management Approaches ........................................................................ 244 
12.2 Urethral Discharge Syndrome (UDS) ....................................................................... 245 
12.3 Vaginal Discharge Syndrome (VDS) ........................................................................ 245 
12.4 Lower Abdominal Pain Syndrome or Pelvic Inflammatory Disease (PID) ............ 246 
12.5 Painful Scrotal Swelling (PSS) ................................................................................. 247 
12.6 Ano-rectal Syndrome (ARS) ..................................................................................... 247 
12.7 Oropharyngeal Syndrome ......................................................................................... 248 
12.8 Genital Ulcer Disease (GUD) ..................................................................................... 249 
12.9 Neonatal Conjunctivitis (Ophthalmia Neonatorum) ............................................... 249 
12.10 Inguinal Bubo (IB) .................................................................................................... 249 
12.11STI/RTI flow charts ................................................................................................... 250 
12.8   Management of other common STI Conditions .................................................... 260 
CHAPTER THIRTEEN ........................................................................................................ 262 
SKIN DISEASES AND ALLERGIC REACTIONS ............................................................... 262 
13.1 Bacterial Skin Infections ........................................................................................... 262 
13.1.1 Impetigo ................................................................................................................... 262 
13.1.2 Folliculitis ................................................................................................................ 262 

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13.1.3 Abscess ................................................................................................................... 263 
13.1.4 Erysipelas and Cellulitis ........................................................................................ 264 
13.1.5 Paronychia .............................................................................................................. 264 
13.2 Fungal Skin Infections .............................................................................................. 265 
13.2.1 Tinea Corporis (Body Ringworm) ......................................................................... 265 
13.2.2 Tinea Capitis ........................................................................................................... 265 
13.2.3 Pityriasis Versicolor ............................................................................................... 265 
13.2.4 Tinea Pedis (Athlete’s Foot) and Tinea Cruris ..................................................... 266 
13.2.5 Candidiasis .............................................................................................................. 266 
13.2.6 Onychomycosis ...................................................................................................... 267 
13.2.7 Chromoblastomycosis ........................................................................................... 267 
13.2.8 Mycetoma (Madura Foot) ....................................................................................... 268 
13.3 Parasitic Infestations ................................................................................................. 268 
13.3.1 Scabies .................................................................................................................... 268 
13.4 Viral Infections ........................................................................................................... 269 
13.4.1 Herpes Simplex ....................................................................................................... 269 
13.4.2 Chickenpox ............................................................................................................. 269 
13.4.3 Herpes Zoster (Shingles) ....................................................................................... 269 
13.4.4 Post-herpetic Neuralgia ......................................................................................... 270 
13.4.5 Molluscum Contagiosum ....................................................................................... 270 
13.4.6 Viral warts ................................................................................................................ 271 
13.5 Eczema (Dermatitis) Conditions ............................................................................... 271 
13.5.1 Contact Dermatitis .................................................................................................. 271 
13.5.2 Atopic Eczema ........................................................................................................ 272 
13.5.3 Seborrheic Dermatitis ............................................................................................ 273 
13.6 Anaphylaxis ................................................................................................................ 273 
13.7 Papulosquamous Disorder ....................................................................................... 273 
13.7.1. Psoriasis ................................................................................................................. 273 

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13.7.2. Lichen Planus ........................................................................................................ 274 
13.7.3 Acne ......................................................................................................................... 275 
13.8 Drug Reactions .......................................................................................................... 275 
13.8.1 Fixed Drug Eruption (FDE) ..................................................................................... 276 
13.8.3 Stevens Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) ..... 276 
13.10 Pellagra ..................................................................................................................... 277 
13.11 Vitiligo ....................................................................................................................... 277 
13.12 Pruritic Papular Eruption (PPE) .............................................................................. 278 
13.13 Oculo-cutaneous Albinism and Xeroderma Pigmentosum ................................. 278 
13.14 Urticaria and Angioedema ...................................................................................... 279 
13.15 Connective Tissue Diseases .................................................................................. 279 
13:16 Autoimmune Blistering Disease ............................................................................ 281 
13.17 Keloids ...................................................................................................................... 281 
13.18 Folliculitis Decalvans .............................................................................................. 281 
13.19 Infantile Haemangioma ........................................................................................... 282 
13.20 Cysts ......................................................................................................................... 282 
13.21 Skin Lightening ........................................................................................................ 282 
CHAPTER FOURTEEN ....................................................................................................... 284 
EYE DISEASES AND CONDITIONS .................................................................................. 284 
14.1 Major Blinding Eye Diseases .................................................................................... 284 
14.1.1 Cataract ................................................................................................................... 284 
14.1.2 Glaucoma ................................................................................................................ 286 
14.1.3 Trachoma ................................................................................................................. 289 
14.1.4 Diseases of the Retina ........................................................................................... 290 
14.1.5 Refractive Errors ..................................................................................................... 294 
14.2 Painful Red Eyes ........................................................................................................ 296 
14.2.1 Ocular Trauma ........................................................................................................ 296 
14.2.2 Herpes Simplex Keratitis ....................................................................................... 299 

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14.2.3 Corneal Ulcer .......................................................................................................... 299 
14.2.4 Uveitis ...................................................................................................................... 300 
14.2.5 Conjunctivitis .......................................................................................................... 301 
14.3 Structural Abnormalities of the Eye ......................................................................... 305 
14.4 Ocular Oncology ........................................................................................................ 305 
14.4.1 Retinoblastoma ....................................................................................................... 305 
14.4.2 Squamous Cell Carcinoma of Conjunctiva .......................................................... 307 
14.5 Dry Eye ....................................................................................................................... 308 
14.6 Herpes Zoster Ophthalmicus .................................................................................... 309 
14.7 Endophthalmitis ......................................................................................................... 309 
14.8 Retinitis ....................................................................................................................... 310 
14.9 Orbital Cellulitis ......................................................................................................... 310 
14.10 Visual Problems ....................................................................................................... 312 
14.11 Onchocerciasis (River Blindness) ......................................................................... 313 
CHAPTER FIFTEEN .......................................................................................................... 315 
EAR, NOSE AND THROAT DISEASES ........................................................................... 315 
15.1 Ear Condition ............................................................................................................. 315 
15.1.1 Circumscript otitis Externa (Furunculosis) .......................................................... 315 
15.1.2 Diffusewer Otitis Externa (Swimmer’s ear) .......................................................... 315 
15.1.3 Necrotizing Otitis Externa ...................................................................................... 316 
15.1.4 Herpes Zoster Oticus (Ramsay Hunt syndrome) ................................................. 317 
15.1.5 Pre-auricular sinus tract infection ........................................................................ 318 
15.2 Trauma of the pinna .................................................................................................. 319 
15.2.1 Hematoma of the pinna ........................................................................................... 319 
15.2.2 Laceration of the Pinna .......................................................................................... 319 
15.2.3 Ear Keloid ................................................................................................................ 319 
15.2.4 Cerumen Impaction ................................................................................................ 320 
15.2.5 Foreign Body in the Ear ......................................................................................... 320 

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15.2.6 Traumatic Tympanic Membrane/ Ear Drum Perforation. .................................... 320 
15.3 Otitis Media (Acute or Chronic) ................................................................................ 321 
15.3.1 Acute Otitis Media .................................................................................................. 321 
15.3.2 Chronic Suppurative Otitis Media ......................................................................... 322 
15.3.3 Mastoditis with Sub-Periosteal Abscess .............................................................. 323 
15.3.4Otitis Media with Effusion ....................................................................................... 323 
15.4 Hearing Loss .............................................................................................................. 324 
15.4.1 Sensorineural hearing loss (SNHL) ...................................................................... 324 
15.4.2 Sudden Sensorineural Hearing Loss .................................................................... 324 
15.4.3 Otosclerosis ............................................................................................................ 325 
15.4.4 Peripheral Vertigo (Meniere’s disease and Benign Paroxysmal Positional 
Vertigo(BPPV) .................................................................................................................... 325 
15.4.5 Vestibular Neuritis /Vestibular Neuronitis and Labyrinthitis .............................. 325 
15.4.6 Vestibular Migraine ................................................................................................. 326 
15.4.7 Tinnitus .................................................................................................................... 326 
15.4.8 Glomus tumours ..................................................................................................... 326 
15.4.9 Vestibular schwannomas ....................................................................................... 327 
15.5 Nose/Paranasal Sinuses Conditions ....................................................................... 327 
15.5.1 Acute Rhinitis .......................................................................................................... 327 
15.5.2 Acute Non-Allergic Rhinitis ................................................................................... 327 
15.5.3 Allergic Rhinitis ...................................................................................................... 328 
15.6 Granulomatous diseases of the nose ...................................................................... 328 
15.6.1 Rhinoscleroma ........................................................................................................ 328 
15.6.2 Tuberculosis of the nose ....................................................................................... 329 
15.6.3 Syphilis of the nose ................................................................................................ 329 
15.6.4 Rhinosporiodiosis .................................................................................................. 329 
15.6.5  Mucormycosis ........................................................................................................ 330 
15.7 Other Conditions of the Nose ................................................................................... 330 
15.7.1 Nasal septal abscess and Hematoma ................................................................... 330 

xvi!
15.7.2 Choanal atresia ...................................................................................................... 331 
15.7.3 Nasal Turbinate hypertrophy ................................................................................. 331 
15.7.4 Nasal bone fracture ................................................................................................ 331 
15.7.5 Nasal Septal deviation(non-traumatic) ................................................................. 331 
15.7.6 Adenoid Hypertrophy ............................................................................................. 332 
15.7.7   Acute Rhinosinusitis ............................................................................................ 332 
15.7.8 Chronic Rhinosinusitis .......................................................................................... 334 
15.7.9 Nasal polyposis ...................................................................................................... 334 
15.7.10 Nose Bleeding (Epistaxis) .................................................................................... 335 
15.7.11 Foreign Bodies in the Nose ................................................................................ 336 
15.8 Throat Conditions ...................................................................................................... 336 
15.8.1 Pharyngotonsilitis ................................................................................................... 336 
15.8.2 Laryngitis ................................................................................................................. 337 
15.8.3 Acute Laryngitis ...................................................................................................... 337 
15.8.4 Chronic Laryngitis .................................................................................................. 338 
15.8.5 Acute Epiglottitis (AE) ............................................................................................ 338 
15.8.6 Non-infectious Chronic Laryngitis ........................................................................ 338 
15.8.7 Recurrent Respiratory Papillomatosis (Laryngeal Papillomas) ......................... 339 
15.8.8 Foreign Bodies in the Throat ................................................................................ 339 
15.8.9 Subglottic hemangioma ......................................................................................... 340 
15.8.9 Laryngomalacia ...................................................................................................... 340 
15.8.10 Vocal cords paralysis ........................................................................................... 341 
15.8.11 Infection of Thyroglossal duct cyst, dermoid cyst, branchial cleft cysts ....... 341 
15.8.12 Deep neck spaces infections ............................................................................... 342 
15.8.13 Peritonsillar Abscess (Quincy) ............................................................................ 342 
15.9 ENT Neoplasms ......................................................................................................... 343 
15.9.1 Juvenile nasopharyngeal angiofibromas (JNA) .................................................. 343 
15.9.2 Salivary Gland Tumors ........................................................................................... 343 

xvii!
15.9.3 Parapharyngeal tumours ....................................................................................... 344 
15.9.4 Cancer of the Larynx .............................................................................................. 344 
15.9.5 Sino-Nasal Malignancy ........................................................................................... 344 
15.9.6 Naso-Pharyngeal Malignancy ................................................................................ 345 
15.9.7 Oropharyngeal Malignancy .................................................................................... 346 
15.9.8 Hypo-Pharyngeal Malignancy ................................................................................ 346 
15.9.9 Metastatic Lymphadenopathy &Neck Masses ..................................................... 347 
15.10 Speech Disorders ................................................................................................... 347 
16.1 Periodontal Conditions ............................................................................................. 348 
16.1.1 Gingivitis ................................................................................................................. 348 
16.1.2 Periodontitis ............................................................................................................ 348 
16.1.3 Acute Necrotizing Ulcerative Gingivitis (ANUG) .................................................. 349 
16.1.4 Stomatitis ................................................................................................................ 349 
16.2 Dental Caries .............................................................................................................. 349 
16.3 Odontogenic and Non-Odontogenic Orofacial Infections ..................................... 350 
16.3.1 Periapical abscess ................................................................................................. 350 
16.3.2 Dental Abscess (Odontogenic Abscess) .............................................................. 351 
16.3.3 Ludwig’s Angina ..................................................................................................... 352 
16.3.4 Pericoronitis ............................................................................................................ 352 
16.3.5 Osteomyelitis of the jaw ......................................................................................... 353 
16.4  Fungal Infections ...................................................................................................... 353 
16.4.1 Oral Candidiasis ..................................................................................................... 353 
16.5 Viral Infections ........................................................................................................... 354 
16.5.1 Herpes Simplex Virus ............................................................................................. 354 
16.6 Aphthous Ulceration ................................................................................................. 355 
16.7 Post Extraction Complications ................................................................................. 355 
16.7.1 Bleeding socket ...................................................................................................... 355 
16.7.2 Infected Socket ....................................................................................................... 356 

xviii!
16.7.3 Dry Socket ............................................................................................................... 356 
16.7.4 Oro-Antral communication .................................................................................... 357 
16.8 Tooth Sensitivities ..................................................................................................... 357 
16.9 Tooth Eruption, Shedding and Edentulousness .................................................... 357 
16.9.1 Eruption of Teeth .................................................................................................... 357 
16.9.2 Shedding of Deciduous Teeth ............................................................................... 358 
16.9.3 Edentulousness ...................................................................................................... 358 
16.10 Malocclusions .......................................................................................................... 359 
16.11 Management of Maxillofacial Trauma .................................................................... 359 
16.11.1 Traumatic Dental Injuries ..................................................................................... 359 
16.11.2 Facial Bones Injuries ............................................................................................ 360 
16.12 Tumours and Tumour-Like Conditions of Oral Cavity and Facial Region ......... 362 
16.12.1 Benign Odontogenic Tumors .............................................................................. 362 
16.12.2 Non Odontogenic Benign Tumours .................................................................... 363 
16.12.3 Benign Soft Tissues Non-Odontogenic Tumours ............................................. 364 
16.12.4 Malignant Soft and Bone Tumours ..................................................................... 364 
16.12.5 Odontogenic and Non- Odontogenic Cysts ...................................................... 365 
16:13 Management of Oral Conditions during Pregnancy ............................................. 367 
16.14 Temporal Mandibular Disorder and Chronic Orofacial Pain ............................... 367 
16.14.1 Chronic Orofacial Pain other than Temporomandibular disorders ................. 367 
16.14.2 Temporomandibular Disorders (TMDs) .............................................................. 368 
16.14.3 Osteoarthritis and Rheumatoid arthritis of TMJ ................................................ 369 
CHAPTER SEVENTEEN ................................................................................................... 370 
MUSCULOSKELETAL DISORDERS ............................................................................... 370 
17.1 Infections .................................................................................................................... 370 
17.1.1   Osteomyelitis ........................................................................................................ 370 
17.1.2   Septic arthritis ....................................................................................................... 371 
17.1.3 Gonococcal arthritis .............................................................................................. 371 

xix!
17.1.4 Post Open reduction and internal fixation or arthroplasty infection ................ 371 
17.1.5 Tropical Pyomyositis ............................................................................................ 372 
17.1.6 Necrotizing fasciitis ............................................................................................... 373 
17.2 Inflammatory Conditions .......................................................................................... 374 
17.2.1 Rheumatoid Arthritis .............................................................................................. 374 
17.2.2 Juvenile Idiopathic Arthritis ................................................................................. 376 
17.2.3. Gout ........................................................................................................................ 377 
17.2.4 Osteoarthritis .......................................................................................................... 378 
17.2.5 Heterotopic Ossification ........................................................................................ 380 
17.2.6 Tendinopathies ....................................................................................................... 380 
17.2.7 Plantar Fasciitis ...................................................................................................... 381 
17.3 Metabolic Bone Diseases ........................................................................................ 382 
17.3.1 Osteoporosis and Brittle Bone Diseases ............................................................. 382 
17.3.2 Hypocholecalciferolemia (Vitamin D Deficiency) ............................................... 383 
17.4.1 Diabetic Foot Ulcers .............................................................................................. 384 
17.5 Affection of the Brain and Spine ..............................................................................385
17.51 Low Back Pain.......................................................................................................385
17.5.2  Cervical Degenerative Disorders ......................................................................... 388 
17.5.3 Pyogenic spondylodiscitis .................................................................................... 390 
17.5.4 Tuberculous spondylodiscitis .............................................................................. 391 
17.5.5 Osteoporotic vertebral compression fractures (VCFs) ...................................... 392 
17.6 Common Congenital Anomalies of Musculoskeletal System .............................. 394 
17.6.1 Talipes equinovarus (congenital clubfoot) .......................................................... 394 
17.8 Angular Deformity of Limbs ..................................................................................... 395 
17.8.1 Rickets ..................................................................................................................... 395 
17.8.2 Physiological Bowing/Knocked Knees ................................................................. 396 
CHAPTER NINETEEN ........................................................................................................ 397 
19.1 Diabetes Mellitus ....................................................................................................... 397 

xx!
19.2 Management of Diabetes During Religious Fasting ............................................... 403 
19.3 Hyperglycaemia in Pregnancy .................................................................................. 404 
19.4 Diabetes and HIV ....................................................................................................... 405 
19.5 Diabetes and Tuberculosis ....................................................................................... 406 
19.6 Hypoglycaemia .......................................................................................................... 406 
19.7 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic States ........................ 407 
19..8 Diabetes and Cardiovascular Diseases .................................................................. 410 
19.9 Diabetic Peripheral Neuropathy ............................................................................... 411 
19.10 Diabetic Nephropathy .............................................................................................. 412 
19.11 Diabetic Retinopathy ............................................................................................... 413 
19.12 Thyroid Disorders .................................................................................................... 414 
19.12.1 Hypothyroidism .................................................................................................... 414 
19.12.2 Hyperthyroidism ................................................................................................... 415 
19.12.3 Toxic Multinodular Goitre or Thyroid Antibody Positive .................................. 415 
19.12.4 Grave’s Hyperthyroidism ..................................................................................... 416 
19.12.5 Thyroid Storm (Crisis) .......................................................................................... 417 
19.13 Cushing's Syndrome ............................................................................................... 434 
19.14 Prolactinoma ............................................................................................................ 435 
19.15 Diabetic Insipidus (DI) ............................................................................................. 435 
19.16 Pheochromocytoma ................................................................................................ 436 
19.17 Disorder of Sexual Development (DSD) ................................................................ 436 
19.8 Obesity in Adults ....................................................................................................... 437 
19.19 Physical Activity ...................................................................................................... 439 
CHAPTER TWENTY ........................................................................................................... 441 
CARDIOVASCULAR DISEASE CONDITIONS .................................................................. 441 
20.1 Prevention of Atherosclerotic Ischaemic Heart Disease and Stroke .................... 441 
20.2 Management of Dyslipidemias ................................................................................. 442 
20.3   Chronic Stable Coronary Artery Disease (CSCAD) / ISCHAEMIC Heart Disease 
(IHD) .................................................................................................................................... 443 

xxi!
20.4    Acute Coronary Syndrome .................................................................................... 444 
20.4.1 Unstable Angina (UA) ............................................................................................. 444 
20.4.2 Non-ST Elevation Myocardial Infarction (NSTEMI) .............................................. 444 
20.4.3 ST Elevation Myocardial Infarction (STEMI) ......................................................... 445 
20.5 Hypertension .............................................................................................................. 447 
20.6   Resistant (Refractory) Hypertension ..................................................................... 454 
20.7 Hypertensive Urgency ............................................................................................... 454 
20.8 Hypertensive Emergency .......................................................................................... 454 
20.9 Heart Failure ............................................................................................................... 454 
20.10   Chronic Heart Failure ............................................................................................ 456 
20.11 Pulmonary Oedema ................................................................................................. 457 
20.12 Infective Endocarditis (IE) ....................................................................................... 458 
20.13 Acute Rheumatic Fever ........................................................................................... 460 
20.14 Pulmonary Embolism .............................................................................................. 462 
20.14.1   Acute Pulmonary Embolism .............................................................................. 462 
20.14.2 Chronic Pulmonary Embolism ............................................................................ 463 
20.15   Cardiac Arrhythmias/ Dysrhythmias .................................................................... 464 
20.15.1 Tachyarrythmias ................................................................................................... 464 
20.15.2   AV Junctional Re-Entry Tachycardias .............................................................. 465 
20.15.3   Wide QRS (Ventricular) Tachyarrhythmias (VTs) ............................................ 466 
20.16   Heart Block (Second & Third Degree) .................................................................. 467 
20.17 Sinus Bradycardia & Sinus Arrest ......................................................................... 468 
KIDNEY AND UROLOGICAL DISORDERS ....................................................................... 469 
21.1 Chronic Kidney Diseases (CKD) .............................................................................. 469 
21.1.1 Diabetic Kidney Disease ......................................................................................... 470 
21.1.2 Hypertension and CKD ........................................................................................... 471 
21.1.3 Dialysis .................................................................................................................... 473 
21.1.4 CKD Associated Metabolic Acidosis .................................................................... 473 

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21.1.5 Hyperkalaemia ....................................................................................................... 473 
21.1.7 Mineral Bone Disease (MBD) ................................................................................. 475 
21.1.8 Haemodialysis (HD) Catheter Related Blood Stream Infection .......................... 475 
21.2 Acute Kidney Disease ............................................................................................... 476 
21.3 Glomerular Diseases (GD) ........................................................................................ 477 
21.3.1 Glomerular disease - Nephritic syndrome ........................................................... 478 
21.3.2 Nephrotic syndrome ............................................................................................... 478 
21.4 Kidney Transplantation ............................................................................................. 481 
21.4.1 Transplant Donor Evaluation ............................................................................... 481 
21.4.2 Transplant Candidate ............................................................................................ 483 
21.4.3 Transplant Recipient .............................................................................................. 483 
21.4.5 Acute Kidney Graft Rejection ............................................................................... 486 
21.4. 6 Other Conditions in Transplantation and their Managements .......................... 487 
21.5 Cystic Kidney Disease .............................................................................................. 488 
21.6 Renal artery stenosis ................................................................................................ 488 
21.8 Reflux nephropathy ................................................................................................... 489 
21.9 Contrast Induced Nephropathy (CIN) ...................................................................... 490 
21.10 Urinary Tract Infection (UTI) ................................................................................... 491 
21.10 Urology Disorders ................................................................................................... 493 
21.10.1 Prostatitis .............................................................................................................. 493 
21.10.2 Benign prostatic hyperplasia (BPH) .................................................................. 493 
21.10.3 Prostate cancer .................................................................................................... 494 
21.10.4 Urolithiasis ............................................................................................................ 495 
21.10.5 Obstructive uropathy ........................................................................................... 496 
21.11 Sexual Dysfunction ................................................................................................. 497 
21.11.1 Female Sexual Dysfunction ................................................................................. 497 
21.11.2 Male sexual dysfunction ...................................................................................... 498 
CHAPTER TWENTY-TWO .................................................................................................. 499 

xxiii!
MALIGNANT DISEASE CONDITIONS ............................................................................... 499 
22.1 Cancer Prevention, Screening and Early Detection ............................................... 499 
22.2 Gynecological Malignancies ..................................................................................... 500 
22.2.1 Cancer of the Uterine Cervix ................................................................................. 500 
22.2.2 Endometrial Cancer ................................................................................................ 501 
22.2.3 Cancer of the Vulva ................................................................................................ 502 
22.2.4.    Gestational trophoblastic disease .................................................................... 503 
22.2.5 Cancer of the Ovary ................................................................................................ 505 
22.3 Breast Cancer ............................................................................................................ 506 
22.4 Cancer of The Skin .................................................................................................... 508 
22.4.1 Non-melanoma Skin Cancers ................................................................................ 508 
22.4.2 Malignant Melanoma .............................................................................................. 509 
22.4.3 Kaposi’s sarcoma (KS) ........................................................................................... 509 
22.5 Head and Neck Cancers ............................................................................................ 510 
22.5.1 Nasopharyngeal Cancer ......................................................................................... 510 
22.5.2 Laryngeal Cancer .................................................................................................... 511 
22.5.3 Hypopharyngeal Cancers: ..................................................................................... 511 
22.5.4 Salivary gland cancer ............................................................................................. 512 
22.5.5 Nasal Cavity and Paranasal Sinus Cancer ........................................................... 512 
22.5.6 Oral Cavity Cancer .................................................................................................. 512 
22.5.7 Oropharyngeal Cancer ........................................................................................... 513 
22.5.8 Thyroid Carcinoma ................................................................................................. 514 
22.6 Gastrointestinal Malignancies .................................................................................. 515 
22.6.1 Esophageal Cancer ................................................................................................ 515 
22.6.2 Gastric Cancer ........................................................................................................ 515 
22.6.3 Hepatocellular Carcinoma ..................................................................................... 516 
22.6.4 Rectal Cancer .......................................................................................................... 518 
22.6.5 Colon Cancer .......................................................................................................... 519 

xxiv!
22.6.6 Anal Cancer ............................................................................................................. 519 
22.7 Lung Cancer ............................................................................................................... 520 
22.7.1 Non-small cell lung Cancer .................................................................................... 520 
22.7.2 Small cell lung cancer ............................................................................................ 521 
22.8 Genitourinary Malignancies ...................................................................................... 521 
22.8.1 Carcinoma of the Prostate ..................................................................................... 521 
22.8.2 Urinary Bladder Cancer .......................................................................................... 523 
22.9 Haematological Malignancies ................................................................................... 524 
22.9.1 Lymphomas ............................................................................................................. 524 
22.9.2 Leukemia ................................................................................................................. 526 
22.9.3 Multiple myeloma .................................................................................................... 528 
22.10 Central Nervous System Maligancies .................................................................... 529 
22.10.1 Meningiomas ......................................................................................................... 529 
22.10.2 Pituitary tumors .................................................................................................... 530 
22.10.3 Gliomas .................................................................................................................. 531 
22.11 Oncological Emergencies ....................................................................................... 533 
22.11.1 Superior vena cava syndrome (SVCS) ............................................................... 533 
22.11.2 Hypercalcaemia .................................................................................................... 534 
22.11.3 Spinal–cord Compression ................................................................................... 534 
22.11.4 Tumor lysis Syndrome ......................................................................................... 535 
20.11.5 Febrile Neutropenia .............................................................................................. 535 
CHAPTER TWENTY-THREE .............................................................................................. 537 
MENTAL HEALTH CONDITIONS ....................................................................................... 537 
23.1 Patients with Aggressive and Disruptive Behaviours ........................................... 537 
23.2 Delirium ..................................................................................................................... 538 
23. 3 Dementia ................................................................................................................... 539 
23.4 Schizophrenia ........................................................................................................... 539 
23.5 Catatonia ................................................................................................................... 541 

xxv!
23.6 Schizoaffective Disorder .......................................................................................... 541 
23.7 Brief or Acute/Transient Psychotic Disorder ......................................................... 542 
23.8 Bipolar Mood Disorders ........................................................................................... 542 
23.9 Major Depressive Disorder ...................................................................................... 543 
23.10 Suicide ..................................................................................................................... 544 
23.11 Generalized Anxiety Disorder ................................................................................ 544 
23.12 Panic Disorder ........................................................................................................ 545 
23.13 Obsessive-Compulsive Disorder .......................................................................... 546 
23.14 Acute Stress Disorder and Post-Traumatic Stress   Disorder ............................ 547 
23.15 Substance Related Disorder .................................................................................. 547 
23.15.1 Substance Use Disorder ..................................................................................... 547 
23.15.2 Substance Induced Disorder ............................................................................... 549 
23.16 Psychiatric Disorders Associated with Epilepsy ................................................. 552 
23.17 Psychiatric Disorders in Pregnancy ..................................................................... 554 
23.17.1 Depression ............................................................................................................ 554 
12.17.2 Panic disorder ....................................................................................................... 555 
12.17.3 Obsessive-compulsive disorder ......................................................................... 555 
12.17.5 Schizophrenia ....................................................................................................... 556 
23.18. Autism Spectrum Disorder .................................................................................... 556 
23.19 Attention Deficit / Hyperactivity Disorder (ADHD) ............................................... 557 
23.20 Enuresis ................................................................................................................... 558 
23.21 Neuroleptic Malignant Syndrome (NMS) .............................................................. 558 
23.22 Somatic Symptom Disorder ................................................................................... 559 
23.24 Conversion Disorder .............................................................................................. 559 
CHAPTER TWENTY-FOUR ................................................................................................ 560 
NUTRITION DISORDERS ................................................................................................... 560 
24.1 Iodine Deficiency Disorders (IDD) ............................................................................ 560 
24.2 Vitamin A Deficiency (VAD) ...................................................................................... 561 

xxvi!
24.3 Vitamin B Deficiencies .............................................................................................. 562 
24.3.1 Vitamin B1/Thiamine Deficiency (Wernicke Encephalopathy and Beriberi) ...... 562 
24.3.3 Vitamin B6/Pyridoxine Deficiency .......................................................................... 562 
24.3.4 Vitamin B12 (Cobalamin) Deficiency ...................................................................... 563 
24.4 Malnutrition ................................................................................................................ 563 
24.5 Growth Faltering/Failure to Thrive ........................................................................... 566 
24.6 Obesity and Overweight ............................................................................................ 567 
24.7 Nutritional Management in TB, HIV and AIDS ......................................................... 568 
24.7.1 Nutrient Requirements and Dietary Management in TB, HIV and AIDS Patients
 ............................................................................................................................................. 569 
24.8 Dumping Syndrome. .................................................................................................. 569 
24.9 Dietary Management in Diabetes Mellitus ............................................................... 570 
24.10 Nutrition Care and Support in the Intensive Care ................................................ 571 
CHAPTER TWENTY-FIVE .................................................................................................. 573 
POISONING ........................................................................................................................ 573 
25.1 Common poisons ...................................................................................................... 573 
25.2 General principles of management of poisoning ................................................... 573 
25.2.1 Management Protocol of a poison (specific and non-specific antidotes) ......... 575 
25.2.2 Management of Ingested Poisons ......................................................................... 576 
25.2.3 Food Poisoning ....................................................................................................... 577 
25.2.4 Herbal Poisoning .................................................................................................... 578 
25.2.5 Management of Skin contamination ..................................................................... 579 
25.2.6 Management of Eye contamination ...................................................................... 579 
25.2.7 Management of Inhaled Poisoning ....................................................................... 579 
25.3 Specific poisons ........................................................................................................ 580 
25.3.1 Corrosive Compounds Poisoning ......................................................................... 580 
25.3.2 Petroleum Compounds Poisoning ........................................................................ 580 
25.3.3 Organo-Phosphorus and Carbamate Compounds Poisoning ........................... 581 
25.3.4 Paracetamol Poisoning .......................................................................................... 584 

xxvii!
25.3.5 Acetylsalicylic acid and other salicylates poisoning. ......................................... 585 
25.3.6 Iron Poisoning ......................................................................................................... 585 
25.3.7 Carbon-monoxide Poisoning ................................................................................. 586 
25.3.8 Opioid Poisoning .................................................................................................... 586 
25.3.9 Heavy Metal poisoning ........................................................................................... 587 
25.4 Prevention of poisoning ............................................................................................ 589 
25.5 Alcohol Intoxication .................................................................................................. 589 
25.6 Bites and stings ......................................................................................................... 589 
25.6.1 Management of Specific Bites/Stings ................................................................... 590 
CONTRIBUTORS ................................................................................................................ 596 

xxviii!
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ACRONYMS AND ABBREVIATIONS 
3D-CRT 
Three-dimensional Conformal Radio-Therapy 
ACS 
Acute Coronary Syndrome 
ACS 
 Acute Chest Syndrome 
ACT 
Artemisinin Combination Therapy 
ADA 
Adenosine Deaminase 
ADH 
Anti-Diuretic Acid 
aHUS 
atypical Hemolytic Uremic Syndrome  
AIS 
Acute Ischaemic Stoke 
ALU 
Artemether Lumefantrine 
AMI 
Acute Myocardial Infarction 
AMPLE  
Allergies, Medications, Past medical history, Last meal and Events leading 
to presentation 
bhCG 
beta human Chorionic Gonadotropin 
BMD 
Bone Mineral Density 
BP 
 Blood Pressure 
BUN 
Blood Urea Nitrogen 
C/T/L 
Cervical, Thoracic, Lumbar 
CAF 
cyclophosphamide, 
doxorubicin 
hydrochloride 
(Adriamycin), 
and 
fluorouracil 
CAH 
Congenital Adrenal Hyperplasia 
CAP 
 Community Acquired Pneumonia 
CAVE 
Cavus, Adductus, Varus, Equinus 
CEF 
 Cyclophosphamide Epirubicin Fluorouracil 
CKD 
Chronic Kidney Disease 
CPP 
Cerebral perfusion pressure  
CRP 
C Reactive Protein 
CVA 
 Cerebral Vascular Accident 
CVD 
Cardiovascular Disease 
CVP 
Central Venous Pressure 
DIND 
Delayed Ischaemic Neurologic Deficit 
DKA 
Diabetic Keto Acidosis 
DME 
Diabetic Macular Edema 
DNS 
Dextrose Normal Saline 
DR-TB 
Drug Resistance Tuberculosis 
DSD 
Disorder of Sexual Development 
DSM-5 
Diagnostic and Statistical Manual of Mental Disorders vol.5 
DST 
Drug Susceptibility Test 
DTLC 
 District Tuberculosis and Leprosy Coordinator 
DWMR 
Diffusion Weighted Magnetic Resonance 

xxix!
!
ECT 
 Electroconvulsive Therapy  
EITB 
Enzyme-linked Immune Transfer Blot 
EMD 
Emergence Medical Department 
ENL 
Erythema Nodosum Leprosum 
ERCP 
Endoscopic Retrograde Cholangiopancreatography 
ESA 
Erythropoietin Stimulating Agent 
ESR 
Erythrocyte Sedimentation Rate 
EVD 
External Ventricular Drainage 
FAO 
Foot Abduction Orthosis 
FAST 
Focus Assessment with Sonography for Trauma 
FAST 
Facial drooping, Arm weakness, Speech difficulties and Time 
FEIBA 
Factor Eight By-passing Agent 
FIGO 
The International Federation of Gynecology and Obstetrics 
FNA 
 Fine Needle Aspiration 
G6PD 
Glucose 6 Phosphatase Dehydrogenase 
GB 
Gall Bladder 
GCS 
 Glasco comma scale 
GUS 
Genital Ulcer Syndrome 
HBA 
 Haemoglobin Adult 
HBS 
Sickle Haemoglobin 
HD: 
Hemo-Dialysis 
HDN 
 Haemolytic Disease of New Bone 
HDU 
 High Dependency Unit 
HEENT 
Head, Eye, Ear, Nose and Throat 
HHS:  
Hyperglycemic Hyperosmolar Syndrome 
HRCT 
 High Resolution Computer Tomograph 
HVL 
 HIV Viral Load 
IBD 
Inflammatory Bowel Syndrome 
ICH 
 Intra Cerebral Haemorrhage 
ICP 
 Intracranial Pressure 
ILAE 
International League Against Epilepsy 
IMCI  
Integrated Management of Childhood Illness 
IOP 
Intraocular Pressure 
IPTP 
 intermittent preventive treatment in pregnancy 
IRIS 
Immune Reconstitution Syndrome 
ITI 
Immune Tolerance Induction 
ITP 
Idiopathic Thrombocytopenia Purpura 
JIA 
Juvenile Idiopathic Arthritis 
LAMM 
 Labyrinthine Aplasia, Microtia And Microdontia 
LAP 
Lower Abdominal Syndrome 

xxx!
!
LFT 
 Liver Function Test 
LKW 
Last Known Well 
LLINs 
Long Lasting Insecticide Nets 
LLQ 
Left Lower Quadrant 
LMWH 
Low Molecular Weight Heparin 
LPR 
Laryngopharyngeal Reflux 
MAP 
Mean Arterial Pressure  
MDMA 
3,4-MethyleneDioxy-MethAmphetamine 
MDR-TB 
Multi-Drug Resistance Tuberculosis 
mRDT 
malaria Rapid Diagnostics Test 
MSM 
Men who have Sex with Men 
MTD 
 Maximum Tolerated Dose 
mTOR 
mammalian Target Of Rapamycin 
MUAC 
Mid-Upper Arm Circumference 
NGT 
Naso Gastric Tube 
NIV 
Non-Invasive Ventilation 
ODS 
Osmotic Demyelination Syndrome 
OI 
Opportunistic Infection 
OPG 
Orthopantomography 
OT 
 Occupational Therapy 
PAD 
Peripheral Artery Disease 
PCV 
Pneumococcal Conjugate Vaccine 
PDMPs 
Plasma-derived medicinal products 
PEFR 
Peak Expiratory Flow Rate 
PEP 
Post Exposure Prophylaxis  
PI 
Protease Inhibitor 
PID 
Pelvic Inflammatory Disease 
pMDI 
Pressurised Metered Dose Inhaler 
PPS 
Parapharyngeal Space 
PPSV 
Pneumococcal Polysaccharide Vaccine 
PrEP  
Pre-Exposure Prophylaxis  
PSA 
Prostate Specific Antigen 
PT 
Physio Therapy 
PUVA 
Psoralens + Ultraviolet radiation 
RAM 
Resistance Associated Mutation 
RBG 
Random Blood Glucose 
RICE 
Rest, Ice, Compression, And Elevation 
RR 
Rifampicin Resistance 
RRT 
Renal Replacement Therapy 
RTLC 
Regional Tuberculosis and Leprosy Coordinator 

xxxi!
!
rtPA 
recombinant tissue Plasminogen Activator 
SAH 
 Subarachnoid Haemorrhage 
SBCC 
Social Behavioural Change 
SLE 
Systemic Lupus Erythematosus 
SMBG 
Self-Monitoring Blood Glucose 
SMFE 
Systemic Marrow Fat Embolism 
SpO2 
Oxygen Saturation 
SSRI 
Selective Serotonin Reuptake Inhibitor 
SSS 
Scrotal Swelling Syndrome 
TBI 
Traumatic Brain Injury 
TFT 
Thyroid Fuction Test 
TIA 
Transient Ischaemic Attack 
TIVA 
Total Intravenous Anaesthesia 
TM 
Tympanic Membrane 
TMD 
Temporomandibular Disorders 
TMJ 
Temporomandibular Joint 
TMP 
Tympanic Membrane Perforation 
TNM 
Tumor Nodes and Metastases  
TPT 
Tuberculosis Preventive Therapy 
TURP 
 Transurethral Resection of the Prostate 
UDS 
Urethral Discharge Syndrome 
UDS 
Urine Drug Screen 
VAP 
Ventilator-Associated Pneumonia 
VDS 
Vaginal Discharge Syndrome 
VTE 
Venous Thrombo-Embolism 
VWF 
Von Willebrand Factor 
WfH 
Weight for Height  
WFNS 
World Federation Neurological Surgeon 
WHZ 
 Weight for Height Z score 
WPW 
Wolff-Parkinson-White Syndrome 
 
 
 
 
 


1!
!
PART I 
THE NATIONAL ESSENTIAL MEDICINES LIST (NEMLIT) 
Background Information 
The National Essential Medicines List (NEMLIT) presents essential medicines, for which health 
facilities at all levels requisite for management of priority diseases. The NEMLIT is based on the 
concept of essential medicines, defined by the World Health Organization (WHO) as those 
medicines that meet priority healthcare needs of the population and intended to be available within 
the context of functioning health systems at all times, with assured quality and at a price the 
individual and the community can afford. The concept emphasizes carefully and systematically 
selection of essential medicines using an evidence-based process with due consideration of clear 
evidence of safety and efficacy and comparative cost effectiveness. The rationale for selecting a 
limited number of essential medicines is to enhance supply, improve rational use, and lower costs. 
 
Categorization of antibiotics 
A new categorization of antibiotics into Access, Watch, Reserve (AWaRe) classification has been 
introduced to guide their prudent use and reduce antimicrobial resistance. 
 
Access Group Antibiotics  
This group includes antibiotics that have activity against a wide range of commonly encountered 
susceptible pathogens while also showing lower resistance potential than antibiotics in the other 
groups.  Access group antibiotics are recommended as essential first or second choice empiric 
treatment options for infectious syndromes. They are essential antibiotics that should be widely 
available, affordable and quality assured. 
 
Watch Group Antibiotics  
This group includes antibiotic classes that have higher resistance potential. These medicines should 
be prioritized as key targets of stewardship programs and monitoring. The selected Watch group 
antibiotics are recommended as essential first or second choice empiric treatment options for a 
limited number of specific infectious syndromes.  
 
Reserve Group Antibiotics  
This group includes antibiotics that should be reserved for treatment of confirmed or suspected 
infections due to multi-drug-resistant organisms. Reserve group antibiotics should be treated as “last 
resort” options. While they must be accessible when required, their use should be limited to highly 
specific patients and clinical settings, when other antibiotic alternatives have failed or are not 
suitable. They should be protected and prioritized as key targets of national and international AMR 
stewardship programmes, involving monitoring and utilization reporting, to preserve their 
effectiveness. 
 
Prescribing of Medicines with Regard to Level of Service Provision and Professional 
Expertise 
Similar to previous editions, the NEMLIT will be used with regard to levels of care. Additionally, a 
new categorization of prescribing medicines with regards to expertise has been introduced to 
facilitate reimbursement of medicines by the NHIF. In summary, stocking and prescribing of 
medicines as per level of care will be: tertiary hospitals (A, B, C, D & S); Regional Referral Hospitals 
(A, B, C & D); District Hospitals (A, B & C); Health Centers (A & B) and dispensaries (A). Additional 
category reflects professional expertise; regardless of level of care: Specialists (A, B, C, D & S); 
Medical Officers (A, B, C & D); Assistant Medical Officer (A, B & C); Clinical Officers (A & B) and 
Assistant Clinical Officers (A). 
 

2!
Table 1: Restrictions for Prescribing Medicines Listed in the NEMLIT 
Level of Medicines with Regard to 
Service Provision 
Level of Medicines with Regard to Professional 
Expertise 
Tertiary Hospital 
A,B,C,D,S 
Specialist 
A,B,C,D,S 
Regional Referral Hospital 
A,B,C,D 
Medical Officer (MO) 
A,B,C,D 
District Hospital 
A,B,C 
Assistant 
Medical 
Officer 
(AMO) 
A,B,C 
Health Centre 
A & B 
Clinical Officer (CO) 
A & B 
Dispensary 
A 
Assistant Clinical Officer (ACO) 
A 
Hence, at tertiary level hospitals (S); the National, Zonal Referral and Specialized hospitals, all 
medicines in the NEMLIT may be stocked; as per hospital needs and specialists may prescribe all 
medicines listed in the NEMLIT. However, level (S) medicines are restricted to other experts. 
Implying that, a Medical Officers at tertiary hospital will be prescribe medicines listed A, B, C and D 
and Assistant Medical Officer A, B, & C but not S.  
At Regional Referral Hospitals (RRH) level, medicines listed as (A, B, C & D) will be stocked. 
Specialists at that level may prescribe medicines at level (A, B, C, D, S) as per their specialty areas 
e.g. cardiologist may prescribe cardiovascular diseases medicines at that level. Medical officer at
RRH will prescribe medicines at level (A, B, C, D). If there is an Assistant Medical Officer at RRH
allowed to prescribe medicines listed (A, B, C) and Clinical Officers (A & B).
At District hospitals level, medicines listed as (A, B & C) will be stocked. Specialists prescribe 
medicines listed (A, B, C, D, S) as above. Medical Officers will prescribe medicines listed (A, B, C, 
D) and AMO (A, B, C). If their Clinical Officers (CO) at that level will be permitted to prescribe
medicines listed A & B only. Health Centers stock medicines listed as A & B and dispensaries A, but
if there is AMO, MO or specialist will prescribe as above.
Note 
•
Different from previous editions, the arrangement of STG/NEMLIT have changed; the
NEMLIT starts followed by chapters of STG to make easy reference of essential medicines 
by users. 
•
All medicines indicated for treatment of various diseases in the STG are listed in the
NEMLIT. 
•
Some medicines are listed in some levels for the treatment of specific disease condition
e.g. cefixime is level (D) but, may be prescribed in lower HFs for treatment of STI only.
•
Medicines in the NEMLIT are grouped according to pharmacological groups and written
alphabetically, in generic names, with their dosage forms and strengths. 
•
All health facilities in the public sector will adhere to the NEMLIT in procurement of
medicines from MSD and other sources. 
•
The NHIF will adhere to the NEMLIT for reimbursement of medicines in both public and
private health facilities. 
•
Special arrangement to quantify and procure medicines, which are not managed at specific
health facilities but are needed due to presence of expertise as stated above; for that case 
the Hospital Pharmacists in collaboration with the Office of Chief Pharmacist shall facilitate 
the process. 
Further recommendations, advices and clarifications of the use of this document are much welcome; 
please, you may communicate with the office of the Director Pharmaceutical Services - Ministry of 
Health, Community Development, Gender, Elderly and Children. We believe that all medicines 
stocked in our health facilities are of assured quality. However, for recommendations and advices 
concerning all aspects of the quality of medicines and any adverse reaction please contact the 
Tanzania Medicines and Medical Devices Authority at www.tmda.go.tz .  

3!
The National Essential Medicines List, 2021 Edition 
Name of drug 
Dosage forms and Strengths 
Level 
1.0 Anasthetics, Preoperative Medicines and Medical Gases 
1.1  General Anaesthetics and Oxygen 
1.1.1 Inhalational Medicines 
Halothane 
Liquid  
for 
inhalation, 
bottle 
250mL 
B 
Isoflurane 
Liquid for inhalation, 250MmL 
B 
Nitrous oxide 
Cylinder (F gas) for inhalation 
C 
Oxygen 
Cylinder (medical gas) 
for inhalation 
B 
Sevoflurane 
Inhalation 
S 
1.1.2 Injectable Medicines and Other Pre-Medication 
Atropine 
Injection 1mg (as sulfate in 1mL ampoule) 
A 
Calcium chloride 
Injection 10mcg/mL 
D 
Clonidine 
Injection 500mcg/mL 
S 
Dexmedetomidine 
Injection 100mcg/mL 
S 
Ephedrine injection 
Injection 30mg/mL 
B 
Flumazenil 
Injection 0.2mg (IV) 
A 
Etomidate 
Injection 20mg/mL 
S 
Glycopyrrolate 
Injection 200mcg/mL in 1mL, 600mcg in 3mL 
S 
Ketamine 
Injection  (hydrochloride), 10mg/mL in 20mL 
B 
Labetalol 
Injection 10mg/mL 
C 
Lipid emulsion 
Solution 20% 
S 
Metaraminol 
Injection 1mg/mL 
S 
Midazolam 
Injection 1mg/mL, 5mg/mL 
D 
Noradrenaline 
Injection 2mg/mL 
S 
Ondansetron 
Injection 2mg/mL 
S 
Phenylephrine 
Injection 10mg/mL 
S 
Propofol 
Injection 10mg/mL, 20mg/mL 
D 
Sodium citrate 
Solution 0.3 moles 
D 
Thiopental 
Injection (sodium salt),  in 20mL 
C 

4!
1.2 Local Anaesthetics 
Bupivacaine 
Injection 
0.5% 
(hydrochloride) 
in 
7.5% 
dextrose spinal  
C 
Bupivacaine 
 Injection  2.5mg/mL, 5mg/mL, 7.5mg/mL 
C 
Lidocaine 
Injection hydrochloride 1%  & 2%;   
A 
Lidocaine 
Gel 2% & 5%; Spray 10% 
B 
Lidocaine in Dextrose 
Injection (hydrochloride), 5% in 7.5% dextrose 
B 
Lidoocaine 
+
epinephrine
(adrenaline) 
Injection (hydrochloride) 2% with adrenaline 
1:100,000 in 2mL ampoule for dental use  
A 
1.3  Muscle Relaxants and Cholinesterase Inhibitors 
Atracurium 
Injection 50mg/5mL 
S 
Baclofen 
Tablet 10mg 
S 
Neostigmine 
Injection 
(hydrochloride 
or 
hydrogen 
tartarate),1mg/mL in 1mL ampoule, Injection 
(hydrochloride 
or 
hydrogen 
tartarate), 
2.5mg/mL in 1mL ampoule  
B 
Pancuronium 
Injection (bromide) 4mg/mL in 2mL ampoule 
C 
Rocuronium 
Injection 50mg/5mL 
S 
Sugammadex 
Injection: 100mg/mL 
S 
Suxamethonium 
Powder for injection (bromide or chloride) 
50mg/mL in 2mL vial  
C 
Tizanidine 
Tablet/Capsule: 2mg; 4mg 
S 
2.0 Medicines for Pain and Palliative Care 
2.1 Non-opioids and Non-steroidal Anti-inflammatory Medicines (NSAIMs) 
Acetylsalicylic acid 
Tablet 300mg 
A 
Dexketoprofen 
Tablet 25mg 
S 
Diclofenac 
Injection 25mg/mL; Recto  
caps 
100mg 
(slow release); Gel.  
A 
Diclofenac 
Tablet (sodium/potassium salt) 50mg, 100mg; 
C 
Ketoprofen 
Tablet/Capsule: 50mg, 75mg, 200mg;  Gel 
2.5% w/w 
S 
Ibuprofen  
Tablet 200mg; 400mg ; Syrup 100mg/5ml 
A 
Mefenamic Acid 
Tablet 500mg 
B 
Meloxicam 
Tablet 7.5mg; 15mg 
D 
Paracetamol 
Tablet 500mg; 
Syrup  125mg/5mL, 
suppositories 125mg 
A 
10 mg/mL Solution for Infusion 
D 

5!
Piroxicam 
Tablet 20mg 
A 
Sulfasalazine 
Tablets 500mg 
D 
2.2 Opioid Analgesics/Antagonists 
Fentanyl 
Injection 100mcg/2mL; Patches 
S 
Methadone 
Tablet: 5mg; 10mg (as hydrochloride); Oral 
liquid: 
5mg/5mL; 
10mg/5mL 
(as 
hydrochloride); Concentrate for oral liquid: 
5mg/mL; 10mg/mL (as hydrochloride)  
C 
Morphine 
Tablet 10mg (morphine hydrochloride or 
morphine sulfate);  Granules (slow-release: to 
mix with water) 20mg-200mg (morphine 
sulfate); 
 
Oral 
liquid: 
(10mg 
morphine 
hydrochloride 
or 
morphine 
sulfate)/5mL; 
Injection: 10mg (morphine hydrochloride or 
morphine sulfate) in 1mL ampoule  
C 
Naloxone 
Injection (hydrochloride) 0.4mg/mL in 1mL 
ampoule  
B 
Pethidine 
Injection (hydrochloride) 50mg/mL in 1mL and 
2mL ampoule  
B 
Tramadol 
Tablet  
50mg; Injection 50mg/mL in 2mL 
B 
2.3 Medicines for Other Common Symptoms in Palliative Care 
Amitriptyline 
Tablet 25mg 
A 
Haloperidol 
Injection: 5mg/1mL ampoule; Tablet 5mg 
B 
Hydrocortisone 
Powder for injection (as sodium succinate) 
100mg in vial  
A 
Hyoscine butyl bromide 
Tablet 10mg 
A 
Hyoscine butyl bromide 
Injection: 20mg/mL 
B 
Loperamide 
Tablet 2mg 
B 
Imipramine 
Tablet 25mg 
C 
3.0 Anti-allergies and Medicines Used in Anaphylaxis 
Betahistine 
Tablet as dihydrochloride 16 mg 
C 
Bethametasone 
Injection: 4mg/mL 
D 
Cetirizine 
Oral solution 5mg/5mL; Tablet (hydrochloride) 
10mg  
A 
Chlorpheniramine 
Injection (maleate 10mg/mL in 1mL ampoule); 
Elixir (maleate) 2mg/5mL; Tablet (maleate) 
4mg  
A 
Desloratadine 
Tablet:  5 mg film-coated 
S 

6!
Dexamethasone 
Injection: 
4mg/mL 
in 
1mL 
ampoule 
(as 
disodium phosphate salt);  
B 
Epinephrine (Adrenaline) 
Injection: 1mg (as hydrochloride or hydrogen 
tartrate) in 1mL ampoule  
A 
Loratadine 
Syrup 5mg/5mL; Tablet 10mg 
C 
Promethazine 
Injection (hydrochloride) 25mg/mL in 2mL; 
Syrup  5mg/5mL; Tablet (hydrochloride) 25mg  
A 
4.0 Antidotes and Other Substances Used in Poisonings 
4.1 Antidotes (Non-specific) 
Charcoal, activated 
Tablet or Powder, 50g 
A 
Magnesium sulfate 
Powder salt, 5g 
C 
4.2 Antidotes (Specific) 
Acetylcysteine 
Injection: 200mg/mL in 10mL ampoules 
C 
Atropine 
Injection 1mg (as sulfate in 1mL ampoule) 
A 
Calcium gluconate 
Injection 100mg/mL in 10mL 
A 
Deferoxamine 
Injection 500mg (mesylate)in vial 
D 
D-penicillamine
Tablet 250mg 
D 
Dimercaprol 
Injectable 50mg/mL in 2mL ampoule 
D 
Ethylenediaminetetra-acetic 
acid 
(EDTA)  
Injection 200mg/mL in 5mL 
D 
Flumazenil 
Injection:100mcg/mL in 5mL 
D 
Pralidoxime 
Injection 600mg 
S 
Sodium bicarbonate 8.4% 
Injection 10mLs 
C 
Sugammadex 
Injection 100mg/mL 
S 
Succimer 
Capsule 100mg (2,3-Dimercaptosuccinic acid) 
D 
5.0   Anticonvulsants and Antiepileptics 
Carbamazepine 
Syrup 100mg/5mL;  Tablet 100mg;  200mg 
A 
Clonazepam 
Tablet 0.5mg, 2mg 
D 
Diazepam 
Tablet 5mg 
C 
Injection 
5mg/mL  in ampoule  2mL 
A 
Lamotrigine 
Tablet 100mg, 200mg 
S 

7
Levetiracetam 
Injection 
5mg/mL, 
10mg/mL, 
15mg/mL, 
100mg/mL,  Tablet 250mg, 500mg, 750mg, 
1000mg 
S 
Lorazepam 
Injection: 2mg/mL in ampoule; 4mg/mL in 
ampoule, Tablet 1mg/2mg  
C 
Magnesium sulfate 
Injection 50mg/mL in 10mL vial 
A 
Phenobarbital 
Injection  
(as  
sodium  salt), 
100mg in 2mL ampoule; 
A 
Tablet  (as 
sodium)  30mg, 100mg 
A 
Phenytoin 
Suspension (as sodium salt) 30mg/5mL; 
Tablet/Capsule (as sodium salt) 50mg, 100mg, 
Injection 100mg/2mL  
C 
Pregabalin 
Tablet/Capsule 75mg, 100mg; 150mg 
D 
Sodium Valproate 
Tablet 200mg, 500mg 
C 
6.0 Anti-Infective Medicines 
6.1 Antihelminthics 
6.1.1.Intestinal anthelminthics 
Albendazole 
Suspension 100mg/5mL in 30mL bottle; 
Tablet 200mg, 400mg, chewable  
A 
Mebendazole 
Suspension 100mg/5mL in 30mL bottle; Tablet 
100mg, chewable  
A 
6.1.2 Antifilariasis 
Ivermectin 
Tablet 3mg, 6mg 
A 
6.1.3 Anti-schistosomiasis and Other Anti-trematode Medicines 
Praziquantel 
Tablet 600mg 
A 
Albendazole 
 Tablet 
200mg, 
400mg 
A 
6.2 Antibacterial 
6.2.1 Access Group Antibiotics 
Ampicillin 
Powder for injection (as sodium salt) 250mg, 
500mg in vial  
A 
Ampicilin + cloxacillin 
Capsule 250/250mg, injection 
B 
Amoxicillin 
Capsule (as trihydrate) 250mg; Dispersible 
tablet 250mg, 125mg   
A 
Amoxicillin + Clavulanic acid 
Powder for suspension (as trihydrate) 125mg+ 
31.25mg (as potassium salt) in 5mL AND 
250mg 
amoxicillin 
+ 
62.5mg 
clavulanic 
acid/5mL; Tablet (as trihydrate) 500mg + 
125mg clavulanic acid (as potassium salt)   
B 
Amoxicillin + Clavulanic acid 
Powder for injection 500mg (as sodium), + 
100mg (as potassium salt) in vial 
C 

8!
Benzathine benzyl penicillin 
Powder  for  injection 1.44g (2,400,000 IU) in 
vial   
A 
Benzyl Penicillin 
Powder for injection (as sodium or potassium 
salt) 3g (5,000,000 IU) in vial  
A 
Cephalexin 
Capsule 250mg (as monohydrate); Powder for 
reconstitution 125/5mi; 250mg/mL  
B 
Cloxacillin 
Powder for injection (as sodium salt) 250mg, 
500mg in vial  
B 
Doxycycline 
Capsule  (as hydrochloride), 100mg 
A 
Erythromycin 
Powder for suspension (as ethylsuccinate), 
125mg/5mL in 100mL bottle; Tablet (as 
stearate or ethyl succinate), 250mg, film 
coated  
A 
Flucloxacillin + Amoxicillin 
Tablet 
500mg 
(as combination) ; 
C 
Flucloxacillin 
Injection (sodium) 250mg; 125mg/5mL Oral 
solution 
C 
Metronidazole 
Suspension  as (benzoate) 
200mg/5mL 
in 
100mL;   Tablet 200mg  
A 
 Injection (I.V) 5mg/mL in 100mL bottle; 
B 
Nitrofurantoin 
Tablet 100mg 
A 
Phenoxymethylpenicillin 
Powder 
for 
suspension 
125mg/5mL; 
(as 
potassium salt), Tablet 250mg 
A 
Tetracycline 
Capsule 250mg 
S 
Oxytetracycline 
Eye ointment 1% (hydrochloride) 
A 
6.2.2 Watch Group Antibiotics 
Ampicillin + Sulbactum 
Powder for injection (ampicillin 1g/sulbactam 
0.5g), (ampicillin 2g/sulbactam 1g), (ampicillin 
10g/sulbactam 5g) 
C 
Azithromycin 
Capsule/Tablet (as dihydrate) 250mg, 500mg;  
Oral liquid 200mg/5mL  
B ( level A for 
STI only) 
Clarithromycin 
Tablet 250mg, 500mg 
C 
Chloramphenicol 
Oily injection 0.5g (as sodium succinate)/mL 
in 2mL ampoule; Powder for injection (as 
sodium succinate) 1g, 125mg/5mL injection 
(as Phosphate), 150mg/mL in 2mL ampule  
B (Reserved for 
meningitis) 
Ceftriaxone 
Injection 250mg, 500mg, 1g in vial 
B ( level A for 
STI only) 
Ceftriaxone+sulbactam 
Injection 1.5g vial 
D 
Ciprofloxacin 
Tablet (as hydrochloride) 250mg, 500mg 
A 
Ciprofloxacin 
Solution for IV infusion 2mg/mL in 100mL 
C 

9!
Gentamicin 
Injection 
(as 
sulfate) 
40mg/mL 
in 
2mL 
ampoule, 20mg/mL in 2 mL ampoule  
A 
Piperacillin + tazobactam 
Powder for injection 2g (as sodium salt) + 
250mg (as sodium salt); 4g (as sodium salt) + 
500mg (as sodium salt) in vial 
S 
Sulfamethoxazole + triemethoprim 
Suspension (Sulphamethoxazole 200 mg/5mL 
+ trimethoprim 40mg/5mL in 100mL bottle;
Tablet 
480mg; 
Sulphamethoxazole 
400mg/trimethoprim 80mg 
A 
Ceftazidime 
Powder for injection (as pentahydrate) 250mg 
in vial  
D 
Cefixime 
Capsule 200mg/ 400mg 
S (A for STI 
and Typhoid) 
Cefuroxime 
Powder for Injection 250mg, 750mg, 1.5g (as 
sodium salt) in vial 
D 
Oral suspension 125mg/5mL, 250mg/5mL; 
Tablet 250mg, 500mg; injection 
D 
6.2.3 Reserve Group  Antibiotics 
Amikacin 
Injection  250mg/mL  (as sulfate) 
S 
Cefepime 
Injection 1000mg 
S 
Clindamycin 
Capsule 150mg  (as hydrochloride); 
S 
Injection (as phosphate) 150mg/mL in 2mL 
ampule 
S 
Colistin 
Powder for Injection 1MIU per vial 
S 
Dapsone 
Tablet 100mg 
S 
Meropenem 
Injection 500mg, 1000mg 
S 
Vancomycin 
Capsule: 125mg; 250mg (as hydrochloride) 
S 
Powder for injection 250mg (as hydrochloride) 
in vial 
S 
6.2.3 Antileprosy  Medicines 
Clofazimine 
Capsule: 50mg; 100mg 
A 
Dapsone 
Dapsone Tablet 50mg, 100mg 
A 
Rifampicin 
Tablet 25mg; 50mg; 100mg 
A 
6.2.4 Antituberculosis  Medicines 
Ethambutol 
Tablet  
(as 
hydrochloride) 400mg 
A 
Ethambutol+Isoniazide 
Tablet 400mg + 100mg 
A 
Ethionamide 
Tablet 125mg, 250mg 
S 

10!
Isoniazid 
Tablet 100mg 
A 
Pyrazinamide 
 Tablet 500mg 
A 
Rifampicin+Isoniazid 
Capsule/Tablet,150mg+75mg, 50mg+150mg 
A 
Rifampicin+Isoniazid+Pyrazinamid 
e+Ethambutol  
Tablet 150mg + 75mg + 400mg + 275mg 
A 
6.2.5 Reserved Second-line for Treatment of Multidrug Resistance 
Tuberculosis (MDR-TB)  
Cycloserine 
Tablet 250mg 
S 
Bedaquiline 
Tablet 100mg 
S 
Capromycine 
Powder for injection 1g (as sulfate) in a vial 
S 
Delamanide 
Tablet 50mg 
S 
Kanamycin 
Powder for injection: 1g (as 
sulfate) in vial  
S 
Levofloxacin 
Tablet 250mg 
S 
Linezolid 
Injection 
for 
intravenous 
administration: 
2mg/mL in 300mL bag; Tablet 400mg; 600mg  
S 
Moxifloxacin 
Tablet 400mg 
S 
p-Amino salicylic acid (PAS)
Granules 4g in  a sachet; Tablet 500mg 
S 
6.3 Antifungal Medicines 
Amphotericin B 
Amphotericin  B Powder for injection 50mg in 
vial  
S 
Clotrimazole 
Clotrimazole  Vaginal cream 
(nitrate) 
1%, 
10%;  Clotrimazole Pessaries 100mg; 500mg ; 
Topical cream/Ointment 
A 
Fluconazole 
IV infusion 2mg/mL in vial 
C 
Tablet/Capsule  
150mg, 200mg 
A 
Flucytosine 
Isotonic infusion solution containing flucytosine 
(1%)and 0.805% sodium chloride 
S 
Tablet 250mg, 500mg 
S 
Griseofulvin 
Tablet 500mg 
A 
Itraconazole 
Capsule 100mg 
D 
Miconazole 
Miconazole Oral gel 2%; Vaginal Pessaries, 
Topical cream/ointment 
C 
Nystatin 
Suspension oral 100,000 IU/mL 
A 
Terbinafine 
 Tablet 250mg ; Topical cream 
C 
6.4 Antiviral Medicines 
6.4.1 Antiherpes Medicines 

11!
Acyclovir 
Cream  5%; 
Tablet 
200mg, 400mg, 
B 
Injection  500mg/Vial 
D 
Valganciclovir 
Tablet 450mg 
S 
6.4.2 Antiretrovirals (ARVs) 
6.4.2.1 Nucleoside/Nucleotide Reverse Transcriptase Inhibitors 
Abacavir (ABC) 
Tablet: 300mg (as sulfate) 
A 
Lamivudine (3TC) 
Oral Liquid 50mg/mL; Tablet: 150mg 
A 
Tenofovir 
disoproxil 
fumarate (TDF)  
Tablet: 300mg 
A 
Zidovuine (AZT) 
Capsule 250mg; Oral liquid 50mg/5mL 
A 
6.4.2.2 Non-nucleoside Transcriptase Inhibitors 
Efavirenz (EFV) 
Tablet: 200mg; 600mg 
A 
Nevirapine (NVP) 
Oral 
liquid: 
50mg/5mL; 
Tablet 
50mg 
(dispersible); 200mg  
A 
6.4.2.3 Protease Inhibitors 
Atazanavir 
Tablet  
100mg;  300mg  (as sulfate) 
C 
Atazanavir + Ritonavir 
Tablet: 300mg (as sulfate) + 100mg 
C 
Lopinavir + Ritonavir (LPV/r) 
Capsule 40mg + 10mg; Oral liquid 400mg + 
100mg/5mL; Tablet 100mg + 25mg; 200mg + 
50mg  
C 
Ritonavir 
Oral liquid 400mg/5mL; Tablet 25mg; 100mg 
C 
Darunavir 
Tablet 75mg, 400mg, 600mg, 800mg 
S 
6.4.2.4 Integrase Inhibitors 
Raltegravir 
Tablet 25mg, 100mg, 400mg 
S 
6.4.2.5 Fixed Dose Combinations 
Abacavir/Lamivudine 
Dispersible Tablet 60/30mg;  Dispersible tablet; 
120/60mg; Tablet 600/300mg Scored  
A 
Tenofovir /Emtricitabine 
Tablet 300/200mg 
A 
Tenofovir/Emtricitabine/Efavirenz 
Tablet 300/200/600mg 
A 
Tenofovir/Lamivudine/Efavirenz 
Tablet 300/300/600mg 
A 
Tenofovir/Lamivudine/Dolutegravir 
Dispersible 
tablet 
60/30mg; 
Tablet 
300/300/50mg 
A 
Zidovudine/Lamivudine 
Tablet 300/150mg 
A 

12!
Zidovudine/Lamivudine/Nevirapine 
Tablet 300/150/200mg 
A 
6.4.2.6 Medicines for Prevention of Opportunistic Infections 
Isoniazide 
Tablet 300mg 
A 
Pyridoxine 
Tablet 25mg 
B 
Sulphamethoxazole + trimetoprim 
Tablet 400mg + 80mg 
A 
6.4.3 Antihepatitis Medicines 
6.4.3.1 Medicines for  Hepatitis-B  
Entecavir 
Tablet 0.5mg 
S 
Tenofovir 
disoproxil fumarate 
(TDF) 
Tablet: 300mg 
A 
6.4.3.2 Medicines for Hepatitis-C 
Ledipasvir 
Tablet 90mg 
S 
Ribavirin 
Tablet 600mg 
S 
Sofosbuvir 
Tablet 400mg 
S 
6.5 Antiprotozoal  Medicines 
6.5.1 Antiamoebic and Antigiardiasis Medicines 
Metronidazole 
Suspension 200mg/5mL; Tablet 200mg 
A 
Tinidazole 
Tablet 500mg 
B 
6.5.2 Anti-malarial Medicines 
Artemether/Lumefantrine  (ALU) 
Tablet 20mg/120mg 
A 
Artemether 
Injection 80mg/mL ampoules 
B 
Artesunate 
Injection: 
ampoule, 
containing 
60mg 
anhydrous 
artesunic 
acid 
with 
separate 
ampoule of 5% sodium bicarbonate solution  
A 
Dihydroartemisinin+Piperaquine 
(DPQ) 
Tablet  40mg+320mg, 20mg+160mg 
C 
Primaquine 
Tablet (as phosphates) 2.5mg, 7.5mg, 15mg 
A (restricted 
to 
few HFs under 
the project) 
Sulfadiazine 
500mg tablet 
D 
Pyrimethamine 
25mg tablet 
D 
6.5.3 Malaria Prophylaxis 
Sulfadoxine + Pyrimethamine 
Tablet 500mg + 25mg 
A 

13!
7.0 Antimigraine Medicines 
7.1 Medicines for Treatment of Acute Attack 
Acetylsalicylic acid 
Tablet 300mg 
A 
Ibuprofen 
Tablet 200mg; 400mg 
A 
Ergotamine tartarate 
Tablet 1mg, 2mg 
C 
7.2 Medicines for Prophylaxis 
Propranolol 
Tablet  40mg as hydrochloride) 
A 
8. Antineoplastics, Immunosuppressives and Immunomodulators
5-fluorouracil
Injection: 250mg; 500mg;  000mg; 
S 
Abiraterone  acetate 
Tablet 250mg 
S 
Actinomycin D 
Powder for injection: 500 micrograms in vial 
S 
Alfuzocin 
Tablet 10mg 
D 
Allopurinol 
Tablet 100mg; 300mg 
B 
Anastrazole 
Tablet 1mg 
S 
Antithymocite 
globulin 
(ATG) 
(rabbit/horse) 
Injection 25mg/mL in 5mL  
S 
Azacitadine 
Injection 25mg/mL 
S (with  control) 
Azathioprine 
Tablet 50mg, 75mg, 100mg 
S 
basiliximab 
Injection 20mg 
S 
Bicalutamide 
Tablet 150mg, 50mg 
S 
Bleomycin 
Powder for injection: 15 IU (as sulfate) in vial 
S 
Bortezomib 
Injection 3.5mg/vial 
S 
Capecitabine 
Tablet  500mg 
S 
Carboplatin 
Injection 10mg/mL 
S 
Chlorambucil 
Tablet  2mg 
S 
Cisplatin 
Powder for injection 50 mg; 10mg in vial. 
S 
Cyclophosphamide 
Injection 
S 
Cyclosporine 
Injection: 
50 
mg/mL 
in 
1-mL 
ampoule;  
Capsule: 25 mg; 50mg; 100mg 
S 
Dacarbazine 
Powder for injection: 100 mg in vial; 200mg/; 
500mg 
S 
Danazol 
Capsule 100mg 
S 
(hematology 
special) 
Docetaxel 
Concentrate for infusion 120mg; 80mg 
S 
Doxorubicin 
Injection  10mg;  20mg, 50mg 
S 

14!
Dutasteride 
Tablet 0.5mg 
S 
Etoposide 
Capsule: 100 mg;  Injection 100 mg/mL;  
Injection 50mg/5mL  
S 
Everolimus 
Tablet 0.25, 0.5mg 
S 
Febuxostat 
Tablet 40mg; 80mg 
S 
Filgrastim 
Injection 5mcg 
S 
Finasteride 
Tablet 5mg 
D 
Folinic acid 
Tablet 15mg, injection 6mg 
S 
Gemcitabine 
Injection 200mg; 500mg; 1000mg 
S 
Goserelin 
Injection 3.6mg, 10.8mg 
S 
Hydroxychloroquine 
Tablet 200mg 
S 
Hydroxyurea 
Capsule 500mg 
S 
Ifosfamide 
Injection 1g/20mL 
S 
Imatinib  
Tablet 400mg 
S 
Irinotecan  
Injection 180mg/mL 
S 
Lenalidomide 
Tablet 25mg 
S 
Leucovorin 
Injection 200 mg/mL 
S 
Mesna 
Injection, 100mg/mL; Tablet 400mg 
S 
Methotrexate 
Tablet 2.5mg;  Injection 50 mg/5mL 
S 
Mycophenolate Sodium 
Tablet 360mg 
S 
Mycophenolate Mofetil 
Tablet 500mg 
S 
Oxaliplatin 
Powder for injection 50mg; 100mg in vial; 
S 
Paclitaxel 
Injection 260mg  vial 
S 
Rituximab 
Injection 375 mg 
S 
Sirolimus 
Tablet 1mg, 2mg 
S 
Tacrolimus 
Tablet 0.5mg; 1mg; 2mg Ointment 0.1% 
S 
Tamsulosin 
Tablet  0.4mg 
D 
Tamoxifen 
Tablet 20mg 
D 
Temozolomide 
Tablet  200mg 
S 
Thalidomide 
Tablet 200mg 
S 
Trastuzumab 
Injection 440mg; 150mg; 600mg; 500mg 
S 
Vinblastine 
Injection 10mg  
S 
Vincristine 
Powder for injection: 2 mg; 5 mg (sulfate) in 
vial.  
S 
Zolendronic acid 
Injection 4mg; 5mg 
S 

15!
9.0 Hormones and Antihormones 
9.1 Adrenal Hormones and Synthetic Substitutes 
Betamethasone 
Injection 4mg/mL 
D 
Dexamethasone 
Tablet 0.5mg; 4mg 
D 
Injection (as sodium phosphate) 10mg/mL 
B 
Hydrocortisone 
Powder for Solution for Injection/Infusion 100 
mg  (as sodium succinate)  
A 
Methylprednisolone 
1000 mg powder and solvent for solution for 
injection/infusion;  Tablet 4mg; 8mg; 
D 
Metyrapone 
Tablet 250mg 
S 
Prednisolone 
Tablet 5mg 
A 
Triamcinolone 
Injection 40mg/mL; Cream 0.1% 
S 
9.2 Oestrogens 
Ethinyloestradiol 
Tablet 50mcg 
A 
9.3 Ovulation Inducers 
Clomiphene 
Tablet 50mg 
C 
9.4 Progesterone 
Dydrogestrone 
10mg tablet 
S 
Etonorgestrel 
Implant 68mg 
A 
Levonorgestrel 
Tablet 0.03mg,  0.07mg, 0.75mg 
A 
Implant 75mg  
A 
Medroxyprogesterone 
Injection acetate (depot) 150mg 
A 
Norethisterone 
Tablet 5mg 
C 
9.5 Androgens 
Testosterone 
Injection, 
30 
mg/1.5mL;100mg/mL; 
200mg/mL;  Cream 
S 
9.6 Contraceptives 
Ethinyloestradiol + Norgestrel 
Tablet 0.03mg + 0.3mg 
A 
Ethinylestradiol Levonorgestrel 
Tablet 0.03mg + 0.15mg 
A 
Ethinylestradiol Desogestrel 
Tablet 0.03mg + 0.15mg 
A 
9.7 Thyroid, Parathyroid Hormones and Antagonists 
Carbimazole 
Tablet 5mg 
C 
Potassium Iodide Solution 
Iodine 2mg + Potassium Iodide 4mg/g in 
water (prepare from raw material)  
B 

16!
Levothyroxine 
Tablet (sodium salt) 0.05g 
D 
Iodized oil Capsule 
Iodized oil Capsule with nipple  
240mg/0.5mL  
and  
480mg 
iodine/mL  
A 
Iodized oil  
Injection  
C 
Propylthiouracil 
Tablet 50mg 
D 
10. Antiparkinsonism Medicines and Antiprolactenemia
Benzhexol 
Tablet (hydrochloride) 5mg 
B 
Bromocriptine 
 Tablet  2.5mg 
C 
Cabergoline 
Tablet 0.5mg 
S 
Levodopa/Carbidopa 
Tablet 100mg + 25mg 
D 
Selegiline 
Tablet 5mg 
S 
11. Medicines Affecting the Blood
11.1 Antianaemia Medicines 
Erythropoietin 
2000 unit/Ml; 4000 units/mL 
S 
Ferrous 
200mg ( sulfate or as fumarate) 
A 
Ferrous salts 
Oral liquid: Equivalent to 25mg iron (as 
sulfate)/mL;   Tablet: Equivalent to 60mg iron  
A 
Folic acid 
Folic acid Tablet 5mg 
A 
Hydroxocobalamin (Vitamin B12) 
 Injection 1mg/mL  
C 
11.2 Medicines Affecting Coagulation 
Desmopressin 
(Move 
to 
anti- 
diuretics)  
Injection 4mcg/mL, Tablet 0.2mg 
S 
Etamsylate 
Tablet 500mg 
C 
 Low molecular Weight heparin 
Injection 100mg/mL 
S 
Phytomenadione (Vit K1) 
Injection 0.5 mg/mL, 2mg/mL in 2mL ampoule; 
B 
Protamine sulfate 
Injection 10mg/mL in 5mL ampoule 
B 
Rivaroxaban 
 Tablet 15mg, 20mg 
S 
Unfractionated Heparin Sodium 
Injection (sodium salt) 1,000 IU/mL in 5mL 
ampoule  
B (Under 
specialist 
supervision) 
Tranexamic acid 
Injection 100mg/mL in 5mL ampoule; Syrup 
500mg/5mL in 300mL bottle;  Tablet 500mg  
C 
Warfarin 
Tablet: 1mg; 2mg; 5mg (sodium salt) 
C 

17!
12.1 Blood and Blood Components 
Fresh frozen plasma (FFP) 
Fresh frozen plasma (FFP) Bags 
D 
Platelets 
Platelets 
D 
Red blood cells. 
Packed red blood cells. 
D 
Whole blood 
Whole blood 
B 
12.2 Plasma-Derived Medicines 
12.2.1 Human Immunoglobulins 
Anti-rabies immunoglobulin 
A 
Anti-tetanus immunoglobulin 
A 
Human Immunoglobulin G 
S 
12.2.2 Blood Coagulation Factors 
Eltrombopag 
Tablet 25mg 
S 
Factor VIII concentrate 
Factor VIII concentrate 500IU 
S 
Factor IX concentrate 
Factor IX concentrate500 IU 
S 
12.3 Plasma Substitutes 
Albumin 
Infusion 5%; 25% 
S 
Polygeline 
Polygeline IV solution 3.5%, 500mL bottles 
S 
13.0 Cardiovascular Medicines 
13.1 Antianginal Medicines 
Bisoprolol 
Tablet 5mg; 10mg 
S 
Glyceryl trinitrate 
Spray 
400 
micrograms/metered 
dose, 
sublingual spray 
C 
Isosorbide Dinitrate 
Tablet 10mg, 20mg 
C 
Labetalol 
Tablet 100mg, 200mg ; Injection 5mg/mL 
C 
Nifedipine 
Slow-release Capsule/Tablet 10mg; 20mg 
B 
Nitroglycerin 
Injection/Infusion 25mg/250mL; 50mg/250mL; 
100mg/250mL 
S 
Propranolol 
Tablet 40mg 
A 
13.2 Antiarrhythmic Medicines 
Adenosine 
Injection 3mg/mL in Saline 
S 
Amiodarone 
Injection 30mg/mL in 10mL ampoule; Tablet 
100mg   
S 
Sotalol 
Tablet 80 mg, 120 mg, 160 mg, 240 mg; Oral 
solution 5mg/Ml; Injection 15mg/mL 
S with control 
12.0 Blood Products of Human Origin and Plasma Substitute 

18!
Verapamil 
Injection 2.5mg/mL, 2mL ampoule; Tablet 
40mg 80mg  
S 
13.3 Antihypertensive Medicines 
Amlodipine 
Tablet 5mg, 10mg 
C 
Atenolol 
Tablet 50mg 
B 
Candesartan 
Tablet 16mg; Tablet in fixed combination 
S 
Captopril 
Tablet 12.5mg, 25mg 
B 
Carvedilol 
Tablet 6.25, 12.5mg 
C 
Clonidine 
Injection 500mcg/mL; Tablet 0.1 mg, 0.2 mg 
and 0.3 mg 
S 
Diltiazem 
Tablet 60mg 
D 
Doxazosin 
Tablet 2mg,  4mg 
S 
Enalapril 
Tablet 2.5mg, 5mg (as hydrogen maleate) 
C 
Esmolol 
Injection 10g/mL 
S 
Hydralazine 
Tablet 25mg 
B 
 20mg Powder for Injection/Infusion 
C 
Irbesartan 
Tablet 
150mg, 
300mg; 
Tablet 
in 
fixed 
combination 
S 
Lisinopril 
Tablet 5mg, 10mg 
C 
Losartan 
Tablet 50mg; Tablet in fixed combination 
C 
Nimodipine 
Capsule 30mg 
S 
Methyldopa 
Tablet 250mg 
A 
Metolazone 
Tablet 5mg 
S 
Metoprolol 
Tablet 50mg 
C 
 Injection 1mg/mL 
S 
Telmisartan 
Tablet 
40mg, 
80mg; 
Tablet 
in 
fixed 
combination 
S 
13.4 Medicines Used in Heart Failure 
Candesartan 
Tablet 8mg 
C 
Dobutamine 
Injection 250mg/5mL 
S 
Dopamine 
Injection 250mg 
S 
Digoxin 
Injection 250mg/mL 
D 
Tablet 0.25mg 
D 

19!
Ivabradine 
Tablet 5mg 
S 
13.5 Diuretics 
Furosemide 
Injection 10mg/mL; Tablet 40mg 
B 
Eplerenone 
Tablet 25mg, 50mg 
S 
Bendrofluazide 
Tablet 5mg 
A 
Hydrochlorothiazide 
Tablet 25mg; 12.5mg 
D 
Mannitol 
Injectable solution: 10%; 20% 
C 
Spironolactone 
Tablet 12.5mg, 25mg 
C 
Torsemide 
Tablet 2.5mg, 5mg; 10mg 
S 
13.6 Antithrombotic Medicines 
13.6.1 Anti- Platelet Medicines 
Acetylsalicylic acid 
Tablet: 75mg, 100mg 
A 
Clopidogrel 
Tablet: 75mg; 300mg 
D 
Prasugrel 
Tablet 10mg 
S (with special 
permission) 
Ticagrelor 
Tablet 60mg, 90mg 
S (with special 
permission) 
13.6.2 Thrombolytics 
Alteplase 
Powder for injection: 50mg vial 
S 
Streptokinase 
Powder for injection: 1.5 million IU in vial. 
S 
13.7 Lipid Lowering Medicines 
Atorvastatin 
Tablet 10mg; 20mg; 40mg 
B 
Fenofibrate 
Capsule 200mg 
D 
Rosuvastatin 
Tablet: 10mg ; 20mg 
S 
14.0 Dermatological Medicines 
14.1 Antifungal Medicines 
Benzoic acid Compound  (whitfied's) 
3% salicylic acid and 6% benzoic acid 
ointment  
A 
Clotrimazole 
Cream 1% 
A 
Miconazole 
Cream (nitrate) 2% 
C 
Terbinafine 
Cream 1%, 
C 

20!
Fusidic acid 
Cream 2% 
C 
Gentian Violet 
1%, aqueous solution 
A 
Mupirocin 
Ointment 2% 
C 
Potassium permanganate 
Potassium 
permanganate 
Solution 1:4000 
A 
Povidone iodine 
Solution 10% 
A 
Silver Sulfadiazine 
1% Cream 
A 
14.3 Anti-nflammatory and Anti-pruritic Medicines 
Betamethasone 
cream or ointment 0.1% ( as valerate) 
C 
Calamine 
Lotion 15.0% w/v 
A 
Clobetasol propionate 
Cream 0.05%; 0.1% 
D 
Fludrocortisone 
Tablets 0.1 mg (as acetate) 
S 
Hydrocortisone 
Hydrocortisone Cream 0.5% 
A 
Mometasone furoate 
Ointment/Cream containing 0.1% contains 
mometasone furoate, 
S 
Triamcinolone 
Injection 40mg/mL as Acetonide 
S 
14.4 Medicines Affecting Skin differentiation and Proliferation 
All-trans-retinoic acid (ATRA) 
Tablet 10mg, 20mg, injection 
S 
Benzoyl peroxide 
Gel 2.5%, 5% and 10% 
A 
Coal tar 
Solution 5% (prepare from raw materials) 
C 
Isotretinoin 
0.05% cream, Capsule 10mg, 
20mg  
S 
Podophyllin Solution 
 Solution 10-25% (prepare from raw materials) 
D 
Salicylic acid 
Topical 
solution 
5% 
(prepare 
from 
raw 
materials)  
C 
Silver nitrate pencil 
Silver nitrate pencil 
C 
Tretinoin cream 
2.5% cream 
S 
14.5 Scabicides and Pediculicides 
Benzyl benzoate Emulsion 
Emulsion: 25% 
A 
Lindane 
Lotion 1% 
C 
14.6 Sunscreen Protector 
Sunscreen protecting factor (SPF 
30+)  
Sun screen cream 30+ 
C 
14.2 Anti-infective Medicines 

21!
15.1 Antiulcer Medicines 
Antiacid Mixture 
Antiacid 
Mixture 
containing 
magnesium 
trisilicate 
+ 
aluminium 
hydroxide 
and 
Simethicone  
B 
Bismuth Subgallate 
Tablet 200mg 
D 
Esomeprazole 
Tablet 20mg; 40mg 
S 
Lansoprazole 
Tablet 30mg 
C 
Magnesium trisilicate  Tablet 
Tablet (250mg magnesium trisilicate + 120mg 
dried aluminium hydroxide)  
A 
Mesalazine 
Tablet 400mg, 500mg, 800mg 
S 
Octreotide 
Injection 50mcg; 100mcg 
S 
(Special 
permission) 
Omeprazole 
Tablet 20mg 
A 
Pantoprazole 
Tablet 40mg; Powder for injection 40mg 
C 
Terlipressin 
0.12mg/mL  
solution 
for 
injection (acetate) 
S 
15.2 Drugs affecting Intestinal Secretion and Antispasmodics 
Cholestyramine 
Cholestyramine Powder 4g per 
Sachet   
S 
Hyoscine butylbromide Tablet 
Hyoscine butylbromide Tablet 10mg 
A 
Hyoscine butylbromide Injection 
Hyoscine butylbromide Injection 20mg/mL; 
1mL ampoule  
C 
Inflixmab 
Injection 100mg  
S 
(Special 
permit) 
Mebeverine 
Tablet 135mg 
D 
Pancreatic 
Supplement Enzyme 
S 
Ursodeoxycholic acid 
Tablet/capsule 300mg 
S 
15.3 Anti-emetics 
Domperidone 
Tablet 10mg 
D 
Doxylamine 
Tablet 25mg 
C 
Metoclopramide 
Tablet 10mg;  Injection 5mg/mL;  Suspension 
5mg/5mL 
C 
Promethazine 
Tablet 
(hydrochloride/theoclate) 
25mg; 
Injection (as hydrochloride) 25mg/mL; Elixir 
5mg/5mL (as chloral hydrate) 
A 
Ondansetron 
Tablet 8mg, Injection 2mg/mL 
S 
15.4 Cathartics 
Bisacodyl 
Tablet 5mg 
A 
Lactulose 
Solution 3.1 - 3.7g/5mL, 200mL bottle 
C 
15.0 Gastro-Intestinal Medicines 

22!
15.6 Medicines Used in Diarrhoea 
Loperamide 
Tablet/Capsule (hydrochloride) 2mg 
B 
Oral Rehydration Salts (ORS) 
Low osmolality sachet to make 1 litre of 
solution containing Sodium chloride 2.6g, 
Sodium citrate 2.9g, Potassium chloride 
1.5g  
and  
Glucose 20.5g)  
A 
Zinc 
Tablet  
dispersible (equivalent to 20mg 
elemental zinc)  
A 
16.0 Insulin and Medicines Used for Diabetes and Related Disorders 
Empagliflozin 
Tablet 10mg 
S (with special 
permit) 
Glibenclamide 
Tablet 5mg 
A 
Gliclazide 
Tablet 40mg; 80mg; 30mg; 60mg 
A 
Glimepiride 
Tablet  1mg; 2mg 
C 
Glucagon 
Powder  for 
reconstitution 
10mg/vial 
S 
Insulin 
Rapid acting; Injection: 40 IU/mL; 100 
IU/Ml 
Short acting;  Injection: 40 IU/mL; 100 
IU/mL  
A 
Intermediate acting;  Injection: 40 IU/mL; 
100 IU/mL  
A 
Long acting; Injection: 40 IU/mL; 100 
IU/mL 
A 
Pre-Mixed Insulin;  Injection: 40 IU/mL; 
100 IU/Ml 
S 
Metformin 
Tablet 500mg; 750; 850MG; 1000MG; SR 
A 
Pioglitazone 
15mg 
D 
Phenoxybenzamine 
Tablet 10 mg 
S 
Sitagliptin 
Tablet 50mg; 100mg 
S 
17.0 Immunologicals 
17.1 Sera and Immunoglobulins 
Anti D immunoglobulin 
Injection 150mg; 300mg 
C 
Antirabies immune globulin  
Injection 
400IU/mL; 
10,000IU/5mL 
A 
L-Ornithine L-Aspartate
Granules; Injection 
S 
15.5 Anti-Haemorrhoids 
Local anaesthetic + astringent and 
anti-inflammatory  
Suppositories/ointment 
(zinc 
oxide 
25mg
+ bismuth oxide+ bismuth subgallate 
59 mg + balsam Peru)
B 

23!
Anti-venom immunoglobulin 
Snake  
venom polyvalent 
Antiserum 
injection (|Central African type) 
A 
Diphtheria antitoxin 
Injection: 10,000 IU; 20,000 IU vial 
A 
Tetanus Immunoglobulin 
Tetanus  
Immunoglobulin  
(human) – 250 IU/mL,250 IU/2.5mL 
A 
17.2 Vaccines 
17.2.1 For Immunization 
BCG Vaccine 
Injection 20 doses vial (Bacillus Calmette 
Guerin) 
A 
DPT-HepB-Hib Vaccine 
Diphtheria, Tetanus, Pertussis, Hepatitis 
B and Haemophilus Influenza vaccine in 
vials of 10 doses 
A 
Hepatitis B 
Injection 
10mcg/mL, 
20mcg/mL, 
40mcg/Ml 
B 
Human Papilloma Vaccine (HPV) 
Human  
Papilloma  
Vaccine 
(HPV) – 0.5mL per dose  
A 
Inactivated Polio Vaccine (IPV) 
Inactivated Polio Vaccine (IPV) 
A 
Measles-Rubella Vaccine 
Measles-Rubella  
Vaccine 
Injection 10 doses in vial 
A 
Oral Poliomyelitis Vaccine (OPV) 
Oral 
Poliomyelitis 
Vaccine 
(Live 
attenuated) Oral solution 20 doses in vial  
A 
Pneumococcal 
Conjugate 
Vaccine 
(PCV13)  
Pneumococcal 
Conjugate 
Vaccine (PCV13) -4 doses vial 
A 
Pneumococcal polysaccharide vaccine 
(PPSV-23) 
Vial 
S 
Rota Vaccine 
Rota Vaccine Oral solution 
A 
Tetanus (toxoid) Vaccine 
Tetanus  
(toxoid) 
Vaccine 
Injection 20 doses in 10mL vial 
A 
17.2.2  For Specific Groups for Individuals 
Human Diploid Cell Rabies Freeze 
dried rabies vaccine  
Human  Diploid  Cell  Rabies 
Freeze dried rabies vaccine  
A 
Meningitis vaccine 
Injection 
C 
Yellow Fever Vaccine 
 0.5mL dose 
C 
18.0 Muscle Relaxants (Peripherally-Acting) and Cholinesterase Inhibitors 
Neostigmine 
Injection: 
500microgram 
in 
1mL 
ampoule; 
2.5 
(metilsulfate) 
in 
1mL 
ampoule  
C 
Suxamethonium 
Injection: 50mg (chloride/mL in 2mL 
ampoule  
C 

24!
19.1 Anti-infective Agents 
Acyclovir ointment 
Acyclovir Eye ointment 3% 
C 
Ciprofloxacin 
Drops 0.3% 
C 
Chloramphenicol 
Drops 0.5%, 1%;  Eye ointment 1% 
A 
Chlorhexidine 
Drops 0.2% 
S 
Dexamethasone+Chloramphenicol 
Drops 0.1%, 0.5% 
C 
Dexamethasone +Gentamicin 
Drops 0.1, 0.3% 
C 
Econazole 
Drops 5% 
S 
Natamycin 
Drops 5% 
S 
Ofloxacin 
Drops 0.3% 
D 
Oxytetracycline t 
Eye ointment 3% 
A 
Iodine 
Eye drops, 2.5-5% 
A 
19.2 Anti-allergy, Artificial Tears and Anti-inflammatory Agents 
Dexamethasone eye drops 
Drops 0.1% 
D 
Hydroxypropylmethylcellulose 
Drops 0.70% 
C 
Methylprednisolone acetate 
Injection 40mg/mL 
D 
Prednisolone eye drops 
Drops 0.5%, 1% 
D 
Oxymetazoline 
Drops 0.025% 
C 
Sodium cromoglycate drops 
Sodium cromoglycate 2%, 4% eye drops 
C 
Triamcinolone Acetatonide 
Injection 40mg/mL 
S 
19.3 Local and Topical Ocular Anaesthetic Agents 
Amethocaine eye drops 
Drops 0.5%w/v or 1.0%w/v 
A 
Tetracaine  eye drops 
Drops .5%w/v 
C 
19.4 Miotics and Antiglaucoma 
Acetazolamide 
Tablet 250mg 
C 
Acetylcholine 
Injection; 
vial 
contains 
20 
mg 
acetylcholine 
chloride 
and 
56 
mg 
mannitol 
S 
Betaxolol 
Drops 0.25% -0.5% w/v 
D 
Brimonidine 
Drops 0.15 – 0.2% w/v 
D 
Dorzolamide 
Drops 20 mg/ml 
S 
Latanoprost 
Drops 0.005%  w/v 
D 
Pilocarpine hydrochloride 
Drops 2 or 4% w/v 
C 
Prostamide bimatroprost 
Drops 0.03%  w/v 
D 
Timolol 
Drops 0.25%, 0.5% w/v 
C 
19.0 Ophthamological Preparations 

25!
19.5 Mydriatics and Anti-vascular Endothelial 
Atropine 
Drops 0.5%, 1% w/v;  Ointment 1% 
B 
Cyclopentolate 
Drops 0.5%, 1% w/v 
C 
Tropicamide 
Drops 1% w/v 
S 
Tropicamide with Cyclopentolate 
Drops 0.5%, 1%   w/v 
C 
Tropicamide with Phenylephrine 
Drops 0.8% / 5% w/v 
C 
19.6 Other Ocular Preparations 
5 –Fluoro Uracil 
1% eye drops 
D 
Ganciclovir 
Injection 2mg; ophthalmic gel, 0.15% 
S 
Mitomycin C 
5mg/vial, 10 mg/vial 
D 
Silicon Oil 
1000 CS, 1500 CS, 5000 CS 
S 
20.0 Oxytocics and Antioxytocics 
20.1 Oxytocics 
Ergometrine Injection 
Injection (maleate) 0.5mg/mL (hydrogen 
maleate) in 1mL ampoule  
C 
Misoprostol 
Tablet 
200mcg 
(rectal, 
sublingual) 
A 
Oxytocin Injection 
Injection 10 IU in 1mL ampoule 
A 
20.2 Antioxytocics (tocolytics) 
Dicyclomine 
Tablet 20mg; Injection 
B 
Nifedipine 
Immediate – release capsule: 10mg, 
20mg  
B 
Salbutamol Tablet 
Tablet 4mg 
A 
21.0 Dialysis Solution and Other Related Medicines 
Iron Sucrose 
Injection 20mg/Ml 
D 
Intraperitoneal dialysis solution 
Parenteral 
solution 
(of 
appropriate 
composition) 
S 
22.0 Psychotherapeutic and Related Medicines 
22.1 Medicines used in Psychotic Disorders 
Benzhexol 
Tablet 5mg 
C 
Chlorpromazine 
Injection (hydrochloride) 25mg/mL in 2mL 
ampoule; Tablet (hydrochloride) 25mg, 
100mg   
A 
Donepezil 
Tablet 5mg, 10mg 
S 
Fluphenazine 
Injection 25mg/mL  (decanoate) in 1mL 
ampoule  
C 

26!
Haloperidol 
 Injection  5mg/mL  in 1mL ampoule; 
Tablet 1.5mg   
B 
Lorazepam 
Tablet 1mg, 2mg 
C 
Olanzapine 
Tablet 5mg; 10mg 
S 
Risperidone 
Tablet 1mg/2mg 
S 
Zuclopenthixol 
Injection 50mg/mL (Acetate) 
S 
22.2 Medicines Used in Mood Disorders 
22.2.1 Medicines used in Depressive disorders 
Amitriptyline 
Tablet (hydrochloride) 25mg 
A 
Citalopram 
Tablet 20mg 
D 
Fluoxetine 
Capsule 20mg 
S 
Imipramine 
Tablet 25 mg 
C 
Oxybutynin 
Tablet 5mg 
S 
22.2.2 Medicines in Bipolar Disorders 
Carbamazepine 
Tablet 100mg, 200mg 
A 
Lamotrigine 
Tablet 100mg, 200mg 
S 
Sodium Valproate 
Tablet 200mg, 500mg 
C 
22.3 Medicines Used for anxiety Disorders 
Diazepam 
Tablet 5mg 
C 
22.4 Medicines Used for Disorders due to Psychoactive Substance use 
Buprenorphine 
Sublingual Tablets2mg 
S 
Methadone 
Oral 
liquid: 5mg/5mL; 10mg/5mL 
C 
Naltrexone 
Tablet 50mg 
S 
23.0 Medicines Acting on Respiratory Tract 
23.1 Anti-asthmatics 
Budesonide inhaler 
Inhalation 100mcg, 200mcg 
B 
Fluticasone propionate 
Nasal Spray 50mcg 
D 
Ipratropium Bromide Aerosol 
Inhalation 
(aerosol): 
20 
microgram/metered dose; Nebulizer 250-
500mcg  
S 
Montelucast 
Tablet 5mg; 10mg 
D 
Salbutamol 
Tablet (as sulfate) 4mg; syrup (as 
sulfate)  2mg/5mL; Inhalation (as sulfate) 
0.1mg per dose (aerosol inhaler)  
A 
Nebulizer solution 2.5mg/mL; 5mg/mL; 
Injection 0.5mg/mL; img/mL   
B 

27!
Salfolinl 
Inhalation 100mcg, 200mcg 
C 
Tiotropium 
 Inhalation1.25mcg/actuation;   
2.5mcg/actuation 
S ( with special 
permit) 
23.2 Cough Preparations 
Cough syrup 
Containing expectorants/Antitussive 
Lictus  
A 
24.0 Solutions, Correcting Water Electrolyte and Acid-Base Disturbances 
Dextrose 5%; 
Dextrose 5%; 500mL, 1000mL 
A 
Dextrose 10%; 
Dextrose 10%; 500mL 
C 
Dextrose 25%, 
Dextrose 25%,  50mL, 100mL 
C 
Dextrose 50%, 
Dextrose 50%; 50mL, 100mL 
C 
Polystyrene sulfonate 
Solution containing calcium (or sodium) 
D 
Sodium bicarbonate 
Injection 5%, 
C 
Sodium 
lactate 
compound 
Sodium 
lactate 
compound 
(Ringer's 
solution) 500mL, 1000mL.  
A 
Sodium Chloride solution 
0.9% Sodium Chloride 500mL, 
1000mL  
A 
Sodium Chloride solution 
3% Sodium Chloride 500mL, 
1000mL  
C 
Sodium chloride+Dextrose 
Sodium 
chloride+Dextrose 
0.9%+5%; 500mL, 1000mL 
B 
Potassium chloride Solution 
Potassium  chloride  Solution 
7.4% 10mL Vial  
C 
Water for injection 
5mL, 10mL vial 
A 
25.0 Vitamins/Minerals 
Ascorbic acid (Vitamin C) Tablet 
Ascorbic acid (Vitamin C) Tablet 100mg 
and 500mg  
A 
Calcium gluconate 
Injection 100mg/mL in 10mL ampoule 
A 
Calcium Carbonate 
Tablet 500mg 
S 
Calcium 
with vitamins 
C 
Calcium 
with amino acids 
C 
Ergocalciferol (vitamin D) 
Capsule 1.25mg (50, 000IU); Oral solution 
0.25mg/mL (10,000IU/mL)  
C 
Glucosamine +Chondrotin sulphate 
Tablet 
S 
Iron 
with vitamins 
C 
Iron 
with amino acid 
C 
Nicotinamide (Vitamin B3) 
Tablet 50mg 
C 
Potassium chloride 
Tablet (slow release) 600mg ; Injections 
C 

28!
Pyridoxine (Vitamin B6) 
Tablet (hydrochloride) 25mg 
B 
Retinol (Vitamin A) Capsule 
Retinol (Vitamin A) Gelatin Capsule (with 
nipple to allow administration drop by 
drop) 50,000IU, 100,000IU 200, 000IU  
A 
Sodium Hyaluronate 1% 
Injection. 1% 
S 
Thiamine (Vitamin B1) 
 Tablet (hydrochloride) 100mg 
C 
Thiamine (Vitamin B1) 
Injection (hydrochloride) 1000mg/mL in 
1mL ampoule  
C 
Vitamin B complex 
Vitamin B complex Tablet BP (contains 
per Tablet: nicotinamide 15mg, iboflavin 
1mg, thiamine 1mg)  
A 
Syrup 
(contains 
nicotinamide 
15mg, 
riboflavin 1mg, thiamine 1mg/5mL)  
A 
Vitamin B complex 
Injection BP in 10mL vial (contains 
icotinamide 200mg, pantothenol 30mg, 
pyridoxine 
20mg, 
riboflavine 
20mg, 
thiamine 50mg per 1 mL)  
B 
Vitamin E 
Tablet/capsule alpha tocopherol acetate 
500 mg/5 mL  
D 
26.0 Medicines Used in Ear, Nose & Throat Diseases 
26.1 Ear Drops 
Betamethasone 
Ear drops; 0.1% w/v 
Boric acid 
Ear drop; 3% 
A 
Ciprofloxacin 
Ear drops; 0.3% 
C 
Clotrimazole 
Ear drops; 1% 
Chloramphenicol 
Ear drops; 5% w/v 
Dexamethasone + Neomycin 
Ear drops: 0.1% + 0.5% 
C 
Lidocaine 
+ 
Beclometasone
+ 
Clotrimazole + Chloramphenicol 
Ear drop 
D 
26.2 Oral Antiseptics 
Chlorhexidine gluconate Solution 
Chlorhexidine 
gluconate 
Solution 
0.1%;prepare from concentrated solution; 
gel  
B 
Potassium permanganate Solution 
Potassium 
permanganate 
Solution 
1:4000; 
prepare 
from 
powder/crystals 
A 
26.3 Nasal Preparations 
Ephedrine 
Nasal drops 0.5% and 1% 
B 
Normal saline 
Nasal drop 0.9% 
A 
Mometasone 
Nasal spray 50 micrograms/dose (as 
furoate) 
S 
Xylometazoline 
Nasal spray 0.05% 
S 

29!
27.0 Disinfectants and Antiseptics 
Chlorhexidine + Cetrimide 
Solution 
concentrated 
containing 
chlorhexidine digluconate 1.5%+ 15% 
cetrimide  
A 
Chloroxylenol 
Solution 4.9% BP 
A 
Cresol saponated 
Solution 3% BP 
A 
Formaldehyde 
Solution 36 - 
37% stabilized 
B 
Glutaraldehyde 
Activated solution 2% 
C 
Hydrogen peroxide 
Solution 3% 
A 
Hydrogen peroxide 
Solution 6% 
A 
Methylated spirit 
Solution 70% 
A 
Potassium permanganate 
Potassium  
permanganate 
Solution 1: 4000 
A 
Povidone-Iodine 
Solution 10% 
A 
Sodium dichloroisocyanurate 
Tablet, 1.67g (equal to 1g available 
chlorine)  
A 
28.0 Miscellaneous 
Sildenafil 
Tabet 50mg 
S 

30!
PART II 
THE STANDARD TREATMENT GUIDELINE (STG) 
Standard Treatment Guidelines provide standardized guidance to health professionals on diagnosis 
and treatments. It provides invaluable assistance to practitioners especially those with lower skills or 
new in the field. STG are systematically developed statements to assist practitioners/prescribers in 
making decisions about appropriate treatment for specific clinical conditions. The statements contain 
information on: clinical conditions, diagnosis criteria, non- pharmacological, medicines of choice (and 
alternatives) for the medical condition, important prescribing information—dose, duration, 
contraindications, side effects, warnings, medicine interactions and the referral criteria. 
The STGs should be updated regularly to reflect changes in accepted treatment strategies. The 
2021 edition of STG have been updated to reflect new therapeutic options and to include new 
emerging diseases. In the development process, the use of evidence-based medicine was 
overemphasized and each chapter was revised by a Lead Reviewer, an expert on the specific 
disease condition. The STG has covered the priority disease conditions in the country arranged in 
twenty-six chapters namely: 
•
Emergency and Critical Care
•
Anaesthesia
•
Haematological Disease  Conditions
•
Notifiable Diseases
•
Malaria
•
HIV/AIDS
•
TB and Leprosy
•
Nervous Disease  Conditions
•
Respiratory Disease Conditions
•
Gastrointestinal Disease Conditions
•
Obstetrics, Gynaecology  and Contraception
•
Sexually Transmitted Infections
•
Skin Disease and Allergic Reactions
•
Eye Disease Conditions
•
Oral and Dental Conditions
•
Ear, Nose and Throat Diseases
•
Musculoskeletal Disorders
•
Trauma and Injuries
•
Metabolic  and Endocrine Disease Conditions
•
Kidney and Urological Disorders
•
Malignant Disease Conditions
•
Mental Health Conditions
•
Nutrition Disorders
•
Poisoning
Note 
•
All medicines indicated for treatment of various diseases in the STG are listed in the
NEMLIT. 
•
The referral criteria in the STG meant to refer the patient to the next level of care; with the
fact that expertise to manage a patient/diagnosis capacity may lack at that level. 

31!
CHAPTER ONE 
APPROACH TO PATIENTS WITH EMERGENCY CONDITIONS 
1.1 The Concept of Emergency Care and Resuscitation 
Emergency care and Resuscitation involves rapid assessment and early intervention. Approach to 
Emergency care and resuscitation needs to be systematic hence the use of the ABCs approach. 
The ABCs approach provide the framework for evaluation and treatment of severely ill patients.  
Primary survey 
I.
Airway
Assess the airway to establish patency of the airway. This includes:
•
Looking for signs of airway obstruction (signs of trauma, swelling, secretions,
presence of foreign body).
•
Listen for abnormal sounds like stridor, snoring.
If there are signs of airway obstruction intervene by positioning, opening and clearing the airway. 
Perform chin lift or jaw thrust manoeuvre to open the airway (If suspecting cervical spine injury use 
the jaw thrust manoeuvre). Use sunction to remove the secretions. Airway adjuncts like 
oropharyngeal or nasopharyngeal airway can be used. 
Note 
•
Remember to reassess the airway after performing interventions
•
Some patient may require use of advance airway devices like endotracheal intubation or
surgical airway
II.
Breathing
Upon completing airway assessment and intervention, assess for presence of breathing, signs
of respiratory distress such as tachypnea, hypoxia, cyanosis, apnoea and abnormal breath
sounds.Provide oxygen when oxygen saturation is below 92% or the patient is dyspnoeic.
Oxygen can be administered using the nasal prong, simple face mask, non-rebreather mask or
ambubag. Advance interventions include: mechanical ventilation.
III.
Circulation
Check for pulse (central pulse) for not more than 10 seconds. If absent start CPR (Refer
cardiopulmonary resuscitation section below). Assess for signs of poor peripheral perfusion
(shock) such as cold extremities, prolonged capillary refill, dry mucous membrane and
hypotension. If there are signs of shock, establish two (2) IV large bore cannula and give IV
fluids (crystalloids) bolus (2lts in adults and 20mls/kg in pediatrics). Limit fluids to individuals
whom you suspect to have heart failure, renal failure or malnourished children.
IV.
Disability
This involves rapid assessment of the neurological status. This includes assessment for the
level of consciousness (use of AVPU or Glascow coma scale), signs of convulsions, random
blood glucose level, examination of the pupils and presence of focal neurological
deficit.Interventions that can be performed during the disability assessment include: correction
of hypoglycemia, airway protection, stopping the convulsions by administering anticonvulsant
V.
Exposure
This involves fully exposing the patient and rapid assessment of the body for signs of trauma,
rashes or infection.
Secondary survey 
After assessment and stabilization of ABCs during the primary survey, focus is turned into 
secondary survey. The secondary survey is a systematic assessment of the rest of the body to 
identify injuries and illnesses. Common approaches include a head to toe or organ –system based 
assessment. It is important to note that the secondary survey is performed after the primary 
assessment and interventions. When performing a secondary survey, if the patient condition 
changes then you must stop immediately and redo the primary survey and necessary interventions. 

32!
Note: 
All patients with compromised airway, breathing, circulation or disability must be attended in the 
resuscitation rooms. (Refer Triage overview section) 
1.2 Cardiac Arrest and Cardiopulmonary Resuscitation 
Cardiopulmonary resuscitation is an Emergency lifesaving procedure performed when there is 
sudden cessation of heart beats. It involves the combination of chest compressions and artificial 
ventilation to preserve blood flow to the organs including the brain function. Early initiation of CPR 
can double or triple the chances of survival after cardiac arrest. 
Note: HIGH QUALITY CPR 
•
Compressions:
•
Infant: 2 finger compression (if alone) or thumb encircling technique (if you have
assistance)
•
Child: 1 or 2 hand
•
Adult: Two hands
•
Compression rate: 100-120/min
•
Compression depth: approximately 1/3 antero-posterior diameter of the chest
•
Compression/ventilation ratio: 30:2 (adults and children), 30:2 (If alone) and 15:2 (If
you have assistance)
•
Allow chest recoil
•
Minimize interruptions
•
Adequate ventilation
Clinical presentation 
•
Unresponsiveness (sudden loss of consciousness)
•
Absence of central pulse (carotid pulse/femoral pulse or brachial pulse in infants)
•
Loss of spontaneous respiration
Investigations 
While continuing with CPR, point of care (POC) tests are conducted while looking for the reversible 
causes of the cardiac arrest (Hypovolemia, hypoxia, hypo/hyperkalemia, acidosis, hypothermia, 
hypoglycemia, tension pneumothorax, toxins, thrombi, cardiac tamponade). These includes: 
•
POC Blood gases
•
POC Bicarbonates
•
POC Electrolytes- Potassium, sodium, Calcium, Chloride,
•
POC Creatinine, POC urea
•
POC RBG
•
Bedside ultrasound- looking for pneumothorax, cardiac tamponade or thrombi
•
POC Toxicology screens (If available)
•
POC ECG (if there is return of spontaneous circulation)
•
POC lactate
•
POC Troponin
 Management 
•
HAZARDS- ensure safety and use of PPEs
•
HELLO- Check for responsiveness, Carotid pulse (not more than 10 seconds) and
breathing
•
CPR starts with early recognition (unresponsiveness, loss of spontaneous breathing and
absence of carotid pulse. In infant’s CPR is initiated when the heart rate is below 60
beats/min
•
Call for HELP and immediately start chest compression. As more members arrives to help
assign different roles including airway and breathing management, time recording,
documentation, AED/monitor, medications
•
Open the airway by performing chin lift or jaw thrust (if suspecting C spine injury). Use
airway adjuncts to open the airway.
•
Give 2 breaths using bag valve mask connected to oxygen source and observe for chest
rise

33!
•
Establish IV access for administration of fluids and medications, if failed perform
Intraosseous access
•
After FIVE cycles of compressions/ventilation (2 minutes), check for pulse and use
AED/Defibrillator to analyze rhythm if there is a need to deliver shock
•
If no need for shocking continue with CPR for another 2 minutes (FIVE cycles)
Pharmacological Treatment 
A: adrenaline (IV) Adult: 1mg, Pediatrics0.01mg/kg (repeat every 3-5 minutes) 
AND 
A: 0.9% sodium chloride (IV):Adult 2000mls, pediatrics 20mls/kg; if suspecting 
hypovolemia as a cause of the arrest 
AND 
A: dextrose 5% (IV) if needed to correct hypoglycemia 
OR 
C: dextrose 10%, 25% or 50% (IV) if needed to correct hypoglycemia 
AND 
C: sodium bicarbonate 1mmol/kg (IV) push (if needed to correct acidosis) 
*Additional medications maybe required depending on cause of the cardiac arrest (the
reversible cause)
Disposition 
Upon achieving return of spontaneous circulation (ROSC), definitive airway is achieved by 
performing endotracheal intubation for mechanical ventilation and patient must be admitted to the 
ICU or transferred to a facility with an ICU capacity. 
1.3 Approach to Stridor 
Stridor is an abnormal, high-pitched sound produced by turbulent airflow through a partially 
obstructed airway. Stridor is a dangerous finding and may indicate imminent airway obstruction. It 
can be inspiratory, expiratory or biphasic. 
 Clinical presentation: 
•
Hypoxia
•
Respiratory distress
•
Altered mental status
•
Inability to speak
•
Inability to swallow
 Differential diagnoses 
Infectious causes- croup, epiglottitis, peri-tonsillar abcess, retropharyngeal abcess 
Non- infectious causes- Foreign body obstruction, burns, trauma, anaphylaxis, malignancy, 
laryngotracheomalacia, stenosis 
Investigations 
Blood gases analysis, Lateral neck X ray (for foreign body, masses or soft tissue swelling), CXR 
(foreign body, evidence of aspiration), CT- scan, Blood Sugar, Lactate, Electrolyte analysis and/or 
Serum creatinine and urea  
Non pharmacological  
Keep the patient calm by allowing the patient to assume their most comfortable position. Give 
oxygen if there are signs of increased work of breathing. 
Pharmacological treatment 
A: adrenaline (nebulization) 0.5mls/kg 
AND  
A:  prednisolone (PO) 1-2mg/kg stat 
OR 
D: dexamethasone (PO) 0.6mg/kg stat 

34!
Referral: All patients with stridor whom the cause has not yet been established must be referred to 
higher health facilities  
1.4 Approach to Upper Gastrointestinal Bleeding 
Upper GI bleeding is any GI bleeding originating proximal to the ligament of Treitz. 
 Clinical Presentation 
Hematemesis and coffee-ground emesis suggest a UGI source. On physical examination, vital signs 
may reveal obvious hypotension and tachycardia. Cool, clammy skin is an obvious sign of shock. 
Abdominal examination may disclose tenderness, masses, ascites, or organomegaly. Perform rectal 
examination to detect the presence of blood and its appearance, whether bright red, maroon, or 
melanotic. Other findings include, the presence of spider angiomas, palmar erythema, jaundice, and 
gynecomastia which may suggest liver disease while petechiae and purpura may suggest an 
underlying coagulopathy.  
Differential diagnosis 
Peptic ulcer disease, upper GI malignancy, oesophageal or gastric varices, esophagitis, Mallory-
Weiss tear, Boerhaave syndrome and arteriovenous malformation 
Investigations 
ABO Grouping and cross-matching, Complete Blood Count, Hemoglobin Level, Blood Urea Nitrogen 
and Creatinine, Electrolytes, (Sodium, Potassium, Calcium Chloride), PT, PTT, INR, Liver Function 
Tests, Lactate levels, Obtain an ECG in patients with underlying coronary artery disease and/or 
Bedside Ultrasound 
Non Pharmacological treatment 
Maintain ABCs, give oxygen if needed 
Pharmacological Treatment 
Give blood If severe pallor, ongoing bleeding, Hb < 5g/dl and Hb < 7g/dl (with active bleeding) 
•
Adults 2 units within 1hour and Paediatric 20ml/kg 1hour (whole blood) or 10ml/kg (pRBC)
•
If ongoing indication for blood, start transfusion in the following ratio:  1unit pRBCs
(20ml/kg in Paediatric): 1unit FFP (20mls/kg in Paediatric): 1unit PLT (20ml/kg in
Paediatric)
 Give 
A: 0.9% sodium chloride (IV) 
OR 
A: compound sodium lactate (IV); Adult 2000mls and Paediatrics 20ml/kg 
AND 
C: 
pantoprazole 
(IV); 
Adult 
80mg 
stat, 
then 
infusion 
8mg/hour 
for 
3days, 
Paediatrics1mg/kg stat (max 80mg) then infusion 1mg/kg/hour for 3days  
OR 
S: esomeprazole (IV) 40mg 24hourly for 3days 
For patients with suspected variceal bleeding give: 
S: octreotide (IV) Adult 50mg slow bolus, then infusion 50mcg/hour for 5days; 
Paediatrics1mcg/kg/hour (maximum 50mcg/hour) for 5days  
If features suggestive of cirrhosis; give 
C: ciprofloxacin (IV) 500mg 12hourly for 7days 
OR  
B: ceftriaxone (IV) 2g 24hourly for 7days 
DEFINITIVE CARE: Early Endoscopy and Intensive care unit admission (Refer Gastrointestinal 
disease chapter)  
Note 
Administer IV fluids (if signs of shock) – refer section on the management of shock 

35!
1.5 Approach to Seizure and Status Epilepticus 
Status epilepticus is a single seizure ≥5 minutes in length or two or more seizures without recovery 
of consciousness between seizures.Status epilepticus is a neurologic emergency, and treatment 
should be initiated in all patients with continuous seizure activity lasting more than 5 minutes.  
Clinical presentations 
•
Abrupt onset seizures
•
Altered mental status
•
Postictal drowsiness
•
Tongue biting
Differential diagnoses 
Epilepsy, meningitis, encephalitis, malaria, space occupying lesion, alcohol withdrawal, isoniazid 
toxicity, intracranial hemorrhage, metabolic abnormalities- hyponatremia, eclampsia, acute 
hydrocephalus. 
Investigations: 
Blood Glucose, Electrolytes: (Sodium, Potassium, Chloride, Magnesium and Calcium), ECG, 
Bedside ultrasound, Blood gases, Malaria Test, Serum creatinine and urea, Lactate levels, 
Pregnancy test (females), Toxicology screening and/orCT Head 
Non-pharmacological management 
•
Protect patient from injury (If possible place in left lateral position to reduce aspiration
risks), Don’t place tongue depressor
•
Perform both primary and secondary assessment and provide necessary interventions
•
Give Oxygen if needed
•
Do bedside random blood sugar test
•
Establish IV access for administration of anticonvulsants, if unable use the rectal route
•
Connect the patient to the cardiac monitor to obtain vital signs
Pharmacological management 
I.
Active seizure 0-5minutes
Supportive care: 
IV access, monitors, maintain airway, oxygen therapy. Check point-of-care glucose and provide: 
A: dextrose 5%(IV); if glucose is ≤ 3.5mmol/L 
AND 
A: diazepam (IV) 0.15-0.2mg/kg. Maximum 10mg (Rectal dose: 0.2-0.5mg/kg) repeat 
every 5 minutes up to 3 doses 
OR 
D: midazolam (IV): 0.1mg/kg repeat every 5 minutes up to 3 doses 
II.
Established Status Epilepticus 5-10 min
B: phenobarbitone (IV):  Adults 20mg/kg slowly (max 50mg/min); Paediatrics 20mg/kg
slowly (max 30mg/min) 
OR 
C: phenytoin (IV) Adults 20mg/kg slowly (max 50mg/min); Paediatrics 20mg/kg slowly 
(max 30mg/min) 
Consider INTUBATION if patient still seizing 
C: thiopental (IV):  Adult 3-6mg/kg loading dose then 25-100mg infusion as needed; 
Paediatrics 2-5mg/kg loading dose  
OR 
D: propofol (IV): Adults 2mg/kg loading dose then 2-10mg/kg/hour; Paediatrics 3mg/kg 
loading dose, then 7.5-18mg/kg/hr  
OR 
 
D: midazolam (IV): Adult 0.2mg/kg loading dose then 0.1-0.2mg/kg/hour; Paediatrics 
0.1mg/kg then infusion 0.06 – 0.4mg/kg/hour 
 
Disposition:Intensive care unit admission or refer to the higher health facility with ICU/HDU 
capacity 

36!
1.6 Approach to Altered Mental Status 
This is the acute alteration in brain function and may include alteration of arousal or awareness, 
thought content, memory or attention. 
Clinical presentation 
Depending on the cause but may include: agitated, Restlessness, Hemiparesis, visual deficit, 
dysphasia 
Differential diagnosis 
The mnemonic AEIOU TIPS is widely preferred in the emergency department when considering a 
broader differential. Alcohol/acidosis, Epilepsy/Electrolytes, Insulin/Inborn Errors of Metabolism, 
Oxygen/Overdose, 
Uremia, 
Trauma, 
Infection, 
Psychiatric/Poisoning, 
Stroke/Subarachnoid 
Hemorrhage/Shock 
Investigations 
POC Glucose, Rapid Malaria test, Blood gases, Serum Electrolytes, POC ECG, Bedside ultrasound, 
Serum Creatinine and Urea, Lactate, Complete Blood Count, Liver function tests, Head CT-scan, 
Chest Xray and/orToxicology screening (If highly suspiciousness of intoxication) 
Non pharmacological treatment: 
•
If aggressive/ restless consider restraining- mechanical or chemical (medications)
•
Obtain set of vital signs including random blood glucose
•
Perform both primary and secondary assessment and provide necessary interventions.
•
Give Oxygen if Hypoxic or dyspnoeic
•
Connect the patient to the cardiac monitor to obtain vital signs
 Pharmacological treatment 
A: diazepam (IV):Adult 5-10mg loading dose, maintenance 0.03-0.1mg/kg every 30 
minutes to 6 hours; Paediatrics 0.1-0.15mg/kg stat, may repeat after 3-5 minutes 
OR 
B: haloperidol (IV): Adult 0.5-10mg *** (If concerned about psychiatric disorder)Child: 
safety and effectiveness not established 
OR 
B: ketamine (IV) 1-2mg/kg and 2-4mg/kg for IM 
OR 
D: midazolam (IV): Adults 5mg stat, maintenance 20-100mcg/kg/hr. infusion; Paediatrics 
0.05-0.1mg/kg stat 
Note 
Additional pharmacological treatment will depend on the cause of the altered mental status 
Consult/refer to a higher center with a psychiatrist if concerned about psychiatric disorder 
1.7 Approach to Difficult in Breathing 
Shortness of breath or breathlessness may result from a range of pulmonary, cardiac and central 
nervous system causes. It is important to look for the underlying cause for immediate intervention. 
Clinical presentation 
•
Increased work of breathing
•
Altered mental status
•
Diaphoresis
•
Additional souds- stridor, wheezes
Differential diagnosis 
•
Pulmonary embolism
•
Pulmonary oedema
•
Myocardial infarction
•
Asthma
•
Anaphylaxis
•
Airway obstruction
•
Tension pneumothorax

37!
•
Cardiac tamponade
•
Acute chest syndrome
•
Pneumonia
•
Pericarditis
Investigations 
Blood gases, Serum Electrolytes, Serum Creatinine and Urea, Troponins, Chest X-ray, POC ECG, 
Bedside Ultrasound, Lactate, Troponin, Random blood glucose  
Non pharmacological treatment 
•
Perform both primary survey (ABCs) and secondary survey and provide necessary
interventions
•
Obtain Vital signs
•
Position the patient
•
Give Oxygen if hypoxic or increased work of breathing
 Pharmacological treatment 
Pharmacological management will depend on the underlying cause of difficulty in breathing. (Refer 
Asthma-respiratory chapter and Acute chest syndrome and Pulmonary embolism-
hematology chapter) 
1.8 Anaphylaxis 
Anaphylaxis is a severe, life-threatening, generalised or systemic hypersensitivity reaction 
characterised by rapidly developing life-threatening airway (pharyngeal or laryngeal edema) and/or 
breathing (bronchospasm and tachypnea) and/or circulation (hypotension and tachycardia) 
problems usually associated with skin and mucosal changes. 
Clinical presentation 
•
Hives
•
angioedema
•
wheezes
•
Difficult breathing
•
Diarrhoea
•
Hypotension
Anaphylaxis is a clinical diagnosis and should be suspected when: 
•
Acute onset involving skin, mucosal tissue with either respiratory compromization or blood
pressure reduction (or syncope)
•
Hypotension after exposure to a known allergy for the patient (SBP <90mmHg or >30%
from baseline)
•
Respiratory compromise (i.e dyspnoea, stridor, wheeze, hypoxemia)
•
Exposure to a likely allergen causing involvement of the skin, mucosal, respiratory
compromization or blood pressure reduction
Investigations 
Blood gases, Serum Electrolytes, POC ECG, Troponin, CXR and/or POC USS 
Non pharmacological management 
•
Perform both primary and secondary assessment. If patient has signs of severe respiratory
distress perform early intubation/surgical airway
•
Give oxygen if hypoxic (spO2 below 95%) or severe respiratory distress
•
Insert TWO large bore IV cannulas or obtain intraoseous access
Pharmacological Management 
A: adrenaline (IM): Adult 0.3-0.5mg (maximum 0.5mg) every 5-15min as soon as possible. If 
inadequate response, start adrenaline (IV) 2-10mcg/min in 0.9% sodium chloride (IV) OR 
Ringer lactate (IV) 1-2 litres. If hypotensive. Repeat IV fluids as needed; Paediatric 0.01mg/kg, 
every 5-15min as soon as possible.  If inadequate response, start adrenaline (IV) 0.05-
1mcg/kg/min in 0.9% sodium chloride (IV)ORcompound sodium lactate (IV) 20mls/kg if 
hypotensive. Repeat IV fluids as needed 

38!
OR 
A: hydrocortisone (IV)200mg stat 
OR 
B: salbutamol (nebulisation) 10mg and equal volume of water for injection (This is useful to 
patients with refractory bronchospasm).   
OR  
D: methylprednisolone (IV) 1-2mg/kg/day 
Disposition 
All patient with severe and moderate symptoms which required repeated doses of adrenaline or 
didn’t respond to treatment must be admitted or referred to higher health facility. Those with mild 
response which responded to IM adrenaline may be discharged after 4 hours’ observation at the 
health facility. 
1.9 Cardiac Tamponade 
Cardiac tamponade is the result of compression of the myocardium by fluid, gas, pus, blood, or a 
combination of substances. It occurs in a physiologic continuum reflecting the amount of fluid, the 
rate of accumulation, and the nature of the heart.  
The result is increased pericardial pressure, which causes decreased ventricle compliance and 
decreased flow of blood into the right ventricle which eventually leads to a decreased cardiac output. 
Conditions that may predispose a patient to pericardial effusion and tamponade include; trauma, 
radiation exposure, Tb pericarditis, renal failure (uremic pericarditis), autoimmune diseases, drugs 
that induce a lupus-like syndrome, hypothyroidism, or ovarian hyperstimulation syndrome.  
Clinical presentations 
•
Chest pain and dyspnea
•
Pulsus paradoxus >10 mm Hg
•
Beck’s triad includes low blood pressure, elevated jugular venous distention, and
decreased heart sounds.
•
In the absence of hypotension and tension pneumothorax in a patient with PEA, consider
the diagnosis of cardiac tamponade.
 Investigations 
Bedside ultrasound, POC ECG, Blood gases, Serum Electrolytes, Troponins, Pericardial fluid 
analysis- biochemistry, microbiology and cytology, Serum creatinine and urea and/or Chest Xray 
Non pharmacological and pharmacological treatment 
•
Perform both primary and secondary assessment and provide appropriate interventions.
•
Give oxygen if hypoxic or increased work of breathing
•
Connect the patient to a cardiac monitor and obtain vital signs
•
Pericardiocentesis is the definitive management
Pharmacological treatment 
A: 0.9% sodium chloride (IV): Adults 1-2 lts, Paediatrics 20ml/kg) to increase right sided 
filling pressure 
Disposition 
All patients with cardiac tamponade require inpatient management in an intensive care unit 
setting/HDU.  
1.10 Pulmonary Edema 
Life threatening condition that occurs due to abnormal fluid build-up in the lungs leading to impaired 
gaseous exchange, acute respiratory distress and may cause respiratory failure. Can be classified 
as cardiogenic pulmonary edema; due to increased hydrostatic pulmonary pressure (HF) and Non 
cardiogenic pulmonary edema; due to increased permeability (acute lung injury and allergic 
alveolitis). 

39!
Note 
Cardiogenic and non-cardiogenic pulmonary edema have no clear cut differences in clinical 
presentation, however identifying the specific underlying cause of pulmonary edema is 
significant for therapeutic and prognostic purposes. 
Clinical presentation 
Shortness of breath, use of accessory muscles, diaphoresis, tachypnoea and crepitations 
Investigations 
Chest X-ray, Blood gases, Serum Creatinine and Urea, POC ECG, POC troponin, Serum 
electrolytes and/orBedside Ultrasound 
Non Pharmacological management 
•
Perform both primary and secondary assessment and provide necessary interventions
•
Give high flow oxygen therapy
•
Put patient on cardiac monitor (if available) and obtain vital signs
•
Position patient at 45° angle or sitting upright position
•
Perform ECG (rule out ischemia, dysrhythmia)
•
Perform bedside ECHO (to rule out cardiac causes- contractility, pericardial effusion)
•
Perform chest ultrasound (comet tails and B lines)
Pharmacological management 
Control hypertension (for SBP>90mmHg) 
S:  nitroglycerin (IV): Adult loading 100mcg/min titrate rapidly to 400mcg/min over 2 
minutes 
CAUTION! 
Beware of preload sensitive condition example inferior or right ventricular myocardial infarction, 
phosphodiesterase inhibitors use 
Reduce intravascular volume if fluid overloaded 
B: furosemide (IV/IM):  0.5-1mg/kg over 20minutes (maximum 120mg) or infusion IV 5-10mg/kg 
(maximum 120mg)  
CAUTION! 
Beware of renal insufficiency and volume depleted patients, check size of IVC 
Ventilation 
Oxygen therapy (target saturation>95%); CPAP or BiPAP (for persistent respiratory distress, 
hypoxia or acidosis despite high flow oxygen therapy); Intubation and mechanical ventilation (for 
respiratory failure despite CPAP/BiPAP) 
 Disposition 
Goal of treatment - Relieve hypoxemia (improve oxygenation); Reduction of pulmonary capillary 
pressure and improve perfusion.Admit all patients with pulmonary edema to HDU/ICU or transfer the 
patient to a health facility with ICU/HDU capacity 
1.11 Approach to Shock 
Shock is a state of acute circulatory failure leading to decreased organ perfusion, with inadequate 
delivery of oxygenated blood to tissues and resultant end-organ dysfunction and it is an emergency 
condition. Adherence to evidence-based care of the specific causes of shock can enhance a 
patient’s chances of surviving. 
Clinical presentation 
•
Low blood pressure (systolic BP below 80 mmHg) is the key sign of shock
•
Weak and rapid pulse
•
Rapid and shallow breathing
•
Restlessness and altered mental state

40!
•
Weakness
•
Low urine output
Table 1.1: Types of shock & Additional Symptoms 
Type 
of 
shock 
Description 
Additional 
symptoms 
Initial Management 
Hypovolemic 
Most 
common 
type of shock 
Primary cause is 
loss of fluid from 
circulation due to 
haemorrhage, 
burns, 
diarrhoea 
etc. 
Weak 
thread 
pulse, cold and 
clammy skin. 
-Ensure patency of the airway
- assess breathing and administer oxygen if
indicated
-Place two large bore cannula and initiate 2lts of
saline/crystalloids 
(20mls/kg 
in 
pediatrics).
Reassess after giving fluids
- Assess for mental status
-blood products (RBC,plasma,platelets) 1:1:1 if no
improvent then refer
Cardiogenic 
shock 
Caused 
by 
the 
failure of heart to 
pump 
effectively 
e.g. in myocardial
infarction, cardiac
failure etc. systolic
blood 
pressure
less than 80 or
90mmhg
Distended neck 
veins, weak or 
absent pulses 
-Ensure patency of the airway
- Assess breathing and administer oxygen if
indicated
-Place two large bore cannula and AVOID giving
IV fluids, if needed give small volume (adult:
250mls-500mls and pediatrics: 5mls/kg)
- Assess for mental status
-
Inotropes (Dobutamine 2-20mcg/kg/min or
vasopressor (Dopamine 1-50mcg/kg/min)
- Give blood if needed
Septic shock 
Caused 
by 
an 
overwhelming 
infection, leading 
to vasodilatation. 
Elevated body 
temperature 
-Ensure patency of the airway
- Assess breathing and administer oxygen if
indicated
-Place two large bore cannula and initiate 2lts of
saline/crystalloids (20mls/kg in pediatrics)
- Assess for mental status
-Empirical antibiotic therapy within 1hr
Neurogenic 
shock 
Caused by trauma 
to the spinal cord, 
resulting 
in 
sudden decrease 
in 
peripheral 
vascular 
resistance 
and 
hypotension. 
Warm and dry 
skin 
-hypotension
-bradycardia
-hypothermia
-Ensure patency of the airway
- Assess breathing and administer oxygen if
indicated
-Place two large bore cannula and initiate 2lts of
saline/crystalloids (20mls/kg in pediatrics)
- Assess for mental status
-
Inotropes (Dobutamine 2-20mcg/kg/min or
vasopressor (Dopamine 1-50mcg/kg/min)
- Give blood if needed
Anaphylactic 
shock 
Caused by severe 
allergic reaction to 
an 
allergen, 
or 
drug. 
Bronchospasm, 
angioedema 
and/or Urticaria 
Refer anaphylaxis section 
 Investigations 
The following investigations can be performed depending on the type of shock 
•
Basic serum chemistry (including renal function)
•
Liver function tests
•
Blood culture
•
POC Ultrasound- lungs, IVC, Cardiac
•
Echocardiography
•
CSF analysis if a patient is suspected with meningitis
•
Troponins
•
Blood gases
•
Serum Electrolytes
•
Lactate
•
Hb Level

41!
Non-pharmacological Treatment 
Prompt diagnosis of underlying cause is essential to ensure optimal treatment. 
•
Perform ABCD approach. Intervene when needed
•
Maintain open airway
•
Administer oxygen with face mask and if needed after intubation with assisted
ventilation
•
Check for and manage hypoglycemia
Pharmacological Treatment 
Treatment depends on the type of shock. Intravenous fluid therapy is important in the treatment of 
all types of shock except for cardiogenic shock. 
A: 0.9% sodium chloride (IV): Adultgive 2 litres bolus infusion. Repeat bolus until blood 
pressure is improved. Transfuse blood and plasma expanders in hemorrhagic shock. 
Paediatrics give 20ml/kg as a slow infusion. 
All children with shock which is not obviously due to trauma or simple watery diarrhea should receive 
antibiotic cover for probable septicemia. 
If the pressure doesn’t improve after two bolus of IV Fluids (4lts in adults and 40mls/kg in 
pediatrics), administer Ionotropes/vasopressors (Refer Sepsis and septic shock topic section) 
CAUTION! 
•
Do not administer calcium containing fluids, e.g. Ringer Lactate, within 48 hours of
administering ceftriaxone
•
Do not administer IV fluids in case of cardiogenic shock but maintain IV line
•
If patient develops respiratory distress, discontinue fluids but maintain IV line
•
Ceftriaxone is contra-indicated in neonatal jaundice
Referral: Refer the patient urgently with the escort of a nurse to high level facility to establish 
the cause and address all medication given in the referral letter. 
1.12  Sepsis and Septic Shock 
Septicaemia (Sepsis) is defined as life-threatening organ dysfunction caused by a dysregulated host 
response to bacterial infection (commonly) and fungal or viral infections (leastly).  Organ dysfunction 
can be represented by an increase in the Sequential [Sepsis-related] Organ Failure Assessment 
(SOFA) score of 2 points or more, with an in-hospital mortality greater than 10%.  
Septic Shock is defined as a subset of sepsis in which particularly profound circulatory, cellular, and 
metabolic abnormalities are associated with a greater risk of mortality than 40%. 
Clinical presentation 
•
Temperature of >38oC or <360C; Heart rate of >90/min; Respiratory rate of >20/min or
PaCO2 <32 mm Hg
•
Above features plus evidence of organ dysfunction (hypotension, jaundice, oliguria, or
altered state of consciousness from altered sensorium like drowsiness/lethargy
Investigations 
Blood gases analysis, Bedside ultrasound- accessing the inferior venacava and the lungs, POC 
ECG, Urine dipstick, Chest Xray- if suspecting pneumonia, Complete blood count, Qualitative or 
quantitative CRP or Procalcitonin in centres available, Serum Electrolytes, Creatinine and Urea, 
Liver function tests- liver enzymes, bilirubin, clotting time, Blood culture and antimicrobial 
susceptibility testing. Primary source of infection’s clinical sample culture (e.g. urine, pus, sputum, 
Note 
•
Septicaemia and septic shock are invariably fatal unless timely investigated and promptly
managed using specific antimicrobial therapies and other supportive management.
•
Identification of the primary source/focus of infection is mandatory to eliminate the infection
and ensure favorable treatment outcomes.Neonates may present atypically with inability to
feed, respiratory distress/cyanosis or abdominal distension.

42!
CSF etc) and antimicrobial susceptibility testing and/or RNA/DNA PCR for viral pathogens (where 
indicated) 
Diagnostic criteria 
Sepsis: Q-SOFA in settings with limited laboratory infrastructures: two or more SOFA score namely: 
Respiratory rate ≥22/min, Altered mentation and Systolic blood pressure ≥100 mm Hg) ± bacteria or 
fungal proven blood culture and susceptibility testing are recommended to make a definitive 
diagnosis.  
Septic shock:Sepsis diagnostic criteria above and vasopressor therapy needed to elevate MAP ≥65 
mmHg and lactate >2 mmol/L (18 mg/dL) despite adequate fluid resuscitation. 
Non-pharmacological Treatment 
•
Nutritional support
•
Control measures focused to the primary focus of infection.
•
Perform primary and secondary assessment and provide necessary interventions
•
Ensure patency of the airway and give oxygen if hypoxic or increased work of breathing
•
Connect the patient to the cardiac monitor and obtain vital signs
Pharmacological Treatments 
A: 0.9% sodium chloride (IV) (ADULT: 2litres; CHILD: 20mls/kg) 
OR  
A: compound sodium lactate (IV): Adult 2litres; paediatrics 20mls/kg) in 20minutes as first 
bolus followed by second bolus of 2litres/20mls/kg (use small boluses in CCF). 
OR   
S: dobutamine (IV) 2-20mcg/kg/min can be given for patients in shock not responding to 
fluids or when there is poor cardiac output.  
OR 
S: noradrenaline (IV) 5-20mcg/min for patients in septic shock not responding after 4litres 
of IVF to maintain the mean arterial pressure (MAP) of ≥ 65mm Hg  
AND  
A: hydrocortisone (IV) 200mg stat. 
Note: Transfuse blood  (If hemoglobin is < 7g/dl) 
Antimicrobial therapies (broad spectrum antibiotics must be started within the first hour): 
A: ampicillin (IV) 150-200mg / kg/day divided 6hourly a day 
AND  
B: cloxacillin (IV) 50-100mg / kg/day 6hourly a day 
AND 
A: gentamicin (IV) or (IM) 120mg [For children 7.5mg/kg] 24hourly for 5 days. 
 If no improvement in vital signs within 24 hours (Temp, HR, RR and altered state of consciousness), 
give: 
B: ceftriaxone (IV) 1 gm [For children 100 mg/kg (IV) or (IM)] 24hourly for 4-14 days 
AND 
A: gentamicin (IV) or (IM) 120mg [For children 7.5mg/kg] 24hourly for 5 days 
Refer immediately. 
D:  ceftriaxone +salbactum (FDC) (IV) or (IM) 75-120 mg/kg 24hourly for 4-14 days 
AND  
A: gentamicin (IV) or (IM) 120mg [For children 7.5mg/kg] 24hourly for 5days 
OR 
S**: piperacillin+tazobactum (FDC) (IV) (4g+0.5g) administered 8hourly [For children 100 
mg Piperacillin+12.5mg Tazobactam per kg body weight 8hourly] for 7-10days 
AND  
A: gentamicin (IV) or (IM) 120mg [For children 7.5mg/kg] 24hourly for 5days. 
Alternatively, (for patients who have evidence of not improving on the treatment above and referred 
to a zonal/tertiary hospital with judicious decision from a medical specialist or medical super-
specialist): 

43!
!
 
S**: meropenem 2g (IV) 8hourly in adults and adolescents [40 mg/kg 8hourly in children] 
for 7-14days 
OR 
S**: vancomycin (IV) 15 to 20 mg/kg body weight 8 -12hourly (not to exceed 2 g per dose) 
for 7-14days.  
 
Note 
In renal insufficiency vancomycin can be adjusted for dose and dose interval. These antimicrobial 
agents are usually reserved for Gram negative and Gram positive pathogen(s), respectively 
supported by culture and antimicrobial susceptibility testing 
 
For suspected co-existing anaerobic infections, an additional to all regimes above of  
B: metronidazole (IV) 500mg 8hourly [In children 7.5 mg/kg 8hourly] for 7days  
OR 
S: clindamycin 600mg-1.2g/day diluted infusion in two or three doses [In children 15-
25mg/kg/day in three equal doses] for 7-10days is recommended. 
 
For the rare cases of sepsis or septic shock due to carbapenem-resistant Gram negative 
bacteria or vancomycin-resistant Gram positive bacteria, give: 
S**: colistin (IV) 2.5-5mg/kg/day 8-12 hourly for 5days  
AND  
S**: linezolid (PO/IV) 400-600mg 12hourly for 10-14 days respectively or other non-beta 
lactam antibiotics may be considered based on culture and antimicrobial susceptibility 
testing results. 
 
In case there is/are risk factors for invasive Candida infections like in immunocompromised 
states, prolonged invasive vascular, necrotizing pancreatitis, then antifungal therapies should 
be added. 
C: fluconazole (IV) 800mg 24hourly on the first day then 400mg 24hourly for 14days [In 
children 6-12mg/kg/day for 14days]  
 
1.13  Approach to Pain 
 Pain is an unpleasant sensation or emotional experience associated with actual or potential tissue 
damage, or described in terms of such damage. Any pain of moderate or higher intensity is 
accompanied by anxiety and the urge to escape or terminate the feeling. Pain is subjective and 
unique perceptual experience with multiple dimensions that may not directly be observed by others 
or measured by physiological tests. Assesment is almost entirely self-reported. 
 
Assessment of pain. 
Self-report is the key to pain assessment. In non- or pre verbal children, facial expression is the 
most valid indicator of pain; therefore, use faces pain scale to assess severity. Pain should be 
assessed by: 
• 
Duration 
• 
Severity, e.g. does the patient wake up because of the pain 
• 
Site 
• 
Characteristics, e.g. stabbing, throbbing, crushing, cramp like 
• 
Persistent or intermittent 
• 
Relieving or aggravating factors 
• 
Accompanying symptoms 
• 
Distribution of pain 
• 
In children pain can be assessed by child’s crying voice, posture, movement and colour 
1.13.1 Approach to Chest Pain 
The approach to non-traumatic chest pain requires early recognition of life threatening conditions. 
Patients with life threatening conditions may have stable initial vital signs. 
For a patient presenting with chest pain, the following are the list of differential diagnoses 
• 
Acute coronary syndrome 
• 
Cardiac tamponade 
• 
Pericarditis 
• 
Myocarditis 
• 
Myocardial infarction  
• 
Aortic dissection 

44!
!
• 
Pulmonary embolism 
• 
Tension pneumothorax 
• 
Acute chest syndrome (sickle cell 
patients) 
• 
Lung infection (pneumonia) 
• 
Esophageal perforation 
• 
Reflux Esophagitis 
• 
Musculoskeletal pain 
 
Investigations 
Depending on the clinical presentation, the following investigations maybe required:  
POC ECG, Bedside USS-(cardiac, lungs, pleural, IVC, Abdominal aorta, kidneys etc),Serum 
electrolytes, POC Troponin, Blood gases, Serum creatinine and urea, Urine pregnancy test, 
Radiological investigations- Chest X-ray and/or CT scan- chest. 
Pharmacological Treatments 
Treat the underlying cause as indicated in specific chapters. The following analgesia may be used to 
relieve the pain: 
A: paracetamol (PO) 1g6hourly for 24hrs 
OR 
A: ibuprofen (PO )400mg 8hourly for 24hours 
OR 
A: diclofenac (IM) 50-100mg stat  
 
For those patients who are unable to take oral medications 
B: tramadol (IV) 50-100mg stat 
OR 
C: morphine (IV) 0.1mg/kg stat 
OR 
D: paracetamol (IV) 1g stat 
 
If myocardial ischemia is highly suspected give:  
                   A: acetylsalicylic acid (PO)325mg stat  
AND  
D: clopidrogel (PO) 300mg stat 
 
Referral: Refer to higher facility with expertise when failed to establish the cause of the chest pain. 
1.13.2 Approach to Abdominal Pain 
Abdominal pain is among the common complaints of patients presenting to the Emergency 
Department. While majority have benign and self-limited etiology, the goal is to identify those with 
serious or life threatening etiologies so as to perform early intervention. 
Differential Diagnoses: 
Surgical causes: 
• 
Abdominal aortic aneurysm 
• 
Mesenteric ischemia 
• 
Perforation 
(PUD, 
bowel, 
esophagus, appendix) 
• 
Intestinal obstruction 
• 
Upper GI bleeding 
• 
Lower GI bleeding 
• 
Splenic rupture 
• 
Acute appendicitis 
• 
Pancreatitis 
• 
Gallbladder diseases 
 
Genito-urinary causes 
• 
Ectopic pregnancy 
• 
Torsion (Testicular, ovarian) 
• 
Dysmenorrhoea 
• 
Endometriosis 
• 
Ureteric and kidney stones 
• 
Urinary tract infection 
• 
Pelvic inflammatory disease 
 
Medical causes 
• 
Myocardial infarction 
• 
Peptic ulcer disease 
• 
Gastro esophageal reflux disease 
• 
Inflammatory bowel syndrome 
• 
Gastritis 
• 
Hepatitis
Investigations 
Depending on the clinical presentation, the following investigations may be required: 

45!
!
ECG, Bedside USS- (gall bladder, liver, lungs, IVC, Abdominal aorta, kidneys etc), Serum 
electrolytes, Troponin, Blood gases, Lactate, Serum Creatinine and Urea, Urine pregnancy test, 
Radiological investigations (Chest and Abdomen X-ray and/or CT scan- Abdomen). 
Pharmacological Treatments 
For pain control, the following analgesia maybe used: 
A: paracetamol (PO)1g 6hourly for 24hours  
OR 
A: diclofenac (IM) 50-100mg stat. 
OR 
A: hyoscine butyl bromide (PO) 10mg 8hourly for 24 hours 
 
For those patients who are unable to take oral medications 
B: tramadol (IV) 50-100mg stat 
 
 
OR 
C: morphine (IV) 0.1mg/kg stat 
OR 
B: hyoscine butyl bromide (IM) 10mg stat 
 
 
OR 
D: paracetamol (IV) 1g stat 
 
1.13. 3 Headache 
Approach to acute headache 
Headache is a challenging complain as it requires balancing symptomatic control with rapid 
assessment for life threatening diagnoses. Headaches can be categorized into primary and 
secondary. Primary causes are neurologic and include: tension, cluster and migraine. Secondary 
headaches are as a results of an underlying pathological process such as malignancies, infections 
and other organic causes. 
Differential diagnoses 
Sudden onset severe headache 
• 
Subarachnoid hemorrhage 
• 
Cerebral venous thrombosis 
• 
Hypertension emergency 
• 
Adrenal and pituitary emergencies 
 
Altered:
• 
Meningitis 
• 
Encephalitis 
• 
Intracranial tumor 
• 
Space occupying lesions 
• 
Stroke 
• 
Subarachnoid hemorrhage 
• 
Hypoglycemia 
• 
Fever 
• 
Meningitis 
• 
Malaria 
• 
Brain abscess 
  
Investigations 
Will be specific basing on the clinical presentation of the patient. These may include: 
• 
Malaria test 
• 
Random blood glucose test  
• 
Blood Gases 
• 
POC Urine dipstick  
• 
Urinalysis 
• 
CSF analysis 
• 
POC ECG 
• 
Bedside USS 
• 
Serum Electrolytes 
• 
Serum Creatinine and Urea 
• 
POC Lactate  
• 
Urine pregnancy test 
• 
Radiological investigations- X-ray, 
CT scan 
Pharmacological Treatment 
A: paracetamol (PO): Adult 1g 8hourly for 3days; Paediatrics 15mg/kg 6hourly when 
required to a maximum of 4doses per 24hours 
OR 
A: ibuprofen (PO): Adult 400mg 8hourly for 3days; Paediatics   5–10mg/kg 8hourly for   
24hours 

46!
For severe pain or if the patient is unable to take orally, IV/ IM analgesia administration may be 
administered. These includes: 
For those patients who are unable to take oral medications 
B: tramadol (IV) 50-100mg stat 
C: morphine (IV) 0.1mg/kg stat 
D: paracetamol (IV) 1g stat 
1.13.4 Other Pains 
Other pains may include: 
•
Generalized body ache
•
Joint pain
•
Pain due to local infections
•
Pains due to injury
•
Eye pains
•
Ear pains
Non-pharmacological and Pharmacological Treatments 
Perform the primary and secondary assessment with interventions when needed. 
For generalized pain give analgesics, advise the patient to rest and make a follow-up. For joint, 
infections, injury, eye and ear pains treat as for main disease. 
CAUTION! 
•
Do not use acetlysalicylic acid for abdominal pain or if a patient is vomiting or has nausea
and do not use acetlysalicylic acid in children below 12years. Patients with peptic ulcers
should not be given acetlysalicylic acid tablets.
•
Refer the patients when pain persists despite of medication given for pain relief for further
investigation.
Referral:  
Refer patients if: 
•
Children with moderate and acute severe pain
•
No response to oral pain control
•
Uncertain diagnosis
•
All acute abdominal pain accompanied by vomiting and no passing of stool
•
Pain requiring definitive treatment for the underlying disease
•
Pain requiring opioids
1.14  Approach to Fever (Pyrexia) 
Fever is abnormal elevation of body temperature that occurs as part of a specific biologic response 
that is mediated and controlled by central nervous system and is usually a symptom of an infection. 
It is characterized by an elevation of body temperature above the normal range of 36.5–37.5 0C
 Clinical presentation 
•
Depression
•
Lethargy
•
Anorexia
•
Sleepiness
•
Hyperalgesia
•
Inability to concentrate
•
Feeling cold
•
Increased muscle tone
•
Shivering
•
Irritability
Note 
Fever alone is not a diagnosis 
 Investigations 
Will be specific basing on the clinical presentation. These may include: 
•
Rapid Malaria test
•
Blood slide for malaria parasites
•
POC Urine dipstick
•
POC ECG
•
Bedside USS- Gall bladder, Liver,
spleen, Abdominal aorta, kidneys
etc
•
Serum Electrolytes
•
Serum Creatinine and Urea

47!
!
• 
Radiological investigations- X-ray, 
CT scan 
• 
Complete blood count  
• 
Lactate 
 
Non-Pharmacological Treatment 
• 
Perform both primary and secondary assessment. Intervene whenever necessary. 
• 
Advise patient for bed rest 
• 
Ask patient to take plenty of fluids (If able to take orally) 
 
Note 
• 
In children, temperature >400C need urgent lowering. However, lukewarm sponging and 
evaporative cooling are not recommended.  
• 
Fevers caused by virus are usually self-limiting but all other fevers need treatments. 
 
Pharmacological Treatment 
Give antipyretic medicines: 
A: paracetamol (PO): Adult1g 6hourly when required, Paediatrics 15mg/kg 6hourly when 
required OR suppository 125mg–250mg, 6hourly 
OR 
A: ibuprofen (PO): Adult 400mg 8hourly when required; Paediatrics 5-10mg/kg 8hourly 
when required 
 
For patient who are unable to take oral medications, give: 
D: paracetamol 1gm (IV) 
 
Referral 
Refer the patient to the next facility with adequate expertise and facilities. 
• 
If no diagnosis is established 
• 
If no improvement of fever after the use of antibiotics 
• 
Fever that recurs 
1.15  Cough 
Cough is a common reflex action that clears the throat of mucus, allergens, dusts or other foreign 
irritants. A cough can be caused by several conditions both temporary and permanent. Frequently 
coughing indicates the presence of disease. 
 
Characteristics of cough/sputum 
• 
If cough is dry without sputum and fever, it is probable an allergic condition or mild 
upper respiratory illness (e.g. allergic rhinitis or allergic bronchitis)  
• 
If cough is dry without sputum or fever and is associated with other congestive 
symptoms it may be due to Congestive Cardiac Failure (CCF) 
• 
If it is a repeated attack cough with wheezing but without fever, it is likely to be 
bronchial asthma 
• 
If it is a cough with fever, rapid breathing and chest in-drawing, it is likely pneumonia 
• 
If it is cough with sputum which is yellowish pus-like and there is fever, it is likely 
acute bronchitis or pneumonia 
• 
If it is cough with blood in sputum and/or irregular fever with loss of weight and 
appetite, it is a suspected tuberculosis 
• 
If it is cough with large quantity of sputum, very foul smelling it is likely lung abscess 
or bronchiectasis 
 
Pharmacological Treatment 
Causative/precipitating factors e.g. CCF, asthma; allergies must be established and treated 
accordingly. (Refer respiratory disease condition chapter 9) 
 
Note 
Refer to high facility with expertise when cough persist and failed to establish the cause or when 
association with fever. 
 

48!
!
1.16 . Approach to the Trauma Patient  
 
 
 
 
 
 
Table 1.2: Approach to Trauma Patient 
PREPARATION 
Mobilise medical emergency team 
Prepare 
equipment, 
examples; 
monitors, 
ultrasound, Consider high-risk mechanisms of 
injury 
High Risk Mechanisms of Injury 
• 
High speed motor vehicle accident 
• 
Pedestrian accidents 
• 
Ejection   
• 
Fall > 3m in height 
• 
Penetrating injuries 
INITIAL RESUSCITATION 
Airway: Protect as appropriate and ensure Cervical-spine immobilization. 
Breathing: Give oxygen and titrate to SpO2 (above 92%). If no air entry or if hyper-resonance present, 
insert chest drain. If patient is showing signs of obstructive shock or deviated trachea, needle 
decompression can be used initially before definitive decompression with a chest drain. 
Circulation: Insert 2 large bore IV Cannula. Resuscitate with crystalloid solutions according to BP. If not 
responding to crystalloids, patient should be resuscitated with blood. Control all external bleeding 
immediately. 
 
Disability: Check GCS and document this regularly to check for any changes in conscious state. 
Perform a brief neurological examination. Check pupillary response. Check RBG. 
 
Exposure: Expose patient to check for other injuries. Prevent against hypothermia. 
SECONDARY SURVEY 
HEENT – check for scalp 
haematomas, 
depressed 
skull fractures, facial bony 
tenderness, eye injuries, 
otorrhea, haemotypanum, 
tracheal deviation. 
Spine – Must log-roll 
patient 
and 
palpate 
spinous 
processes 
of 
C/T/L-spine and check 
for any tenderness or 
stepping. 
Chest 
– 
look, 
palpate, 
auscultate. Check for signs 
of 
pneumothorax, 
haemothorax, ribs fractures, 
flail 
chest. 
If 
failing 
to 
ventilate 
or 
oxygenate, 
consider NIV or intubation. 
Pelvis 
– 
careful 
examination for bony pelvic 
ring movement. If concerns 
re pelvic fractures, a pelvic 
binder (sheet) must be 
placed on the patient. 
Abdomen 
– 
careful 
examination 
for 
guarding / tenderness / 
bruising in all quadrants. 
Ensure 
FAST 
examination performed 
in all trauma patients. 
Extremities – examine all 
peripheries for bony injury, 
compartment 
syndrome, 
muscular or soft tissue 
damage, 
neurological 
changes. 
 
CHECKLIST :( Before patient leaves EMD) make sure: 
• 
Airway is patent/protected 
 
 
• 
Tension pneumo-haemothorax? Sp02>92% 
• 
Large-bore IV placed and fluid given 
 
• 
Control of external bleeding 
• 
Pelvic fracture assessment done  
• 
Assessment for internal bleeding done 
• 
Spinal immobilization done 
 
 
• 
Neurovascular status of all limbs assessed 
• 
Does the patient need chest tube, NGT or catheter? 
 
 
 
1.17  Approach to Dehydrated Patient 
It refers to the loss of body water, with or without salt at a rate greater than the body can replace it. 
The cause of dehydration is a combination of physiological and disease processes. Persons at 

49!
greatest risk for dehydration include persons with diarrhoea, vomiting, fever, diabetes or infections, 
impaired level status.  
Table 1.3: Types of Dehydration 
Mild 
Moderate 
Severe 
Consciousness 
Is normal 
May be irritable but is 
conscious 
Unconscious 
Skin pinched up 
Becomes 
normal 
immediately 
Takes two seconds for 
folds to disappear 
Remain in folds for 
over two seconds 
Eyes 
Moist 
and 
tears 
are 
present 
Sunken, tears and/or 
absent 
Sunken and tearless 
Mouth 
Not dry 
Is dry 
Is dry 
Urine output 
Decreased 
Oliguria 
Oliguria/anuria 
Fontanel 
Normal 
Depressed 
Sunken 
Blood Pressure 
Normal 
Normal but orthostasis 
Decreased 
Capillary refill 
2s 
2-4s
More than 4s 
Investigations 
•
Blood chemistry (to check
electrolytes, 
especially 
sodium, 
potassium, 
and 
bicarbonate levels) 
•
Blood urea nitrogen (BUN) and
creatinine
•
Bedside USS- IVC
•
Complete blood count
•
Urine specific gravity
•
Blood Gas analysis
•
Lactate
Other tests may be done to determine the cause of the dehydration (for example, blood sugar level 
to check for diabetes). 
Non-pharmacological Treatment 
•
Perform both primary and secondary assessment and provide the necessary interventions.
•
Give oxygen if hypoxic or increased work of breathing
•
Put TWO large bore IV cannulas for fluid resuscitations
The treatment for minor dehydration often considered the most effective, is drinking water and 
stopping fluid loss. 
Pharmacological Treatment 
In more severe cases, correction of a dehydrated state is accomplished by the replenishment of 
necessary water and electrolytes. 
A: oral rehydration salt (ORS) 
OR 
A: 0.9% sodium chloride (IV): Adult 1-2litres; Paediatrics 20mls/kg) 
OR 
A:compound sodium lactate (IV): Adult 1-2litres; Paediatrics 20ml/kg 
Remember to do reassessment after fluids resuscitations. If there is no electrolyte loss; give 
A: dextrose (IV) 5% 
If the underlying disease condition is diagnosed; treat as per specific condition in guidelines. 
Referral: Refer to high center with expertise if no improvement. 
Note 
•
Dehydration in Children refer to Plan A,B and C in IMCI guideline

50!
1.18  Hyponatremia 
Defined as serum sodium (Na+) levels less than 135mEq/L. It can be classified as: Mild 
hyponatremia (130-135 mEq/L), Moderate hyponatremia (125 -129 mEq/L), Severe hyponatremia (< 
125mEq/L). 
Clinical presentation 
Clinical signs generally will occur once levels are <125mEq/L. The following are symptoms related to 
hyponatremia: 
•
Nausea and vomiting
•
Fatigue
•
Dizziness
•
Headache or confusion
•
Tremulousness or seizures
•
loss of consciousness or coma
•
Cramps or muscle spasms
•
Irritability and restlessness
•
Weakness
•
Thirst and anorexia
Investigations 
Based on classification and patients’ clinical findings, the following investigations maybe necessary: 
•
POC RBG
•
Urine dipstick
•
Electrolytes
•
Creatinine and Urea
•
LFTs
•
Serum Osmolality
•
Urine Na+
•
Urine Osmolality
•
Thyroid profile
•
CT 
brain 
(suspected 
cerebral
process)
•
CXR 
(suspected 
pulmonary 
infection/edema – related to renal 
failure, CCF) 
Non-pharmacological Treatment: Nutritional measures adjusted to patients need 
-
Salt containing foods
-
Rehydration therapy
-
Dietary modification
The goal of acute management is treatment of serious complications and careful restoration of 
serum sodium concentration. Management depends on the cause, severity and time course. Based 
on duration of development, hyponatremia can be (i) acute or (ii) chronic 
Table 1.4: Pharmacological Treatment for Hyponatremia 
ACUTE HYPONATREMIA 
CHRONIC HYPONATREMIA 
usually symptomatic and onset <48 hours 
Symptoms: neurologic deficit, seizures, 
coma and confusion 
usually asymptomatic and onset > 48hours 
Requires immediate treatment 
Give: 
C: 3% sodium chloride (IV) at rate of 1-
2mEq/L/hr 
Alternative: 
C: sodium bicarbonate (IV) 8.4% 50ml over 
5min 
Do NOT raise serum Sodium by > 6mmol/L 
in 6hrs  
Stop 
infusion 
when 
symptoms 
have 
resolved 
Manage seizures and coma as appropriate 
No specific treatment if mild and asymptomatic 
If moderate to severe:  
Give:  
    A: 0.9% sodium chloride (IV) 
Do NOT raise serum Sodium by over 12mmol/L 
in the first 24 hours 
Stop 
correction 
when 
Sodium 
reaches 
130mEq/L 
Once symptoms have resolved 
Assess volume status using point of care Ultrasound (POCUS) for IVC as well as vitals 
assessment and quantify as either (i) Hypovolemic hyponatremia, (ii) Euvolemic hyponatremia 
and (iii) Hypervolemic hyponatremia 

51!
Severe Hyponatremia: (seizures, coma, signs of brainstem herniation), consider treatment for 
cerebral edema and elevated ICP; give: 
•
3% Sodium Chloride 3-5mls/kg over 15 to 60minutes to increase sodium by 2-4mmol/l
•
Close monitoring of Serum sodium initially hourly with target correction rate of no more
than 8-10mmol/l/day and less than 0.5mmol/l/hour over 1-2hours
Hypovolemic Hyponatremia: 
•
Determine Sodium deficit: Total body Sodium deficit = (Desired sodium – actual plasma
Sodium) x Total body water{0.6 x weight (kg) Men OR 0.5 x weight (kg) women}
•
Replace with 0.9% sodium chloride (IV)
•
Correct at no more than 0.5mmol/l/ hour
 Disposition 
Symptomatic Hyponatremia, Severe hyponatremiamust be admitted to the HDU/ ICUfor continuous 
biochemical and clinical monitoring. If not available refer the patient to a higher health facility with 
HDU/ ICU capabilities. 
1.19  Hypokalaemia 
Is defined as plasma potassium below 3.5mmol/l. It includes: Weakness, constipation, paralysis, 
bradycardiaand reduced tendon reflexes. 
Investigations 
POC ECG, serum creatinine and urea, serum electrolytes and/or bedside ultrasound 
Additional investigations may be required basing on the clinical presentation. 
Non-pharmacological Treatment 
•
Perform both primary and secondary assessment and provide necessary interventions
needed.
•
Give oxygen if hypoxic or increased work of breathing
•
Connect the patient to the monitor and obtain Vital signs
•
Place IV access
Possible causes: 
-Dehydration 
(vomiting, 
diarrhea, 
sweating, 
third 
spacing, 
hydration with hyperosmolar 
fluids) 
Possible causes: 
-Psychogenic polydipsia
-Iatrogenic
-Syndrome of inappropriate
ADH secretion)
Possible causes: 
-Renal Failure
-Cirrhosis
- Nephrotic syndrome
-Congestive Cardiac Failure
-MDMA (Ecstasy use)
-Hypothyroidism
-Psudohyponatremia
-Give 
compound 
sodium
lactate 
or 
0.9% 
sodium
chloride (IV) 250 – 500mls or
0.5-1ml/kg/hour (guided by
BP response)
-Prevent
further 
exacerbation
of 
hyponatremia
-Prevent
rapid 
overcorrection
-Insert Foleys catheter to
monitor output
-Nil per oral, restrict fluids
- Furosemide (IV) 40mg daily
until fluid volume is corrected.
Note 
•
Look for complications of over-correction such as Osmotic demyelination syndrome
(ODS)
•
Hyponatremia can also lead to cerebral edema which may lead to increased Intra
cranial pressure (ICP)
•
Exercise associated hyponatremia is common in athletes and the cause is over
hydration and not excessive water loss
•
Psychogenic polydipsia caused by over ingestion of large quantity of water in
psychiatric patients or those on SSRI’s.
(i) HYPOVOLEMIC
(ii) EUVOLEMIC
(iii) HYPERVOLEMIC

52!
!
Pharmacological management 
Mild (3.0-3.5mmol/l) 
C: potassium chloride (PO): Adult 20-40 mEq 8hourly (dissolved in 100-150mL water); 
Paediatrics 2 mEq/kg 8hourly diluted in oral fluids or food. In case of diarrhea, give ORS 
(5ml/kg/hr) 
Moderate (2.5-2.9mmol/l) 
C:potassium chloride (IV): Adult 10mEq/hour; Paediatrics 0.5 mEq/kg/hour diluted in 25-
50mls of 0.9% sodium chloride or DNS or 5% dextrose solutions via peripheral vein.  Do 
not exceed 10 mEq/hour. 
 
Severe (<2.5mmol/l) 
Both IV & Oral Replacement 
C: potassium chloride(PO): Adult (28mmol K+) per hour if tolerated (dissolved in 100-
150mL water) dilutedpotassium; Paediatrics (PO) 2mEq/kg 8hourly. 
OR 
C:potassium chloride (IV): Adult 20 mEq in 100mL fluid over 1 hour via cubital fossa vein. 
Continue to measure serum potassium every 1 to 2 hours until K+ > 2.8 mmol/L. 
Paediatrics 1mEq/kg/hour.  
 
The calculated hourly dose is multiplied by 12.5ml volume for dilution with NS/DNS/D5%. 
Do not exceed 10 mEq/hr 
 
Note 
• 
20 mEq of Potassium will raise K+ by 0.25 mEq/L. Aim to replace 25% of K+ deficit in 6 
hours 
• 
potassium chloride must never be given as IM or IV push 
• 
Oral potassium (Slow K) 600mg tab is equivalent to 8 mEq 
• 
Injection potassium chloride 7.5% 1ml = 1 mEq  
 
Role of Magnesium 
Magnesium should be checked. IF LOW, give Magnesium as follows: 
A: magnesium sulphate 50% (IV): Adult Initially give 4ml diluted to 10ml with 0.9% sodium 
chloride run over 20 minutes, then potassium chloride infusion, then magnesium sulphate 
50% (IV) 0.12ml/kg/day; Paediatrics 0.1 ml/kg/dose administered over 2hours 
 
Hypokalemia in CARDIAC ARREST in Adults: KCl 10 mEq IV over 5 min; the dose may be repeated 
once 
 
Note: ECG changes in hypokalemia 
• 
Increased P wave amplitude, Prolonged PR interval, 
• 
ST segment depression, 
• 
QT prolongation, flattening or T wave inversion, and prominent U waves. 
 
 
1.20  Triage Overview 
Triage is the process of determining the priority of a patient to medical care based on the acuity 
(severity of condition) and capacity of the system to address the condition, so as to 
optimizeoutcome. 
Importance of triage  
Triage enables quick identification of patients who need immediate attention, and can thus 
improve patient outcomes by avoiding potentialdelays. It helps in organizing, monitoring, 
evaluating and determining the department resources that patientsmight need. 
 

53!
Triage system 
The triage system is based on recommendation of Emergency Medicine expert’s basic principles of 
triage, which uses specific criteria to categorize patients into three main levels of acuity:  
•
Emergency: all patients with immediate life or limb threats who are deemed
salvageable, but likely to further decompensate without immediate intervention
will be triaged in thislevel. This category can also be labeled as RED
•
Priority:those seriously injured/ill patients with potential to decompensate if not
treated within 1 hour are triage as prioritycases. This category can also be
labeled as YELLOW
•
Queue: this level includes all the walking wounded or those with less serious
injury/sickness who are unlikely to decompensate. Patients in this category can
safely wait for their turn. However, they should be monitored as their conditions
may change and warrant immediatecare. This category is also labeled as
GREEN.
Figure 1. Summary of triage flow and timelines of care 

54!
Unresponsive 
Pregnant with Heavy bleeding 
Stridor 
Pregnant with Severe abdominal pain 
SpO2 <90% 
Pregnant with Seizures 
Respiratory distress or cyanosis 
Pregnant with Severe headache 
Weak pulse or Capillary refill>3 sec 
Pregnant with Visual changes 
Hear rate <50 or > 150 
Pregnant with SBP≥160 or DBP ≥110 
Heavy bleeding 
Pregnant with Active labour 
Active convulsions 
Pregnant with Trauma 
Hypoglycemia 
Age < 2years with Temp <36oC or > 39oC 
High-risk trauma* 
Child <14 with severe dehydration 
Poisoning 
or 
dangerous 
chemical 
exposure*  
Adult with signs of meningitis 
Threatened limb* 
Acute chest or abdominal pain (>50 years 
old) 
Snake bite 
ECG with acute ischaemia 
Violent or aggressive 
Other 
(state):____________________________ 
PRIORITY CRITERIA (Tick here if Yes) 
Vomits everything or ongoing diarrhoea 
(adult) 
Severe pain (no Red criteria) 
Unable to feed or drink 
Visible acute limb deformity 
Severe pallor 
Open fracture 
On-going 
bleeding 
(no 
emergency 
criteria)) 
Suspected dislocation 
Recent fainting 
Other trauma/burns (no Red criteria) 
Altered mental status (no emergency 
criteria)) 
Sexual assault 
Acute general weakness 
Acute testicular/ scrotal pain or priapism 
Acute focal neurology 
Unable to pass urine 
Acute visual disturbance 
Wheezing (no Red criteria) 
New rash worsening over hours or peeling 
(no emergency criteria) 
Exposure 
requiring 
time- 
sensitive 
prophylaxis 
(example: 
animal 
bite, 
needle-stick injury) 
Any infant 8 days to 2 months old 
Child below 14 years old with malnutrition 
Child below 14 years old with dehydration 
Child below 14 years old with ongoing 
diarrhoea 
Referral patient (no emergency criteria) 
Other, 
state: 
__________________________ 
QUEUE CRITERIA (Tick here if Yes) 
Patient with no Emergency or priority criteria indicated in above tables 
EMERGENCY CRITERIA (Tick here if Yes) 

55!
!
 
 
CHAPTER TWO 
ANAESTHESIA 
 
Anaesthesia is a state of controlled reversible loss of consciousness usually accompanied by 
analgesia, muscle relaxation, amnesia and areflexia. It is usually induced for the purpose of 
facilitating surgery and other therapeutic or diagnostic procedures. 
 
Anaesthesia may be achieved with either: 
• 
Regional anaesthesia alone e.g. spinal/epidural anaesthesia, arm block 
• 
General anaesthesia 
• 
A combination of regional and general anaesthesia 
• 
Regional anaesthesia with sedation 
• 
Local anaesthesia through topical application/spray or infiltration of local anaesthetics 
 
Note 
• 
Anesthetic medicines and sedatives MUST be provided by medical practitioners who are 
properly trained and have appropriate experience with their use 
• 
Medicines and equipment for resuscitation should be immediately available whenever 
general anaesthesia, regional anaesthesia or sedation is administered. 
 
2.1   General Anaesthesia 
Medicines used in general anaesthesia include the following pre-medications: 
Sedation and Anxiolytics 
A: diazepam (IV) 0.05 – 0.1mg/kg 
OR 
C: diazepam (PO) 0.5 – 0.75mg/kg 
 
 
 
OR      
C: lorazepam (IM) 0.05mg/kg or 0.04mg/kg (IV)  
OR 
D: midazolam (IV) 0.05–0.1mg/kg 
 
If there is an overdose with benzodiazepines use the following antidote: 
A: flumazenil (IV): 0.2mg stat over 30 seconds. Repeated dose of 0.2mg may be given at 
1minute intervals until desired level of consciousness is achieved; do not exceed 
4doses (1mg). 
 
If there is bradycardia, salivary secretion or other muscarinic side effects give 
A: atropine (IV) 0.01mg/kg 
 
OR 
S: glycopyrrolate (IV) 0.2–0.4mg (0.2mg for every 1mg of neostigmine). Alternatively, a 
dose of 10–15 µg/kg (0.01–0.015mg/kg) (IV) with 50 µg/kg (0.05mg/kg) neostigmine or 
equivalent dose of pyridostigmine 
Antiemetics are indicated for prevention of Post-Operative Nausea and Vomiting (PONV) 
B: dexamethasone sodium phosphate (IV) 4–5mg for PONV prevention 
 
 
OR 
C: metoclopramide (IV) 10mg  
 
 
 
OR 
S: ondansetron (IV)4mg administered over 2–5minutes 
Antacidsare given to patients at risk of aspiration, such as pregnant women, before Caesarean 
section. 
B: sodium citrate (PO) 0.3moles, 30ml. Not more than 30 minutes pre–induction of 
anaesthesia 
OR 

56!
!
C: pantoprazole (IV) 40 mg as soon as the possibility of surgery is known in cases of 
emergency procedures 
General anaesthetics are used for induction of anaesthesia as boluses or for maintenance of 
anaesthesia as continuous infusions in Total Intravenous Anaesthesia (TIVA). 
B: ketamine (IV) 1–2mg/kg (Forinduction, however can be used for maintenance under 
TIVA, but contraindicated in those who a significant rise in BP/IOP/ICP would constitute a 
serious hazard) 
 
 
 
OR 
C: thiopental (IV) 3–5mg/kg (For induction, however can be used for maintenance under 
TIVA) 
 
 
 
OR 
D: propofol (IV) 1.5–2.5mg/kg for induction of anaesthesia and 6–12mg/kg/hour infusion 
for maintenance in TIVA. 
propofol is contraindicted to Patients with risk of hypotension, use volatile agent for 
maintenance of anaesthesia  
 
 
 
OR 
S: etomidate (IV) 0.3mg/kg (between 0.2–0.6mg/kg) for induction (cardiostable, it affects 
cortisol production) 
 
Inhalational anaesthetic agents (for induction and/or maintenance) 
B: halothane 2–4% in air, oxygen or oxygen/nitrous oxide and maintenance 0.5–1.5% 
(Nitrous oxide is delivered in a ratio of 70:30 Mix with oxygen, reduce the requirement 
of a more toxic anaesthetic/ potent agent) 
 
 
OR 
B:  isoflurane1.2–2.5% titrates to desired effect 
 
 
OR 
S:  sevoflurane 5–7%  
Maintenance: 0.5–3% sevoflurane with or without the concomitant use of nitrous oxide.  
 
Muscle Relaxants 
B: suxamethonium (IV) 1–1.5mg/kg for induction 
OR  
C: pancuronium (IV) 0.04–0.1mg/kg for maintenance. 
OR 
S: atracurium (IV) 0.4–0.5mg/kg over 60 seconds followed by 0.08–0.1mg/kg 20–
45minutes after initial dose for maintenance or infusion at 0.05–0.1 mg/kg/min (For 
patients with renal impairment) 
OR 
S: rocuronium (IV) 0.6 -1 mg/kg can be used for induction if sugammadex (reversal agent) 
is available, it has minimal side effects, can be used in case suxamethonium is 
contraindicated. 
 
 
Contraindications 
Suxamethonium is contraindicated  in patients with risk for developing hyperkalaemia or with 
upper/lower motor neuron defect, prolonged chemical denervation, direct muscle trauma, tumour or 
inflammation, thermal trauma, disuse atrophy, severe infection 
 
Medicines for Reversal of Neuromuscular Blockade 
B: neostigmine (IV) 50µg/kg with atropine (IV), 20µg/kg (maximum 1.2mg)  
OR  
S: glycopyrrolate (IV)10 µg/kg  
 
 
OR 
S: sugammadex (IV) 2–4mg/kg  
 

57!
!
Analgesics for Pain Management in Peri–operative Period 
Non–Opiod Analgesics 
B: paracetamol (IV) 15mg/kg 8hourly  
Opioid analgesics 
 
B: tramadol (IM/IV) 50mg 6hourly 
OR 
C: morphine (IV/IM) 3–5mg as a single dose, then further boluses of 1–2mg/minute. 
                        Maximum dose of morphine 0.1–0.2mg/kg, and monitor vitals closely 
 
 
OR 
B: pethidine (IV/IM) 1–2mg/kg (used for analgesia during anaesthesia, and during labour) 
OR 
S: fentanyl (IV) 1–2µg/kg  
 
Antagonists of Opioids 
For opioid over–dosage 
B: 
naloxone 
(IV) 
0.4mg–2mg, 
alternatively 
may 
be 
given 
intramuscularly 
or 
subcutaneously. For reversal of opioid sedation initial dose 0.1–0.2mg (IV) at 2–3 
minutes’ intervals to the desired degree of reversal. 
2.2   Local Anaesthesia 
Medicines used as local anaesthetics cause revisable absence of pain sensation, although other 
senses are often affected as well. Also, when it is used on specific nerve pathways, paralysis can 
also be achieved.  
A: lidocaine (site): Maximum 4.5mg/kg without vasoconstrictors (adrenaline) or 7mg/kg 
with vasoconstrictors (Not for Spinal Anaesthesia) 
 
 
OR 
C: bupivacaine (site): 625µg/ml(0.0625%)1.25mg/ml(0.125%) 
 
 
OR 
C: bupivacaine + glucose: bupivacaine hydrochloride 5mg/ml (0.5%) with 80 mg/ml 
glucose (specific gravity of 1.026). The addition of glucose produces a hyperbaric 
solution relative to cerebrospinal fluid.  
 
Medicines for Local Anaesthetics Overdose 
S: Lipid emulsion (intralipid 20% or 30% solution) for severe local anaesthetic toxicity with 
cardiovascular or neurological impairment. 
Dose: 
1.5ml/kg (IV) over 1min, then continuous infusion 0.25ml/kg/min. Repeat bolus 1–2times 
for persistent cardiovascular collapse. Double infusion rate to 0.5ml/kg/min if BP remains 
low. Continue infusion for at least 10 minutes after cardiovascular stability attained. 
Recommended upper limit: approximately 10ml/kg lipid emulsion over the first 30 minutes. 
Epidural and combined spinal-epidural anaesthesia Techniques 
Epidural anaesthesia is a type of neuraxial anaesthesia; local anaesthetic (LA) is injected into the 
epidural space to anaesthetize the spinal nerve roots that traverse the space. Epidural anaesthesia 
is used for anaesthesia of abdominal, pelvic, and lower extremity procedures and, less commonly, 
thoracic procedures.  
 
A: lidocaine 1 to 2 %(Epidurally) 
 
OR 
C: bupivacaine 0.25 to 0.75% (Epidurally) 
 
 
Epidural Labour Analgesia (Local Anaesthetics, Adjuvant Drugs) 
D: bupivacaine 0.1-0.25% with or without Fentanyl 50 – 100µg (Epidurally).  e.g. 
(Bupivacaine 0.1% Plus Fentanyl 2µg/ml at   infusion rate of 0-12mls/hour)  
Peripheral nerve blocks 
Peripheral nerve blocks are widely used for surgical anaesthesia as well as for both postoperative 
and nonsurgical analgesia. 

58!
!
Blocks are often used to avoid the effects of alternative anesthetics or analgesics. The most 
common rationale for their use is to avoid side effects and complications of general anaesthesia 
(GA), particularly respiratory-related effects, and to provide analgesia while minimizing opioid use. 
 
Local Anaesthetics 
B:  lidocaine (Perineurally) 1 to 2%  
OR 
C: bupivacaine (Perineurally) 0.25 to 0.75%  
OR 
C:bupivacaine+glucose(Perineurally) 0.25 to .75%  
 
Adjuvants 
A: adrenaline (Perineurally) Typical Concentration 5-10µg  
OR 
B: dexamethasone (Perineurally) 4-10mg 
OR 
S: clonidine (perineurally) 0.5-2µg  
Topical Anaesthesia 
B: lidocaine gel (Topically) 2 to 5%  
OR  
B: lidocaine topical spray 2% and 10% solutions for topical anaesthesia of the upper 
airway (i.e., oropharynx and vocal cords), the trachea, and nasal passages.  
2.3 Sedation 
The aim of providing sedation is to reduce anxiety, agitation and pain so as to tolerate unpleasant 
medical procedures or intervention while the patient retains control of airway, breathing and blood 
pressure. This procedural sedation and analgesia is commonly used in emergency units, 
radiological /diagnostic units, dentistry and for certain endoscopic and gynaecological procedures. 
 
Minimal Sedation/Anxiolysis (no analgesic effect is required) 
A: diazepam (IV) 0.1mg/kg (In a 60kg patient, give boluses of 2mg every minute; may 
require up to 10mg)  
OR   
C: nitrous oxide inhaled 20 to 50%, in oxygen (will also provide some analgesia) 
OR 
D: midazolam (IV) 0.05mg/kg (In a 60 kg patient, give boluses of 1 mg every minute; may 
require up to 3mg) 
 
Medicines for moderate sedation & analgesia 
If analgesia is required, one of the above is usually combined with an opiate. However, ketamine 
has analgesic activity and can be used on its own or combined with a benzodiazepine. 
B: ketamine (IV) 0.5mg/kg. Repeat doses of 0.5mg/kg as required, every 5-10minutes 
OR 
C: morphine(IV) 0.1mg /kg in increments of 2mg every 5minutes 
OR 
S: fentanyl (IV) 0.25µg/kg  
 
Alternative medicines 
D: propofol (IV) 0.5mg/kg. Repeated as 0.25mg/kg boluses every 5minutes as required 
 
 
 
OR 
S: etomidate (IV) 0.1mg/kg. Repeat doses of 0.05 mg/kg (IV) every 5minutes, as required. 
But it is more likely to cause myoclonus  
 
Medicines for Deep Sedation & Analgesia: This is usually achieved with either higher doses of 
medications used for moderate sedation, or by combining an opiate, a benzodiazepine, and either 
Propofol or Etomidate. When agents are combined, lower doses may be adequate. 

59!
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Supplemental Analgesia: Simple analgesics can be given before or after the procedure: 
A: paracetamol (PO): 1g 4-6 hourly when required to a maximum of 4doses per 24hours. 
Maximum dose: 15mg/kg/dose. Maximum dose: 4 g in 24 hours. 
OR 
A: ibuprofen (PO) 400mg 8hourly with meals after the procedure. 
 
Note 
Sedation in intensive care 
• 
Indications for sedation in intensive care needs to be defined for each patient, and may include 
one or more of anxiolysis, analgesia, agitation control, or to help patients tolerate 
uncomfortable situations or procedures (e.g. intubation and ventilation) 
• 
Sedation requirements fluctuate rapidly so, it warrants regular review 
• 
Adequate pain control is often more efficacious than sedatives for reducing agitation. Delirium 
should be considered and managed appropriately.  
 
Short–term and long–term sedation 
Medicines for short–term sedation (less than 24 hours) 
C: midazolam (IV) 0.05–0.2mg/kg/hour. 
OR 
D: propofol (IV) 0.5mg/kg/hour.  
Due to high fat solubility, midazolam also becomes ‘long acting’ after infusions of more than 24 
hours 
 
Medicines for longer–term sedation (72 hours or more)   
C: lorazepam (IV) 0.1mg/kg/hour. 
OR 
D: midazolam (IV) 0.2mg/kg/hour.  
 
Lorazepam (0.1 mg/kg/hour) is as effective (and as easy to wean) as midazolam 0.2 mg/kg/hour) but 
more difficult to titrate. 
 
Supplemental analgesia 
C: morphine (IV) 0.1–0.2mg/kg/hour.  
OR 
S: fentanyl (IV) 1 µg/kg/hour (also becomes long acting after prolonged infusion due to fat 
solubility) 
2.4 Anaesthesiain Special Conditions 
2.4.1 Surgery in Diabetic Patient 
Diabetes leads to increased surgical morbidity, mortality and length of hospital stay. Perioperative 
Hyperglycemia is associated with increased risk of infection, medical complications and death. The 
following shall be considered:   
• 
Ideally, the elective patient should have a preoperative glycated haemoglobin less than 9% 
or blood glucose fasting 10 mmol/l of random 13 mmol/l.   
• 
Screen for nephropathy, cardiac disease, retinopathy and neuropathy and inform surgical 
team. 
• 
If on oral hypoglycemic therapy and well controlled and surgery is minor, omit therapy on 
morning of surgery and resume therapy when eating normally.  
• 
If on insulin adjust depending on the type of surgery and expected fasting period as 
follows:  
 
Minor surgery (duration < 3hours)   
Insulin: in the morning intermediate–acting insulin, 1/2 to 2/3 of total daily dose.   
• 
If blood glucose is above 20 mmol/l, give a small dose short–acting insulin.  
• 
In the evening give intermediate–acting insulin, 1/3 of daily dose.   
Fluid: 5% dextrose (IV), volume according to age. 

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Blood glucose monitoring: every 1–2 hours’ values between 10–14 mmol/l. 
 
Major surgery (duration > 3hours) Involve a general anesthesia and therefore a period 
of fasting.   
• 
Insulin and fluid: infusion solution containing 5% glucose and 20 mmol/l potassium 
chloride (maintenance volume)   
• 
Insulin infusion 0.05 IU/kg/hour. 
• 
Blood glucose monitoring: every 1–2 hours; values between 6–14 mmol/l, if < 5 
mmol/l reduce infusion rate, continue infusion therapy intraoperatively.   
• 
Post operatively: give 5–10% dextrose (IV) 1 Litre + 20ml potassium chloride + 2/3 of 
total daily dose of insulin over 8hours and repeat to maintain infusion therapy until 
food intake is re–established. 
 
2.4.2 Surgery in Hypertensive Patient 
• 
Monitor BP, scan monitors for HR, ECG rhythm, EtCO2, temperature 
• 
Provided the patient is adequately oxygenated & ventilated, deepen anesthetic 
• 
Examine patient: 
o 
Pupils (high ICP) 
o 
Diaphoresis & flushing (carcinoid, pheochromocytoma, hyperthyroidism) 
o 
Rigidity (malignant hyperthermia, serotonin syndrome) 
o 
Bladder distension 
o 
Hot (thyroid storm, malignant hyperthermia, serotonin syndrome) 
• 
Examine drugs & equipment: 
o 
Potential drug error 
o 
Possible TIVA or circuit disconnect (awareness) 
o 
Tourniquet (pain) 
o 
Equipment error (falsely high reading) 
Give 
C: hydralazine (IV) 5-20mg (max 30mg) slow IV push every 20minutes 
OR 
C: labetalol (IV) 5-20mg every10min (max total 300mg) 
OR 
S: esmolol (IV) 0.5mg/kg over 1minute; start infusion at 50mcg/kg/min 
OR 
S: nitroglycerin (IV) 50-100mcg; start infusion at 10mcg/min  
• 
Treat underlying cause i.e., pain.  
 
2.4.3 Surgery in Asthmatic Patient 
Considerations 
• 
Risk of perioperative respiratory complications: 
o 
Bronchospasm, mucous plugging, pneumothorax, atelectasis, pneumonia 
• 
Possible pulmonary hypertension & RV failure  
• 
Need for preoperative optimization: 
o 
Treatment of bronchospasm, infection, atelectasis 
• 
Avoidance of triggers & exacerbating factors: 
o 
Avoid general anesthesia, endotracheal intubation, histamine releasing 
medications, light anesthesia 
• 
Medication management: 
o 
Continue usual inhalers pre-operatively 
o 
Stress dose steroids (STEROID COVER) if recent high dose steroid use  
 
Severe Asthma Exacerbation Treatment Options  
Refer to asthma section. 
Anesthetics 
B: ketamine (briochodilator effect) 
 
OR 
D: propofol(bronchodilator effect) 
• 
Volatiles all are bronchodilators but sevoflurane is likely best choice  
• 
Always consider noninvasive PPV as rescue before intubation  
• 
If intubation & ventilation: 

61!
!
o 
Use permissive hypercapnia 
o 
Use low respiratory rates: start at 10-12 breaths/minute but may need lower 
rates  
o 
Use prolonged expiratory time (e.g. I: E ratios 1:3, 1:4, or even 1:5)  
o 
Tidal volume 6-8cc/kg  
o 
FiO2 to achieve PaO2>60mm Hg 
 
2.4.4 Surgery in Sickle Cell Patient 
• 
Avoid precipitants of sickle cell crisis: 
o 
Hypoxia 
o 
Vascular stasis 
o 
Hypothermia 
o 
Hypovolemia/hypotension 
o 
Acidosis 
• 
Optimize perioperative pain control  
• 
Monitor for: 
o 
Vaso-occlusive crisis 
o 
Acute chest syndrome 
o 
Aplastic crisis 
o 
Splenic sequestration syndrome 
o 
Right upper quadrant syndrome  
 
Optimization (in consultation with hematology)  
Risk factors for acute pain crises: 
• 
Age, frequency of hospitalizations &/or transfusions for episodes of crisis, evidence of 
organ damage (e.g., low baseline oxygen saturation, elevated creatinine, cardiac 
dysfunction), history of central nervous system events, concurrent infection 
• 
Procedural risk for complications: 
o 
Low: minor surgery (e.g., inguinal hernia & extremity surgery) 
o 
Intermediate: intra-abdominal operations (e.g., cholecystectomy) 
o 
High: intracranial & intrathoracic procedures, hip surgery 
• 
Hematology consult, optimize treatment: 
o 
Hydroxyurea to ↑ fetal hemoglobin production 
o 
Cancel non-emergent cases if patient experiencing a crisis 
o 
IV fluid to avoid dehydration while NPO 
• 
Preoperative transfusion therapy: 
o 
Controversial without good evidence 
o 
Purpose is to correct pre-existing anemia, ↓ hemoglobin S concentration 
& ↑ adult hemoglobin 
o 
Consider target hemoglobin 6 -10 for surgery & always have blood available for 
any surgery 
o 
Exchange transfusions are not routinely recommended 
• 
Treatment of Pain:  
o 
Rest, warmth, reassurance, analgesia, fluid replacement: 
o 
Oral analgesics may be sufficient for minor attacks 
o 
Opioids (IM, SC, IV, PO) 
o 
PCA opioids with baseline analgesia provided by background infusion or fentanyl 
patch 
o 
Paracetamol & NSAIDs 
o 
NSAIDS particularly good for bone pain 
o 
Ketamine as adjunct 
o 
Regional blocks as appropriate, epidural use has been reported 
 
 
 
 

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CHAPTER THREE 
HAEMATOLOGY AND BLOOD TRANSFUSION 
3.1 Anaemia 
3.1.1 Iron Deficiency Anaemia 
A lack of iron in the body (mainly due to nutritional deficiency, chronic blood loss, malabsorption and 
hookworm infestations and increased demand such as during pregnancy). 
 
Clinical presentation: fatigue, palpitation, dizziness, glossitis, koilonychias (spoon shaped nails) 
and pica 
 
Investigations  
• 
Full blood picture (FBP) 
• 
Peripheral smear 
• 
Iron studies- serum iron levels, total iron binding capacity, serum ferritin   
• 
Stool analysis for hookworm ova and occult blood. If stool for occult blood is positive, do 
Oesophagoduodenoscopy (OGD) to confirm upper gastrointestinal bleeding 
 
Non-Pharmacological Treatment  
 
• 
To prevent iron deficiency; 
o 
Eat a variety of iron rich foods like meat, eggs, legumes (dried beans, lentils, peas), 
spinach and dark green leafy vegetables, iron fortified breads and cereals, nuts and 
seeds. 
• 
To help in iron absorption from diet; 
o 
Avoid drinking tea/coffee with meals 
o 
Increase intake of vitamin C rich foods (e.g. citrus fruit, broccoli, cauliflower, guavas, 
tomatoes, bell peppers and strawberries) with meals to maintain iron in its reduced 
state 
 
Pharmacological Treatment  
Treat the undelying cause of iron deficiency anaemia. 
Adults  
 
A: ferrous sulfate (PO) 200mg 8hourly for 3months.  
Children: 
A: ferrous sulphate (PO) 5mg/kg 8hourly. Continue for 3months after the normal hemoglobin 
has been achieved.  
 
 
 
OR 
B: Blood transfusion (is only indicated if anaemia is life threatening; e.g anaemia in failure, 
hypoxia.) 
 
 
 
OR 
D: Iron sucrose (IV) 200mg in 100ml0.9% sodium chloride running for 15 minutes once a day 
three times a week for 2 weeks.  
 
Parenteral iron is indicated in patients who can not tolerate or are refractory to oral iron. 
• 
Total cumulative dose = number of 100mg ampoules for Hb increase 
• 
Divide the total cumulative dose in 200mg doses, given 24hourly 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

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Table 3.1: Number of 100mg/ampoules of iron sucrose needed for Hb increase based on the 
body weight. 
 
• Duration of treatment may extend to 4 weeks based on the total cumulative dose required. 
• Monitor blood counts and clinical assessment monthly. 
 
Note 
 Formulations of iron combined with other nutritional supplements (vitamins, 0.4mg-5mg folic acid, zinc 
and amino acids) are recommended to enhance absorption of iron and correct combined nutritional 
deficiencies.  
 
3.1.2 Megaloblastic Anemia 
This is a condition whereby the bone marrow usually produces large, structurally abnormal, 
immature red blood cells (megaloblasts) often due to inadequate intake or malabsorption of vitamin 
B12 or folate.  
 
Clinical presentation  
Pallor, depression, hair loss, pins and needles, numbness in hands or feet, tremors and palsies, 
mildly jaundiced (lemon yellow tint), beefy tongue, darkening of palms and ataxic gait. 
 
Investigations 
• 
FBC-Low Hb, sometime pancytopenia, raised mcv but maybe low or normal if coexisting 
with iron deficiency (combined deficiency anaemia) 
• 
Peripheral smear 
• 
Serum vitamin B12,  
• 
Serum folate level,  
• 
TSH 
• 
Reticulocyte count 
• 
Bone marrow aspiration may be indicated 
 
Pharmacological Treatment 
Vitamin (B12 deficiency anaemia) and other macrocytic without neurological involvement.  
C: hydroxycobalamine (IM) initially 1mg 3times a week for 2weeks then 1mg (IM) every 
3months.  
Review the patient’s blood counts and clinical assessment every 3months.   
 
Pernicious Anaemia (B12 deficiency) with neurological symptoms and signs  
C: hydroxycobalamine (IM) initially 1mg on alternate days until no further improvement 
(maximum reversal or neuro-psychiatric signs and symptoms are achieved) then 1mg 
every 2-3months 
 
 
AND 
A: folic acid (PO) 5mg 24hourly for at least 3months this must be started simultaneously 
with injection vitamin B12 
 
 
 
AND 
A: ferrous sulphate (PO) 200mg 8hourly for at least 3months.  
 

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3.1.3 Haemolytic Anaemia 
Haemolytic anaemia results from an increase in the rate of red cell destruction in the intravascular or 
in the reticuloendothelial system in some pathological disorders 
Clinical presentation: 
•
Pallor, jaundice, splenomegaly
•
Anaemia, Reticulocytosis, indirect hyperbilirubinemia, and haemoglobinuria
Pharmacological Treatment 
Immunosuppressants 
A: prednisolone (PO) 1–1.5mg/kg/day for 1-3 weeks until Hb > 10g/dl 
 
AND/OR 
S: cyclosphophamide (IV) 50mg/kg/day for 4days 
If no response; 
A: folic acid (PO) 5mg 24hourly should be given for 1to 3months. 
 
OR 
B: blood transfusion if anaemia is severe 
 
OR  
S*: High dose human immunoglobulin G (IV) 400mg/kg/day for 5days 
Surgical Management 
Splenectomy may be considered in those who fail to respond to pharmacological treatment. 
3.1.4   Sickle Cell Disease (SCD) 
Clinical presentation 
The clinical manifestations of SCA are variable; 
•
Symptoms usually occur after 6 months of life.
•
acute onset of unexplained illness, including acute pain, anaemia, acute neurological
symptoms, loss of vision, respiratory infections, hepatosplenomegaly, jaundice, swollen
limbs and sepsis.
•
Four types of crises occur in SCD; vaso-occlussive crisis, hemolytic crisis, sequestration
crisis, aplastic crisis.
Investigations 
Screening test: sickling test, isoelectric focusing (electrophoretic separation) 
Confirmatory Tests: Sickle Scan, haemoglobin electrophoresis, HPLC (High performance Liquid 
Chromatography) 
Other ancillary laboratory investigations useful in detection and monitoring of the disease include: 
•
FBP, Reticulocyte count, Peripheral
blood film, 
•
Blood culture and sensitivity,
•
LDH, total and indirect bilirubin,
liver and renal profile, 
•
POC blood gases, ECG,
•
mRDT, RBG,
•
Blood grouping and cross match,
•
Imaging eg CXR, ECHO,
Ultrasounds (abdominal and 
transcranial doppler TCD USS), 
and CT Scan head if suspicious of 
stroke.

65!
Note 
Confirmatory test should be done to all patients with positive screening tests and those with 
negative screening test results but have clinical presentation suggestive of SCD. 
Screening 
From the age of 10 years, screen for renal disease (proteinuria by urine dipstick) and retinopathy 
annually 
Annual screening for risk of stroke by transcranial Doppler from the age of 2years to 16years. 
Pharmacological Treatment 
A: folic acid (PO) 5mg 24hourly 
Prophylaxis against Pneumococcal Infection 
A: phenoxymethyl penicillin (PO) 125mg for children younger than 3years; phenoxymethyl 
penicillin (PO) 250mg for children 3 years and older twelve hourly until 5years of age in all 
children with SCA.  
Immunisation against pneumococcal infection 
A: pneumococcal conjugate vaccine (PCV-13) from two months of age, 3 doses 8 weeks 
apart (i.e at age 2months, 4 months and 6 months) and a booster dose between 12-15 
months. If the child has not previously received this vaccine, then at least one dose should 
be given between 6-18 years. PCV-13 and vaccine against H. influenza is incorporated in 
Tanzania EPI schedule. 
S: pneumococcal polysaccharide vaccine (PPSV-23) - at 2 years then after every 5 years 
for life. 
Table 3.2: Analgesia for General Pain Relief 
Severity 
Management 
Mild 
Reassurance, hot packs, reposition, massage, distraction (stories, play) 
Child: A: paracetamol (PO) 15mg/kg 6hourly 
Adult: A: paracetamol (PO) 1g 6hourly 
Moderate 
As for mild pain, PLUS 
Child: A: ibuprofen (PO) 5mg/kg 8hourly 
Adult: A: ibuprofen (PO) 400mg 8hourly  
Severe 
As for moderate pain PLUS 
Child:C: morphine (PO) 0.5mg/kg 3–4 hourly as needed 
Adult: C: morphine (PO) 5–10mg, 3–4 hourly as needed 
If unable to take orally, administer paracetamol (IV) 1g 6-8hourly and morphine 
0.1mg/kg 8-12hourly 
If morphine is not available, tramadol may be used. 
B: tramadol (PO) 50-100mg 6hourly as needed 
Hydration: Encourage oral fluids first; it should be used whenever possible. Give IV fluids, 
preferably normal saline, if the patient is unable to drink well, has severe pain, or abdominal 
symptoms. 
Body weight (kg) 
Fluids (ml/kg/day) 
<10 kg 
150ml/kg/day 
11 – 20kg 
75ml/kg/day for every kilogram above 10kg 
ADDED to 1500ml for the first 10kg of weight 
> 20kg
30ml/kg for every kilogram above 20kg 
ADDED to 225Oml for the first 20kg of weight 
Divide the total daily volume by 24 hours to obtain hourly fluid rate 
Indications for use of Hydroxyurea Include: 
All children older than nine months with proven SCD; and 
In adolescents and adults with the following;  

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!
• 
Recurrent vaso-occlussive crisis (3 or more severe episodes requiring admission in the 
last 12 months), 
• 
Severe and/or recurrent acute chest syndrome (ACS) (2 or more episodes in a lifetime), 
• 
Severe symptomatic chronic anemia that interferes with daily activities or quality of life,  
• 
Where chronic transfusion therapy is not feasible use it as an alternative to prevent new or 
recurrent stroke,  
• 
Silent infarcts, stroke and in patients with abnormal TCD (199cm/sec), 
• 
Recurrent priapism,  
• 
Chronic kidney disease on erythropoietin to improve anaemia. 
 
Principle of Dosage Initiation and Monitoring: 
S: hydroxyurea (PO) 15 mg/kg/day 24hourly; (5–10 mg/kg/day if patient has chronic kidney 
disease).  
S: hydroxyurea (PO) 20mg/kg/day, starting dosage for infants and children.   
 
Increase the dose by 2.5–5 mg/kg/day every 3 months,Maximum tolerated dose (MTD) should not 
exceed 30mg/kg/day.  
Blood work monitoring 
• 
Bi-monthly FBP, reticulocyte count for 1 month, then monthly for 3months, then once 
every 3months if blood counts remain stable. 
• 
HbF % analysis, liver function test, serum creatinine and urea every 6months. 
• 
Weigh patient every three months and adjust the dosage accordingly. 
 
Threshold for dose reduction 
• 
Neutrophil ANC < 1.5 X109/L 
• 
Reticulocyte count < 80 X1012/L 
• 
Platelet count < 80 X109/L 
• 
Hb < 6g/dl 
 
If haematologic toxicity occurs; 
• 
Discontinue hydroxyurea until counts recover, usually 1-2 weeks, 
• 
Reinitiate hydroxyurea at a dose 2.5 mg/kg/day less than the dose given before onset of 
cytopenias to achieve the maximum tolerable therapeautic dose,  
• 
Do FBP according to the initiation schedule. 
Note 
• 
Clinical response to treatment with hydroxyurea may take 3-6months. A 6month trial on 
MTD is required before considering discontinuation due to treatment failure. 
• 
Hydroxyurea should be stopped at least three months prior to conception in both males 
and females  
• 
Hydroxyurea should be discontinued in all pregnant women 
• 
Hydroxyurea should be discontinued in all breastfeeding women 
 
Blood transfusion in SCA 
Simple (Top-Up) Blood Transfusion:  
Indicated in symptomatic anaemia, orhaemoglobin level has dropped by > 2g/dl below the steady-
state value.  
 
Exchange Blood Transfusion:  
Aim to reduce HbS to 30%.  
 
Indications for Exchange Blood Transfusion 
• 
Cerebrovascular Accidents (CVAs)  
• 
Acute Chest Syndrome (ACS)  
• 
Prior to major surgery  
• 
Multi-organ failure, including Systemic Marrow Fat Embolism (SMFE)  
• 
Multiple pregnancies  
• 
Prevention of recurrent stroke.  

67!
Relative Indications for Exchange Blood Transfusion 
•
Intractable or very frequent severe crises
•
Major priapism unresponsive to other therapy.
Note 
•
Because the cardiovascular system adjusts to the chronic anaemia, blood transfusion is not
routinely indicated in steady state SCD simply for the reason that haemoglobin level is below 8–
10g/dl.
•
Packed red cells transfusion is preferred to minimize the risk of fluid overload
SCD in pregnancy 
•
Stop hydroxyurea 3 months before conception
•
Educate the patient about the risks associated with pregnancy in SCD.
•
Determine the haemoglobinopathy status of the partner.
•
Document pre-pregnancy baseline results if any.
•
Refer the patient to a high-risk antenatal clinic for proper follow up
•
Prescribe routine prenatal vitamins, see under Obstetric and gynaecology chapter
•
Prophylactic blood transfusion is not recommended.
•
Vaginal delivery is preferred unless there is indication for caesarian section.
•
Prescribe prophylaxis for venous thromboembolism (VTE) for patients with additional risk
factors for VTE e.g history of VTE. See details under coagulation disorders section 3.5
•
Monitor hydration status, warmth and give analgesia as needed after delivery.
•
Assess and manage neonatal opioid dependency and withdrawal all infants with history of
in utero opioid exposure.
Pharmacological Treatment. 
A: acetylsalycylic acid (PO) 75mg 24hourly, starting from the second trimester to reduce 
the risk of pre-eclampsia.  
SCD emergency conditions 
Acute chest syndrome 
•
Life threatening – admit the patient in a high dependency unit or ICU,
•
Diagnostic criteria – respiratory distress (fast breathing, SPO2<95% on air) and/or pleuritic
pain, cough, fever, tachycardia, infiltrates on CXR,
•
Investigations – arterial blood gases, creatinine, electrolytes, ALT, FBP, malaria test, blood
and urine culture and sensitivity, CRP, CXR, HPLC,
•
Management – Give supplemental oxygen to maintain SPO2>95%, analgesia for pain
relief, fluids per hydration protocol, broad spectrum antibiotics while awaiting culture and
sensitivity results, top up blood transfusion or exchange transfusion if expertise available.
Acute anaemia 
•
Haemoglobin < 5g/dl or recent acute drop in Hb >2g/dl below steady state.
•
Causes – infection, splenic sequestration, haemolytic crisis and aplastic crisis.
•
Investigations – do FBP, reticulocyte count, creatinine, bilirubin, ALT, LDH, malaria test,
urine and blood culture and sensitivity, blood grouping and cross-matching,
•
Management – immediately transfuse packed red cells 10mls/kg over 4hours, repeat
transfusion as needed as per transfusion protocol, treat the underlying cause, document
size of liver and spleen.
Stroke 
•
See management details under central nervous system chapter,
•
Exchange transfusion or top up transfusion to prevent recurrent stroke.

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3.1.4 G6PD Deficiency 
G6PD is an inherited X-linkded recessive genetic disorder, haemolysis results from oxidative 
damage to RBCs due to loss of protective effect of the enzyme G6PD. 
 
Clinical presentation 
• 
Usually asymptomatic but liable to haemolysis (acute anaemia) if infection, incriminated 
drugs (e.g. sulphonamides, chloroquine, primaquine or proguanil). or foods (e.g. fava 
beans) are taken. 
• 
Pallor,  
• 
Jaundice and  
• 
Dark urine (Coca-colored urine) 
 
Investigations:  
• 
FBP, peripheral smear, reticlocyte count,  
• 
Methaemoglobin reduction (G6PD) test.  
 
Pharmacological Treatment 
A: folic acid (PO) 5mg 24hourly for 1 to 3 months.  
 
 
 
AND 
B: Transfusion of packed red blood cells in severe anaemia. Give 10ml/kg body weight. 
Then assess the level of haemoglobin and clinical presentation. 
 
 
 
 
3.1.5   Aplastic Anaemia (Bone Marrow Failure) 
Aplastic anaemia is defined as pancytopenia resulting from aplasia of the bone marrow. it can be 
inherited (Fanconi anaemia) or acquired (idiopathic, chemical or drug induced). It is one of 
haematological emergency. 
 
Clinical presentation 
Vary with severity but include;  
• 
Anaemia, easy bruising/bleeding, recurrent infection;  
• 
splenomegaly is not a feature. 
 
Diagnostic Criteria 
• 
Pancytopenia,  
• 
Bone marrow hypocellularity of < 30% hematopoietic cells. 
 
 
Investigations 
• 
FBP, peripheral smear, reticulocyte count,  
• 
Viral screening (HIV, Hepatitis B and C),  
• 
Bone marrow aspiration and trephine biopsy. 
 
Pharmacological Treatment 
Supportive treatment 
B: blood transfusion (preferred irradiated, leucodepleted) when Hb<7g/dl 
 
 
 
OR 
S: platelet transfusion if bleeding or if platelet count is <10 X109/L. see dosage under  
blood transfusion section 3.6 
 
 
 
AND 
Prophylactics antibiotics, hygiene, isolation of the patient, and use of masks to prevent neutropenic 
sepsis in patients with ANC of less than 0.5 X 109/L. 
 
Note 
Culture and sensitivity in patients with neutropenic sepsis. Refer to management of neutropenic 
sepsis under malignant diseases chapter. 
 
Definitive treatment 
Allogeneic haematopoietic stem cell transplantation is indicated in patients younger than 45yrs.  
Immunosuppressive Therapy 
 
S: anti-thymocyte globulin (ATG) (IV) 40mg/kg/daily 4-10days 

69!
 
AND 
S: cyclosporine (PO)2-10mg/kg/day 12hourly for 6-24months 
 
AND 
S: eltrombopag (PO): Children <5years; 2.5mg/kg 24hourly, 6-11years; 75mg 24hourly, >12 
years; 150mg 24hourly for 6months 
For patients who develop cyclosporine toxicity (nephrotoxicity, hypertension, gingival hypertrophy 
and hirsutism), the following drugs may be used although the response rate is low. 
D: methylprednisolone (PO) 5–10mg/kg for 3–14days 
OR 
S: cyclophosphamide (IV) 45mg/kg /day for 4days 
OR 
S: danazol (PO) 5mg/kg/day for 6months 
Note 
Give supportive therapy and refer patients to higher health facility with adequate expertise and 
facilities. 
Monitor blood counts bi-monthly for outpatients, and as needed for admitted patients. 
3.1.6 Myelodysplastic syndrome (MDS) 
Pre-malignant condition, primarily disease of the old people. 
Investigations: similar to aplastic anaemia, plus analysis of 5q deletion. 
Pharmacological treatment 
B:blood transfusion for symptomatic treatment 
AND 
S: azacitidine (SC) 75mg/m2 24hourly for 7days, repeat after every 28days 
3.2    Bleeding Disorders 
3.2.1 Hereditary Bleeding Disorders 
Hereditary bleeding disorders includes haemophilia A and B, Von Willebrand disease 
3.2.1.1 Haemophilia 
Haemophilia is an inherited, X-linked lifelong bleeding disorder which affects males almost 
exclusively. 
Clinical presentation 
•
Spontaneous muscle and joint bleeding without injury,
•
Prolonged bleeding after injury,
•
Epistaxis and easy bruising.
•
Complication includes arthropathy and disability.
Haemophilia A (Factor VIII deficiency) 
Is the most common of the hereditary clotting factor deficiencies and are caused by deficiency of 
factor VIII. 
Haemophilia B (Factor IX deficiency) 
•
It is caused by deficiency of clotting factor IX
•
Presentation as in Haemophilia A, this is less common 20%.
Classification of Haemophilia 
Haemophilia is classified as mild, moderate or severe according to the levels of circulating factor VIII 
or IX and indicates the expected frequency of bleeding. 

70!
Classificati
on 
Haemophilia A 
Factor 
VIII 
level 
Haemophilia B 
Factor IX level 
Clinical features 
Severe 
<1% of normal 
≤ 0.01 U/ml 
≤ 1% of normal 
≤ 0.01U/ml 
•
Spontaneous haemorrhage
•
Frequent spontaneous haemarthrosis
Moderate 
2-5%of normal
0.01-0.05 U/ml
•
Haemorrhage secondary to trauma or
surgery
•
Occasional 
spontaneous
haemarthrosis
Mild 
5-40%of
normal 
5-40% of normal
• Haemorrhage post trauma or surgery
• Rare spontaneous
Investigations 
•
Prolonged aPTT but normal PT and Platelets counts
•
Confirm by factor VIII or IX assay
Non-pharmacological Treatment 
•
Avoid I.M injections and use small gauge needles if necessary
•
Inform the patient and parents thoroughly on the problem, and provide means of alerting
other medical/pharmaceutical personnel
•
Genetic counselling
•
For Acute Bleeding episodes (RICE): Rest, Ice/cold pack – 5 minutes on, 10 min off,
Compression and Elevate the joint.
For haemarthrosis – AVOID incising or aspiration of the affected joint.  Treat by replacing the 
specific factor e.g factor 8 or 9 concentrate if available or FFP (10 - 15ml/kg), joint support and tabs 
Paracetamol for pain. 
Pharmacological Treatment  
Avoid use of NSAIDs, instead use paracetamol 
Haemophilia A (Factor VIII Deficiency) no Inhibitor 
Dose depends on bleeding severity 
Minor bleed: 
S: Factor VIII (IV) 20–40IU/kg. 
Major bleed: 
S: Factor VIII (IV) 50–100 IU/kg 12hourly for 3-5days or until bleeding stops 
Expected response: 1IU/kg = 2% rise in factor VIII level 
Half life Factor VIII: 8–24hours 
Haemophilia B (Factor IX deficiency) no inhibitor 
Dose depends on bleeding severity 
Minor bleed: 
S: Factor IX (IV) 20-50IU/kg 
Major bleed:  
S: Factor IX (IV) 100IU/kg 
Expected response: 1IU/kg= 1.5 rise in the factor IX level 
Half-life Factor IX: 16–24 hrs 
D: Fresh frozen plasma (FFP) can be used where factor concentrate is unavailable. 
Average dose 10-15mls/kg 
Note 
•
If there is no response to appropriate replacement therapy tests for inhibitors (an inhibitor is
formed when one develops antibodies against factor concentrates)
•
Detection of inhibitor is by aPTT mix study and confirmed by Bethesda assay (BU)
Factor VIII Inhibitor Management Options 
• High dose factor concentrate infusion
• Use by-pass agent like FEIBA (Factor Eight Inhibitor By-passing Agent)
Table 3.3: Classification of Haemophilia 

71!
!
• Immune tolerance induction therapy (ITI) 
• In case of emergency surgery consider plasmapheresis 
• Adjuvant antifibronolytic agents eg Tranexamic acid can used with either of the above 
 
Note 
• 
All patients suspected with haemophilia A or B refer to higher facility with adequate expertise 
or consult haematology Unit. 
• 
Children with severe haemophilia are recommended to be on low dose prophylaxis of factor 
concentrate 
• 
Male circumcision should be done at a hospital where factor concentrate is available. 
Concentrate should be given before and after the procedure. 
 
3.2.2 Von Willebrand Disease (VWD) 
Von Willebrand Disease is inherited disease due to deficiency of vWF. It is the commonest bleeding 
disorder in the population especially in women. 
 
Clinical presentation 
• 
History of easy bruising,  
• 
Menorrhagia 
• 
Gum bleeding 
• 
Joint bleeding in severe cases 
 
Investigations 
• 
Confirmatory test: VWF level assay. 
• 
PT, aPTT, and platelet count are normal except in severe cases.  
 
Pharmacological Treatment 
 
 
 
C: etamsylate (PO) 500mg 8hourly until the bleeding stop 
 
 
 
OR 
 
C: tranexamic acid (PO) 500mg 8hourly until bleeding is stopped. 
 
If no response   
 
S: Desmopresin (IV) 0.3µg/kg IV stat. Max. Dose20µg. 
 
Note: 
• Patient unresponsive to DDVAP may be treated with virus-inactivated vWF containing 
FVIII concentrate. 
• Never give Etamsylate or Tranexamic acid to patients bleeding per urethral  
 
3.2.3 Acquired Bleeding Disorders/Platelet Disorders 
3.2.3.1 Disseminated Intravascular Coagulation (DIC) 
Clinical features 
• Usually are related to the underlying disorder. 
• Bleeding manifestation, 
• Extensive organ dysfunction,  
• Shock, renal cortical ischemia, coma, delirium and focal neurological symptoms. 
 
Pharmacological Treatment 
Rapid and appropriate treatment of the underlying disorder including; 
• Antibiotics for infection, 
• Surgical debridement of necrotic tissues,  
• Chemotherapy for malignant causes,  
• Evacuation of dead fetus;  
• Platelets transfusion for thrombocytopenia,  
• Fresh frozen plasma (FFP) for coagulation factor depletion.  
• Monitor prothrombin time (PT), international normalized ratio (INR), activated partial 
thromboplastin (aPTT), platelet count and fibrinogen. 
 

72!
Note: If patient is not bleeding Platelets concentrate is contraindicated. If DIC is severe enough to 
cause multiorgan dysfunction, management in an intensive care unit is required. 
3.2.3.2 Idiopathic Thrombocytopenic Purpura (ITP) 
Clinical features: 
•
long history of Purpura, menorrhagia, epistaxis and gingival haemorrhage.
•
Intracerebral haemorrhage occurs infrequently but is the most cause of death
•
overt bleeding is rare unless thrombocytopenia severe (less than 10 X109/L)
Note 
A palpable spleen strongly suggests that ITP is NOT the cause for thrombocytopenia. 
Non-pharmacological Treatment 
•
Patients with platelet counts over 50 X109/L usually do not have spontaneous bleeding and
may undergo invasive procedure.
•
Emergency treatment of acute bleeding caused by severe thrombocytopenia need
immediate platelet transfusion
Pharmacological Treatment 
A: prednisolone (PO) 1mg/kg/day for 3–6 weeks, then taper 10mg weekly (For all patients 
with platelet counts below 30 X109/L) 
OR  
B: dexamethasone (IV) 40mg in 500ml Normal saline running for 4hours once a day for 
4days. 
If no response; 
S:human Immunoglobulin G (IV) 0.4g/kg/day for 5days, 
OR 
S:human Immunoglobulin G (IV) 1g/kg/day for 2days followed by immediately platelets 
transfusion 
3.3 Coagulation Disorders 
Venous thromboembolism (VTE) is a common disorder that comprises deep vein thrombosis (DVT) 
and pulmonary embolism (PE). In most cases, pulmonary embolism arises from proximal deep vein 
thrombosis i.e. popliteal, femoral or iliac veins in at least 90%. 
3.3.1 Deep Vein Thrombosis (DVT) 
Clinical presentation 
•
Leg pain, tenderness and swelling.
•
A palpable cord representing thrombosed vessels.
•
Discoloration, venous distention and prominence of superficial veins and cyanosis.
•
The clinical diagnosis of DVT is highly nonspecific.
Investigations 
•
D-dimer,
•
Doppler USS,
•
PT, INR, Aptt
Pharmacological Treatment 
Long term anticoagulation is required to prevent a frequency of symptomatic extension of 
thrombosis and/or recurrent venous thromboembolic events. Warfarin is started with initial 
unfractionated heparin or enoxaparine therapy and then overlapped for 5days. 
C: warfarin (PO) 5mg 24hourly for 5days, then adjust the dose according to INR 
levels for 3-6 months. 
AND 

73!
S: Low Molecular weight heparin (SC)1mg/kg 24hourly for 5days 
OR 
S: Unfractionated heparin (IV) by 75units/kg followed by continuous infusion of 
18units/kg/hrs. 
Adolescents or children: loading dose 75units/kg then 15–25 Units /kg/hr by IV infusion or 
250units/kg 12hourly by SC injection. 
S: rivaroxaban (PO) 15mg 12hourly for 21days, then rivaroxaban (PO) 20mg 24hourly for 
the remaining duration of treatment. 
Pregnant women 
Warfarin is teratogenic, therefore low molecular weight heparin is recommended during pregnancy. 
D: Low Molecular weight heparin (SC) 1mg/kg 12hourly for the whole duration of treatment. 
3.3.2 Pulmonary Embolism (PE) 
It is a medical emergency.  
Clinical presentation 
•
Transient dyspnea and tachypnea in the absence of other clinical features
•
Pleuritic chest pain, cough, haemoptysis, pleural effusion, and pulmonary infiltrate
•
Severe dyspnea and tachypnea and right-side heart failure
•
Cardiovascular collapse with hypotension, syncope, and coma
•
Several less common and nonspecific presentation including unexplained tachycardia or
arrhythmia, resistant cardiac failure, wheezing, cough, fever, apprehension and confusion.
Investigations 
•
PT, INR, aPTT, D-dimer, CXR and CT angiography
Pharmacological Treatment
Treat as Deep Vein Thrombosissection 3.3.1 
Note 
•
Warfarin therapeutic INR ranges from 2 to 3 for VTE, and 2.5 -3.5 for patients with
mechanical heart valves
•
Warfarin therapy should be monitored by INR after 5–7 days of treatment, then as needed
throughout the duration of treatment.
•
If the cause of VTE is acquired thromboembolism, treatment lasts for 3-6 months, BUT if the
cause is inherited thrombophilia, treatment is lifelong.
•
Warfarin interacts with many drugs therefore precaution should be taken when administered
with other drugs.
•
If warfarin overdose/toxicity occurs, stop warfarin and give FFP 10-15mls/kg and vitamin K
5mg IV stat. Reinitiate warfarin after bleeding has stopped and INR is within therapeutic
range, using the lower dosage.
•
For VTE prophylaxis in bedridden patients, give enoxaparin 40mg SC OR Rivaroxaban
10mg orally once a day until ambulation resume.
•
Unfractionated heparin should be monitored by aPTT before and during treatment.
3.4 Blood Transfusion 
Blood components 
A single donation of blood can be separated into several blood components. Currently in Tanzania 
the following blood components are available for transfusion: packed red blood cells, Fresh Frozen 
Plasma, single unit platelet (plasma rich) and whole blood units. 
I.
Whole blood
One unit contains 450mls of blood. It is poor in platelets and clotting factors and can be stored
for 35days at 2-6°C.
Indications: Exchange transfusion, open heart surgery, and in the absence of PRBCs in
patients with acute blood loss and hypovolaemia.

74!
It can be stored for 35days at 2-6°C. One unit increases haemoglobin (Hb) level by approximately 
1g/dl in adult, whereas in children, a dose of 10-15mls/kg will increase the Hb by about 3g/dl. 
Indications: acute blood loss, exchange transfusion, cardiac patients with Hb level <8g/dl, chronic 
symptomatic anaemia with Hb <5g/dl, preoperative patients with Hb level <8g/dl, pre-radiotherapy 
patients with Hb level <10g/dl, pre and post chemotherapy patients with Hb <9g/dl, and patients 
admitted to ICU with Hb <7g/dl. 
III.
Platelets
A single random donor platelet (RDP) from one whole blood unit and contains about 5.5X109/L
platelets in 50ml unit. It is stored at room temperature (20-24°C) and has a life span of 5days.
Dosage: 50mls per 10kg i.e 5-6 RDP units in adults. In infants < 10kg, the dose is 5mls/kg, one
adult therapeutic dose increases platelet counts by approximately 20-40 X109/L.
Indications 
•
Therapeautic: thrombocytopenia of platelet counts< 50X109/L with clinical evidence of
bleeding.
•
Prophylactic in patients with platelet counts of:  <10 X109/L, <20X109/L with additional risk
factor of bleeding, <50X109/L and planned for minor surgery, <100X109/L with multiple
injuries, or microvascular bleeding, or planned for major surgery. Also, in massive
transfusion to maintain a platelet count of >50X109/L.
Contraindications: Absolutely contraindicated in heparin induced thrombotic thrombocytopenia 
(HITT) and thrombotic thrombocytopenic purpura (TTP). Relatively contraindicated in idiopathic 
thrombocytopenia (ITP) unless a life-threatening bleeding is anticipated. 
IV.
Fresh frozen plasma (FFP)
FFP prepared from one unit of whole blood contains about 200-300mls of plasma. It is stored at -
18°C and contains all clotting factors in physiological levels except factors V and VIII which are
present in slightly reduced amount. It has a life span of 12 months. Thaw FFP in water bath at 30-
37°C and transfuse within 30 minutes after thawing. It expires 24 hours after thawing.
Dosage: 10-20ml/kg, approximately 4-6 units for adult, this will raise a minimum of 30% of plasma 
clotting factors. 
Indications: haemophilia if factor concentrates not available, patients with significant coagulopathy 
eg DIC, Vitamin K deficiency and massive transfusion, thrombotic thrombocytopenic purpura (TTP) 
or haemolytic uremic syndrome (HUS) as top up or exchange plasma transfusion, scoline apnoea, 
haemorrhagic disease of the newborn. 
 Investigations 
•
Before transfusion:FBC, ABO and Rh-blood grouping and crossmatch (cross matching not
needed for platelets and FFP transfusion),
•
If transfusion adverse reaction occurs: Assess for haemolysis (FBC, peripheral smear,
direct antiglobulin test, serum bilirubin, serum LDH), re-grouping and crossmatch, other
tests depending on the type of transfusion reaction.
 Types of blood transfusion 
I.
Acute simple/episodic transfusion
Used in management of symptomatic patients with anaemia or bleeding tendencies 
II.
Chronic/top up transfusion
Used as prophylactic to prevent complications, eg. In patients with sickle cell anaemia (SCA) 
III.
Exchange blood transfusion
Used in management of severe neonatal jaundice, in patients with SCA with acute chest syndrome, 
suspected acute stroke or transient ischaemic attack. 
II.
Packed red blood cells (PRBCs)

75!
Transfusion of blood volumeto patient equivalent to his/her total blood volume in less than 24 hours, 
or 10 units or more in 24 hours. Administer in parallel a 1:1:1 ratio of 6 Units of RBCs, 6 Units of FFP 
and 6 Units of Platelets. The target is to achieve 1:1:1 ratio over 6 hours. Aim the PT, PTT <1.5x 
control mean, fibrinogen >1 g/L, target platelet > 100x109/L if pts has CNS trauma, eye and > 
50x109/L for other type of injuries.  
Plasma Derived Medicinal Products (PDMPs) available from commercial outlets 
•
Haemosolvate factors VIII and IX used in management of haemophilia
•
Immunoglobulins used in immune-mediated conditions
•
Albumin used in management of hypovolaemia, hypoalbuminaemia and in therapeautic
plasma exchange.
Therapeautic phlebotomy 
Indications: Polycythemia, and in hereditary iron overload. 
Table: 3.4 Adverse effects of blood transfusion 
Reaction 
Transfusion 
Management 
Acute 
immunologic 
reactions 
Acute 
haemolytic 
transfusion reaction 
Stop transfusion, supportive care to maintain hemodynamics. 
Regroup and crossmatch donor and recipient’s samples. 
Assess for haemolysis. 
Allergic reactions 
Stop 
transfusion, 
administer 
antihistamine 
eg 
Chlorphenamine 4mg PO as needed +/- steroid eg 
Hydrocortisone 100mg IV stat, resume transfusion if 
symptoms 
subside. 
If 
anaphylactic 
reaction, 
add 
vassopressors eg epinephrine and supportive care. 
Febrile 
non-haemolytic 
transfusion reaction 
Stop transfusion, administer antipyretics A: Paracetamol 1g 
PO as needed+/- steroid eg Hydrocortisone 100mg IV stat, 
resume transfusion if symptoms subside 
Transfusion-related 
acute 
lung 
injury 
(TRALI) 
Stop transfusion, oxygen supplementation and mechanical 
ventilation if required. 
Transfusion associated 
graft-versus-host 
disease (TA-GVHD) 
Supportive care 
Delayed 
immunologic 
reactions 
Delayed 
hemolytic 
transfusion reaction 
Symptomatic treatment, request extended cross match for 
additional transfusions. 
Post-transfusion 
purpura 
Self limiting,  
S: IV immunoglobulin 0.4g/kg/day IV for 5days or plasma 
exchange may be needed in severe cases. 
Acute 
non-
immunologic 
reactions 
Transfusion-related 
circulatory 
overload 
(TACO) 
Stop transfusion, administer diuretics, manage as cardiac 
failure. See details under cardiovascular diseases chapter. 
Bacterial contamination 
Stop transfusion, antibiotics and supportive care 
Delayed non-
immunologic 
reactions 
Infectious 
disease 
transmission 
Manage the infection accordingly eg HIV, Hepatitis B & C. 
see details under respective chapters 
Iron overload 
Iron chelation with deferroxamine 
Blood transfusion in Jehovah’s witness 
•
Blood transfusion is a medical treatment, and therefore patients have the right to refuse
treatment.
•
Inform the patient of the benefits and risks of transfusion.
•
Enable the patients to understand the consequences of not receiving blood.
•
Inform the patients of any alternatives to transfusion available eg autologous transfusion
and plasma derived medicinal products.
•
Guarantee strict clinical confidentiality
IV.
Massive blood transfusion

76!
Include the following; 
•
Leukaemia – acute and chronic leukaemia
•
Lymphomas – Hodgkin’s and Non-Hodgkin’s lymphoma
•
Multiple myeloma
These are discussed in details under malignant disease chapter. 
Haematological malignancies 

77!
CHAPTER FOUR 
NOTIFIABLE DISEASES 
Notifiable Diseases, conditions and events usually pose a great public health threat, with a potential 
of international spread. They require immediate notification by health personnel (clinical, laboratory, 
environmental, etc.), to health authorities, as required by the International Health Regulations (IHR 
2005). Notification is mandatory, in order to ensure prompt and effective response, to avoid further 
spread and to prevent deaths.   
Note: 
•
Immediately notify the Public Health Authorities using the electronic reporting system for
priority diseases, i.e. the electronic Integrated Disease Surveillance and Response (e-
IDSR) System
•
Ensure that the disease, condition or event is recorded in the Health Facility e-IDSR
reporting booklet
•
Manage patients on site, in an isolation ward/room or an established isolation centre
•
Use Personal Protective Equipment (PPE) before attending a suspected patient
•
Strictly apply principles of IPC during patient management and waste disposal
4.1 Bacterial Infections 
4. 1.1 Cholera
Cholera is an acute gastrointestinal infection caused by Vibrio cholerae. Infection occurs through 
ingestion of contaminated water or food by Vibrio cholerae leading to severe diarrhoea and emesis 
associated with body fluid and electrolyte depletion. 
Clinical Presentation 
•
A sudden onset of painless watery diarrhoea that may quickly become severe with profuse
watery stool, vomiting, severe dehydration and muscular cramps, leading to hypovolemic 
shock and death 
Case Definition 
•
Suspected cholera case: In areas where a cholera outbreak has not been declared: Any
patient aged two years and older presenting with acute watery diarrhoea and severe 
dehydration or dying from acute watery diarrhoea 
•
In areas where a cholera outbreak is declared: any person presenting with or dying from
acute watery diarrhoea 
•
Confirmed cholera case: A suspected case with Vibrio cholerae O1 or O139 confirmed by
culture or PCR (Polymerase Chain Reaction). 
Laboratory Investigation 
•
Specimen: Liquid stool or rectal swab
•
Diagnostic test: Isolate V. cholerae from stool culture and determine O1 serotype using
polyvalent antisera for V. cholerae O1. If desired, confirm identification with Inaba and 
Ogawa antisera. 
•
If specimen is not serotypable, consider, V. cholerae O139
•
Antibiotic Susceptibility Testing   before provision of antibiotics; Follow up 48 -72 hours
after antibiotic initiation 
Note 
•
For confirmation at the beginning of an outbreak, rectal swab or stool specimen should
be taken from first 5 to 10 suspected cases. 
•
If any are positive, every tenth case will be sampled for specimen throughout the
Note 
Rational approaches to case management of cholera with oral and intravenous rehydration therapy 
have reduced the case fatality of cholera from more than 50% to much less than 1%. When a case 
of cholera is suspected at home, advise to rehydrate the patient using ORS if available while 
preparing to take the patient to the nearest health facility or Cholera Treatment Centre 

78!
outbreak 
•
Manage a suspected cholera case in an isolation ward or in an established Cholera
Treatment Centre 
Prevention 
•
Drink treated or boiled water from safe sources (taps, decontaminated deep wells, bottles)
•
Boil water or treat to kill bacteria and make it safe for drinking and for other domestic uses
•
Wash hands with liquid soap and running water after visiting the toilet, before preparing
foods, and before eating 
•
DO NOT eat uncooked food from the street and do not eat cooked food that is no longer
hot 
•
DO NOT eat street prepared fruits. Always eat home prepared fresh fruits
Management 
Pharmacological Treatment 
Cholera requires immediate treatment because the disease can cause death within hours. There are 
three elements of treatment: Rehydration, Antibiotic Treatment, Zinc and Folic Acid Supplements. 
i. Rehydration
•
Assess the patient's level of dehydration as per National Guidelines for Prevention and
Control of Cholera. It is of paramount importance to make correct diagnosis and administer 
the right treatment. 
o
plan A: No dehydration,
o
plan B: Moderate dehydration and
o
plan C: Severe dehydration.
For Severe dehydration: 
•
Administer intravenous (IV) fluid immediately to replace fluid deficit; Use Ringer Lactate
solution or, if that is not available, 0.9% sodium chloride solution. Give 100 ml/kg IV in 3
hours, 30 ml/kg as rapidly as possible (within 30 min) then 70 ml/kg in the next 2.5 hours.
•
After the initial 30 ml/kg has been administered, the radial pulse should be strong and
blood pressure should be normal. If the pulse is not yet strong, continue to give IV fluid
rapidly. Administer ORS solution (about 5 ml/kg/hour) as soon as the patient can drink, in
addition to IV fluid.
•
If the patient can drink, begin giving A: oral rehydration salt solution (ORS) by mouth while
the drip is being set up; ORS can provide the potassium, bicarbonate, and glucose that
saline solution lacks.
Note 
When using 0.9% sodium chloride solution there is a possibility of hyper-metabolic Acidosis causing 
kidney injury 
ii. Antibiotic treatment
Antibiotic treatment to patients with severe dehydration is as follows: 
Adults (Not for pregnant women) 
A: doxycycline (PO) 300 mg or 5mg/kg stat then 200mg (PO) 12 hourly for 7 days 
OR 
A: ciprofloxacin (PO) 1g stat then 15mg/kg 12 hourly for 7 days   or 500mg (PO) 12 hourly 
for 7 days  
OR 
A: azithromycin (PO) 500mg once a day for 7 days 
Expectant mothers: 
A: erythromycin (PO) 500mg 8 hourly for 7 days 
Children: 
A: erythromycin syrup (PO) 12.5mg/kg 6 hourly for 5 days 
OR 
A: Azithromycin 250mg (PO) once a day for 7 days 

79!
For adolescents: 
A: ciprofloxacin (PO) 12mg/kg2 times for 5 days 
OR 
A: doxycycline (PO) 300mg as stat or 5mg/kg (PO) stat 
OR 
A: azithromycin (PO) 500mg once a day for 7 days 
Note 
•
Ciprofloxacin was previously contraindicated to children under 12 years. Recent studies
have shown it to be safe for use in children
•
Start feeding 3-4 hours after oral rehydration begins. Preferably, give antibiotics with food
to minimize vomiting
For moderate Dehydration 
•
Give oral rehydration, approximately 75-100ml/kg in the first four hours
•
Reassess after four hours; if improved, continue giving WHO based ORS, in quantity
corresponding to losses (e.g. after each stool) or 10 to 20ml/kg. If not improved, treat as
severe dehydration.
If no signs of dehydration 
•
Patients who have no signs of dehydration when first observed can be treated at home
•
Give these patients ORS packets to take home, enough for 2 days
•
Demonstrate how to prepare and give the solution
•
Instruct the patient or the caretaker to return if any of the following signs develop;
increased number of watery stools repeated vomiting or any signs indicating other
problems (e.g. fever, blood in stool)
For each loose stool or vomiting give; 
•
50-100 ml (¼ - ½ cup) of ORS solution for a child less than 2 years old.
•
100-200 ml for older children. Adults can take as much as they want
Note 
Prophylactic treatment of cholera contacts with antibiotics is not recommended. Routine treatment of 
a community with antibiotics, or mass chemoprophylaxis, has no effect on the spread of cholera, can 
have adverse effects by increasing antimicrobial resistance and provides a false sense of security. 
iii. Zinc and Folic Acid Supplements
•
Zinc (PO) 20mg once daily decreases diarrhea and shortens the duration of illness in
children with cholera.
•
Provide zinc supplementation, at a dosage of 20 milligrams per day for children older than
six months or 10 mg per day for those younger than six months, for 10–14 days. 
•
Folic acid (PO)2.5mg once daily for children < 6 months, or 5mg once daily for children >6
months for the duration of the treatment. For Pregnant women use Folic acid (PO) 5mg
once daily for the duration of the treatment.
Public Health Control Measures 
•
Establish treatment centre in locality where cases occur. Treat cases onsite rather than
referring them to treatment centers elsewhere.
•
Initiate a line listing of suspected and confirmed cases and ensure laboratory results are
linked with cases
•
Strengthen case management
•
Mobilize community early to enable rapid case detection and treatment.
•
Work with community leaders to limit the number of large gatherings, if seen mandatory,
establish by-laws
•
Ensure availability and continuous access to clean and safe water.
•
Promote safe preparation of food, including fruits, and vegetables
•
Promote safe disposal of human waste.
•
Ensure adequate collaboration with various sectors including water and sanitation to
ensure appropriate interventions are addressed.

80!
Note 
Cholera Vaccine is available however its utilization must be accompanied with strategies to 
improve water and sanitation 
4.1.2 Anthrax 
Anthrax is a bacterial disease caused by the spore forming Bacillus anthraces, a gram positive, rod-
shaped bacterium. It is a zoonotic disease whereby man is infected directly through contact with 
infected hides or inhalation of spores in the lungs or ingestion of infected meat. It can be manifest on 
the skin (Cutaneous Anthrax) in the lungs (Pulmonary / Inhalation Anthrax), and/or intestinal 
(Gastrointestinal Anthrax and Oropharyngeal anthrax) or CNS (Meningeal Anthrax). 
Clinical Presentation 
Cutaneous Anthrax 
•
Itching
•
Pruritic papule or vesicle
•
Characteristic depressed black eschar surrounded by moderate to severe edema
•
A malignant pustule,
•
Pyrexia
Inhalation Anthrax 
Mild inhalation Anthrax 
•
Cough, Fever, Fatigue, Myalgia, can resemble a viral respiratory illness, Pulmonary and
gastrointestinal signs may occur together 
• 
Severe inhalation Anthrax 
•
Diaphoresis, Stridor, Dyspnea, Hypotension, Acute respiratory distress
These patients may develop sepsis accompanied by cyanosis, shock, and hemorrhagic pneumonia. 
Hemorrhagic pleural effusions often develop. 
Gastrointestinal Anthrax 
•
Fever, Abdominal pain, Vomiting, Diarrhea Bloody stool.
Oropharyngeal anthrax 
Signs of oropharyngeal anthrax may include Dysphagia with posterior oropharyngeal necrotic ulcers, 
Unilateral neck swelling, Cervical adenopathy, Edema, Pharyngitis fever. 
Meningeal Anthrax 
Hemorrhagic meningoencephalitis that involves both 
•
Deep brain parenchymal hemorrhagic lesions
•
Infection of the cerebrospinal fluid (CSF) in the subarachnoid space
Case Definition 
Suspected Case: Any person with acute onset illness characterized by several clinical forms which 
are: 
•
Cutaneous form: Any person with skin lesion evolving over 1 to 6 days from a papular
through a vesicular stage, to a depressed black eschar invariably accompanied by oedema
that may be mild to extensive. 
•
Gastro-intestinal:Any person with abdominal distress characterized by nausea, vomiting,
anorexia and followed by fever 
•
Pulmonary (inhalation): Any person with brief prodromal resembling acute viral
respiratory illness, followed by rapid onset of hypoxia, dyspnoea and high temperature, 
with X-ray evidence of mediastinal widening 
•
Meningeal: Any person with acute onset of high fever possibly with convulsions, loss of
consciousness, meningeal signs and symptoms; commonly noted in all systemic 
infections, but may present without any other clinical symptoms of anthrax. 
AND 
Has an epidemiological link to confirmed or suspected animal cases or contaminated animal 
products? 

81!
!
Confirmed case: A confirmed case of anthrax in a human can be defined as a clinically compatible 
case of cutaneous, inhalational or gastrointestinal illness that is laboratory-confirmed by: 
(a) Isolation of B. anthracis from an affected tissue or site; or 
(d) Other laboratory evidence of B. anthracis infection based on at least two supportive 
laboratory tests. 
 
Laboratory Investigation  
• 
Isolation of Bacillus anthracis from a clinical specimen (e.g. blood, lesions, 
discharges) 
• 
Demonstration of B. anthracis in a clinical specimen by microscopic 
examination of stained smears (vesicular fluid, blood, cerebrospinal fluid, 
pleural fluid, stools)  
• 
Positive serology (ELISA, Western blot, toxin detection, chromatographic 
assay, fluorescent antibody test). 
• 
Detection of nucleic acid by PCR. 
 
Other supporting tests 
• 
Measurement of antibodies or toxin in blood 
• 
Chest X-ray  
• 
Computerized tomography (CT) scan 
• 
Detection of B. anthracis by nucleic acid test (NAT) covering the genes coding for capsule 
and virulence factors;  
 
Prevention: Post Exposure Prophylaxis 
• 
A: Initial 10-day exposure: ciprofloxacin (PO)500 mg 12hourly for5 daysor doxycycline100 
mg(PO)  
12 hourly (or, if pathogens are documented to be susceptible phenoxymethyl penicillin) 
may be used 
Adults: phenoxymethyl penicillin(PO) 250-500 mg 6 hourly.  
Children 1-5 years: phenoxymethyl penicillin(PO)125 mg 6 hourly. 
 6-12 years: phenoxymethyl penicillin(PO)250 mg6 hourly 
48 hours’ exposure:  
OR 
• 
S: clindamycin(PO) 150 to 300 mg 6 hourly for 5days 
OR  
• 
S: levofloxacin(PO)500 mg 12hourly for5 daysare alternative antimicrobial prophylaxis to 
the local population within 48 hours of the initial exposure  
 
Pharmacological Treatment  
A: benzylpenicillin(IV)0.6 MU 6 hourly until local oedema subsides then continue with 
A: phenoxymethy lpenicillin (IV)250 mg 6 hourly for 7 days 
 
If not responding change to  
A: doxycycline(PO)200mg initial dose then 100mg 12 hourly for 7 days  
OR  
A: ciprofloxacin(PO)500mg12 hourly for 7 days 
AND  
A: paracetamol(PO)15mg/kg 8 hourly for 5days 
In severe forms ADD  
Dexamethasone(PO) 0.6 mg/kg per day in divided doses every 8 hours for 4 days 
 
Public Health Control Measures 
• 
Standard infection control precautions (IPC) should be used when managing patients with 
particular attention to body fluid spills, as organisms which remain on surfaces may form 
spores which are infectious 
• 
Personal protective equipment should be used in situations where there is potential for 
splashes and inoculation injuries.  
• 
Mobilize the community for early detection and care. 
• 
Ensure proper burial or cremation (if practiced) of dead bodies (humans and animals) 

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• 
Conduct 
community 
education 
on 
the 
disease 
symptoms 
and 
signs, 
early 
reporting/seeking of medical care, disease transmission and prevention, application of 
infection prevention and control for home care setting,  
• 
Conduct active search for additional cases that may not come to the health care setting 
(older women or small children patients, for example) and provide a door to door 
information about prevention and when to seek care. 
• 
Ensure adequate collaboration with other sectors such as livestock, agriculture, 
environmental and sanitation, to ensure appropriate interventions are addressed. 
• 
Request additional help from district/regional/national levels as needed 
 
4.1.3 Plague 
A zoonotic systemic bacterial infection caused by Yersinia pestis (plague bacillus) usually 
transmitted to humans by rodent fleas or by handling an infected animal.  There are 3 forms of 
plague infection, depending on the route of infection:  
• 
Bubonic plague is the most common, caused by the bite of an infected flea. Y. pestis, 
which enters the body at the bite site and travels through the lymphatic system to the 
nearest lymph node, replicates itself and causes the lymph node to be inflamed, tense 
and painful, turning into open sores with pus. 
• 
Septicaemic plague occurs when infection spreads through the bloodstream, following 
untreated bubonic plague causing bleeding, tissue necrosis and shock. 
• 
Pharyngeal and or Pneumonic plague is the most virulent form and is rare. It is 
typically caused by spread to the lungs from advanced bubonic plague. Untreated 
pneumonic plague can be fatal. 
 
Human to human transmission only occurs with the pneumonic form of plague by infectious 
droplets. Incubation period is 2 to 6 days and case fatality rate (CFR) may exceed 50-60% in 
untreated bubonic plague and is nearly 100% in untreated pneumonic or septicaemic plague. 
However, it is usually <1% with appropriate and timely treatment. Currently, plague is one of the 
most important reemerging bacterial zoonoses in the world. 
 
The main risk factor is exposure to infected populations of wild or domesticated rodents and 
their fleas in plague endemic areas. 
 
Case Definition 
Bubonic Plague 
Suspected case; Any person with a very painful swelling of lymph nodes – buboes And Fever (or 
history of fever) or at least 3 of the following: headache or chills or generalized or severe asthenia 
and consistent epidemiological features, such as exposure to infected animals and/or evidence of 
flea bites and/or residence in or travel to a known endemic area within the previous 10 days. 
 
Confirmed case: Any person with suspected case confirmed by isolation of Yersinia pestis from 
blood or aspiration of buboes, or specific seroconversion or rapid diagnostic test detecting the Ag F1 
in endemic areas 
 
Pneumonic Plague 
Suspected case: Anyone, of any age, with coughs of less than 5 days with one of the following 
signs: Striated sputum from blood or dyspnea or chest pain and Fever (or history of fever) or at least 
3 of the following: headache or chills or generalized or severe asthenia and Epidemiological context 
(contact with suspect or confirm pneumonic plague case, etc). 
Confirmed caseof pneumonic plague: Any suspected case of plague in which Yersinia pestis has 
been isolated in culture 
Or Suspect plague case with positive F1 rapid diagnostic test (RDT) and positive PCR or 
Seroconversion or increase in IgG antibody titre by 4 to 15 days 
Suspicious death of plague: Anyone who died suddenly without apparent cause but with an 
epidemiological link to plague established and without biological sampling 
 
Probable case of plague: Any suspected case of plague alive or deceased with F1 rapid diagnostic 
test (RDT) Or 

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Positive PCR alone 
 
Note: 
Human plague remains a public health concern in Tanzania despite its quiescence in most foci for 
years, considering the recurrence nature of the disease. Plague hosts comprises about  50% of all 
the animals trapped in West Usambara Mountains in north-eastern Tanzania. 
 
Clinical Diagnostic Criteria 
• 
Sudden onset of fever, chills, head and body aches 
• 
Weakness, vomiting and nausea. 
• 
Yersinia pestis is identified by laboratory testing from a sample of pus from a bubo, 
blood or sputum.  
A specific Y. pestis antigen can be detected by different techniques.  
 
 
Note:  
Differential diagnosis Bubonic plague may be confused with streptococcal or staphylococcal 
lymphadenitis, infectious mononucleosis, cat-scratch fever, lymphatic filariasis, tick typhus, tularemia 
and other causes of acute lymphadenopathy 
 
Laboratory Investigation  
• 
Aspiration after an injection of 1-2 ml of saline through an 18-22-gauge needle. Suitable 
microbiological culture media (e.g. brainheart infusion, broth, sheep blood agar, or 
MacConkey agar) should be inoculated with a portion of each specimen.  
• 
Smears should be examined with Wayson or Giemsa stain and with Gram=s stain to show 
Small gram-negative and/or bipolar-staining coccobacilli 
• 
smears should also be submitted for direct fluorescent antibody testing (anti-F1 antibody) 
• 
Serological testing - anti-F1 antigen titre by agglutination  
• 
Molecular biological techniques based on PCR and DNA Hybridization 
 
Note 
Anti-F1 rapid diagnostic test (RDT) positive alone is not a confirmed case.  Culture and PCR tests 
need to done at the appropriate facility. 
 
Prevention:  
• 
Inform people of the presence of zoonotic plague and advised to take precautions 
against flea bites 
• 
Do not handle animal carcasses and avoid direct contact with infected body fluids and 
tissues 
• 
Apply standard precautions when handling potentially infected patients and while 
collecting specimens 
 
Vaccination: Not recommended except for high-risk groups (such as laboratory personnel who are 
constantly exposed to the risk of contamination, and health care workers). 
 
Pharmacological Treatment 
A: streptomycin (IM)30 mg/kg/day (up to a total of 2 g/day) in divided doses, to be 
continued for 10 days of therapy or until 3 days after the temperature has returned to 
normal.  
OR  
A: erythromycin (PO) 500 mg (or 12.5 mg/kg) 8 hourly for 14 days 
OR  
A: doxycycline (PO) 200mg 12 hourly for 14 days 
 
Public Health Control Measures 
• 
Remove trash, food sources, and rat harborages to control rodent populations 
• 
Protect against fleas with insect repellent on skin and clothing 
• 
Conduct environmental flea control in houses, seaports and airports 
• 
Isolate patients with pneumonic plague with precautions against airborne spread until at 
least after 48 hours of appropriate antibiotic therapy.  
• 
Always observe the standard infection prevention and control (IPC) measures. 

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• 
Conduct community education on the disease symptoms and signs, early 
reporting/seeking of medical care, disease transmission and prevention, application of 
infection prevention and control for home care setting, 
• 
Mobilize community to enable rapid case detection and treatment 
• 
Provide chemoprophylaxis using tetracycline (PO) 15-30 mg/kg or chloramphenicol (PO) 
30 mg/kg daily in 4 divided doses for 1 week after exposure ceases. 
• 
Ensure adequate collaboration with other sectors such as livestock, agriculture, 
environmental and sanitation sectors to ensure appropriate interventions are addressed. 
 
4.1.4 Bacterial Cerebro-Spinal Meningitis 
Bacterial epidemics for Cerebro-Spinal Meningitis are commonly caused by Neisseria meningitidis. 
Other common bacteria are Haemophilus influenza, Staphylococcus aures and Streptococcus 
pneumoniae. Human-to-human disease transmission is via large respiratory droplets from the nose 
and throats of infected people. Incubation period is 2 to 10 days. Attack rates are highest among 
children aged less than 15 years. Case fatality rates are usually 8-15% among treated patients, and 
>70% among untreated cases. Many survivors suffer long-term sequelae including mental 
retardation, hearing loss and loss of limb use. Further information on Meningitis for Nervous system 
related management  
 
Case Definition 
Suspected meningitis case: Any person with a sudden onset of fever (>38.5 °C rectal or 38.0 °C 
axillary), and neck stiffness or other meningeal signs and in case of infants, a bulging fontanelle. 
 
Probable meningitis case: Any suspected case with macroscopic aspects of cerebrospinal fluid 
(CSF) (turbid, cloudy or purulent); or with a CSF leukocyte count >10 cells/mm3 or with bacteria 
identified by Gram stain in CSF; or positive antigen detection (for example, by latex agglutination 
testing) in CSF 
 
In infants: CSF leucocyte count >100 cells/mm3; or CSF leucocyte count 10–100 
cells/mm3 and either an elevated protein (>100 mg/dl) or decreased glucose (<40 
mg/dl) level. 
 
Confirmed meningitis case: Any suspected or probable case that is laboratory confirmed by 
culturing or identifying (i.e. polymerase chain reaction) a bacterial pathogen (Neisseria meningitidis, 
Streptococcus pneumoniae, Haemophilus influenzae 
type b) in the CSF or blood 
 
Clinical Diagnostic Criteria 
• 
Sudden fever 
• 
Neck stiffness,  
• 
Intense headache, nausea and vomiting,  
• 
Altered consciousness and convulsions, Bulged anterior fontanelle (in infants)  
 
Laboratory Investigation  
• 
Lumbar puncture for Cerebrospinal Fluid Analysiswith a median opening pressure  
• 
CSF leukocyte count in episodes with CSF leak–associated meningitis  
• 
CSF Culture and Sensitivity  
• 
Elevated white blood cell count (WBC) in CSF of over 1000 cells/mm3  
• 
Glucose concentration, <1.9 mmol/L 
• 
Ratio of CSF glucose concentration to blood glucose concentration, <0.23;  
• 
Protein concentration 
• 
WBC count, >2000 cells/mLCSF neutrophil count, >1180 cells/mL 
 
 
 
 
 
 
 
 

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Table 4.1: Cerebrospinal Fluid Analysis Findings 
CSF 
Characteristic 
Normal Range  
 
Suggestive 
of 
Bacterial 
Meningitis 
Suggestive of Viral 
Meningitis 
Colour  
Clear 
Cloudy 
Cloudy 
RBC Count  
None 
None 
None 
Gram stain 
Negative 
Usually Positive 
Usually 
Negative 
(60%-90%) 
Pressure* 
20–30 
cmH2O 
(16–24 
mmHg or 2.1–3.2 kPa) 
with the patient sitting up 
Above > 42 cm H2O   Normal 
Protein  
15 to 20.2 milligrams per 
deciliter (mg/dL) or 0.15 to 
0.6 milligrams per milliliter 
(mg/mL) 
Above 
20.2 
milligrams 
per 
deciliter 
(mg/dL) 
,>2.20 g/L 
Above 20.2 milligrams 
per deciliter (mg/dL) 
,>2.20 g/L 
Glucose 
50-75 mg/dL (around 1.9 
mmol/L) 
50 to 75 mg/dL (or greater 
than 2/3 of the blood 
sugar level). 
Below normal (<1.9 
mmol/L) 
Usually 
normal 
or 
below normal 
Lymphocytic 
pleocytosis 
None 
Positive 
with 
neutrophilic 
pleocytosis 
Positive 
with 
lymphocytic 
pleocytosis 
*Measured by recording the height of CSF in the manometer tube with the patient's leg 
gently and return the neck to a neutral position with the head supported with a pillow 
 
Use intravenous tubing sets and a ruler to measure cm of pressure if manometer is not 
available 
Prevention  
• 
Vaccines targeted against N. meningitidis serogroups A or C, or a tetravalent A, C, Y, and 
W135 vaccine are useful for immunocompromized children.  
• 
Hib conjugate vaccine is useful for immunocompromized children  
 
Pharmacological Treatment 
A: benzathine penicillin(IV/IM) 300,000U/kg/day with a maximum dose of 24MU/day for 10-
14 days, give 4 million units 4 hourly IV in adults and pediatric patients older than 1 month 
for 10-14 days. 
AND 
A: chloramphenicol (IV) 50 to 100mg/kg/day with a maximum dose of 4 g/day give in 
divided doses at 8 hourly intervals for 10-14 days. 
o 
Serum concentrations requires monitoring due to chloramphenicol toxicity 
o 
Recommended therapeutic levels include a trough of 5 to 10 mcg/mL and a peak of 
10 to 20 mcg/mL 
 
If no improvement in 3 days’ give 
• 
C: ceftriaxone (IV) 2g (50 mg/kg in pediatric patients older than 1 month) 12 hourly for 10-
14 days OR cefotaxime (IV)2 g (50 mg/kg in pediatric patients older than 1 month) 6 hourly 
for 10-14 days. 
• 
C: ceftriaxone (IV or IM) 2g for Adults daily for 10-14 days is preferred for patients with 
central nervous system involvement 
AND  
B: dexamethasone (IV/IM) 0.15mg/kg with a maximum dose of 10mg 8hourly for 3 days 
 
Public Health Control Measures 
• 
Mass vaccination within 4 weeks of crossing the epidemic threshold*** 
• 
Mobilize community to permit early case detection, treatment, and improve vaccine 
coverage during mass vaccination campaigns for outbreak control. 
• 
Conduct 
community 
education 
on 
the 
disease 
symptoms 
and 
signs, 
early 
reporting/seeking of medical care, disease transmission and prevention. 

86!
•
Maintain regular collection of 5-10 CSF specimens per week throughout the epidemic
season in all affected districts to detect possible serogroup shift. Distribute treatment to
health centres
•
Treat all cases with appropriate antibiotics as recommended by National protocol.
***If a neighbouring area to a population targeted for vaccination is considered to be at risk
(cases early in the dry season, no recent relevant vaccination campaign, high population
density), it should be included in a vaccination programme.
4.1.5 Neonatal Tetanus 
A neuromuscular toxin-mediated illness caused by the anaerobic spore-forming soil bacterium 
Clostridium tetani. The disease is transmitted when spores enter open wounds (injections, cutting 
the umbilical cord) or breaks in the skin. While tetanus may occur in adults, infection primarily affects 
newborns. Neonatal tetanus has decreased dramatically in countries with improved maternal 
tetanus immunization rates. Maternal and neonatal tetanus is targeted for elimination in the WHO 
African Region, aiming to achieve neonatal tetanus incidence rates of less than 1 case per 1000 live 
births. Incubation period is 3 to 21 days, with an average of approximately 6 days. Usually occurs 
through introduction of tetanus spores via the umbilical cord during delivery through the use of an 
unclean instrument to cut the cord, or after delivery by “dressing” the umbilical stump with 
substances heavily contaminated with tetanus spores.   
Clinical Diagnostic Criteria 
•
Sudden inability of a newborn to suck/feed between 2nd and 28th day after birth
•
Generalized stiffness
•
Convulsions
Laboratory Investigation 
•
Diagnosis is mainly clinical as there are no reliable laboratory tests for confirming tetanus
•
Blood counts and blood chemical findings are unremarkable.
•
Peripheral leukocytosis may be suggestive
Prevention 
•
Immunize women of reproductive age with TTCV, either during pregnancy or outside of
pregnancy. This protects the mother and also her baby through the transfer of tetanus 
antibodies to the fetus. 
•
Good hygienic practices when the mother is delivering a child are also important to
prevent neonatal and maternal tetanus. 
To be protected throughout life, WHO recommends that an individual receives 6 doses (3 
primary plus 3 booster doses) of TTCV through routine immunization. 
Non-pharmacological Treatment 
•
Rigorously cleanse the umbilical stump to stop the production of toxin at the site of
infection 
Pharmacological Treatment 
A: For children amoxycillin-clavulanate(PO) via Nasal Gastric Tube 20–30 mg/kg/day 
divided 8 hourly for 7 days 
For Adults amoxycillin-clavulanate (PO) via Nasal Gastric Tube 500mg 8 hourly for 7days 
AND 
A: metronidazole (PO) 7.5mg/kg for postnatal age ≤7days: Weighing 1200–2000g: 7.5 
mg/kg/day(PO) given every 24 hours >2000 g: 15 mg/kg/day (PO) in divided doses every 
12 hours. Postnatal age >7days: 1200-2000g: 15 mg/kg/day (PO) in divided doses every 
12 hours >2000 g: 30 mg/kg/day(PO) in divided doses every 12 hours for 7 days 
For Adults Metronidazole 400mg (PO) 8hourly for 7days 
OR 
C: ceftriaxone (IV) 2g (50 mg/kg in pediatric patients older than 1 month) 12hourly for 
7days 
      For Adults ceftriaxone(IV) 2g once or in 2 divided doses for 7days 

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OR  
C:cefotaxime) (IV) 2g (50 mg/kg) in pediatric patients older than 1 month 6hourly for 5days. 
For Adults Cefotaxime 2g (IV) 24hourly or 1g 12hourly for 7days 
OR  
Immunotherapy to neutralise circulating toxin  
B: Administer human antitetanus immunoglobulin TIG, (IM) 100–300IU/kg stat, with the 
dose divided into two different muscle masses to the confirmed infected patients (Don’t 
give vaccine to the confirmed infected patients) 
AND         
A: diazepam (PO) 0.5mg/Kg 8hourly as the effective management of muscle spasm, 
give a sedative cocktail of ALL the following via NGT:  
 
AND  
A: chlorpromazine (PO) 2mg/kg 8 hourly 
AND  
B: phenobarbitone (PO) 6mg/kg 12 hourly 
 
Table 4.2: Guidelines for Dosage Administration** 
Time (hours)  
0 
3 
6 
9 
12 
15 
18 
21 
24 
Diazepam  
* 
* 
 
* 
 
* 
 
* 
* 
Chlorpromazine  
 
* 
 
* 
 
* 
 
 
 
Phenobarbitone  
* 
 
* 
 
 
 
 
* 
 
** These are general guidelines. Frequency of drug administration should be titrated vs clinical 
condition 
 
• 
Airway / respiratory control 
Provide mechanical ventilation.  
• 
Provide adequate fluids and nutrition, as tetanus spasms result in high metabolic 
demands and a catabolic state.  
 
Public Health Control Mesures 
The WHO global target for neonatal tetanus elimination is to reduce the incidence of neonatal 
tetanus to less than 1 case of neonatal tetanus (NT) per 1000 live births in every district of every 
country.  To meet the target 
• 
Immunize the mother and other pregnant women in the same locality as the case with at 
least 2 doses of tetanus toxoid. 
• 
Conduct a supplemental immunization activity for women of childbearing age in the 
locality. 
• 
Improve routine vaccine coverage through IVD and maternal immunization program 
activities. 
• 
Educate birth attendants and women of childbearing age on the need for clean cord cutting 
and care. Increase the number of trained birth attendants. 
 
 
4.1.6 Tick-Borne Relapsing Fever (TBRF) 
A bacterial infection caused by bacteriaBorrelia duttonii, are known zoonoses transmitted to humans 
through the bite of infected “soft ticks” Ornithodoros spp that live within rodent burrows feeding on 
the rodent. Humans typically come into contact with soft ticks when they sleep in rodent-infested 
cabins.  
 
Common Symptoms  
• 
Recurring episodes of fever, Non-specific headache, Non-specific Muscle pain, Non-
specific Joint pain, Non-specific Chills, Non-specific Vomiting, and Abdominal pain. 
 
Bacteremia tends to be greater among pregnant women, and may sometimes result in more severe 
infection. Symptoms tend to develop within 7days after the tick bite. Long-term sequelae of TBRF 
are rare but include iritis, uveitis, cranial nerve and other neuropathies. 
 
Clinical Diagnostic Criteria 
• 
Recurring episodes of high fever, headache, muscle and joint aches, and nausea 

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• 
Recurring symptoms, producing a telltale pattern of fever lasting roughly 3 days, followed 
by 7 days without fever, followed by another 3 days of fever. Without antibiotic treatment, 
this process can repeat several times. 
 
Laboratory Investigation 
• 
Microscopy from the peripheral blood smear will reveal a long and spiral-shaped 
bacteriumSpirochetemia (spirochetes in blood) in TBRF patients often reaches high 
concentrations (>106 spirochetes/ml). Direct microscopic observation of relapsing fever 
spirochetes using dark field microscopy or stained peripheral blood smears 
 
Prevention 
• 
Avoid sleeping in rodent-infested buildings whenever possible. Although rodent nests may 
not be visible, other evidence of rodent activity (e.g., droppings) are a sign that a building 
may be infested. 
• 
Prevent tick bites. Use insect repellent (on skin or clothing) or permethrin (applied to 
clothing or equipment). 
 
Pharmacological Treatment 
A: erythromycin(PO) 500mg (or 12.5 mg/kg) 8 hourly for 14days 
A: tetracycline(PO)500mg 6hourly for 14days 
C: ceftriaxone (IV or IM) 2 grams daily for 10-14days is preferred for patients with central 
nervous system involvement 
 
Public Health Control  
• 
Provide public education, awareness, preventive control measures, and avoidance of 
areas where infected ticks are most abundant. 
• 
Assessing evidence of rodent activity in and around structures of infected people 
• 
Removal of rodents and their nests 
• 
Reduce tick exposures by removing tick infested structures with an appropriate pesticide 
applied by a professional pest control operator who is familiar with the types of “crack and 
crevice” treatments used to control cockroaches or other wall-dwelling pests 
 
4.2 Viral Infections 
4.2.1 Viral Haemorrhaghic Fevers (VHF) 
Viral Haemorrhagic Fever (VHF) is a general term for a severe illness caused by viruses and 
sometimes associated with bleeding. Their distribution is dependent on the ecology of reservoir 
hosts with a potential to cause life-threatening illness in humans. Diagnosis and management is 
challenging due to the non-specificity of early symptoms, limited laboratory facilities in endemic 
areas, severity of disease, lack of effective therapy, strict infection control requirements and 
propensity to cause epidemics with secondary cases in healthcare workers. 
 
Primary transmission is from animal to human, through contact with an infected animal or its 
product. Secondary transmission is from person to person through: 
• 
Contact with a sick person or direct contact with the blood and/or secretions or with 
objects, such as needles that have been contaminated with infected secretions of an 
infected person. 
• 
Breast feeding 
• 
Sexual contact   
 
Public Health Control measures  
• 
Maintain strict viral haemorrhagic disease (VHD) infection prevention and control (IPC) 
practicesthroughout the outbreak. 
• 
Mobilize the community for early detection and care and conduct community education 
about how the disease is transmitted and how to implement IPC in the home care setting 
and during funerals and burials. Consider social distancing strategies. 
• 
Conduct contact follow-up and active searches for additional cases that may not come to 
the health care setting. 
• 
Establish an isolation ward or treatment centre to handle additional cases that may come 
to the health centre and ensure strict IPC measures to avoid transmission in health care 
settings. 

89!
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• 
Suspected cases should be isolated and treated for more common conditions with similar 
symptoms, which might include malaria, typhoid, louse borne typhus, relapsing fever or 
leptospirosis. Ensure a barrier is instituted between suspected and confirmed cases. 
• 
Provide psychosocial support for the family, community and staff. 
• 
Consider quarantine for high risk contacts with home support during the incubation period 
and ensure daily follow up of their movements. 
• 
There are promising vaccine candidates under development for some VHDs that might be 
useful to be used in the event of outbreak in a ring vaccination approach and for health 
care workers. 
• 
Treat conservatively the symptoms which might be presented; severe cases require 
intensive support care; if dehydrated ensure fluid replacement with fluids that contain 
electrolytes. 
 
4.2.1.1 Ebola 
Ebola Virus Disease (EVD) is a deadly disease in people and non-human primates. The viruses that 
cause EVD are located mainly in sub-Saharan Africa. People can get EVD through direct contact 
with an infected animal (bat or nonhuman primate) or a sick or dead person infected with Ebola 
virus. Symptoms appear from 2 to 21 days after contact with the virus, with an average of 8 to 10 
days. 
 
Case Definition:  
Suspected case: Illness with onset of fever and no response to treatment of usual causes of fever in 
the area, and at least one of the following signs: bloody diarrhoea, bleeding from gums, bleeding 
into skin (purpura), bleeding into eyes and urine. 
 
Confirmed case: A suspected case with laboratory confirmation (positive IgM antibody, positive 
PCR 
or viral isolation), or epidemiologic link to confirmed cases or outbreak. 
 
Note 
During an outbreak, case definitions are likely to be adapted to new clinical presentation(s) or 
different modes of transmission related to the local event. In outbreak setting, the following standard 
case definitions apply; 
 
Suspected case: Any person, alive or dead, suffering or having suffered from a sudden onset of 
high fever and having had contact with: - a suspected, probable or confirmed Ebola case; - a dead 
or sick animal  
OR 
• 
Any person with sudden onset of high fever and at least three of the following symptoms: - 
headaches - lethargy - anorexia / loss of appetite - aching muscles or joints - stomach pain - 
difficulty swallowing - vomiting - difficulty breathing - diarrhoea - hiccups;  
• 
OR 
• 
Any person with inexplicable bleeding; OR 
• 
Any sudden, inexplicable death; OR 
• 
A person (alive or dead) suffering or having suffered from a sudden onset of high fever and 
having had contact with: a dead or sick animal.  
 
Clinical Diagnostic Criteria 
A combination of symptoms suggestive of EVD AND a possible exposure to EVD within 21 days 
before the onset of symptoms is suggestive of Ebola.  
 
Symptoms 
• 
Fever 
• 
Aches and pains, such as severe headache, muscle and joint pain, and abdominal 
(stomach) pain 
• 
Weakness and fatigue 
• 
Gastrointestinal symptoms including diarrhea and vomiting 
• 
Abdominal (stomach) pain 
• 
Unexplained hemorrhaging, bleeding or bruising 
Other symptoms may include red eyes, skin rash, and hiccups (late stage) 

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An exposure may include contact with: 
• 
Blood or body fluids from a person sick with or who died from EVD, 
• 
Objects contaminated with blood or body fluids of a person sick with or who died from 
EVD, 
• 
Infected fruit bats and non-human primates (apes or monkeys), or 
Semen from a man who has recovered from EVD. 
 
Laboratory Investigations 
Ebola virus can be detected in blood after onset of symptoms. It may take up to three days after 
symptoms start for the virus to reach detectable levels. Investigations includes: 
• 
Blood for RT-PCR 
• 
Antigen detection or IgM (ELISA)  
 
Note 
Do not take specimen before wearing appropriate PPE and ensuring the patient is in an  Isolation  
Ward/ Centre  
 
Pharmacological Treatment 
A: paracetamol (PO/IV) 15mg/kg 8 hourly for 3 days 
B: Give oxygen and manage hypoglycaemia if present 
 
Fluid and electrolyte balance 
 
A: compoundsodium lactate OR NS intravenously if cannot take fluids orally  
 
B: Give Oxygen therapy to maintain oxygen status. 
 
A: compoundsodium lactate (Ringers Lactate), NS intravenously if cannot take fluids orally. 
Provide IV fluids and electrolytes (body salts) through infusion into the vein (intravenously) 
 
A: Manage hypoglycaemia with 5% DNS or 25% Dextrose Solution if hypoglycaemia is 
shown by RBG testing  
A: Using medication to support blood pressure, reduce vomiting and diarrhea and to manage fever 
and pain. 
A: Treating other infections or any complicating infection and co-morbid condition 
A: Psychological support is given to patient and family 
C: Refer for Provision of Mechanical ventilation, renal dialysis, and anti-seizure therapy may be 
required. 
 
Prevention 
• 
Isolate person with signs of EVD and has had a possible exposure from other people 
• 
Notify the public health authorities  
• 
Blood samples from the patient should be collected and tested to confirm infection 
• 
Prompt identification of cases, contact tracing, and monitoring of high-risk individuals are 
essential to stopping Ebola virus from spreading 
• 
Early recognition of EVD is critical for infection control. However, because early symptoms 
are not specific to EVD, it can be hard to distinguish it from other illnesses, 
including malaria, leptospirosis, influenza (flu), yellow fever, dengue and other viruses 
spread by insects, or viral or bacterial infections of the intestines, like typhoid fever. 
• 
EVD should be considered when clinical illness is combined with an epidemiologic risk 
factor, like direct contact with a suspected or confirmed case or travel to an Ebola-affected 
area. 
• 
Once a case of EVD is identified, everyone who has come in direct contact with the sick 
patient is traced  
• 
Contacts are watched for signs of illness for 21 days from the last day they came in 
contact with the Ebola patient. If the contact develops a fever or other EVD symptoms, 
they are immediately isolated, tested, and provided care.  
4.2.1.2 Marburg Haemorrhagic Fevers  
Marburg virus belongs to the family Filoviridae, divided into three genera: ebolaviruses, 
marburgviruses, and cuevaviruses. The reservoir host of Marburg virus is the African fruit 

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bat, Rousettus aegyptiacus. Fruit bats infected with Marburg virus do not to show obvious signs of 
illness. Primates (including humans) can become infected with Marburg virus, and may develop 
serious disease with high mortality. The disease can spread rapidly within the health care setting. 
The virus enters through broken skin, mucous membrane or exchange of bodily fluids or ingestion, 
inhalation and injection of infectious material 
 
Case Definition 
Suspected case: Illness with onset of fever and no response to treatment of usual causes of fever 
in the area, and at least one of the following signs: bloody diarrhea, bleeding from gums, bleeding 
into skin (purpura), bleeding into eyes and urine. 
 
Confirmed case: A suspected case with laboratory confirmation (positive IgM antibody, positive 
PCR 
or viral isolation), or epidemiologic link to confirmed cases or outbreak. 
 
In an outbreak setting, the following standard case definitions apply; 
 
Suspected case: Any person, alive or dead, suffering or having suffered from a sudden onset of 
high fever and having had contact with: - a suspected, probable or confirmed Marburg case; - a 
dead or sick animal  
OR 
Any person with sudden onset of high fever and at least three of the following symptoms: - 
headaches - lethargy - anorexia / loss of appetite - aching muscles or joints - stomach pain - 
difficulty swallowing - vomiting - difficulty breathing - diarrhoea - hiccups; OR 
• 
Any person with inexplicable bleeding OR 
• 
Any sudden, inexplicable death; OR 
• 
A person (alive or dead) suffering or having suffered from a sudden onset of high fever and 
having had contact with a dead or sick animal  
 
Non-Pharmacological Treatment: 
Supportive therapy includes:   
• 
Mechanical ventilation, renal dialysis, and anti-seizure therapy may be required. 
• 
Management of complications symptomatically 
• 
Maintaining Oxygen status and Blood Pressure  
 
 
 
 
 
Pharmacological Treatment 
There is no specific treatment for Marburg Haemorrhagic Fever.  
A: paracetamol (PO/IV) 15mg/kg 8hourly for 3days 
B: Give oxygen and manage hypoglycaemia if present 
If there is Fluid and electrolyte imbalance: 
A: compound sodium lactate (Ringers Lactate), NS intravenously if cannot take fluids orally  
B: Give Oxygen therapy to maintain oxygen status. 
A: sodium lactate compound (Ringers Lactate), NS intravenously if cannot take fluids orally. Provide 
IV fluids and electrolytes (body salts) through infusion into the vein (intravenously) 
A: Manage hypoglycaemia with 5% DNS or 25% Dextrose Solution if hypoglycaemia is shown by 
RBG testing  
A: Using medication to support blood pressure, reduce vomiting and diarrhea and to manage fever 
and pain. 
A: Treating other infections or any complicating infection and co-morbid condition 
A: Psychological support is given to patient and family 
D: Refer for Provision of Mechanical ventilation, renal dialysis, and anti-seizure therapy may be 
required. 
 
4.2.1.3 Rift Valley Fever 
Rift Valley Fever (RVF) is a viral disease that affects mainly animals and occasionally humans. The 
virus is a member of the Phlebovirus genus, one of the five genera in the family Bunyaviridae. The 
disease is frequently reported following heavy rainfall and floods.  RVF is mainly transmitted from 
animals (sheep, cattle, goats, camels) to humans through close contact with infected animals (such 
as handling meat and body fluids and consumption of raw milk). During established RVF outbreaks 
in animals, humans can also get infected through bites of infected mosquitoes and other biting 
insects. 
 

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The incubation period of RVF varies from 2 to 6 days. These symptoms usually last from 4 to 7 
days. Most of the infected people recover on their own. However, a small proportion gets 
complications such as vomiting blood, nose bleeding and passing bloody stool. Rift Valley fever is 
difficult to distinguish from other viral haemorrhagic fevers as well as many other diseases that 
cause fever, including malaria, shigellosis, typhoid fever, and yellow fever. 
 
Case Definitions 
Suspected case: Early Disease:  Acute febrile illness (axillary temperature >37.5 ºC or oral 
temperature of >38.0ºC) of more than 48 hours’ duration that does not respond to antibiotic or 
antimalarial therapy, and is associated with: 
• 
Direct contact with sick or dead animal or its products AND / OR 
• 
Recent travel (during last week) to, or living in an area where, after heavy rains, livestock 
die or abort, and where RVF virus activity is suspected/confirmed AND / OR 
• 
Abrupt onset of any 1 or more of the following: exhaustion, backache, muscle pains, 
headache (often severe), discomfort when exposed to light, and nausea/vomiting AND / 
OR: 
• 
Nausea/vomiting, diarrhoea OR abdominal pain with 1 or more of the following:  
• 
Severe pallor (or Hb < 8 gm/dL) 
• 
Low platelets (thrombocytopenia) as evidence by presence of small skin and 
mucous membrane haemorrhages (petechiae) (or platelet count < 100x109 / 
d 
• 
Evidence of kidney failure (edema, reduced urine output) (or creatinine > 150 
mol/L) AND / OR 
• 
Evidence of bleeding into skin, bleeding from puncture wounds, from mucous 
membranes or nosefrom gastrointestinal tract and unnatural bleeding from 
vagina AND / OR 
• 
Clinical jaundice (3-fold increase above normal of transaminases) 
 
Late stages of diseases or complications 
(2-3 weeks after onset) 
• 
Patients who have experienced, in the preceding month a flu-like illness, 
with clinical criteria, who additionally develop the following: 
o 
CNS manifestations which resemble meningo-encephalitis AND/OR: 
o 
Unexplained visual loss OR 
o 
Unexplained death following sudden onset of acute flu-like 
illness with haemorrhage, meningo-ecephalitis, or visual loss 
during the preceding month. 
Confirmed case: 
Any patient who, after clinical screening, is positive for anti-RVF IgM ELISA 
antibodies (typically appear from fourth to sixth day after onset of symptoms) or 
tests positive on reverse transcriptase polymerase chainreaction (RT-PCR). 
 
Transmission to human is mainly through direct or indirect contact with blood or organs of infected 
animals. The virus can be transmitted to human through; 
• 
Handling of animal tissue during slaughtering or butchering, assisting with animal births, 
conducting veterinary procedures.  
• 
Inoculation e.g via wound from infected knife or through contact with broken skin or 
through inhalation of aerosols produced during the slaughter of an infected animals.  
• 
Infected mosquito. 
Human become viraemic; capable of infecting mosquitoes shortly before onset of fever and for the 
first 3–5 days of illness. Once infected, mosquitoes remain so for life. 
 
Clinical Diagnostic Criteria 
• 
Acute febrile illness that does notrespond to antibiotic or antimalarial therapy,  
• 
Exhaustion, backache, muscle pains, headache (often severe),  
• 
Photophobia 
• 
Nausea/vomiting 
• 
Evidence of bleeding into skin, bleeding from puncture wounds, from mucous membranes 
or nose, from gastrointestinal tract and unnatural bleeding from vagina 

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• 
Clinical jaundice (3-fold increase above normal of transaminases) 
Clinical diagnosis is difficult, because RVF symptoms can be mild and non-specific, especially early 
in the course of the disease.  
 
Laboratory Investigations 
Definitive diagnosis of RVF involves laboratory testing of blood (during illness) or other tissue 
samples (postmortem tissue).  
• 
The virus detection in the blood then virus isolation in cell culture  
• 
Molecular techniques (reverse transcriptase polymerase chain reaction or RT-PCR). 
• 
Antibody testing using Enzyme-Linked ImmunoAssay (ELISA) confirms infection with 
RVFV  
• 
IgM antibodies reflect a recent infection and IgG antibodies persist for several years 
(Detection of anti-RVF IgM suggests an ongoing transmission of RVFV in humans during 
inter-epidemic periods.).  
• 
FBC  
o 
Low Hb [Hb<8gm/dL - Severe pallor 
o 
Low platelet < 100 x109 /Dl (Thrombocytopenia) – small skin and mucous 
membrane hemorrhages (Petechiae))   
• 
Serum Creatinine  
 
Note 
Acute RVF can be diagnosed using several different methods 
1. 
Serological tests such as ELISA may confirm the presence of specific IgM antibodies 
to the virus. The virus itself may be detected in blood during the early phase of illness 
or in post-mortem tissue using a variety of techniques including, antigen detection 
tests by ELISA, RT-PCR, virus propagation (in cell cultures), Immunohistochemistry in 
formalin-fixed tissues 
2. 
ELISA IgG can be used for retrospective diagnostic.  
 
Management  
Management of RVF in humans is mainly supportive as there is no definitive treatment for RVF. 
Early detection and management of the disease is important. Human control of RVF is through 
control of the disease in animals through a sustained vaccination program and limiting human-
animal contact. Use of insecticide treated nets and mosquito repellents can also reduce infections in 
human. In addition to human suffering and death, RVF has far reaching economic implications to the 
Livestock industry. In outbreak settings, the disease manifestation includes non-haemorrhagic 
febrile syndromes, and laboratory testing should be considered among persons with milder 
symptoms suggestive of viral illness. 
 
Prevention 
People living in or visiting areas with RVF shall be protected from the RVF infection with these 
steps: 
• 
Protect people from contact with blood, body fluids, or tissues of infected animals. (Use 
PPEs like gloves, boots, long sleeves, and a face shield)  
• 
Protect people from unsafe animal products. All animal products (including meat, milk, and 
blood) should be thoroughly cooked before eating or drinking. 
• 
Protect people from mosquitoes and other bloodsucking insects. Use insect repellents and 
bed nets, and wear long sleeved shirts and long pants to cover exposed skin. 
 
No vaccines are currently available for vaccination in people at risk of RVF infection. 
 
Public Health Control Measures 
• 
Mobilize the community for early detection and care. 
• 
Conduct community education about the confirmed case, how the disease is 
transmitted, and how to prevent contact with tissues of infected animals and avoid 
mosquito bites. 
• 
Provide information about prevention in the home and when to seek care. 
• 
Provide supportive treatment to all cases identified 
• 
Collaborate with the animal health specialists to search and document cases 
among animals as well. 
 

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4.2.1.4 Yellow Fever 
Yellow fever virus is an RNA that belongs to the genus Flavivirus and is related to West Nile, St. 
Louis encephalitis, and Japanese encephalitis viruses.  It is transmitted human-to-human via the 
domestic species of Aedes mosquitoes (Urban epidemics) or to humans from primate reservoir via a 
forest mosquito species (Sylvatic cycle). About 15% of infections progress to fever and jaundice. 
While only the minority of cases are severe, case fatality rate may be 25% to 50% among patients 
with syndrome of haemorrhage, jaundice, and renal disease. A small proportion of patients develop 
“toxic phase” with jaundice (yellowing of the skin and eyes, hence the name ‘yellow fever’), dark urine 
and abdominal pain with vomiting. Bleeding can occur from the mouth, nose, eyes or stomach and 
half of those die within 7 to 10 days. 
 
Risk factor: Sporadic cases often linked to occupation or village location near woods or where 
monkeys are numerous, also non-vaccinated persons. Infection and disease can be prevented 
by vaccination. With a vaccine efficacy > 95% and duration of immunity is life time 
 
Case definition 
Suspected case: Any person with acute onset of fever, with jaundice appearing within 14 days of 
onset of the first symptoms. 
 
Probable case: A suspected case with one of the following; 
• 
Epidemiological link to a confirmed case or an outbreak 
• 
Positive post-mortem liver histopathology 
 
Confirmed case: A probable case with one of the following; 
• 
Detection of YF-specific* IgM 
• 
Detection of four-fold increase in YF IgM and/or IgG antibody titres between 
acute and convalescent serum samples 
• 
Detection of YFV-specific* neutralizing antibodies 
 
*YF-specific means that antibody tests (such as IgM or neutralizing antibody) for other 
prevalent flavivirus are negative. This testing should include at least IgM for Dengue and 
West Nile and may include other flavivirus depending on local epidemiology.  
OR 
One of the following 
• 
Detection of YF virus genome in blood or other organs by PCR 
Detection of yellow fever antigen in blood, liver or other organs by immunoassays Isolation of the 
yellow fever virus 
 
Laboratory Investigations 
• 
ELISA for the presence of yellow fever Specific IgM and IgG antibodies. 
• 
Exclusion of Dengue, West Nile virus and other locally prevalent flavivirus will be 
necessary for the confirmation of yellow fever. 
• 
PCR, YF specific seroneutralization, virus isolation or histopathology 
 
Management  
Non-Pharmacological Treatment 
No specific anti-viral treatment, supportive therapies are recommended. Good and early supportive 
treatment for dehydration, liver and kidney failure, and fever improves outcomes. Associated 
bacterial infections can be treated with antibiotics 
 
Prevention 
Prevention and Control involve mosquito control and provision of Yellow Fever vaccine. The yellow 
fever vaccine is safe, affordable and a single dose provides life-long protection against yellow fever 
disease. 
 
Indication of Yellow Fever Vaccination 
• 
Persons ≥ 9 months of age 
• 
Planning travel to or residence in an endemic area 
• 
Planning travel to a country with an entry requirement 
Needs to be given ≥ 10 days prior to arrival in endemic area 
 

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Contraindications of Yellow Fever Vaccination  
• 
Infants aged less than 9 months; 
• 
Pregnant women – except during a yellow fever outbreak when the risk of infection is high; 
• 
People with severe allergies to egg protein; and 
People with severe immunodeficiency due to symptomatic HIV/AIDS or other causes, or 
who have a thymus disorder 
 
Public Health Control Measures 
• 
Identify all cases and provide clinical, epidemiological and laboratory evidences  
• 
Identify contacts, screen and test for confirmation 
• 
Educate the communities affected on mosquito control  
• 
Destroy known sources of standing water and any newly discovered sites for the presence 
of mosquito larvae. 
• 
Surveillance of Mosquito by Mosquito control professionals 
 
4.2.1.5 Dengue Fever 
Dengue virus is an arbovirus transmitted by aedes mosquitoes (both Ae. aegypti and Ae. 
albopiticus). Dengue fever is caused by four serologically distinct, but closely related Dengue 
viruses: dengue virus (DENV) 1, 2, 3, and 4 of the Flaviviridae family. Dengue fever is an emerging 
pandemic that has spread globally during the past 30 years as a result of changes in human 
ecology. Dengue haemorrhagic fever (DHF) is a potentially deadly complication that has become a 
leading cause of hospitalization and death among children in Asia and Africa. There is good 
evidence that sequential infection with the different serotypes of dengue virus increases the risk of 
more severe disease that can result in dengue shock syndrome (DSS) and death.  
 
Infected humans are the main carriers and multipliers of the virus, serving a source of the virus for 
uninfected Aedes aegypti mosquitoes which maintain the urban dengue transmission cycle. The 
virus circulates in the blood of infected human for 2-7 days, at approximately the same time that they 
have a fever. A sylvatic transmission cycle has been documented in West Africa where DENV-2 has 
been found in monkeys. There is no evidence of person-to-person transmission. 
 
DENV is frequently transported from one place to another by infected travelers; when susceptible 
vectors are present in these new areas, there is the potential for local transmission to be 
established. 
 
Case Definition 
Dengue Fever Suspected case: Any person with acute febrile illness of 2-7 days duration with 2 or 
more of the following: headache, retro-orbital pain, myalgia, arthralgia, rash, haemorrhagic 
manifestations, leucopenia. 
 
Dengue Fever Confirmed case: A suspected case with laboratory confirmation (positive IgM 
antibody, four-fold or greater rise in IgG antibody titres, positive PCR or viral isolation). 
 
Dengue Haemorrhagic Fever: A probable or confirmed case of dengue with bleeding tendencies 
as evidenced by one or more of the following: positive tourniquet test; petechieae, ecchymoses or 
purpura; bleeding: mucosa, gastrointestinal tract, injection sites or other; haematemesis or melaena; 
and thrombocytopenia (100,000 cells or less per mm3) and evidence of plasma leakage due to 
increased vascular permeability, manifested by one or more of the following: 20% rise in average 
haematocrit for age and sex, 20% drop in haematocrit following volume replacement therapy 
compared to baseline, signs of plasma leakage (pleural 
effusion, ascites, hypo-proteinaemia). 
 
Dengue Shock Syndrome: All the above criteria, plus evidence of circulatory failure manifested by 
rapid and weak pulse, and narrow pulse pressure (≤ 20 mm Hg) or hypotension for age, cold, 
clammy skin and altered mental status. 
 
Laboratory Investigations 
• 
Reverse Transcriptase–Polymerase Chain Reaction (RT–PCR) 
• 
Rapid Tests for Dengue NSI antigen 
Serological methods, such as Enzyme-Linked Immunosorbent Assays (ELISA) for IgM and IgG 
anti-dengue antibodiesFBP 

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Management  
There is no specific treatment for dengue, but appropriate medical care frequently saves the lives of 
patients with dengue haemorrhagic fever. 
 
Non-Pharmacological Treatment 
No specific treatment is available for Dengue fever.  
 
Pharmacological Treatment:  
A:  paracetamol (PO/IV) 15mg/kg 8hourly for 3days 
A: Maintainance fluid (Ringers lactate, NS) intravenously if one cannot take enough fluid orally  
B: Blood transfusion and clotting factors. 
B: Oxygen and manage hypoglycaemia if present 
 
Note 
• 
No antibiotics are of proven value.  
• 
Children below 12 years require close monitoring for dangerous form.  
• 
Steroids should not be used. 
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) such as ibuprofen and aspirin should 
be avoided. These anti-inflammatory drugs act by thinning the blood, and in a disease 
with risk of hemorrhage, blood thinners may exacerbate the prognosis 
 
Prevention 
At present, the only method of controlling or preventing dengue virus transmission is to 
combat the vector mosquitoes using environmental management and chemical methods. 
• 
Prevent 
dengue 
by avoiding 
mosquito 
bites 
by 
Aedes. 
aegypti and Aedes. 
albopictus bite during the day and night (Using mosquito repellant, bed nets and 
removing reservoirs). 
• 
All 
four 
dengue 
viruses 
are 
spread 
primarily 
through 
the 
bite 
of 
an 
infected Aedes mosquito. 
• 
A dengue vaccine is available for use in some parts of the world 
 
Public Health Control Measures 
• 
Wear full sleeve clothes and long dresses to cover the limbs 
• 
Use mosquito repellents 
• 
Use mosquito nets – to protect babies, old people and others, who may rest during the 
day. Effectiveness of such nets can be improved by treating them with permethrin 
(pyrethroid insecticide). Curtains (cloth or bamboo) can also be treated with insecticide and 
hung at windows or doorways, to repel or kill mosquitoes 
 
4.2.1.6 Chikungunya Fever 
Chikungunya Virus Disease is the arthropod-borne virus caused by Chikungunya Virus (CHIKV), 
transmitted by the Aedes aegyptiand Aedes albopictus mosquitos the same which transmit Dengue 
virus, West Nile and Yellow Fever viruses. Chikungunya disease (Seroprevalance 7.7% to 26.9% in 
Tanzania) does not often result in death, but the symptoms can be severe and disabling. People at 
risk for more severe disease include newborns, older adults (≥65 years), and people with medical 
conditions such as high blood pressure, diabetes, or heart disease. The word "Chikungunya" is 
Makonde for "that which bends up," in reference to the stooped posture of patients afflicted with the 
severe joint pain associated with the disease. Epidemics of fever, rash and arthritis, resembling 
Chikungunya fever were recorded as early as 1779. However, the virus was first isolated between 
1952-1953 from both man and mosquitoes during an epidemic in Tanzania. 
 
Case Definition 
Acute clinical case 
• 
Clinical criterion: Fever >38.50 C (101.30F) and joint paina (usually incapacitatingb) with 
acute onseta AND 
• 
Epidemiological criterion: resident or visitor in areas with local transmission of 
Chikungunya on the last 15 days (suspected case for epidemiological surveillance) b OR 
• 
Laboratory criterion: confirmation by laboratory: PCR, serology or viral culture (confirmed 
case for epidemiological surveillance) 

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• 
Usually accompanied by exanthema, myalgia, back pain, headache and, occasionally, 
vomiting and diarrhoea (pediatric age group). 
• 
In children aged <3 years, joint pain is expressed as inconsolable crying, irritability, 
rejection to mobilization and/or walking 
 
Atypical case 
Clinical case of laboratory confirmed Chikungunya accompanied by other manifestations: 
neurological, cardiological, dermatological, ophthalmological, hepatic, renal, respiratory, or 
haematological, among others. 
 
Severe acute case 
Clinical case of laboratory-confirmed Chikungunyapresenting dysfunction of at least one organ or 
system that threatens life and requires hospitalization 
 
Suspected and confirmed chronic cases 
Suspect chronic case: Person with previous clinical diagnosis of chikungunya after 12 weeks of the 
onset of the symptoms presenting with at least one of the following articular manifestations: pain, 
rigidity, or edema, continuously or recurrently. 
Confirmed chronic case: Every chronic case with a positive chikungunya laboratory test 
 
Laboratory Investigations 
Chikungunya is a biosafety level-3 (BSL-3) 
• 
Detection of Chikungunya virus (CHIKV) viral culture of blood in the first 3 days 
• 
RT-PCR for Viral RNA from the serum collected <6 days after onset of illness. 
Serological tests show a four-fold rise in antibody titer to Chikungunya virus;  
Non-Pharmacological Treatment: 
The mainstay treatment for Chikungunya is the supportive symptomatic treatment.  
A: Assure plenty of rest to patients 
 
Pharmacological Treatment 
A: Maintain body fluids Sodium Lactate Compound (Ringers Lactate) intravenously. 
A: Control Fever and Pain by giving paracetamol (PO/IV]15mg/kg 8hourly for 3days 
 
Note 
• 
No antibiotics are of proven value.  
• 
Steroids should not be used. 
• 
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) such as ibuprofen and aspirin should 
be avoided. These anti-inflammatory drugs act by thinning the blood, and in a disease 
with risk of hemorrhage, blood thinners may exacerbate the prognosis 
• 
Do not use products containing oil of lemon eucalyptus (OLE) or para-menthane-diol 
(PMD) on children under 3 years old. 
• 
Do not apply insect repellent to a child’s hands, eyes, mouth, cuts, or irritated skin 
 
 
Prevention  
The most effective way to prevent infection from Chikungunya virus is to prevent mosquito bites 
during the day and night.  
• 
Use insect repellent (DEET, Picaridin (known as KBR 3023 and icaridin IR3535, Oil of 
lemon eucalyptus (OLE), Para-menthane-diol (PMD), 2-undecanone) 
• 
Modification of the mosquito bleeding sites 
• 
Wear long-sleeved shirts and pants,  
• 
Treat clothing and gears with permethrin 
• 
Take steps to control mosquitoes indoors and outdoors 
 
Public Health Control Measures 
• 
Symptomatic treatment for mitigating pain and fever using non-steroidal anti-inflammatory 
drugs along with rest usually suffices. Persistent joint pain may require analgesic and long- 
term anti-inflammatory therapy. 
• 
Prevention is entirely dependent upon taking steps to avoid mosquito bites and elimination 
of mosquito breeding sites. 

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• 
To avoid mosquito bites: 
o 
Wear full sleeve clothes and long dresses to cover the limbs 
o 
Use mosquito repellents 
o 
Use mosquito nets – to protect babies, old people and others, who may rest 
during the day. 
o 
The effectiveness of such nets can be improved by treating them with permethrin 
(pyrethroid insecticide). Curtains (cloth or bamboo) can also be treated with 
insecticide and hung at windows or doorways, to repel or kill mosquitoes 
 
4.2.2 Measles (Rubeola) 
Measles is an acute, highly communicable (contagious) infectious viral disease caused by Measles 
virus (MeV) which is the member of the family Paramyxoviridae, genus Morbillivirus. The mode of 
transmission is airborne, by droplet spread through coughing or sneezing, or by direct contact with 
nasal or throat secretions of infected persons. It is the fourth leading cause of death in children 
less than 5 years of age in many African countries. 
 
Case Definition 
Suspected case: 
Any person with fever and maculopapular (non-vesicular) generalized rash and cough, coryza or 
conjunctivitis (red eyes) or any person in whom a clinician suspects measles. 
Confirmed case: 
A suspected case with laboratory confirmation (positive IgM antibody) or epidemiological link to 
confirmed cases in an outbreak. 
 
Clinical Diagnostic Criteria 
• 
Generalized, reddish (erythematous), blotchy (maculopapular) rash;  
• 
History of fever usually above 38˚C (if not measured, then "hot" to touch); 
• 
Dry cough; Sore throat; Runny nose (coryza); 
• 
Inflamed eyes (conjunctivitis), tiny white spots with bluish-white centers on a red 
background found inside the mouth on the inner lining of the cheek- also called Koplik's 
spots.  
• 
In addition, children with measles frequently exhibit a dislike of bright light (photophobia), 
and often have a sore red mouth (stomatitis). 
Symptoms usually develop 10–12 days after exposure to an infected person and last 7–10 days 
 
Laboratory Investigation 
With coordination from the WHO, the Global Measles and Rubella Laboratory Network (GMRLN) 
performs case-based laboratory surveillance standardized methods to confirm Measles Infection by  
• 
Detection of viral RNA by RT-PCR (increasing role in case confirmation),  
• 
Enzyme Immunoassay (EIA) for immunoglobulin M (IgM)  
 
Pharmacological Treatment 
Note 
No specific antiviral treatment exists for measles virus  
 
Adults:  A: paracetamol(PO) 1g 8hourly for 5days 
AND 
A: vitamin A (PO) 200000 IU stat 
 
In case of ocular involvement, add  
A: oxytetracycline eye ointment 1% apply once daily for 7 days  
 
Children: 
A: paracetamol (PO) 10–15mg/kg 8hourly for 5days  
A: vitamin A if less than 1 year give 100,000IU (PO) start and if over 1 year give 200,000IU   
 
Prevention 
Routine measles vaccination for children combined with mass immunization campaigns  
• 
Administration of the first dose of measles-containing vaccine (MCV) at 9 months and 18 
months in measles-endemic regions (Tanzania) and at 12–15 months in non-endemic 
regions. 

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• 
Accelerated immunization activities have had a major impact on reducing measles deaths. 
• 
The World Health Organization (WHO) defines measles elimination as “the absence of 
endemic measles virus transmission in a defined geographical area (e.g. region or country) 
for at least 12 months in the presence of a surveillance system that has been verified to be 
performing well. 
 
Public Health Control Measures 
Efforts to reduce the secondary spread of measles include; 
• 
Improve routine vaccine coverage through the IVD, and lead supplemental vaccination 
activities in areas of low vaccine coverage. 
• 
Mobilize the community early to enable rapid case detection and treatment. 
• 
Provide Vitamin A: Dose 1: immediately, Dose 2: next day 
 
4.2.3 Rabies 
Rabies is a zoonotic disease (a disease that is transmitted to humans from animals) that is caused 
by a virus. Rabies infects domestic and wild animals, and is spread to people through close contact 
with infected saliva (via bites or scratches) The rabies virus infects the central nervous system, 
causing disease in the brain and, eventually, death. Early symptoms in people include: fever, 
headache, and general weakness or discomfort. As the disease progresses, symptoms include; 
insomnia, anxiety, confusion, slight or partialparalysis, excitable behaviour, hallucinations, increase 
in saliva, difficulty swallowing, and fear of water (hydrophobia). 
 
In unvaccinated humans, rabies is almost always fatal if post-exposure prophylaxis is not 
administered before the onset of severe symptoms. Death usually occurs within days of the onset 
of neurological symptoms. Dogs are the main carrier of rabies in Africa and are responsible for 
most (approximately 97%) of the human rabies deaths worldwide WHO estimates approximately 
55,000 human deaths worldwide due to rabies each year; in Africa the annual death toll is 24,000. 
 
Case Definition 
Suspected: A person with one or more of the following: headache, neck pain, nausea, fever, fear of 
water, anxiety, agitation, abnormal tingling sensations or pain at the wound site, when contact with 
a rabid animal is suspected. 
Confirmed: A suspected case that is laboratory confirmed 
 
Laboratory Investigation  
Human rabies is confirmed by intra-vitam and post mortem diagnostic techniques that detect whole 
viruses, viral antigens, or nucleic acids in infected tissues (brain, skin or saliva). E.g. Direct 
fluorescent antibody (DFA) test, which targets rabies virus antigens in brain tissue, Identification of 
viral nucleic acid by reverse transcriptase PCR on fixed tissue collected post mortem or in a clinical 
specimen (brain tissue or skin, cornea or saliva) or Detectable rabies-neutralizing antibody titre in 
the CSF of an unvaccinated person. 
 
Pharmacological Treatment 
Post-exposure prophylaxis (PEP) is the immediate treatment of a bite victim after rabies exposure by 
• 
Extensive washing and local treatment of the bite wound or scratch as soon as possible 
after a suspected exposure; 
• 
Providing effective rabies vaccine that meets WHO standards 
• 
Administration of rabies immunoglobulin (RIG), if indicated. 
 
Local wound therapy: -wash wound thoroughly with running water and soap for 10 minutes, and 
repeat process with:  
 
A: 10% Povidone iodine; to prevent secondary bacterial infection. 
If patient present with Anxiety, Agitation, Seizures,  
A: diazepam Adults 10mg IV slowly in 3–5minutes (0.1–0.3 mg/kg in 3–5 min) 10mg in 3–
5minutes, repeated 1–4 hourly Paediatrics 0.1–0.3 mg/kg in 3–5min, repeated 1–4 hourly 
to provide (total 2.4–12 mg/kg IV for 24 h) 
                 OR  
A:diazepam (IV) slowly in 3–5minutes, repeated 1–4hourly for 24hours 

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                OR 
A:  diazepam (IM) 20mg 2hourly for 24hours 
                OR 
A:  diazepam (Intrarectally) 10mg 1–4 hourly for 24 hours 
OR 
A: lorazepam 25–50mcg/kg 6 hourly for 24 hours  
OR 
C: midazolam 0.08 – 0.2mg/kg (IV) repeated 1–4 hourly for 24 to 48 hours 
              OR 
C: midazolam (intrarectally)10–30mg over 24 hours by pump for 24 to 48 hours 
 
 
If patient present with Anxiety 
A: Haloperidol 5mg (IM or SC) hourly until calm, then 4 or 6 hourly and when necessary 
            OR 
A: haloperidol 5 mg (IV) 5–15mg/24 hours 
OR  
A: chlorpromazine (IM) 25–50mg/6–8 hourly for 48hours 
 
Table 4.3: Support for Patient with Fever, Hypersecretion and Pain 
Indication 
Drug 
Route 
of 
administration 
Dose: adult 
Dose: paediatric 
Fever 
A: paracetamol 
iv infusion over 
15 minutes 
1 g every 8 h, 
maximum 
3-4 
g/24 h 
 
intrarectal 
1g every 4–6h, 
maximum 
3-4  
g/24 h 
10–15mg/kg (PO)  
every 8 hours for 
5 days 
A: ibuprofen 
intrarectal 
300–400 mg 8 
hourly 
 
A: aspirin 
intrarectal 
450–900mg 
4hourly, 
maximum 
3.6 
g/day 
 
Hypersecretion 
A: 
Hyoscine 
(scopolamine) 
hydrobromide 
sc or iv injection 
400 
mcg 
4 
hourly 
10 
mcg/kg 
4–
8hourly 
sc infusion 
1.2–2 mg/24 h 
40–60 mcg/kg/24h 
Pain 
C: morphine 
slow iv, sc or im 
10 mg 4hourly 
 
intrarectal 
15–30 
mg 
4hourly 
100 mcg/kg 
S: fentanyl 
transdermal 
patch 
12–25 
mcg/h 
every 72 h 
12 mcg/h every 
72h 
 
Prevention 
• 
Rabies can be prevented by  
• 
Vaccinating pets 
• 
Staying away from wildlife 
• 
Seeking medical care after potential exposures before symptoms start 
• 
Immunization  
 
Immunization  
Active Immunization  
Pre-exposure immunization is recommended for people in certain high-risk occupations such as 
laboratory workers handling live rabies and rabies-related (lyssavirus) viruses; and people (such as 
animal disease control staff and wildlife rangers)  
Active immunization: Human Diploid Cell Vaccine (HDCV) –either ID or IM 
 
A: anti-rabies Vaccines (2- 3 IU/dose)  
o 
IM: 1ml on days 0, 3, 7, 14, 28 (5 doses)  

101!
!
o 
ID: 0.2ml by dividing 0.1 ml on left shoulder and 0.1ml on right shoulder, on days 0, 3, 
7 and 28 (4 doses). Intradermal (ID) is mostly advised. 
In addition, patients should receive rabies immune globulin with the 1st dose (day 0) 
 
Passive Immunization  
B: anti-rabies human immunoglobulin 20 IU/kg half the dose given parenterally and the other 
half injected into and around the wound for victims suspected to be infected  
 AND 
A: tetanus toxoid vaccine, please refer to the section on Tetanus 
 
Note 
Treat the person immediately after the animal bite, before onset of symptoms    
Corticosteroid therapy generally is not considered for the management of brain edema in rabies. 
 
Public Health Control Measures 
• 
Post exposure prophylaxis to prevent rabies 
• 
Isolate patient and immunize contacts to prevent infection of others 
• 
Vaccinate local dogs and cats to prevent outbreaks 
• 
Promote public awareness of rabies 
• 
Target immunization campaign for domestic or wild animals in high-risk areas 
• 
Maintain active surveillance of rabies in animals 
 
4.2.4   Zika Virus Disease 
Zika virus is a flavivirus that is transmitted primarily through the bite of an infected mosquito, 
primarily Aedes aegypti, and also Aedes albopictus, the same mosquitoes that transmit dengue, 
chikungunya, and yellow fever. Zika virus can also be transmitted in-utero from mother to fetus, and 
through sexual contact, blood transfusion, and organ transplantation. Zika virus infections are 
usually asymptomatic. When symptoms occur, they tend to be mild and include mild fever, rash, 
conjunctivitis, and muscle and joint pain that last for 2 to 7 days. There is no specific treatment but 
symptoms can be treated with common fever medicines, rest and drinking fluids. 
 
Zika virus infection during pregnancy can result in preterm birth, fetal loss, stillbirth, and congenital 
malformations including microcephaly, limb contractures, eye abnormalities, brain calcifications, and 
other manifestations of Congenital Zika Syndrome. 
Zika virus is also associated with an increased risk of Guillain-Barré syndrome, and other 
neurological complications requiring close medical management and possibly intensive care and 
mechanical ventilation. 
 
Case Definition 
Suspected Case: Any person presenting with rash and/or fever and at least one of the following 
signs or symptoms: 
• 
arthralgia; or 
• 
arthritis; or 
• 
conjunctivitis (non-purulent/hyperaemic). 
 
Probable case: A suspected case with presence of IgM antibody against Zika virus and an 
epidemiological link (with no evidence of infection with other flaviviruses). 
 
Confirmed case: Any person with laboratory confirmation of recent Zika virus infection presence of 
Zika virus RNA or antigen in serum or other samples (e.g. saliva, urine, tissue, whole blood); or IgM 
antibody against Zika virus positive and Plague Reduction Neutralizing Test (PRNT90) for Zika virus 
with titre ≥20 and Zika virus PRNT90 titre ratio ≥ 4 compared to other flaviviruses; and exclusion of 
other flaviviruses. 
 
Clinical Diagnostic Criteria: 
• 
Fever, skin rashes, conjunctivitis,  
• 
Joint pain, malaise, Headache - usually mild and last for 2–7 days.  
• 
Neurological and auto-immune complications of Zika virus disease, babies born with 
microcephaly (Observed in northeast Brazil).  
 
 

102!
Laboratory Investigations 
•
Reverse transcriptase-polymerase chain reaction (RT-PCR) for viral RNA
•
Serology for IgM detection
•
Plaque reduction neutralization test (PRNT)
Non-Pharmacological Treatment: 
The mainstay treatment for Zika Virus is the supportive symptomatic treatment. 
•
A: Assure plenty of rest to patients
Pharmacological Treatment 
•
A: Maintain body fluids Sodium Lactate Compound (Ringers Lactate) intravenously.
•
A: Control Fever and Pain by giving Acetaminophen or Paracetamol 15mg/kg (PO/IV) 8
hourly for 3 days 
Note 
•
No antibiotics are of proven value.
•
Steroids should not be used.
•
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) such as ibuprofen and aspirin should be
avoided. These anti-inflammatory drugs act by thinning the blood, and in a disease with
risk of hemorrhage, blood thinners may exacerbate the prognosis
•
Do not use products containing oil of lemon eucalyptus (OLE) or para-menthane-diol
(PMD) on children under 3 years old.
•
Do not apply insect repellent to a child’s hands, eyes, mouth, cuts, or irritated skin
Prevention 
•
Vector control: - removal and modification of breeding sites and reducing contact between
mosquitoes and people
•
Wearing clothing (preferably light-coloured) that covers as much of the body as possible;
•
Using physical barriers such as window screens and closed doors and windows;
•
Applying insect repellent to skin or clothing that contains DEET, IR3535 or icaridin
Public Health Control Measures 
•
Strengthen event-based surveillance to detect the emergence of clusters of cases
presenting with rash and febrile syndrome of unknown aetiology.
•
Actively engage other sectors (e.g., environment, agriculture, tourism) to respond to Zika
virus through a multi-sectoral approach (One Health approach).
•
Enhance surveillance of Zika virus disease and of the conditions that may be associated
with it, including microcephaly and congenital Zika syndrome and Guillain-Barré syndrome
(GBS).
•
Enhance surveillance at prenatal and postnatal clinics to monitor possible congenital
infections and complications.
•
Conduct community-based assessments to determine the abundance of vector
mosquitoes, identify the most productive larval habitats, promote and implement plans for
appropriate vector control.
•
Report any identified unusual increase in the incidence of congenital neurological
malformations including microcephaly in neonates and adverse pregnancy outcomes not
explained through alternate causes, to the relevant public health authorities using IDSR
framework.
•
Intensify of efforts to reduce mosquito populations including elimination of potential
breeding sites (e.g., removal of trash and standing water sites around homes, covering
home water storage containers, and use of larvicides) and adult mosquito control methods.
•
Promotion of personal protection measures such as use of light-coloured protective
clothing (long sleeves and pants), insect repellent, and physical barriers such as screens,
closed doors and windows, and sleeping under mosquito nets including during the day
when Aedes mosquitoes are most active.
•
Develop risk communication messages to address population concerns, enhance
community engagement, improve reporting, and ensure application of vector control and
personal protective measures targeting reduction of contact with the vector.

103!
•
Provide women of childbearing age and particularly pregnant women with the necessary
information and materials on family planning and to reducing risk of exposure.
•
Provide clinical and psychosocial support services for affected children and families.
•
Zika can be transmitted through blood and blood products. Precautions already in place for
ensuring safe blood donations, transfusions, and prevention of bloodborne pathogens
should be followed.
•
Zika can be transmitted sexually. Men and women need to get counselling on safer sexual
practices, and be offered condoms and full range of contraceptive methods.
•
Ensure that pregnant women who have been exposed to Zika virus be counselled and
followed for birth outcomes based on the best available information and national practice
and policies.
•
Refer most severe cases with complication to hospitalized cares.
4.2.5 COVID-19 
Coronavirus Disease 2019 (COVID-19) is a recently discovered disease, caused by a Coronavirus, 
named SARS-CoV-2, which is genetically related to the virus causing Severe Acute Respiratory 
Syndrome (SARS) of 2003 and Middle East Respiratory Syndrome (MERS). This virus belongs to 
the family Coronaviridae, of the order Nidoviralessuspected to originate from an animal host 
(zoonotic origin) followed by human-to-human transmission. The disease was first detected in 
Wuhan, the capital city of Hubei, China, in December of 2019 and declared by the WHO to be a 
Public Health Emergency of International Concern, in 11 March 2020 due to its evident rapid 
disease spread worldwide in less than 6 months. Most estimates of the incubation period for COVID-
19 range from 1-14 days, most commonly around five days. 
Current evidence suggests that COVID-19 spreads between people through direct, indirect (through 
contaminated objects or surfaces), or close contact with infected people via mouth and nose 
secretions (saliva, respiratory secretions or secretion droplets). 
People with the virus in their noses and throats may leave infected droplets on objects and surfaces 
(called fomites) when they sneeze, cough on, or touch surfaces, such as tables, doorknobs and 
handrails. Other people may become infected by touching these objects or surfaces, then touching 
their eyes, noses or mouths before cleaning their hands. 
Case definition 
The case definitions are based on the current information available and might be revised as new 
information accumulates. 
Suspect case: A patient with acute respiratory illness (fever and at least one sign/symptom of 
respiratory disease, e.g., cough, shortness of breath), AND a history of travel to or residence in a 
location reporting community transmission of COVID-19 disease during the 14 days prior to 
symptom onset. 
OR 
A patient with any acute respiratory illness AND having been in contact with a confirmed or probable 
COVID-19 case (see definition of contact) in the last 14 days prior to symptom onset; 
OR 
A patient with severe acute respiratory illness (fever and at least one sign/symptom of respiratory 
disease, e.g., cough, shortness of breath; AND requiring hospitalization) AND in the absence of an 
alternative diagnosis that fully explains the clinical presentation. 
Probable case: Any suspect case for whom testing for COVID-19 is inconclusive or is tested positive 
using a pancoronavirus assay and without laboratory evidence of other respiratory pathogens. 
OR 
A suspect case for whom testing could not be performed for any reason 
OR 
Any suspect case or death with epidemiologic link to confirmed cases or outbreak 
OR 
Any suspect case with typical appearance of COVID-19 in Chest Computed Tomography (CT) or 
chest x-rays. 
Confirmed case: An individual (contact or suspect case) with a laboratory-confirmed COVID-19 by 
real-time reverse-transcription polymerase chain reaction (rRT-PCR). 

104!
OR 
A suspect case with a strong epidemiological link to COVID-19 patient and detection of antigen 
using validated/adequate direct SARS-CoV-2 antigen detection tests. 
OR 
A suspect case with a strong epidemiological link to COVID-19 patient and detection of exposure to 
virus (Antibodies – IgM and/or IgG, IgA) using validated/adequate serology tests (indirect antibody 
detection tests). 
Clinical Diagnosis 
Most common symptoms: 
•
Fever, Dry Cough and Tiredness
Less common symptoms: 
Headache, Sore throat, Loss of taste or smell,Chills, Runny nose, Headache, Chest pain , 
Muscle aches, Diarrhea,, Conjunctivitis, Skin rash , or Discoloration of fingers or toes 
Serious symptoms- Severe Acute Respiratory Infection (SARI): 
•
Difficulty breathing or shortness of breath
•
Chest pain or pressure
•
Loss of speech or movement
The risk of serious illness from COVID-19 includes serious heart diseases, such as heart failure, 
coronary artery disease or cardiomyopathy, Cancer, Chronic obstructive pulmonary disease 
(COPD), Type 2 diabetes, Type 1 diabetes, Asthma, Liver Disease, Cystic Fibrosis, Severe obesity, 
Chronic kidney disease, Sickle cell disease, Immunocompromized patients by solid organ 
transplants, bone marrow transplant, HIV or cancer medications. 
Laboratory Investigation 
Rule out Community-Acquired Pneumonia (Streptococcus pneumonia, Haemophilus influenza type 
b, Staphylococcus aureaus, Klebsiella pneumoniae, Legionella pneumophila, Influenza viruses, and 
Respiratory Syncytial virus). 
Specimen collection, processing, and laboratory testing shall follow biosafety procedures. 
• Collect blood cultures for bacteria that cause pneumonia and sepsis, ideally beforeantimicrobial
therapy.
• DO NOT delay antimicrobial therapy while waiting for blood culture results.
•
Collect specimens from BOTH the upper respiratory tract (URT; nasopharyngealand
oropharyngeal) AND lower respiratory tract (LRT; expectorated sputum, endotracheal aspirate, or
Broncho alveolar lavage) for SARS-CoV-2testing by RT-PCR.
Clinicians may elect to collect only LRT samples when these are readily available (for example, in
mechanically ventilated patients).
• Use appropriate PPE for specimen collection (droplet and contact precautions forURT specimens;
airborne precautions for LRT specimens).
• When collecting URT samples, use viral swabs (sterile Dacron or Rayon, not cotton) and viral
transport media.
Where feasible both URT and LRT specimens can be tested for other respiratory viruses 
like Influenza A and B (including zoonotic influenza A), Respiratory syncytial virus, 
Parainfluenzaviruses, Rhinoviruses, Adenoviruses, Enteroviruses (e.g. EVD68), Human meta 
pneumovirus, and Endemic human coronaviruses (i.e. HKU1, OC43, NL63, and 229E). 
Note 
Do not take sample from the nostrils or tonsils 

105!
•
Routine confirmation of cases of COVID-19 is based on detection of unique sequences of
virus RNA by Nucleic acid amplification tests (NAAT) such as real-time reverse-
transcription polymerase chain reaction (rRT-PCR).
•
Serological testing (indirect antibody detection tests) can aid investigation of an ongoing
outbreak and retrospective assessment of the attack rate or extent of an outbreak.
•
Viral sequencing to providing confirmation of the presence of the virus, regular
sequencing of a percentage of specimens from clinical cases can be useful to monitor for
viral genome mutations
•
Viral culture is not recommended as a routine diagnostic procedure.
Severity of Illness Categories 
• Asymptomatic or Pre-Symptomatic Infection: Individuals who test positive for SARS-CoV-2 using a
virologic test (i.e., a nucleic acid amplification test or an antigen test), but who have no symptoms
that are consistent with COVID-19.
• Mild Illness: Individuals who have any of the various signs and symptoms of COVID-19 (e.g., fever,
cough, sore throat, malaise, headache, muscle pain, nausea, vomiting, diarrhea, loss of taste and
smell) but who do not have shortness of breath, dyspnea, or abnormal chest imaging.
• Moderate Illness: Individuals who show evidence of lower respiratory disease during clinical
assessment or imaging and who have saturation of oxygen (SpO2) ≥94% on room air at sea level.
• Severe Illness: Individuals who have SpO2 <94% on room air at sea level, a ratio of arterial partial
pressure of oxygen to fraction of inspired oxygen (PaO2 /FiO2) <300 mmHg, respiratory frequency
>30 breaths per minute, or lung infiltrates >50%.
• Critical Illness: Individuals who have respiratory failure, septic shock, and/or multiple organ
dysfunction.
Management 
•
All patients with suspected COVID-19 who have severe acute respiratory infection should
be triaged and isolated at the first point of contact with the health care system. 
•
Emergency treatment should be started based on disease severity.
•
For those presenting with mild illness, hospitalization may not be required unless there is
concern about rapid deterioration. If there is only mild illness, providing care at home may 
be considered if available. 
•
Moderate to severe and critical cases must be admitted for management.
•
Admitted cases must be monitored for early identification of deterioration and appropriate
treatment offered as per national treatment protocol for moderate to severe COVID-19 
patients. 
•
Oxygen is the mainstay of therapy for those whose SpO2 drops according the guideline.
•
Recovered patients may be discharged if 2 RT-PCR taken at least 24 hours apart are
negative with clinical recovery (temperature resolved for more than 48 hours and no need 
for oxygen therapy). 
Note 
• All areas for treatment of COVID-19 patients should be equipped with pulse oximeters, functioning
oxygen systems and disposable, single-use, oxygen-delivering interfaces (nasal cannula, simple
face mask, and mask with reservoir
bag).
• Use contact precautions when handling contaminated oxygen interfaces of patients with SARS-
CoV-2 infection.
Early General Supportive Therapy and Monitoring 
Patients with SARI shall be managed in isolated critical care units 
•
Give supplemental oxygen therapy immediately to patients with SARI and respiratory
distress, hypoxemia, or shock.
o
Initiate oxygen therapy at 5 L/min and titrate flow rates to reach target SpO2≥90%
in non-pregnant adults and SpO2≥92-95 % in pregnant patients.
o
Children with emergency signs (obstructed or absent breathing, severe
respiratory distress, central cyanosis, shock, coma or convulsions) should
receive oxygentherapy during resuscitation to target SpO 2 ≥94%; otherwise, the
target SpO2is≥90%.
Testing

106!
•
Use conservative fluid management in patients with SARI when there is no evidence of
shock.
•
Treat cautiously with intravenous fluids, becauseaggressive fluid resuscitation may worsen
oxygenation, especially in settings limited availability of mechanical ventilation.
•
Give empiric antimicrobials to treat all likely pathogens causing SARI.
o
Azithromycin 500mg (PO) day 1 following initial assessment, then followed by
500mg (PO) 8hourly on Days 2-5 when sepsis or superimposed pneumonia is
suspected (based on the clinical diagnosis). Give Steroids
•
Prednisolone 10mg to 20mg (PO) once a day for 7 days OR Dexamethasone 6mg (PO/ IV)
once a day for up to 7days or until hospital discharge) based on patents conditions in ICU /
Critical Care Units
Give Supplements
•
Magnesium 300mg or 400mg (PO) once a day for 7days
•
Zinc 7mg (PO) for children aged 1– years of age, increasing up to 25mg (PO) for adults
and females of any age who are pregnant or lactating
•
Vitamin C dose of 70-150mg 24hourly for 7 days
Closely monitor the patient’s clinical condition 12 hourly
•
Monitor signs of SARI, clinical deterioration, like rapidly Progressive respiratory failure and
sepsis, and apply supportive care interventions immediately.
Note 
•
Application of timely, effective, and safe supportive therapies is the cornerstone of therapy
for patients that develop severe manifestations ofSARS-CoV-2 infection
•
Do not routinely give systemic corticosteroids for treatment of viral pneumonia.
(No survival benefit and possible harms (avascular necrosis, psychosis, diabetes, and
delayed viral clearance).
•
corticosteroid should be used with caution in the treatment of COVID-19 patients < 7 days:
corticosteroids are not recommended for patients with mild conditions
Focused Supportive Management 
Infection Control: 
•
For health care workers who are performing aerosol-generating procedures on patients
with COVID-19, Using an N95 respirator (or equivalent or higher-level respirator) rather
than surgical masks, in addition to other personal protective equipment (i.e., gloves, gown,
and eye protection such as a face shield or safety goggles)
•
Endotracheal intubation in patients with COVID-19 to be performed by health care
providers with extensive airway management experience, if possible
•
Intubation be performed using video laryngoscopy, if possible
Hemodynamic Support: 
•
Norepinephrine as the first-choice vasopressor
•
For adults with COVID-19 and refractory septic shock who are not receiving corticosteroids
to treat their COVID-19, 
Low-dose corticosteroid therapy (“shock-reversal”) over no corticosteroid therapy 
Ventilatory Support: 
•
For adults with COVID-19 and acute hypoxemic respiratory failure despite conventional
oxygen therapy, high-flow nasal cannula (HFNC) oxygen over noninvasive positive
pressure ventilation (NIPPV) (BI).
•
For patients with persistent hypoxemia despite increasing supplemental oxygen
requirements in whom endotracheal 
intubation is not otherwise indicated, considering a trial of awake prone positioning to 
improve oxygenation 
•
For mechanically ventilated adults with COVID-19 and acute respiratory distress syndrome
(ARDS), use low tidal volume (VT) ventilation (VT 4–8 mL/kg of predicted body weight)
over higher tidal volumes (VT >8 mL/kg)
•
For mechanically ventilated adults with COVID-19 and refractory hypoxemia despite
optimized ventilation, prone ventilation for 12 to 16 hours per day over no prone ventilation

107!
Acute Kidney Injury and Renal Replacement Therapy: 
•
For critically ill patients with COVID-19 who have acute kidney injury and who develop
indications for renal replacement therapy, provide continuous renal replacement therapy
(CRRT), if available. If CRRT is not available or not possible due to limited resources,
provide prolonged intermittent renal replacement therapy rather than intermittent
hemodialysis
Pharmacologic Interventions: 
• For the therapeutic Management of Patients with COVID-19 use of Dexamethasone and
Remdesivir, either alone or in combination.
• In patients with COVID-19 and severe or critical illness, there are insufficient data to
recommend empiric broad- 
spectrum antimicrobial therapy in the absence of another indication. 
Implementation of additional Precautions for suspected SARS-CoV-2infections 
Contact and Droplet precautions for suspected SARS-CoV-2 infection: 
- Place patients in adequately ventilated single rooms. For naturally ventilated general ward rooms
this is considered to be 160 L/second/patient;
- Apply Infection prevention and control measures when providing health care where novel
coronavirus (SARS-CoV-2) infection is suspected, the Interim Guidance is to:
•
Place patient beds at least 1m apart;
•
Where possible, cohort HCWs to exclusively care for cases to reduce the risk of spreading
transmission due to inadvertent infection control breaches;
•
Use of PPE (medical mask, Use eye/facial protection (i.e. goggles or a face shield); Use a
clean, non-sterile, long-sleeved fluid resistant gown; Use gloves)
•
Use either single use disposable equipment or dedicated equipment (e.g. stethoscopes,
blood pressure cuffs and thermometers). If equipment needs to be shared among patients,
clean and disinfect between each patient use (e.g. ethyl alcohol 70%);
•
Refrain from touching eyes, nose or mouth with potentially contaminated hands;
•
Avoid the movement and transport of patients out of the room or area unless medically
necessary.
•
Use designated portable X-ray equipment and/or other important diagnostic equipment.
•
If transport is required, use pre-determined transport routes to minimize exposures to staff,
other patients and visitors and apply medical mask to patient;
•
Maintain a record of all persons entering the patient’s room including all staff and visitors.
Prevention 
Application of Standard Precautions for all patients and people at risks in the public include hand 
and respiratory hygiene; use of Personal protective equipment (PPE) depending on risk; in hospitals 
use safe waste management; environmental cleaning and sterilization of patient-care equipment and 
linen. Ensure the following respiratory hygiene measures. 
- Offer a medical mask (N95) or double cloth mask in health care settings
- Cover nose and mouth during coughing or sneezing with tissue or flexed elbow for others
- Perform hand hygiene after contact with respiratory secretions.
Personal Protective Equipment (PPE) 
Rational, correct, and consistent use of available PPE and appropriate hand hygiene helps to 
reduce the spread of the pathogens. PPE effectiveness depends on adequate and regular supplies, 
adequate staff training, proper hand hygiene and specifically appropriate human behavior. 
Health care workers and Administrators should ensure that environmental cleaning and disinfection 
procedures are followed consistently and correctly. Thorough cleaning of environmental 
surfaces with water and detergent and applying commonly used hospital level disinfectants (such 
as sodium hypochlorite) is an effective and sufficient procedure. Laundry, food service utensils 
and medical waste should be managed in accordance with safe routine procedures. 

108!
•
Verify the alerts to determine if they meet the standard case definition for COVID-19
•
Respond as for suspected case if they meet the standard case definition
•
Record all alerts in an alert/rumor log sheet.
•
Provide epidemiological information to conduct risk assessment at the national, regional
and global level.
•
Conduct epidemiological investigation to identify risk factors for infection and populations
at risk for severe disease.
•
Maintain strict acute respiratory disease infection control practices throughout the
epidemic.
•
Mobilize the community for early detection and care and conduct community education
about how the disease is transmitted and how to implement IPC at the home care setting
and during funerals and burials. Consider social distancing strategies.
•
Conduct contact follow-up and active searches for additional community cases or deaths
that may not come to the health care setting.
•
Distribute laboratory specimen collection kits to health care facilities
•
Establish treatment unit to handle additional cases that may come to the health center in
line with the national protocols.
•
Maintain strict acute respiratory disease infection control precautions and establish an
isolation ward to manage additional cases who may present for care.
.
Public Health Control Measures 
•
Establish an alert management system e.g call center with hotlines

109!
!
CHAPTER FIVE 
MALARIA 
 
Malaria case definition 
A malaria case is a person with malaria infection, confirmed by microscopy or mRDT, regardless of 
whether fever and other clinical symptoms are present.  
5.1 Asymptomatic Malaria Case 
Asymptomatic malaria case can be found during Active Case Detection (ACD) by health workers in 
the community and in households. Therefore, all patients with parasitemia are considered “malaria 
cases”, regardless of whether clinical symptoms are present or not.   
5.2 Symptomatic Malaria Case 
5.2.1    Uncomplicated Malaria 
Uncomplicated malaria is defined as symptomatic malaria without signs of severity or evidence 
(clinical or laboratory) of vital organ dysfunction. 
 
Clinical presentation  
• 
Fever 
• 
Headache 
• 
Joint pains 
• 
Malaise 
• 
Vomiting 
• 
Diarrhoea 
• 
Body ache, body weakness 
• 
Poor appetite 
• 
Pallor, enlarged spleen 
 
Investigations 
The recommended investigations are: 
• 
Quality malaria microscopy or quality malaria Rapid Diagnostic Tests (mRDTs)  
 
Note 
• 
It is compulsory to test and confirm all suspected malaria patients. Give antimalarial only to 
those who test positive. 
• 
In cases where non-response to malaria treatment (treatment failure) is suspected in 
patients who initially tested positive, microscopy is the recommended laboratory procedure 
as mRDTs are not recommended because parasite antigens persist up to 4 weeks after 
parasitaemia has cleared. 
 
Non-Pharmacological Treatment 
• 
Continue with feeding and fluid intake 
• 
Followed up immediately if the condition worsens or on the fourth day if symptoms persist. 
 
Pharmacological Treatment 
Drug of choice for treatment of uncomplicated malaria is: 
A: Artemether+Lumefantrine (FDC) (PO) 20mg+120mg   
Common formulations:  
• 
Fixed formulation Artemether 20mg, Lumefantrine120mg; 6, 12, 18 and 24 tablets blister 
• 
Fixed formulation Artemether 80mg, Lumefantrine 480mg; 6 tablets blister 
 
Dispersible tablets: Fixed formulation for children 
A: Artemether 20mg + Lumefantrine120mg; 6 tablets blister (5–14kg): 1 tablet; 15–24 kg: 2 
tablets)  
 
Table 5.1: Dosage regimen forALu (artemether 20mg/lumefantrine 120mg) 
 
 
 
Day 1 
Day 2 
Day 3 
 
Kg 
Dose 
1st 
2nd 
3rd 
4th 
5th 
6th 
Hours 
0 (*) 
8 
24 
36 
48 
60 
Age (years) 
Tablets 
Tablets 
tablets 
tablets 
tablets 
Tablets 
up to 15 
0 to 3 
1 
1 
1 
1 
1 
1 

110!
15 up to 25 
3 up to 8 
2 
2 
2 
2 
2 
2 
25 up to 35 
8 up to 12 
3 
3 
3 
3 
3 
3 
35 
and 
above 
12 
and 
above 
4 
4 
4 
4 
4 
4 
(*) 0 hours means the time of starting medication 
Table 5.2: The recommended dosing schedule for ALu strength 80/480 mg 
Day 1 
Day 2 
Day 3 
Kg 
Dose 
1st 
2nd 
3rd 
4th 
5th 
6th 
Hours 
0 (*) 
8 
24 
36 
48 
60 
Age 
(years) 
tablets 
Tablets 
Tablets 
Tablet
s 
tablets 
Tablets 
35 and 
above 
12 and 
above 
1 
1 
1 
1 
1 
1 
(*) 0 hours means the time of starting medication 
For practical purposes, a simpler dosage regimen is recommended in order to 
improve compliance: the first dose should be given as DOT; the second dose 
should strictly be given after 8 hours; subsequent doses could be given 12hourly 
in the second and third day of treatment until completion of 6 doses 
The alternative medicines for the treatment of uncomplicated malaria, where there is no response to 
Artemether-Lumefantrine or it is contraindicated, is Dihydroartemisinin-Piperaquine.  
C: dihydroartemisinin+piperaquine (FDC) (PO). 
Adult formulation containing 40 mg Dihydroartemisinin + 320 mg Piperaquine.  Paediatrics formulation 
contains a fixed combination of 20 mg of Dihydroartemisinin +160 mg Piperaquine.
Table 5.3: Dose Schedule for Dihydroartemisinin + Piperaquine 
Body 
Weight (kg) 
Daily dose (mg) 
Tablet strength 
Number 
of 
tablets 
per dose 
Dihydro 
artemisinin 
Piperaquine 
5 to <8 
20 
160 
20mg / 160mg 
1 tablet 
x 3 days 
8 to <11 
30 
240 
20mg / 160mg 
1 ½ 
tablet x 
3 days 
11 to <17 
40 
320 
40mg / 320mg 
1 tablet 
x 3 days 
17 to <25 
60 
480 
40mg / 320mg 
1 ½ 
tablet x 
3 days 
25 to <36 
80 
640 
40mg / 320mg 
2 tablets 
x 3 days 
36 - <60 
120 
960 
40mg / 320mg 
3 tablets 
x 3 days 

111!
!
Body 
Weight (kg) 
Daily dose (mg) 
Tablet strength 
Number 
of 
tablets 
per dose 
Dihydro 
artemisinin 
Piperaquine 
60 to <80 
160 
1,280 
40mg / 320mg 
4 tablets 
x 3 days 
>80 
200 
1,600 
40mg / 320mg 
5 tablets 
x 3 days 
 
Management of fever 
Patients with high fever (38.50C and above) should be given an anti-pyretic medicine like 
paracetamol (Error! Reference source not found.) or acetylsalicylic acid every 4 to 6 hours 
(maximum 4 doses in 24 hours) until symptoms resolve, usually after two days.  
Note 
Children below 12 years should not be given acetylsalicylic acid because of the risk of developing 
Reye's syndrome. 
 
Table 5.4: Treatment Schedule for Paracetamol (500mg) Tablets Children 
10mg/kg body weight 
Age (years) 
Weight (Kg) 
Dose 
2 months up to 3 yrs 
4 up to 14 
¼ 
3 up to 5 
14 up to 19 
½ 
5 up to12 
19 up to 35 
1 
12 up to 14 
35 up to 45 
11/2 
14 and above 
45 and above 
2 
 
5.2.2    Severe Malaria 
In a patient with P. falciparum asexual parasitaemia and no other obvious cause of symptoms the 
presence of one or more of features listed below classify the patient as suffering from severe 
malaria. 
 
Clinical presentation 
• 
Prostration/extreme weakness 
• 
Impaired consciousness 
• 
Change of behaviour 
• 
Convulsions 
• 
Respiratory distress (due to lactic 
acidosis 
and/or 
pulmonary 
oedema) 
• 
Jaundice 
• 
Circulatory collapse/shock 
• 
Vomiting everything 
• 
Inability to drink or breast feed 
• 
Bleeding tendency/DIC 
 
Investigations 
In severe malaria, blood slide (BS) is a recommended malaria test as it quantifies parasitemia. In 
severe ill patients receiving injectable antimalarial, serial BS investigations monitors level of 
parasitemia to verify malaria recovery, or if clinical condition is not improving to rule out another 
serious condition. 
• 
Blood film for malaria parasites 
• 
Blood glucose estimation in patients with altered consciousness 
• 
Haematocrit and/or haemoglobin estimation 
• 
Lumbar puncture to exclude meningitis (if facilities for LP assessment are available) 
• 
Serum creatinine or urea– to assess Kidney function 

112!
!
• 
Electrolytes– for early detection of acute renal failure 
• 
Full blood cell count and differential white cell count for additional diagnosis of other 
infectious diseases 
• 
Blood gases, pH and anion gap– to diagnose acidosis  
• 
Radiological investigation: Chest X–ray; look for pulmonary oedema or lobar consolidation 
• 
Blood culture and sensitivity where feasible  
 
Non-Pharmacological Treatment 
A rapid assessment must be conducted including airway, breathing, circulation, coma, convulsion, 
and dehydration status.  
 
Referral: If effective management of severe malaria and supportive care for complications is not 
possible, patients should be given pre-referral treatment and referred immediately to an appropriate 
facility for continued treatment. 
 
Pharmacological Treatment 
A: Parenteral artesunate 
Dosage: 
• 
2.4 mg/kg in body weight. (IV) or (IM) given on admission (time = 0 hour), then at 12 hours 
and 24 hours for a minimum of 3 injections in 24 hours regardless of patient’s recovery. 
• 
Children weighing less than 20 kg Dosage: 3 mg/kg/dose (or higher). Same schedule as 
indicated above (0, 12, 24 hours) 
• 
Complete artesunate injection treatment by giving a complete course (3days) of 
artemether-lumefantrine (ALu) or other ACT. 
Consider broad spectrum antibiotic as treatment of septicemia. 
 
Administration and dosage (30 mg, 60mg and 120mg strength): Injectable artesunate has 2-steps 
dilutions. 
• 
Step 1: The powder for injection should be diluted with 1ml of 5% sodium bicarbonate 
solution (provided in each box) and shaken vigorously 2–3 minutes for better dissolving 
until the solution becomes clear. 
• 
Step 2: For slow intravenous infusion (3–4 minutes), add 5 ml of 5% dextrose or normal 
saline, to obtain artesunate concentration of 10 mg/ml. For deep intra–muscular injection, 
add 2 ml of 5% dextrose or normal saline to obtain artesunate concentration of 20 mg/ml. 
 
Table 5.5: Dilution of Artesunate for Injection 
Route 
IV injection 
IM injection 
Strength 
30 mg 
60 mg 
120 mg 
30 mg 
60 mg 
120 mg 
Sodium bicarbonate 5% 
0.5 
1 
2 
0.5 
1 
2 
Normal saline or 5% of glucose 
2.5 
5 
10 
1 
2 
4 
Total (ml) 
3 
6 
12 
1.5 
3 
6 
Artesunate concentration (mg/ml) 
10 
10 
10 
20 
20 
20 
 
Table 5.6: Dosage Schedule for Artesunate Injection 
Weight 
Dose 
ml per dose strength 60mg 
Vials of Artesunate 60mg 
needed** 
Kg 
mg/kg 
IV 
IM* 
 
10 mg/ml 
20 mg/ml 
 
<5 
3.0 
1.5 
1 
1 
5–8 
3.0 
2 
1 
1 
9–12 
3.0 
4 
2 
1 
13–16 
3.0 
5 
3 
1 
17–20 
3.0 
6 
3 
1 
21–25 
2.4 
6 
3 
1 
26–29 
2.4 
7 
4 
2 
30–33 
2.4 
8 
4 
2 
34–37 
2.4 
9 
5 
2 
38–41 
2.4 
10 
5 
2 
42–45 
2.4 
11 
6 
2 

113!
46–50 
2.4 
12 
6 
2 
51–54 
2.4 
13 
7 
3 
55–58 
2.4 
14 
7 
3 
59–62 
2.4 
15 
8 
3 
63–66 
2.4 
16 
8 
3 
67–70 
2.4 
17 
9 
3 
71–75 
2.4 
18 
9 
3 
76–79 
2.4 
19 
10 
4 
80–83 
2.4 
20 
10 
4 
84–87 
2.4 
21 
11 
4 
88–91 
2.4 
22 
11 
4 
92–95 
2.4 
23 
12 
4 
96–100 
2.4 
24 
12 
4 
*Half the dose is rounded up to 1ml; **Full vial (s) might not be required for a given weight band. The 
left–over solution must be discarded within 1hr of preparation and must not be reused
If the patient can tolerate oral medication after 24 hours provide a full treatment course of AL. Initiate 
the first dose of AL 8 hours after the last injection.  
Alternative 
C: Injectable Artemether 
Injectable Artemether is to be used when Artesunate is contraindicated (in case of allergy, medicine 
interaction or non- response) and when not available. Artemether should be administered in a dose 
of 3.2mg/kg loading dose IM stat (0hour) then 1.6mg/kg (24hours and 48hours). 
Table 5.7: Artemether Injectable Dosage by Weight 
Loading dose 
Second and subsequent doses 
0 hour 
24, 48, hours 
Dose 
Strength 
Dose 
Strength 
Weight 
3.2 mg/Kg 
80 mg/ml 
1.6 mg/kg 
80 mg/ml 
Kg 
Mg 
ml 
mg 
ml 
<5 
16 
0.2 
8 
0.1 
5-8
26 
0.3 
13 
0.2 
9-12
38 
0.5 
19 
0.2 
13-16
51 
0.6 
26 
0.3 
17-20
64 
0.8 
32 
0.4 
21-25
80 
1.0 
40 
0.5 
26-29
93 
1.2 
46 
0.6 
30-33
106 
1.3 
53 
0.7 
34-37
118 
1.5 
59 
0.7 
38-41
131 
1.6 
66 
0.8 
42-45
144 
1.8 
72 
0.9 
>45
160 
2.0 
80 
1.0 
If the patient can tolerate oral medication after 24 hours provide a full treatment course of ALu. 
Initiate the first dose of ALu 8hours after the last injection. 
Management of complications 
To reduce the unacceptably high mortality of severe malaria, patients require intensive care. Clinical 
observations should be made as frequently as possible. Airway maintenance, nurse on side, fanning 
if hyperpyrexia is present, fluid balance review: 

114!
Coma (cerebral malaria): maintain airway, nurse on side, and exclude other causes of coma (e.g. 
hypoglycemia, bacterial meningitis); avoid giving corticosteroids. 
Dehydration: Correct dehydration 
Hyperpyrexia: fanning, paracetamol if patient can swallow 
Convulsions: maintain airways; treat with 
Adult 
A: diazepam (IV) 0.15 mg/ kg (maximum 10 mg) slow bolus IV injection. 
Children 
A: diazepam (rectal) 0.5–1.0 mg/ kg1. 
If convulsions persist after 10 minutes repeat rectal diazepam treatment as above. Should 
convulsions continue despite a second dose, give a further dose of rectal diazepam  
OR  
A: phenobarbitone (IM/IV) 20 mg/ kg after another 10 minutes. 
Hypoglycemia: remains a major problem in the management of severe malaria especially in young 
children and pregnant women. It should be deliberately looked for and treated accordingly. Urgent 
and repeated blood glucose screening. 
In children:  
B: dextrose 10% (IV) 5 ml/kg 
OR 
C: dextrose 25% (IV) 2.5ml/kg as bolus;  
If 50%dextrose solution is available, it should be diluted to make 25% by adding an equal volume of 
water for injection or normal saline.  
In adults:  
B: dextrose 10% (IV) 125ml 
OR 
C: dextrose 25% (IV) 50ml as bolus. 
Where dextrose is not available, sugar water should be prepared by mixing 20g of sugar (4–level 
teaspoons) with 200ml of clean water. 50ml of this solution is given ORALLY or by nasogastric tube 
if unconscious. 
Severe anaemia: Refer to haematologychapter 
Acute pulmonary oedema: Refer to respiratory conditions chapter 
Acute renal failure: Refer to cardiovascular disease condition chapter 
Shock: Refer to emergency and critical care chapter 
5.3 Management of Malaria in Special Groups 
5.3.1    Malaria in Pregnancy (MIP) 
The effects of malaria in pregnancy are related to the malaria endemicity, with abortion more 
common in areas of low endemicity and intrauterine growth retardation more common in areas of 
high endemicity.  
5.3.1.1 Uncomplicated Malaria in Pregnancy  
In high-transmission areas (moderate to high immunity); malaria is usually asymptomatic in 
pregnancy or is associated with only mild, non-specific symptoms. (See section 5.1 above) 
Pharmacological Treatment  
Artemether/Lumefantrine (ALu) is the recommended treatment of choice of a confirmed 
uncomplicated malaria to pregnant women in all trimesters. 
1Draw&the&IV&preparation&into&a&small&syringe&and&remove&the&needle.&Insert&5&cm&of&a&nasogastric&tube&into&the&rectum.&Inject&
the&diazepam&into&the&nasogastric&tube&and&flush&it&with&5&ml&of&water.&If&a&nasogastric&tube&is&not&available,&use&a&syringe&
without&a&needle.&Hold&buttocks&together&for&few&minutes&to&ensure&retention&and&absorption&of&the&medicine&

115!
5.3.1.2 Severe Malaria in Pregnancy 
In low-transmission areas (low malaria immunity); women in the second and third trimesters of 
pregnancy are more likely to develop severe malaria than other adults, often complicated by 
pulmonary oedema and hypoglycaemia.  
The following are common features of severe malaria during pregnancy:  
•
High fever
•
Hyperparasitemia
•
Low blood sugar
•
vere haemolytic anaemia
•
Cerebral malaria
•
Pulmonary oedema
Pharmacological Treatment Intramuscular/ intravenous Artesunate is the drug of 
choice for treatment of severe malaria in all trimesters. 
5.3.1.3 Intermittent Preventive Treatment in Pregnancy (IPTp) 
Malaria parasites can easily accumulate and multiply in the placenta leading to placenta malaria 
infections, resulting to complications such as maternal anaemia, low birth weight, premature 
delivery, congenital infection and/or perinatal death. 
Note 
IPTp is an administration of antimalarial in full therapeutic doses at predetermined intervals during 
pregnancy 
individuals with no signs/symptoms of malaria. The aim is to prevent above mentioned 
complications with adverse 
effects to both mother and fetus3 
The medicine of choice for IPTp 
A: sulphadoxine+pyrimethamine (FDC) (PO) 500mg +25mg 
•
The dose is 3 tablets once
•
A minimum of 3 doses in entire pregnancy period
•
The first dose should be administered from 14 weeks of pregnancy onwards
•
Each dose should be given at least 4 weeks apart
•
The last dose can be administered up to the time of delivery, without safety concerns
Note: 
•
SP should not be administered to women receiving cotrimoxazole prophylaxis or pregnant
women who are taking folic acid at a daily dose equal or above 5 mg, as it counteracts its
efficacy
•
SP can be administered safely with combined ferrous sulphate 200mg + folic acid 0.25mg
•
If malaria is diagnosed to a scheduled pregnant woman for IPT with SP; SP should not be
given, instead a full treatment with antimalarial should be given
5.3.2 Management of Malaria in Neonates 
Neonatal malaria is defined as symptoms attributable to malaria with evidence of ring forms of 
malaria parasite in the blood of an infant within the first twenty-eight days (4 weeks) of life. 
Congenital malaria is defined as symptoms attributable to malaria with evidence of ring forms of 
malaria parasite in the blood of an infant within the first seven days (1 week) of life. The signs and 
symptoms resemble those seen in the new-born with septicemia 
Clinical presentation 
•
Fever
•
Lethargy
•
Unable to breastfeed
•
Vomiting
•
Irritability
•
Respiratory distress
•
Seizures
•
Jaundice
•
Pallor
•
Hepatosplenomegaly
•
Laboratory findings will include the
presence of malaria parasites.

116!
Investigations 
•
Full blood picture
•
blood sugar
•
blood culture and sensitivity, blood smear for malaria parasite, serum electrolytes
•
CSF for analysis
Management of neonatal malaria 
•
Neonatal malaria should always be considered as severe malaria
•
Neonates with suspected malaria should be admitted to hospital immediately as they can
deteriorate quickly and die at home
•
Parental Artesunate is recommended treatment of choice for neonates. Injectable Artemether
can be used as an alternative if Artesunate is not available
•
Broad spectrum antibiotic as majority of severe malaria accompanied with septicemia. Refer
septicemia treatment section.
Nursing care and monitoring 
•
Monitor vital signs (PR, RR & Temperature)
•
Monitor input/output
•
Check BS for malaria parasite daily
•
Ensure feeding
•
Advise on use of LLINs
5.3.3 Management of Malaria in HIV and AIDS Patients 
If malaria is diagnosed, depending on classification of the malaria diagnosis, a full treatment with 
antimalarial should be given according to the malaria classification. 
However, it should be noted that, clearance of parasitaemia may not necessarily be accompanied by 
clearance of symptoms (fever) due to the presence of other underlying opportunistic infections. HIV 
and AIDS infected adults with low CD4 cell counts may be more susceptible to treatment failure of 
anti-malaria drugs. 
Note 
•
In suspected cerebral malaria in a HIV and AIDS patient, cerebrospinal fluid (CSF)
examination to rule out other life-threatening conditions such as bacterial and cryptococcal
meningitis

117!
CHAPTER SIX 
HIVA ND AIDS 
AIDS is defined as Acquired Immuno- Deficiency Syndrome caused by Human Immunodeficiency 
Virus (HIV). Clinical features are usually due to immune system suppression. 
Clinical presentation 
•
Fever, diarrhoea, weight loss, skin rashes, sores, generalized pruritis, altered mental
status, persistent severe headache, oral thrush or Kaposi’s sarcoma may be found in
patients with advanced disease
•
Opportunistic infections e.g. tuberculosis, candidiasis or pyogenic infections, Advanced
HIV Disease
6.1 Treatment of HIV and AIDS in Adults and Adolescents 
•
All HIV infected individuals are eligible for ART. Early initiation of combination treatment
(ART) is associated with health benefits in terms of reduced morbidity and mortality in all
age groups.
•
Antiretroviral therapy (ART) has dramatically reduced HIV-associated morbidity and
mortality and has transformed the HIV disease into a chronic, manageable condition. In
addition, treatment of HIV infected individuals with ART is highly efficient at preventing
transmission to sexual partners and mother to child transmission (MTCT).
Evaluation to be done before Initiating ART 
From the moment a patient tests HIV positive, he/she should be linked to the Care and Treatment 
Clinic (CTC). In health facilities where ART is being initiated at RCH and TB clinics, patients can be 
managed at those clinics. Mobile outreach clinics can also be used for key and vulnerable 
population and hard to reach areas.    
6.1.1 First-Line Regimens for Adults and Adolescents 
Table 6.1Recommended First-Line Regimens for Adults and Adolescents 
Patient group 
Preferred (Default) Regimen 
Alternative Regimen 
Adults and adolescents (>15 
years), 
Pregnant/lactating 
mothers 
A: TDF +3TC +DTG (TLD) 
A: ABC + 3TC+ DTG  
A: TDF + 3TC +EFV (TLE 600 or TLE 
400) 
Special situations: 
A:AZT + 3TC + DTG 
HIV and TB co-infections 
A: TDF + 3TC +DTG (Double 
dosage of DTG) 
A: TDF + 3TC +EFV (TLE600) 
A: ABC + 3TC+ DTG (Double dosage of 
DTG) 
Special situations: 
A:AZT + 3TC + DTG (Double dosage of 
DTG) 
People who Inject Drugs 
(PWID) 
A: TDF + 3TC +DTG 
A: ABC + 3TC+ DTG 
A: TDF + FTC +ATV/r 
6.1.2 ART in Women of Childbearing Potential or Pregnant Women 
Mother-to-child transmission (MTCT) of HIV refers to the transmission of HIV infections from HIV-
infected mothers to their infants. MTCT can occur during pregnancy, labour and delivery, and 
breast-feeding. Without intervention, the overall risk of MTCT is approximately 20%–45%. However, 
with interventions, this risk can be reduced to less than 5%. Transmission of HIV from mother to her 
child accounts for over 90% of all HIV infections in children aged below 15 years. 

118!
Figure 6.1 Estimated HIV Outcomes for Infants Born to Mothers Living with HIV 
6.1.3 Prevention of Mother to Child Transmission 
All HIV infected pregnant women and lactating mothers are eligible for ART regardless of CD4 cell 
count and clinical stage. The pregnant or breast-feeding women with HIV should be started on 
lifelong ART at the time of diagnosis. 
The recommended first line regimen is once a day fixed dose regimen of TDF + 3TC + DTG. 
Although TDF+ 3TC + EFV may be an option for use during the pre-conception period through the 
first eight weeks of pregnancy to avoid potential risk of neural tube defects.Then TLD should be 
continued postpartum 
•
A women-centered approach is adopted. Women of childbearing potential including those
who are using long term effective contraception should be given adequate information to
enable making informed decision and choice.
•
Women should receive on-going counselling support to continue with HIV care and
treatment in order to maintain good health and to reduce the risk of HIV transmission to
others.
Available alternative first-line ART regimen includes 
A:TDF+FTC+EFV600mg (FDC) 
OR 
A: ABC+3TC+EFV600 or DTG 
OR 
A: AZT+3TC+EFV600 or DTG 
Prophylaxis for HIV Exposed Infants 
•
Administer NVP syrup immediately after birth to all HIV exposed infants and continue until
six weeks of age
•
In case a high risk HIV exposed infant is identified, administer duo prophylaxis containing
NVP syrup (once daily) and AZT syrup (twice daily) for the first 6 weeks of life, then
continue with daily NVP alone up to 12 weeks of life
High-risk infants are those who are:
o
Born to women diagnosed to be living with HIV during current pregnancy or breast-
feeding period.
o
women known to be HIV positive but not yet on ART or
o
already on ART but with high viral load (≥50/UL of blood)
•
Infant prophylaxis is most effective when given as soon as possible after birth, preferably
within 6–12 hours
•
HIV exposed infants identified beyond the age of 4 weeks should not be given ARV
prophylaxis
100 infants born to HIV-infected mothers 
who breastfeed
55–80 infants will 
NOT be HIV-
infected 
10-15 infant
infected
during
pregnancy
10-15 infants 
infected 
during 
labour and 
delivery
5-20 infants 
infected 
during breast-
feeding 
25-50%infants%will%be%HIV-infected

119!
!
 
 
 
Table 6.2: NVP Dosing Recommendation 
 
Based on the dosing required to sustain exposure in the infant of >100 ng/mL with the fewest dose 
changes 
Low birth weight infants <2000g should receive mg/kg dosing; suggested starting dose is 2mg/kg 
once daily.   
 
6.1.4 Second-line ART in Adults and Adolescents 
Before treatment failure is confirmed every effort should be made to rule out causes other than drug 
resistance.  
 
Table 6.3: Recommended Second-Line Regimens for Adults and Adolescents 
Patient group 
Preferred 
(Default) 
Regimen 
Alternative Regimen 
Adults, 
adolescents 
(>15 
years) 
and 
Pregnant 
women 
/ 
breastfeeding mothers 
A: AZT+3TC+ATV/r: if TDF 
was used in first line 
 
A: TDF+FTC+ATV/r:  if AZT 
was used in first line 
 
A: ABC+3TC+ATV/r 
A: ABC+TC+LPV/r 
A: TDF+FTC+LPV/r 
 
A: AZT + 3TC + DTG (For patients who did 
not use DTG in the first line) 
HIV 
and 
TB 
co-
infection 
A: AZT+3TC+LPV/r 
 
 
 
A: ABC+3TC+LPV/r
a 
A: TDF+FTC+LPV/r 
a 
 
Note: double dosage of LPV/r to 800/200mg 
for Rifampicin based TB treatment 
People 
Who 
Inject 
Drugs (PWID) 
A: AZT+3TC + DTG 
 A: AZT+3TC+ ATV/r 
A: ABC+3TC +ATV/r 
 
The second line NRTI choice for adults and adolescents depends on the first line regimen. For 
patients on TDF based regimens in first line, the preferred second line option is AZT plus 3TC 
combined with a ritonavir-boosted PI, preferably ATV/r because it is dosed once daily and has fewer 
metabolic complications and side effects. The same NRTIs, with exception of 3TC and FTC used in 
previous regimen should not be used in subsequent regimens during switching due to treatment 
failure. LPV/r can be used as an alternative to ATV/r in patients using anti-TB drugs (with ritonavir 
super boosting) and children below six years. Also, ATV/r (300/100mg) cannot be used in children 
below 30kg.  
 
For patients who were on AZT and had never used TDF regimen, the default second line option will 
be TDF or ABC based regimen combined with a boosted PI (TDF+FTC+ATV/r). 
For patients who were introduced to TDF in first line due to AZT toxicity, the default second line 
option is to use ABC plus 3TC combined with a ritonavir-boosted PI ATV/r or LPV/r. (ABC+3TC + 
LPV/r or ATV/r). However, ABC may be rendered ineffective due to cross resistance with TDF 
associated resistance mutations.  
 
6.1.5 Third-line Antiretroviral Therapy 
Patients failing 2nd line regimens may have extensive NRTI and NNRTIs associated resistance 
mutations (RAMS) which preclude/minimise their use in third-line regimens. Therefore, 3rd line 
Infant age 
NVP daily dosing 
Birth to 6 weeks 
§ 
Birth weight 2000–2499g 
§ 
Birth weight ≥2500g 
 
10mg (1 ml) once daily 
15mg(1.5ml) once daily 

120
regimens, in order to have at least two or preferably three effective drugs, need to be constructed 
using other new classes of drugs or second-generation formulations of previous drugs. These 
second-generation drugs usually have a higher genetic barrier to resistance and their efficacy is not 
compromised by RAMs associated with the first-generation formulations. 
Therefore, this guideline recommends the use of: 
• 
Integrase Strand Transfer Inhibitors (INSTIs) or Integrase Inhibitors Dolutegravir 50mg 
(DTG) and Raltegravir 400mg (RAL), 
• 
Second generation PIs Darunavir 800mg /Ritonavir 100mg (DRV/r), 
 
Table 6.4: Recommended Third-Line Regimens for Adults and Adolescents 
Patient group 
Preferred 
(Default) 
Regimen 
Alternative Regimen 
Adults, 
adolescents 
(>15 
years)  
S: DTG + DRV/r + AZT/3TC 
RAL + DRV/r + AZT/3TC 
 
Pregnant 
women/breastfeeding 
mothers 
S: (DTG or RAL) + DRV/r + 
AZT/3TC 
DTG + DRV/r (AZT/3TC) 
HIV and TB co-infection 
S: DTG (BD) + LPV/r + 
(AZT/3TC or TDF/FTC) 
RAL+(AZT/3TC or 
 TDF/FTC) +LPV/r 
People Who Inject Drugs 
(PWID) 
S: DTG+DRV/r+ AZT/3TC 
DTG+ATV/r+ AZT/3TC 
Note 
• 
DTG in third line regimen should be given twice daily for clients who were previously exposed to 
INSTIs. 
• 
For TB and HIV co-infected patients on LPV/r should be switched to DRV/r after completion of TB 
treatment  
• 
For second- and third-line regimens which are non TDF based, in case of new Hepatitis B co -
 
infection 
TDF with FTC should be added to the new regimen as treatment of Hepatitis B. 
 
6.2 Changing Antiretroviral Therapy 
6.2.1 Drug Specific Adverse Events-Toxicities 
• 
Intolerable side effects 
• 
Drug interactions 
Treatment failure 
• 
Clinical failure-occurrence or persistence of HIV related OIs 
• 
Immunological failure 
• 
Virological failure 
 
Changing ART due to toxicity 
From a clinical perspective, it is generally recommended that when changing a client’s regimen due 
to toxicity, only the toxic drug(s) should be replaced, wherever possible, by a drug without 
overlapping toxicities. Table 6.5 provides guidance on ARV drug combinations with some common 
toxicity substitution within first-line regimens. 
 
 
 

121!
!
Table 6.5: Types of toxicities associated with first and second-line ARV drugs (Refer to 
National Guidelines for Management of HIV and AIDS 7th Edition 2019) 
 
ARV 
Major types of toxicity 
Risk factors 
Suggested management 
and substitution 
TDF 
Tubular 
renal 
dysfunction, 
Fanconi syndrome 
Underlying renal disease 
Older age 
BMI <18.5 (or body weight 
<50kg) 
Untreated diabetes mellitus 
Untreated hypertension 
Concomitant use of 
nephrotoxic 
drugs 
or 
a 
boosted PI 
 
If TDF is being used in first-
line ART, substitute it with 
AZT or ABC 
 
If TDF is being used in 
second-line ART (AZT use in 
first line ART), substitute it 
with ABC 
Decreases in bone mineral 
density 
History of osteomalacia and 
pathological fracture 
Risk factors for osteoporosis 
or bone loss 
Lactic acidosis or severe 
hepatomegaly with steatosis 
Prolonged 
exposure 
to 
nucleoside analogues 
Obesity 
Exacerbation of hepatitis B 
(hepatic flares) 
Discontinuation of TDF due to 
toxicity 
No available alternative drug 
in the country for treatment 
of hepatitis B e.g. Entecavir 
ABC 
Hypersensitivity reaction 
Genetic predisposition (HLA-B 
5701 gene) 
If ABC is being used in first-
line ART, substitute with TDF 
or AZT 
AZT 
Anaemia, neutropaenia, 
myopathy, 
lipoatrophy 
or 
lipodystrophy 
Baseline 
anaemia 
or 
Neutropaenia 
CD4 cell count ≤200 cells/mm
3 
If AZT is being used in first-
line ART, substitute it with 
TDF or ABC 
 
If AZT is being used in 
second-line ART, substitute it 
with ABC 
Lactic acidosis or severe 
hepatomegaly with steatosis 
BMI >25 (or body weight >75 
kg) 
Prolonged 
exposure 
to 
nucleoside analogues 
 
 
 
 
LPV/r 
Hepatotoxicity 
 
Underlying hepatic disease 
HBV and HCV co-infection 
Concomitant 
use 
of 
hepatotoxic drugs 
 
 
 
 
Replace it with ATV/r 
 
Pancreatitis 
Advanced HIV disease 
Lipoatrophy 
or 
metabolic 
syndrome 
dyslipidaemia, 
severe diarrhea and risk of 
prematurity 
Risk factors unknown 
ATV/r 
Indirect 
hyperbilirubinaemia 
(clinical jaundice) 
 
 
Underlying hepatic disease 
HBV and HCV co infection 
Concomitant 
use 
of 
hepatotoxic drugs 
Indirect hyperbilirunemia 
is 
usually transient and ATV/r 
can be continued, however, if 
severe 
jaundice 
develops 
and 
is 
associated 
with 
significantly 
raised 
transaminases, then ATV/r 
should 
be 
replaced 
with 
LPV/r  
 
Nephrolithiasis and risk of 
prematurity 
Risk factors unknown 
Replace it with LPV/r 
 
 
 
 
 
 
EFV 
 
Persistent central nervous 
system 
toxicity 
(such 
as 
dizziness, abnormal dreams, 
depression 
or 
mental 
confusion) 
Depression or other mental 
disorder 
(previous 
or 
at 
baseline) 
Taking with high fat meal 
Replace it with DTG or NVP. 
If the person cannot tolerate 
either INSTI or NNRTI, use 
boosted PIs 
Hepatotoxicity 
Underlying hepatic disease – 
HBV and HCV co infection 

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Concomitant 
use 
of 
hepatotoxic drug 
Convulsions 
History of seizure 
Hypersensitivity 
reaction, 
Stevens-Johnson syndrome 
 
 
Risk factors unknown 
Male gynaecomastia 
NVP 
Hepatotoxicity 
Underlying 
hepatic 
disease 
HBV and HCV co-infection 
Concomitant 
use 
of 
hepatotoxic drugs 
CD4 
>250 
cells/mm3 
in 
women 
CD4 >400 cells/mm3 for men 
First month of therapy (if lead-
in dose is not used) 
EFV. If the person cannot 
tolerate either NNRTI, use 
DTG or a boosted PI 
Severe skin rash and 
hypersensitivity 
reaction 
(Stevens-Johnson syndrome) 
Risk factors unknown 
DTG 
Increase in cholesterol levels; 
mild elevated liver enzymes; 
significant rises in creatinine 
levels; 
Insomnia 
and 
headache 
may 
also 
be 
experienced.  
History 
of 
dyslipidemia, 
diabetes, hypertension 
Monitor cholesterol levels; 
monitor 
Liver 
function 
especially in HBV and HCV. 
Provide 
symptomatic 
treatment 
RAL 
Increased Cholesterol levels, 
Glucose, Aspartate Amino 
Transferase 
(AST), 
and 
Bilirubin. 
Rash, 
Cough, 
Fatigue, 
dizziness 
and 
insomnia 
History 
of 
dyslipidemia, 
diabetes, hypertension 
In case of severe adverse 
effects, switch to DTG if 
patient is >12 years old 
DRV/r 
Increased Cholesterol levels, 
triglycerides; 
Diarrhea, 
Headache, Rash, Abdominal 
pain and Nausea 
History of dyslipidemia 
Monitor 
severity 
and 
occurrence 
of 
fever 
and 
other 
symptoms. 
Provide 
symptomatic treatment 
 
 
Figure 6.2: Substitution within first-line Antiretroviral Regimens 
 
 
 
 
 
Note 
For TB co-infected patients, the dose for DTG should be given twice daily i.e. 50mg  
 
 
 
 
 

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6.2.2 Changing ART due to Treatment Failure 
 
Table 6.6: WHO definitions of treatment failure in chronological order of occurrence: 
virological, immunological and clinical failure for the decision to switch ART regimens 
 
Failure 
Definition 
Comments 
Virological 
Plasma viral load above 
1000 copies/ ml based on 
two consecutive viral load 
measurements 
after 
3 
months, 
with 
adherence 
support 
An individual must be taking ART for at least six 
months before it can be determined that a regimen has 
failed.  
Immunological  
CD4 cell count falls to the 
baseline (or below)  
or Persistent CD4 levels 
below 100 cells/mm
3 
Without concomitant or recent infection or steroid use 
to cause a transient decline in the CD4 cell count 
Immunological and clinical characteristics of treatment 
failure develop much later after virological failure. 
Immunological and clinical criteria of treatment failure 
may also misclassify treatment failure and lead to 
unnecessary ARV switch to subsequent (line of 
treatment) regimen 
Clinical  
New or recurrent clinical 
event 
indicating 
severe 
immunodeficiency 
(WHO 
clinical stage 4 conditions) 
after six months of effective 
treatment. 
The condition must be differentiated from IRIS 
 
 
Switching to Third-line ARV regimens 
It is crucial that before a regimen is declared to have failed, a multidisplinary switch team is 
convened to rule out non-adherence which is the commonest cause of reduced CD4 cell count and 
a VL rise but is often not associated with HIV drug resistance. This team will also plan for enhanced 
adherence and support, for a period of 3 months before a second VL test. In case of non-adherence, 
these measures will lower the VL, increase CD4 cell count and avert a switch to a subsequent 
regimen   
 
Before switching to third-line ARV regimens, genotypic HIV drug resistance is recommended to rule 
cross resistance between 1st and 2nd generation drugs and assist in the determination of whether 
treatment failure is from non-adherence. Genotyping will also inform possibility of recycling drugs 
used in previous regimens i.e. some drugs used in 1st or 2nd regimens may still be effective in third-
line. 
 
6.3 Monitoring Patients on Antiretroviral Therapy 
Monitoring of patients on ART is based on clinical and laboratory parameters. Refer table 6.7 
 
Table 6.7 Clinical and laboratory monitoring of patients on first line drug regimen 
 
Regimens 
Monitoring Tests 
Frequency 
Rationale 
TDF+3TC+DTG 
ABC+3TC+DTG 
AZT+3TC+ (EFV or NVP) 
TDF+FTC+ (EFV or NVP) 
HVL (All Clients) 
For HVL monitoring, 
refer to HVL algorithm 
ART monitoring 
CD4 (All clients) 
Baseline (All) 
After every six months if 
CD4 is <350 cells/ml 
ART monitoring 
FBP/Hb (All clients) 
If a client has Hb 
Baseline, week 4, 
thereafter six monthlies 
Anaemia monitoring 

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<8.5g/dl avoid AZT 
Serum Creatinine 
(For patients on 
TDF) 
Baseline, and after 
every six months and 
whenever symptomatic 
Screening for early renal 
toxicity 
ALT (For patients 
on DTG or NVP) 
Baseline, one month, 
after every six months 
and whenever 
symptomatic 
Liver toxicity 
AZT+3TC+ATV/r 
TDF+FTC+ATV/r 
ABC+3TC+LPV/r or DTG 
Bilirubin (For all 
clients on ATV/r) 
Baseline, 6 months or 
whenever symptomatic 
Indirect hyper-
bilirubinaemia 
 
 
Note 
Clinical evaluation will determine more frequent laboratory tests if required. 
 
Laboratory monitoring of patients on second line drugs 
The following laboratory tests are recommended for Monitoring of patients on second line drugs: 
• 
FBC, baseline, then monthly for 3 months, then after every 6 months (with CD4 and viral 
load) 
• 
Fasting cholesterol and triglyceride, baseline, 6 months and thereafter every 12 months 
• 
Liver function tests, (ALT) 6 monthly 
• 
Fasting glucose, every 12 months 
• 
Urinalysis at baseline and after every 3 months 
• 
Serum creatinine at baseline and once a year. 
 
When changing treatment, the following should be observed: 
• 
Never change a single drug in the combination if the reason for changing is treatment 
failure. Change at least two drugs, preferably change all three drugs 
• 
If changing due to toxicity, change only the drug suspected to be causing the problem. 
• 
Never change to monotherapy (i.e. single drug)  
• 
When selecting drugs, choose drugs that have not been used before, drugs which do not 
have cross-resistance/or no overlapping toxicities or drug-drug interactions.  
• 
Lamivudine has advantage of decreasing viral fitness therefore it may be retained when 
changing the failing regimen 
6.4 Immune Reconstitution Inflammatory Syndrome (IRIS) 
IRIS is a phenomenon associated with the occurrence or worsening of opportunistic 
infections/malignancies which can occur early after initiation of ART or at later (several months) 
during ART. There is an increased risk for occurrence of IRIS in the following situations:  
• 
Treatment naïve patients  
• 
Patients with advanced HIV disease with CD4 cell count < 50 cells/mm3  
• 
Patients with undiagnosed and untreated opportunistic conditions 
• 
Patients who have been introduced on ART before or shortly after initiation of treatment of 
opportunistic infection/malignancy 
• 
In the advent of DTG use, there is increased likelihood for IRIS because of rapid HIV viral 
load suppression. 
 
Note 
Any OI, malignancy and autoimmune diseases may present as IRIS 
 
Diagnostic Criteria: 
The criteria for making a diagnosis of IRIS are delineated below 
 

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Diagnosis of IRIS would require: 
Both major (A plus B) criteria or criterion A plus 2 minor criteria 
Major criteria 
A. A typical presentation of “opportunistic infections or tumours” in patients responding to anti-
retroviral therapy (ART) includes: 
• 
Localized disease e.g. lymph nodes, liver, spleen 
• 
Exaggerated inflammatory reaction e.g. severe fever, with exclusion of other causes of 
painful lesions 
• 
Atypical inflammatory response in affected tissues e.g. granulomas, suppuration, necrosis, 
perivascular lymphocytic inflammatory cell infiltrate 
• 
Progression of organ dysfunction or enlargement of pre-existing lesions after definite, 
clinical improvement with pathogen specific therapy prior to commencement of ART and 
exclusion of treatment toxicity and new diagnoses 
• 
Development or enlargement of cerebral space occupying lesions after treatment for 
cerebral cryptococcus or toxoplasmosis 
• 
Progressive pneumonitis or the development of organizing pneumonia after treatment of 
pulmonary-TB or PCP 
• 
New onset or worsening of uveitis/vitritis after resolution of CMV retinitis 
• 
Fever and cytopenia after treatment for disseminated Mycobacterium avium complex 
(MAC) disease 
• 
Enlargement of Kaposi’s sarcoma lesions and subsequent resolution or partial regression 
without 
• 
Commencement of radiotherapy, systemic chemotherapy or intralesional therapy 
B. Decrease in plasma HIV-RNA level by > 1 log base ten copies/ml (1 log drop = 9/10 of Baseline 
VL copies). This applies in settings where baseline VL is performed. 
 
 
Minor criteria 
• 
Increased blood CD4+ cell count after initiation of ART 
• 
Increase in immune response specific to the relevant pathogen e.g. delayed type 
hypersensitivity to mycobacterial antigens (PPD conversion) 
• 
Spontaneous resolution of disease without specific antimicrobial therapy or tumour 
chemotherapy with continuation of anti-retroviral therapy. 
 
Treatment of IRIS 
Mild to moderate forms: 
• 
Reassure the patient and do not stop ART 
• 
Provide specific treatment for the opportunistic infections/malignancies or other diseases 
 
Severe life-threatening IRIS 
• 
Reassure the patient and Stop ART temporarily 
• 
Provide high doses of prednisolone 1mg/kg for 4 weeks then taper down the dose.  
• 
Provide other appropriate supportive measures such as management of fever, oxygen 
therapy, i.e. fluids 
• 
Restart ART when the patient stabilizes. 
 
Note 
When using high dose steroids, it is important to rule out Strogyloides stecolaris infection to avoid 
disseminated strongylodiasis.  
 
6.5   Antiretroviral Therapy in Children and Adolescents Living with HIV 
ART in children has been proven to increase survival and decrease HIV-related morbidity and 
mortality. Children should be started on ART as soon they are diagnosed including those who are 
presumably diagnosed. 
 
 
 

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Table 6.9: When to start ART in Children Under 15 Years 
 
Age 
When you start 
Children 0-15 years 
Treat all of them regardless of WHO clinical stage or CD4 
cell count 
Children below 18 months old who qualify for 
presumptive diagnosis 
Start ART while awaiting for DNA-PCR confirmation test 
results. 
Children <18 months of age with a positive 
DNA/RNA PCR test 
Start ART while waiting for the second DNA/RNAPCR test 
result 
 
 
Table 6.10: First-Line ARV Regimens in Infants and Children under 15 years 
 
Patient 
group 
Preferred 1
stLine 
Regimen 
Justification 
Alternatives 
Comments 
Infants 
and 
Children 
weighing 
<20kg 
 
 
ABC+3TC+LPV/r 
Higher 
genetic 
resistance barrier 
Avoids 
NNRTI 
transmitted resistance 
from 
mother 
during 
PMTCT 
Potential for malaria 
prevention 
Spares 
AZT 
for 
second line 
AZT+3TC+LPV/r 
 
AZT/3TC+DTG 
(25mg 
or 
10mg 
DTG if available) 
 
LPV/r is available in 
three 
formulations 
(syrup, granules and 
tablets) 
- LPV/r oral solutions 
for 
younger 
infants 
until they can take 
granules 
- LPV/r granules for 
infants and younger 
children  
-LPV/r 
100mg/25mg 
heat stable tablets for 
children 
10kg 
and 
above and able to 
swallow whole tablets 
Children and 
adolescents 
weighing 
≥20kg 
ABC+3TC 
+ 
DTG 
 
-Lowers 
HIV 
viral 
load very fast 
-Has 
high 
genetic 
barriers to resistance 
compared to both PIs 
and NNRTIs 
-Spares 
AZT 
for 
second line 
ABC+3TC+LPV/r 
 
ABC+3TC 
Dispensable 
Tablet 
120/60mg plus DTG 
50mg 
 
Children and 
Adolescents 
weighing 
≥30 kg 
TDF+3TC+DTG 
 
Higher 
genetic 
resistance barrier 
Avoids 
NNRTI 
transmitted 
resistance 
from 
mother 
during 
PMTCT 
Possibility of malaria 
prevention 
Spares 
AZT 
for 
second line 
ABC+3TC+DTG 
TDF+3TC+EFV600 
or EFV400 
 
TLD 
Fixed 
Dose 
Combination 

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For TB and 
HIV 
co-
infected 
children 
already 
on 
LPV/r-based 
regimen 
ABC+3TC+LPV/r 
Continue 
with 
ABC+3TC+LPV/r but 
the dose of LPV/r 
should be doubled 
due to the interaction 
between ritonavir and 
rifampicin 
 
ABC+3TC+LPV/r 
in 
the morning and only 
LPV/r in the evening 
For TB and 
HIV 
co-
infected 
children 
already 
on 
DTG based 
regimen 
ABC+3TC+DTG 
For children 20-25   
kg who get TB/HIV 
co-infection 
it 
is 
advisable 
to 
give 
them ABC+3TC+EFV 
for the time of the TB 
treatment then revert 
to 
ABC+3TC+DTG 
after completion of 
TB Treatment 
For children > 25 kg  
Continue 
with 
ABC+3TC+DTG but 
the dose of DTG 
should be doubled 
due to the interaction 
between ritonavir and 
rifampicin 
 
ABC+3TC+DTG 
in 
the morning and only 
DTG in the evening 
For TB and 
HIV 
co-
infected on 
TLD 
TDF+3TC+DTG 
 
For children 20-25   
kg who get TB/HIV 
co-infection 
it 
is 
advisable 
to 
give 
them TDF+3TC+EFV 
for the time of the TB 
treatment then revert 
to 
TDF+3TC+DTG 
after completion of 
TB Treatment 
For children > 25 kg  
Continue 
with 
the 
same 
regimen, 
Double dose of DTG 
 
TLD in the morning 
and 
only 
DTG 
(50mg) 
in 
the 
evening  
 
 
For dosing of ARV regimens see Annex 6, Paediatric Antiretroviral Dosing 
 
Note 
Children with weight above 30kg can use TDF as a fixed dose combination with 3TC. 
 
Special Considerations for LPV/r syrup, granules and tablets 
• 
The LPV/r liquid requires a cold chain only during storage at the facility  
• 
After dispensing, the liquid is stable at room temperature for 1 month so patients should be 
given a maximum of 1-month supply   
• 
Patients do not have to refrigerate the LPV/r liquid  
• 
LPV/r granules for infants who can safely swallow LPV/r granules but who are unable to 
swallow LPV/r tablets whole.  

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• 
LPV/r tablet is heat stable but must be swallowed whole and should not be split or crushed 
as it loses effectiveness  
 
6.6. Changing ART in Children Under 15 Years 
 
I. 
Drug toxicity 
 
The principles for changing ARVs and the managing drug toxicity in children are like those applied to 
adults. 
 
II. 
Treatment failure 
Virological treatment failure: Viral load is the most reliable method to detect early treatment 
failure. Virological treatment failure is recognized if the child is adherent to the current ART regimen, 
for 6 months or more and has two consecutive viral load measurements over 1000 copies/ml at 3 
months apart.   
Immunological treatment failure: If adherence is good, immunological criteria indicating that 
a change to second-line therapy is warranted where/when HVL test is not available includes 
the following: 
 
Table 6.11: CD4 Criteria Suggesting Immunological Failure a 
Immunological failure is recognized as developing or returning to the following age-related 
immunological thresholds after at least 6 months on ART, in a treatment-adherent child: 
<5 years of age 
CD4 count of <200 cells/mm3 or CD4 <10% 
≥5 years of age 
CD4 count of <100 cells/mm3 
a Preferably, at least two CD4 measurements should be available  
  Use of CD4 in children <5 years and absolute CD4 cell counts in those ≥5 years of age is 
preferred. 
If serial CD4 values are available, the rate of CD4 cell count declines from the peak, CD4 cell 
count reached should be taken into consideration. 
 
Note 
CD4 cell percent should not be measured during an inter-current infection but can be determined 
when the child has 
recovered. 
 
If there is a modest decline in CD4 cell count or percent (< 5%); and if there is no failure to thrive do 
not change medication, instead maintain close monitoring. 
 
Clinical Treatment Failure: Clinical conditions indicating that a change to second-line therapy is 
warranted include: 
• 
Poor growth (failure to gain weight, declining or stagnant weight) over a 6-month period, 
after excluding other causes, such as TB, feeding problems and food insecurity 
• 
No improvement of neuro-developmental milestones 
• 
Development of HIV encephalopathy  
• 
Recurrent infections, such as oral candidiasis, persistent diarrhoea, recurrent severe 
bacterial pneumonia 
• 
Advancement from one clinical stage to another or new evidence of new WHO stage 3 or 4 
disease  
 
Note 
• 
Short inter-current episodes of pneumonia, LRTI and gastroenteritis should not be 
regarded as clinical failure 
• 
Pulmonary or lymph node TB, which are clinical stage 3 conditions, are not indications of 
treatment failure, and thus may not require consideration of second-line therapy  
• 
The response to TB therapy should be used to evaluate the need for switching therapy 
• 
Before an ARV regimen is thought to be failing based on clinical criteria, the child should 
have received the regimen for at least 6 months. 
• 
The condition must be differentiated from immune reconstitution inflammatory syndrome. 
 
 

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Table 6.12: Laboratory parameters for monitoring infants and children under 15 years at 
baseline, before and during ART 
Laboratory tests for diagnosis and 
monitoring 
Baseline 
(at 
entry 
into care) 
At initiation of 
first-line 
or 
second-line 
ART regimen 
Every six 
months 
As required or 
symptom- 
directed 
HIV diagnostic testing 
√ 
 
 
 
Haemoglobin 
√ 
√ 
 
√ 
WBC and differential count  
√ 
 
 
√ 
%CD4+ or absolute CD4 cell 
count 
√ 
 
√b 
√ 
Pregnancy testing in adolescent 
girls 
 
√ 
 
√ 
Full chemistry (including, but not 
restricted to, liver enzymes, renal 
function, glucose, lipids, amylase, 
lipase and serum electrolytes) e 
 
√ 
√e 
√ 
HIV VL measurement 
 
 
√d 
√ 
OI screening (where possible) 
√ 
√ 
√ 
√ 
a. 
HIV re-testing for verification before ART initiation, re-testing is not indicated when 
switching to 2nd or 3rd line 
b. 
For children of <5years continue CD4 monitoring every six months 
c. 
CD4 cell count should be taken on emergence of WHO stage 3 or 4 disease 
d. 
Viral load monitoring is done annually if the first two VL results 6th month apart are 
<1000 copies/mL 
e. 
Regular monitoring (every six months) of full chemistry, particularly lipid levels, liver 
enzymes and renal functions, should be considered for infants and children on ART. 
 
Assessment of Infants and Children receiving ARV Therapy 
Important clinical signs of response to ARV therapy in children include improvement in growth and 
development and decreased frequency of infections (bacterial infections, oral thrush, and/or other 
opportunistic infections). 
 
Clinical monitoring of ARV treatment in children should include: 
• 
Feeding practice and nutritional status  
• 
Growth monitoring: weight, height, MUAC (mid-upper arm circumference) 
• 
Head circumference should be monitored in children under 3 years old 
• 
Neurologic symptoms and developmental milestones 
• 
Cotrimoxazole prophylaxis taken daily 
• 
Adjustment of ARV dose based on weight 
• 
WHO disease clinical staging 
• 
Immunization status 
• 
Other medical conditions 
• 
Screening for malaria and TB. 
 
 
 
 
 
 
 
 
 

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Table 6.13: Recommended Second-line ARV regimens for children under 15 years 
Patient group 
If 
is 
on 
the 
following first line 
Preferred 2L 
Comments 
Children 
and 
adolescents 
<20kg   whose 1st regimen 
was EFV or NVP based, then 
transitioned to LPV/r based 
regimen 
ABC/3TC+LPV/r 
 
AZT/3TC+LPV/r 
Maintain PI 
 
AZT/3TC+LPV/r 
-Higher 
genetic 
resistance barrier 
-Spare INSTI for third-
line 
 
Children 
and 
adolescents 
≥20kg whose 1st regimen was 
EFV or NVP based, then 
transitioned to DTG based 
regimen  
ABC/3TC+DTG 
 
AZT/3TC+DTG 
AZT/3TC+ATV/r 
AZT/3TC+DTG 
ABC/3TC+DTG 
(for those who 
cannot 
tolerate 
AZT) 
Maintain DTG in the 
2nd  line due to higher 
genetic 
barrier 
than 
PIs. 
Children 
and 
adolescents 
weighing ≥30kg 
TDF/3TC/DTG 
AZT+3TC+ATV/r 
ABC+3TC+ATV/r 
 
 
Note 
• 
Infant and children take longer time to attain adequate viral suppression. Before confirming 
treatment failure, calculate drop in VL (using 0.5 log two years and above, 0.7log below 2 
years- for further details on how to convert VL into numbers. 
• 
ATV/r can be used as an alternative to LPV/r in children above 6 years old if paediatric 
formulation is available but adolescents >30kg can take adult formulation. 
 
Third-Line ARV regimens in children under 15 years and adolescents 
Clients failing 2nd line regimen have extensive NRTI and NNRTIs associated resistance mutations 
which minimise their use in third-line regimens. Third-line regimen is constructed using new classes 
of drugs or second-generation formulations, in order to have at least two or three effective drugs. For 
examples, Darunavir (DRV) is a second-generation PI without cross resistance to Lopinavir/r used in 
the previous regimens.  
Criteria for Change to Third line  
Failing any 2nd line regimen 
• 
Referral to specialist care is recommended where third line regimen can be chosen 
according to genotype resistance testing and managed by an expert panel at tertiary care 
facilities. 
• 
The criteria for diagnosing second-line failure are the same as those used for diagnosing 
first-line failure.  
 
Eligibility for Third Line Evaluation:  
All clients should have undergone an Enhanced Adherence Counselling  
• 
Failing 2nd line regimens 
• 
Documented virologic failure (VL > 1000) on a PI regimen; except children below 3 years 
 
Third-line Regimens for Children and Adolescents 
Selection of third-line regimen should consider genotype resistance test results as well as treatment 
history. 
 
 
 

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Table 6.14: Third-line Regimens for Children and Adolescents 
Patient group 
3L Options 
Justification 
Children <20kg 
RAL 
+ 
DRV/r 
+ 
AZT+3TC 
DRV/r -High genetic barrier, Effective for patients 
with resistance to LPVr and ATVr, cannot be used in 
children <3 years of age 
RAL-Can be used for children <20 kg 
DTG-Can be used for children >20 kg 
Children >20kg 
and above 
 
DTG 
+ 
DRV/r 
+ 
AZT+3TC 
 
Adverse reactions in childrenand adolescents 
Drug-related adverse reactions while on ART can occur immediately (soon after a drug has been 
administered), early (within the first days or weeks of treatment) or later (after months of treatment). 
Adverse reactions can vary in severity from mild to severe to life-threatening and may be specific to 
the drug or general to the class of drugs in use.  
 
Table 6.15: Major Types of ARV Toxicity in Children and adolescents 
ABC 
 
ABC is associated with hypersensitivity reactions. Patients may have severe skin rashes or 
other non-specific symptoms such as fever, arthralgias and lymph node enlargement. 
 
AZT 
AZT is associated with risk of haematological toxicity which can include anaemia neutropenia 
and thrombocytopenia. Measuring haemoglobin is recommended before initiating ART among 
children with low body weight, low CD4 cell counts and advanced HIV disease. Patients with 
severe anaemia at baseline (haemoglobin < 7.5 g/dL) should avoid AZT as first line therapy. 
TDF 
 
TDF is associated with nephrotoxicity. Nephrotoxicity is more common in elderly patients, but it 
also occurs in children, especially if co-administered with PI based therapy. Monitoring of 
creatinine clearance is recommended. 
 
EFV 
 
EFV’s main type of toxicity is central nervous system side effects, which typically resolve after 
few weeks. However, in some cases, they can persist for months or never resolve at all. 
 
NVP 
 
NVP’s major toxicities include severe skin rash and hypersensitivity reaction (Steven’s Johnson 
syndrome) and hepatotoxicity. Because of the risk of potentially life-threatening hepatotoxicity 
associated with NVP, hepatic dysfunction of any aetiology in a child on NVP requires careful 
consideration of whether NVP should be continued. 
 
LPV/r 
 
LPV/r’s major toxicity includes hepatotoxicity, pancreatitis, diarrhoea and lipoatrophy.  The risk 
of hepatotoxicity is increased in patients with underlying hepatic disease and the risk of 
pancreatitis is increased in patients with advanced HIV disease.  Electro-cardiac abnormalities 
are also possible; patients with pre-existing conduction system disease are at increased risk 
 
ATV/r 
 
Toxicities of ATV/r are like those of LPV/r. ATV/r can cause jaundice (indirect 
hyperbilirubinemia). Jaundice (indirect hyperbilirubinemia) is usually transient and ATV/r can be 
continued. If severe jaundice develops and there are significantly raised transaminases, then 
ATV/r should be replaced with LPV/r 
DRV/r 
 
DRV/r’s major toxicity is hepatotoxicity. Patients with underlying hepatic disease, hepatitis B or 
C co-infection or who are taking other hepatotoxic drugs are at higher risk. The other side effect 
is severe skin and hypersensitivity reactions. Patients with sulphonamide allergy are at higher 
risk 
 
 RAL 
 
RAL’s potential toxicity includes rhabdomyolysis, myopathy and myalgia as well as hepatitis 
and hepatic failure and severe skin rash and hypersensitivity reactions.  
 
DTG 
 
DTG major toxicity is hepatotoxicity and hypersensitivity reactions. Patients with underlying liver 
disease or hepatitis B or C co-infection are at higher risk. 
 
Principles in the management of ARV drug toxicity 
Severe life-threatening reactions:Immediately discontinue all ARV drugs, manage the medical 
event (i.e. provide symptomatic and supportive therapy) and reintroduce ARV drugs using a 
modified regimen (i.e. with an ARV substitution for the offending drug) when the patient is stabilized  
 
 
 

132!
Severe reactions: Substitute the offending drug without stopping ART 
Moderate reactions: Consider continuation of ART if it is feasible. If the patient does not improve on 
symptomatic therapy, consider single-drug substitution 
Mild reactions: Reassure a child and caregiver that while the reaction may be bothersome, it does 
not require a change in therapy; provide counselling and support to mitigate adverse reactions. 
Emphasize on the maintenance of adherence despite mild and moderate reactions. 
Table 6.16: Suggested ARV Substitutions 
Toxicity events 
Responsible 
ARV 
Suggested first-line ARV drug substitution 
Acute 
symptomatic 
hepatitis 
NVP 
EFV 
If the patient cannot tolerate either NNRTI, use 
boosted PI 
Severe or life-threatening 
rash 
(Stevens-Johnson 
syndrome)  
boosted PI 
Hypersensitivity reaction 
ABC 
AZT 
Lipoatrophy/metabolic 
syndrome 
LPV/r 
If LPV/r is used in first line ART for children, use an 
age appropriate NNRTI (NVP for children below 3 
years and EFV for children with 3 years and above) 
ATV/r can be used for children above 6 years 
Severe 
anaemia 
or 
neutropenia 
AZT 
Substitute with ABC if < 35 kg 
Substitute with TDF if > 35 kg 
Severe 
gastrointestinal 
intolerance 
Persistent 
and 
severe 
central nervous system 
toxicity  
EFV 
NVP 
Tubular renal dysfunction 
TDF 
If TDF is being used in first line ART, substitute with 
AZT or ABC 
If TDF is being used in second line ART, substitute 
with ABC 
Note 
Patients on third line ARV regimen who develop toxicities should be referred to next level facility with 
adequate expertise and facilities 
6.7   HIV Prevention 
6.7.1 Post Exposure Prophylaxis (PEP) 
Post Exposure Prophylaxis (PEP) is the immediate provision of preventive measures and medication 
following exposure to potentially infected blood or other bodily fluids in order to minimize the risk of 
acquiring infection. Several clinical studies have demonstrated that HIV transmission can be 
reduced by 81% following immediate administration of antiretroviral agents. 
Effective post-exposure management entails the following elements: 
•
Management of exposure site
•
Exposure reporting
•
Assessment of infection risk
•
Appropriate treatment
•
Follow-up and counselling.
When an exposure occurs, the circumstances and post exposure management procedure applied 
should be recorded in the exposed person’s confidential form for easy follow up and care.  
Evaluation of the Exposed Individuals 

133!
Individuals exposed to HIV should be evaluated within two hours and no later than 72 hours. A 
starter pack should be initiated within 2 hours after exposure and before testing the exposed person. 
Exposed healthcare workers should be counselled and tested for HIV at baseline in order to 
establish infection status at the time of exposure. PEP should be discontinued if an exposed 
healthcare worker refuses to test. Vaccination against Hepatitis B should be considered. 
In addition, rape survivors should be: 
•
Offered counselling, crisis prevention and provision of an on-going psychosocial support to
reduce/minimize immediate rape trauma disorder and long-term post-traumatic stress
disorder should be offered.
•
Referred to mental care, police and legal services, according to the law and regulations.
Evaluation of the Source Person 
Evaluation of the source person should be performed when the exposed individual agrees to take 
PEP. 
•
If the HIV, HBV and HCV status of the source person is unknown perform these tests after
obtaining consent. The exposed healthcare worker should not be involved in obtaining
consent from the source person.
•
If the source person is unknown, evaluation will depend on other risk criteria.
•
Do not test discarded needles or syringes for viral contamination.
ARVs used for HIV PEP 
Adults 
A: TDF 300mg+3TC 300mg+DTG 50mg (FDC) (PO) 24hourly for 4weeks 
Children (based on body weight) 
A: AZT+3TC+LPV/r 12hourly for 4weeks 
Children whose weight is more than 20kg DTG can be used instead of LPV/r and maintain AZT+3TC 
as backbone. 
Note 
If the source is using PI based regimen, then the PEP regimen should be PI based. (Similar to the 
source’s regimen) 
Follow-up of HIV Exposed individuals 
HIV antibody tests should be performed at least after 4–6 weeks’ post-exposure (i.e. at 6 & 12 
weeks). HIV testing should also be performed for any exposed person who has an illness that is 
compatible with an acute retroviral syndrome, irrespective of the interval since exposure. 
If PEP is administered, the exposed person should be monitored for drug toxicity at baseline and 2 
weeks after starting PEP. Minimally, it should include a Full Blood Count (FBC), renal function test 
(RFT-Serum creatinine and urinalysis) and hepatic function tests (LFT- ALT). 
Exposed persons should be re-evaluated within 72 hours, after additional information about the 
source of exposure including serologic status, viral load, current treatment, any resistance test 
results (if available) or information about factors that would modify recommendations, is obtained. 
PEP should be administered for 4 weeks if tolerated. If not tolerated manage symptoms accordingly 
and if intolerance persists, change to more tolerable PI based regimen. If the patient seroconverts 
and the exposed person becomes HIV infected, he/she should be referred to a CTC for proper care 
and treatment service. 
6.7.2 Pre-Exposure Prophylaxis (PrEP) 
Pre-Exposure Prophylaxis (PrEP) is the use of ARV drugs daily by HIV uninfected persons to 
prevent acquisition of HIV before the person becomes exposed to HIV. PrEP is used by people who 
are at substantial risk for HIV acquisition to lower their chances of getting HIV infection. 
Evaluation of the Exposed Individuals 

134
Eligible clients for PrEP 
•
Aged 15 years and older
•
HIV sero negative
•
At substantial risk* of HIV infection
•
No suspicion of acute HIV infection
*Substantial risk of HIV infection means:
•
Vaginal or anal sex without a condom with more than one partner
•
History of a new sexually transmitted infection
•
Use of post exposure prophylaxis for sexual exposure
•
Has a known HIV positive sexual partner(s) who is not on ART/ on ART less than six
months or refuses to report a risk category but still requests PrEP
Clients who are not eligible for PrEP include: 
•
Acute HIV Infection (AHI)
•
Client with eGFR* <60ml/min
•
Significantly mobile persons that will not be able to attend visits as prescribed. For
example:
o
clients who will not be in a region where PrEP can be provided at the next visit
o
clients who do not have contact information
•
Unwilling/unable to take daily medication
•
Allergy or contraindication to any medication within PrEP regimen.
ARVs used for PrEP  
The recommended PrEP regimen in Tanzania is: 
A:Emtricitabine200mg+Tenofovir Disoproxil Fumarate300mg(PO) 24hourly. 
Indications for PrEP discontinuation 
Individuals taking PrEP require ongoing risk assessment and PrEP can be discontinued if individuals 
acquire HIV infection, are no longer at substantial risk for HIV infection or decide to use other 
effective prevention methods and poor adherence. 
Before discontinuation of PrEP, clients should be provided for at least 28 days after the last possible 
exposure to HIV. The client should return after completing the final prescription for an HIV test to 
confirm status. Refer the client to other relevant prevention services.  
Pre 
Exposure 
• Before
• Activity that can lead to HIV infection
•  Prevention
•
Creatinine clearance >60ml/min**
•
Willingness to consent for and use 
PrEP as prescribed 
Prophylaxis 

135!
!
CHAPTER SEVEN 
TUBERCULOSIS AND LEPROSY 
 
7.1General Management of Tuberculosis 
Tuberculosis is chronic airborne infectious disease caused by Mycobacterium tuberculosis. It is 
transmitted from one person to another when a patient is cough, sneezing or singing. 
  
Clinical presentation 
• 
Cough of more than two weeks or of any duration in among PLHIV 
• 
Fever 
• 
Excessive night sweats 
• 
Haemoptysis (sputum mixed with blood stains) 
• 
Loss of weight 
• 
Others includes swelling of lymph nodes, ascites, difficulty in breathing, chest pain, 
swelling of joints etc., depending on the site of the disease 
 
Investigations 
• 
Sputum- smears microscopy or sputum for rapid molecular tests like Gene –Expert 
• 
Culture and sensitivity; this is done for diagnosis of drug resistance and surveillance 
• 
Chest X-rays: done to assist clinical diagnosis of TB or in case of triaging presumptive 
 
Note.  
• 
Conduct HIV provider-initiated testing and counseling (PITC)for all TB patients 
• 
Conduct Provider Initiated TB screening (PITS) for all health facility outpatients and 
inpatients 
 
For detailed diagnosis and investigation of TB refer to ‘Manual for the Management of Tuberculosis 
and Leprosy in Tanzania’. 
 
Pharmacological Treatment  
TB treatment is divided into two phases: 
• 
Initial /intensive phase, which consists of:  
• 
RHZE for 2 months - new and re-treatment cases 
• 
Continuation phase, which consists of: 
• 
RH for 4 months - new and re-treatment cases 
• 
RH for 10 months for severe forms TB such TB meningitis, Miliary TB and TB of the spine  
 
Table 7.1 Recommended daily doses – regimens of first-line anti-TB drugs for adults and 
children 
 
New/Retreatments 
Initial Phase  
Continuation Phase  
New/Retreatments 
Rifampicin + Isoniazid + Pyrazinamide and 
Ethambutol in fixed dose (RHZE) for 2 
months 
Rifampicin + Isoniazid in fixed 
dose (RH) for 4 months 
 
Table 7.2 Daily dosage of anti-TB drugs (FDCs) in new and retreatment adult patients 
 
Body weight 
Number of tablets in initial phase: 2 
months (R150/H75/Z400/E275) mg 
Number of tablets in continuation 
phase: 4 months (R150/H75) mg 
21–30 kg 
2 
2 
31–50 kg 
3 
3 
51–74 kg 
4 
4 
≥75 kg 
5 
5 
 
 
 
 
 
 
 
 

136
Table 7.3 Daily dosages of anti-TB Drugs (FDCs) in new and retreatment paediatric patients 
 
 
Intensive phase * (2 months) 
Continuation phase (4 months) 
Weight (kg) 
RHZ (paediatric) 75/50/150 
mg 
Ethambutol 
100mg 
RH (paediatric) 75/50 mg 
For infants below 2 kg, consult a paediatric specialist, DTLC, and RTLC for treatment advice 
2-2.9kg 
 
 
 
3-3.9kg 
1 
 
1 
4-7.9kg 
1 
1 
1 
8-11.9kg 
2 
2 
2 
12-15.9kg 
3 
3 
3 
16-24.9 kg 
4 
4 
4 
25 kg+ 
Go to adult FDCs dosages 
 
 
Note 
• 
The oral drugs must be swallowed under observation from health facility staff or treatment 
supporter of his/her choice at home  
• 
The oral drugs should preferably be given on an empty stomach in a fixed dose combination 
 
7.1.1 Drug Resistance Tuberculosis (DR-TB) 
It is a laboratory diagnosis confirmed after testing Mycobacterium tuberculosis strains for resistance 
using WHO recommended rapid genotypic tests like gene-expert or conventional phenotypic culture 
and DST. 
 
Clinical presentation 
The features are the same as susceptible tuberculosis but patient’s shows resistance to the first line 
treatments. Signs and symptoms of DR-TB are like those of drug-susceptible TB (cough, bloody 
stained sputum, fever, night sweats and weight loss).  Patients with the following features have high 
DR-TB risk (presumptive DR-TB patients) 
• 
History of previous TB treatment 
o 
Treatment failure after using first-line anti-TB medicines 
o 
Relapse and return after loss to follow-up, without recent treatment failure 
o 
Patients who remain sputum smear-positive at month two or later during 
treatment of TB using first-line anti TB medicines  
• 
Close contact of a known DR-TB case 
• 
Healthcare workers presenting with TB symptoms. 
• 
Vulnerable groups in congregate settings (prisoners, urban poor, miners, PWIDs) 
 
All presumptive DR-TB cases adults and children must receive the Xpert MTB/RIF test as the initial 
diagnostic test to ensure universal coverage of DST 
 
Pharmacological Treatment 
When you diagnose RR/MDR TB communicate with DTLC for initiation of treatment. 
 
 
 
 
 
 
 
 
 
 
 
 

137
Age 
group 
Patient condition 
Proposed regimens 
Intensive phase 
-------------------------------- 
Continuation phase* 
If any of the medicines cannot be used, 
consult the DR-TB consillium to 
consider replacement if needed using 
one or more of the following based on 
DST, prior use and likelihood of efficacy 
(in order of priority) 
Adults and 
children     
>12 yrs 
 
MDR/RR-TB susceptible 
to fluoroquinolone 
  6 Lfx - Bdq - Lzd - Cfz – 
Cs 
12 Lfx - Cfz - Cs 
E, Z, Pto, PAS 
MDR/RR-TB with 
resistance to 
fluoroquinolone (pre-
XDR) or extensive drug 
resistance (XDR-TB)  
  6 Bdq - Lzd - Cfz - Cs – 
Dlm 
14 Lzd - Cfz - Cs 
E, Z, Pto, PAS  
Central nervous system 
disease 
  6 Lfx - Lzd - Cs – Pto – 
Z 
14 Lfx - Lzd – Cs - Z 
INH
HD (if low-level H resistance - inhA 
mutation)
1 
Pregnant RR/MDR-TB 
  20 Lfx - Cs - E -Cfz- Z 
Consult consillium on all pregnant 
cases. Consider strengthening the 
regimen post-partum with the addition of 
Bdq and Lzd (for 6 months; to replace 
Class C medicines if possible). 
 
Table 7.5: Paediatric treatment regimens for children <12 years with non-severe disease 
Age 
group 
Patient condition 
Proposed regimens 
Intensive phase 
------------------------------- 
Continuation phase* 
If any of the medicines cannot be used, 
consult the DR-TB consillium to consider 
replacement if needed using one or more 
of the following based on DST, prior use 
and likelihood of efficacy (in order of 
priority) 
Children  
6 – 12 
yrs  
RR/MDR TB 
susceptible to 
fluoroquinolone 
  6 Lfx – Bdq – Lzd – Cs 
3 Lfx – Lzd – Cs 
Cfz, Dlm
1 (E if documented sensitivity), Z 
(Cfz preferred over Cs if 50mg capsule 
available) 
RR/MDR-TB with 
resistance to 
fluoroquinolone (pre-
XDR) or extensive 
drug resistance (XDR-
TB) 
6 Bdq - Lzd - Cs - PAS 
3 Lzd - Cs - PAS 
Cfz, Dlm
1(E if documented sensitivity), Z 
(Cfz preferred over PAS if 50mg capsule 
available) 
3 – 6 yrs 
RR/MDR TB 
susceptible to 
fluoroquinolone 
  9 Lfx/Mfx - Lzd - Cs - 
Eto  
Cfz, Dlm
1, PAS (E if documented 
sensitivity), Z; Eto should not be used if 
inhA mutation 
(Cfz preferred over Eto if 50mg capsule 
available) 
 
RR/MDR-TB with 
resistance to 
fluoroquinolone 
  6Lzd - Cs – Dlm
1 - Eto 
3 Lzd – Cs - Eto 
Cfz, PAS (E if documented sensitivity), Z; 
Eto should not be used if inhA mutation 
(Cfz preferred over Eto if 50mg capsule 
available) 
< 3 yrs 
RR/MDR-TB 
susceptible to 
fluoroquinolone 
9 Lfx/Mfx - Lzd - Cs - 
Eto 
Cfz, PAS (E if documented sensitivity), Z; 
Eto should not be used if inhA mutation 
(Cfz preferred over Eto if 50mg capsule 
available) 
RR/MDR-TB with 
resistance to 
fluoroquinolone 
6 Lzd - Cs – PAS – Eto 
3 Lzd- Cs - PAS  
Cfz, Dlm
1 (E or Z if documented sensitivity) 
(Cfz preferred over Eto if 50mg capsule 
available) 
 
 
Table 7.4  Proposed MDR TB treatment regimens

138!
!
Table 7.6: Modified Short Treatment Regimen 
Age 
group 
Patient condition  
Proposed regimens 
Intensive phase 
Continuation 
phase 
15 yrs 
and 
above 
 
 
 
Patient eligible for short treatment 
regimen 
6 Bdq – Lzd – Lfx – Cfz – Cs 
– Z 
3-5 Lfx – Cfz – 
Cs – Z 
Patient eligible for short treatment 
regimen but cannot tolerate 
linezolid (Haemoglobin (Hb) < 8 
g/dL, neutrophils <0.75 x109/L or 
platelets <50 x109/L or severe 
peripheral neuropathy grade ≥2 or 
optic neuritis grade ≥2 at baseline) 
6 Bdq – Dlm– Lfx – Cfz – Cs 
– Z 
3-5 Lfx – Cfz – 
Cs – Z 
 
7.1.2 Treatment of Tuberculosis in Special Cases 
Treatment of TB/HIV co-infected patients 
Consideration is needed when handling a patient with TB/HIV co-infection. 
 
Table 7.7 Special considerations for ART in TB/HIV co-infected patients 
Start ART for all TB patients living with HIV 
irrespective of CD4 counts  
Treat TB first and start ART as soon as possible, 
preferably within two weeks of initiating treatment  
Already on ART at TB diagnosis  
Refer to HIV and AIDS chapter   
 
Also, the following shall be considered in treatment of TB patients: 
 
Pregnancy  
Anti-TB is safe during pregnancy and breast feeding. 
 
TB Prevention; 
TPT is offered to: 
• 
Under 5 household contacts of bacteriologically confirmed PTB cases who have no 
active TB. 
• 
All PLHIV who have no active TB. 
 
Dosage 
In adult and adolescent  
A: isoniazid (PO) 300mg 24hourly for 6months to complete one cycle of TPT  
In children 
A: isoniazid (PO) 10mg/kg (10-15 mg/kg) 24hourly for 6months.  
 
Note 
• 
TPT should only be given in one cycle in lifetime and no repeat cycle is needed. 
• 
People living with HIV who successfully completed their TB treatment should immediately 
receive TPT for six months.  
• 
In case of neuropathy due to INH, Pyridoxine should be used for treatment of neuropathy.  
• 
TB Preventive Therapy is not contraindicated in pregnancy and it can be given during any 
trimester. 
 
Breast feeding: In the mothers with pulmonary tuberculosis, the baby should receive INH 
preventive (5mg/kg) for 6 months followed by BCG vaccination.   
 
Oral contraceptives: Rifampicin interacts with oral contraceptives and reduces the efficacy of this 
contraception.  
 

139!
!
Liver disease: Most of anti-TB medicines can cause liver damage. In case a patient develops 
jaundice, treatment should be stopped and restarted as soon as the jaundice resolves. In severely ill 
patients, start moxifloxacin and ethambutol only.  
 
Renal failure: Ethambutol is excreted by the kidneys and should either be avoided or given in a 
reduced dose.   
 
 
 
 
 
 
 
 
 
 
7.2 General Treatment of Leprosy 
Leprosy is a chronic granulomatous disease caused by Mycobacterium leprae. It mainly affects the 
skin, the peripheral nerves and the mucous membranes. Leprosy is the commonest cause of 
peripheral neuritis in the world.  
 
Clinical presentation 
Presence of any one among the three cardinal signs of leprosy below: 
• 
Skin patch with loss of sensation 
• 
One or more enlarged peripheral nerves 
• 
Presence of leprosy bacilli–positive smear  
 
Classification of Leprosy  
Multibacillary (MB) Leprosy  
• 
Patients with six or more leprosy skin lesions  
• 
Positive skin smear  
 
Paucibacillary (PB) Leprosy  
• 
Patients with one to five leprosy skin lesions   
• 
Negative skin smear  
 
Note 
• 
If there is any doubt regarding the classification, the patient should be classified and 
treated as a multi-bacillary case.  
 
Pharmacological Treatment 
Patients should be treated by multidrug combination therapy; dosage may depend with classification 
and whether patient is adult or children 
 
Table 7.8 Treatment of Leprosy 
Classification 
Medicine dosage 
Duration of treatment 
Adult 
MB: 
15years 
and 
above 
Day 1: Rifampicin 600mg (2x 300mg) +Clofazimine 
300mg (3 x 100mg) + Dapsone 100mg. Daily 
Treatment: Day 2–28, Clofazimine 50mg + Dapsone 
100mg   
12 blister packs to be taken 
within a period of between 
12–18 months   
Child 
MB: 
below 15years 
Day 1: Rifampicin 450mg (3 x 150mg) + Clofazimine 
150mg (3 x 50mg) + Dapsone 50mg. Daily Treatment: 
Day 2–28 Clofazimine 50mg every other day + 
Dapsone 50mg daily. 
12 blister packs to be taken 
within a period of between 
12–18 months   
 
Adult 
PB: 
15years 
and 
above 
Day 1: Rifampicin 600mg (2x 300mg) +Clofazimine 
300mg (3 x 100mg) + Dapsone 100mg. Daily 
Treatment: Day 2–28, Clofazimine 50mg + Dapsone 
100mg   
6 blister packs to be taken 
within a period of between 
6–9 months   
Child 
PB: 
below 15years 
Day 1: Rifampicin 450mg (3 x 150mg) + Clofazimine 
150mg (3 x 50mg) + Dapsone 50mg. Daily Treatment: 
Day 2–28 Clofazimine 50mg every other day + 
Dapsone 50mg daily. 
6 blister packs to be taken 
within a period of between 
6–9 months   
 
7.2.1 Treatment of Leprosy in Special Cases 
Tuberculosis: Patients suffering from both tuberculosis and leprosy require appropriate anti-
Tuberculosis therapy in addition to the MDT. Rifampicin must be given in the dose required for the 
treatment of tuberculosis. Once the intensive phase of anti TB treatment is completed, the patient 
should continue with his/her monthly rifampicin for leprosy treatment.  
 
 

140!
!
There are two types of reactions 
• 
Reverse Reaction or type I reaction  
• 
Erythema Nodosum Leprous (ENL) or type II reaction (For detail refer Manual for the 
Management of Tuberculosis and Leprosy in Tanzania)   
 
Treatment of Reaction: Depending on severity, treatment of reverse reaction is by giving anti- 
inflammatory drugs or corticosteroids usually prednisolone for a prolonged period.   
 
Note 
Health care worker should communicate with DTLC and RTLC when suspect leprosy reaction 
 
 
 
 
 

141!
CHAPTER EIGHT 
NERVOUS SYSTEM DISEASE CONDITIONS 
8.1 Infections of the Nervous System 
Infections of the nervous system can arise secondary to bacteria, fungi, protozoa, helminthes or 
viruses. Clinical features will depend on the site of the nervous system involved. 
8.1.1 Bacterial infections 
8.1.1.1 Bacterial Meningitis 
Bacterial meningitis is a serious infection involving layers (meninges) covering the brain and spinal 
cord. Causative bacteria differ among different age groups. 
Clinical presentation 
•
Headache, high grade fever
•
Altered mental status, convulsions, coma.
•
Photophobia
•
Nausea and vomiting
•
Signs of meningeal irritation
Investigations 
CBC, Blood C/S, Lumbar puncture for CSF analysis 
Pharmacological Treatment 
I. 
Where the organism is not known:
A: benzyl penicillin (IV) 5MU 6hourly for 14days. 
AND 
B: chloramphenicol (IV) 1000mg 6hourly for 14days 
Alternatively 
D: ceftriaxone+Sulbactam (FDC) (IV) 1.5g 12hourly for 14days 
Alternatively 
A: ampicillin (IV) 2g 6hourly for 10–14days 
AND 
 
S: cefepime (IV) 2g 8hourly for 10–14days 
Alternatively, and based on C/S results give 
S: meropenem (IV) 2g 8hourly for 10days 
II.
Where the organism is known:
Meningococcal meningitis (Refer to notifiable diseases section)
Haemophilus influenza meningitis 
B: chloramphenicol (IV) 1g 6hourly for 7–10days. 
OR 
D: ceftriaxone+Sulbactam (FDC) (IV) 1.5g 12hourly for 14days 
Pneumococcal meningitis 
A: benzyl penicillin (IV) 5MU 6hourly for 14days 
OR 
D: ceftriaxone + Salbactam (FDC) (IV) 1.5mg 12hourly for 14days 
8.1.1.2 Tuberculous Meningitis 
Tuberculous meningitis (TBM) is the most common form of central nervous system tuberculosis, 
associated with high mortality and morbidity from neurological sequelae.  
Clinical presentation 
•
Headache
•
Low grade fever
•
Altered mental status, coma.
•
Seizures
•
Nausea and vomiting
•
cranial nerve palsies

142!
•
CBC
•
Blood C/S
•
LP for CSF analysis
o
lymphocytic-predominant pleiocytosis usually between 100-500 cells/µL
o
elevated protein levels typically between 100 and 500 mg/dL
o
low glucose-usually less than 45 mg/dL or CSF:Plasma ratio <0.5.
•
CSF GeneXpert
•
CSF for AFB
•
HIV testing
Imaging Investigations 
•
Contrast head CT scan-can demonstrate multiple ring-enhancing lesions, meningeal and
basal cisterns enhancement
•
Contrast brain MRI with diffusion weighted sequences (DWI)
Pharmacological management 
Refer to TB and leprosy chapter  
Non-pharmacological management 
•
Screen for postinfectious hydrocephalus as it is a common complication of all meningitis
cases and can occur early during treatment—monitor for persistent headache, vomiting,
papilledema on fundoscopy and parinauds syndrome.
•
Refer all patients presenting with clinical or radiological features of increased ICP from
hydrocephalus for neurosurgical evaluation directed at treatment of the associated
hydrocephalus by external ventricular drainage (EVD) or VP shunt once CSF is sterile.
•
Monitor urine output and serum sodium levels as syndrome of inappropriate antidiuretic
hormone secretion (SIADH) is a common complication
8.1.1.3 Tetanus 
It is an acute, often fatal disease caused by an exotoxin produced by the anaerobic bacterium 
Clostridium tetani. It is acquired through wounds contaminated with spores of the bacteria and in the 
case of neonates, through the umbilical stump, resulting in neonatal tetanus. 
Clinical presentation 
•
Generalized spasms and rigidity of
skeletal muscles
•
Locked jaws
•
Patients are usually fully conscious
and aware.
•
Dysphagia
•
Diaphoresis
•
Local spasms may also occur
Non-pharmacological Treatment 
•
Admit in intensive care unit (ICU)
•
Nurse in dark, quiet room to avoid unnecessary external stimuli which can trigger spasms
•
Protect the airway (evaluation for early tracheostomy is required)
•
Thorough cleaning of the site of entry site (e.g., wound), leaving it exposed without
dressing
•
Maintenance of fluid balance and nutrition (via NGT)
•
Avoid giving medications via IV/IM route as injections can trigger spasms
•
Sedation (see below) and care as for unconscious patient
Pharmacological Treatment 
Treatment is generally aimed at the following: 
Pain management as the spasms can be very painful 
A: paracetamol (PO/NGT) 1gm 8 hourly for 5 days 
For prevention of further absorption of toxin from the wound 
A: human tetanus immunoglobulin (IM) Adults give 3000IU stat 
AND 
A: amoxicillin (PO/NGT) 500mg 8hourly for 5days 
Laboratory investigations 

143!
 AND 
          A: metronidazole (PO/NGT) 400mg 8hourly for 5days 
Control of spasms: Give a sedative cocktail of the following medications preferably via NGT: 
A: diazepam (PO/NGT) 10-30mg 4-6hourly for 7-14days 
AND 
          A: chlorpromazine (PO/NGT)100–200mg 8hourly for 7-14days 
AND 
          A: phenobarbitone (PO/NGT) 50–100mg 12hourly for 7-14days 
Table 8.1:Guidelines for Dosage Administration** 
Time (Hours) 
0 
3 
4 
6 
9 
12 
15 
18 
21 
24 
diazepam 
* 
* 
* 
* 
* 
chlorpromazine 
* 
* 
* 
phenobarbitone 
* 
* 
Prevention: tetanus (toxoid) vaccine (IM) 0.5ML; repeat after 4 weeks and after 6-12months, then 
boost every 10years thereafter. 
8.1.1.4 Brain Abscess 
Brain abscess is a focal collection of purulent material within the brain parenchyma, which can arise 
as a complication of a variety of local cranial or remote systemic infections, trauma, or surgery. The 
manifestations of brain abscess depend on the site, size, and the immune status of the patient. 
Clinical presentation 
•
Headache
•
Fevers
•
Seizures
•
Focal neurological deficit
•
Altered mental status that may
progress to coma
Imaging Investigations 
•
Contrast head CT scan--can demonstrate a ring enhancing lesion and possible source of
infection e.g., from paranasal sinuses, ear infections
•
Contrast brain MRI with diffusion weighted sequences (DWI)
•
MR spectroscopy to distinguish from brain tumors where diagnosis is unclear
•
CXR
•
ECHO in suspected valvular heart disease
Lab Investigations 
•
Gram stain, C/S of pus from possible sources
•
Purulent aspirate from the abscess for C/S
•
Ziehl Neelsen stain
Non-pharmacological Treatment 
•
Follow the ABCD protocol
•
If unconscious insert NGT for feeding
•
insert urethral catheter
Pharmacological Treatment: 
•
Control fever and pain with IV Paracetamol
•
Manage seizures with antiepileptic drugs
•
Prompt initiation of intravenous antibiotics
•
Steroids in selected case

144!
Table 8.2: Pharmacological management of Brain abscess 
Condition 
Treatment 
Duration 
Brain abscess 
(unspecific bacterial) 
A: benzyl penicillin (I.V) 5MU 6hourly 
          OR 
C: amoxicillin +clavulanate (FDC) (IV) 1.2g 12hourly 
          OR 
D: ceftriaxone+sulbactam (FDC) (IV) 1.5g 12hourly 
          AND 
A: metronidazole (IV) 500mg 8 hourly 
alternative regimen based on C/S results 
S: piperacillin+tazobactam (FDC) (IV) 4.5g 8hourly 
OR  
S: meropenem (IV) 2g every 8hourly 
4-6weeks
4-6 weeks
2weeks 
2weeks 
Brain abscess (Staph. 
aureus) 
S: vancomycin (IV) 1g 12hourly (used 
with cefotaxime or ceftriaxone+Sulbactam) 
4-6weeks
Seizures control 
C: phenytoin (IV) 15mg/kg loading dose infused at 
50mg/min followed by 100mg (IV/PO) 8hourly 
          OR 
A: carbamazepine (PO/NGT) 200mg 12hourly 
          OR 
C: sodium valproate (PO) 250mg 12hourly (escalate 
dose as required based on response) 
Until seizure 
free for at least 
6 months 
ICP control in selected 
cases 
B: dexamethasone (IV) 0.15mg/kg 6hourly 
3-5days
Note: 
If allergic to penicillin, chloramphenicol 500mg IV every 6hours can be used instead.In case 
antiepileptic drugs are used for prolonged durations 5mg daily Folic acid supplement should be 
added for the entire duration of anticonvulsants treatment especially in women of childbearing 
age. 
Surgical management 
•
Refer all patients diagnosed with a brain abscess for neurosurgical evaluation.
•
Surgical options include stereotactic abscess aspiration and craniotomy for abscess
excision. In cases where the source of
infection is paranasal sinuses or ear infection, involve concomitant ENT surgeon
evaluation for primary source control interventions.
8.1.2 Fungal Infections 
Cryptococcus Meningitis (CM) 
CM is the most common form of fungal meningitis worldwide. It often develops in patients who are 
immune compromised e.g., HIV-positive patients with low CD4 cell count, diabetic mellitus and 
iatrogenic immunosuppression, as in post organ transplant patients. 
Clinical features 
•
Headache, fever, intolerance to light
and sound,
•
Neck stiffness, vomiting, seizures,
deafness, impaired vision
•
In advanced stages it may present
with confusion,
•
Altered mental status that may
progress to coma.
Investigations 
•
CSF gram stain
•
CSF India Ink stain test
•
Serum or CSF Cryptococcus antigen (CrAg) test
•
CSF cultures
•
Contrast brain MRI

145!
o
may demonstrate cryptococcomas
o
assist to rule out differential diagnoses
Pharmacological Treatment 
The treatment should be done in 3 phases: 
Phase 1: Induction phase 
S: amphotericin B (IV) 0.7-1mg/kg/day 
AND 
S: 5 flucytosine (PO)100mg/kg/day for 7days followed by 1 week of 
AND 
A: fluconazole (PO): Adult 1200mg/day,  
Children/adolescents 2mg/kg/day, up to a maximum dose of 800mg daily 
In the absence of flucytosine, alternative therapy should be: 
S: amphotericin B (IV) if available give 3-6mg/kg for 10days 
AND 
A: fluconazole (PO) 1200mg once daily for 14days 
OR 
C: fluconazole (IV) 1200mg once daily for 14days 
Phase 2: Consolidation phase 
A: fluconazole (PO) 800mg/day for 8weeks or until CSF is sterile. 
Phase 3: Maintenance phase 
A: fluconazole (PO) 200mg 24hourly for 1year 
Discontinue maintenance treatment if CD4 ≥100 with undetectable (<50 copies), viral load or CD4 ≥ 
200 if viral load monitoring not available. 
Note 
•
It is recommended to initiate ART 5 weeks after initiation of Cryptococcal meningitis
treatment in ART naïve patient to prevent IRIS and reduce mortality.
•
Monitor creatinine, BUN, serum Potassium and magnesium in all patients on Amphotericin
B every 24hours.
Non-pharmacological Treatment 
•
Refer to section on bacterial meningitis in unconscious patients.
•
Perform serial Lumbar puncture for management of increased ICP in cryptococcal
meningitis. Opening pressure should be measured during LP and therapeutic CSF
drainage done (20-30ml per session) for pressures >25cm H2O.
•
Failure to control ICP after several LPs (recommended 3 attempts) should prompt
neurosurgical evaluation for ventriculoperitoneal shunt insertion to divert CSF.
Note 
The usage of Mannitol, Hypertonic saline, acetazolamide, or corticosteroids to manage increased 
ICP in Cryptococcal meningitis is ineffective and NOT recommended. 
8.1.3 Protozoa infections 
Toxoplasmosis 
Immunocompetent persons with primary infection are usually asymptomatic, but latent infection can 
persist for the life of the host. In immunosuppressed patients, especially patients with AIDS, the 
parasite can reactivate and cause disease, usually when the CD4 lymphocyte count falls below 100 
cells/mm3. 
Clinical presentation 
•
Altered mental status
•
Focal neurological deficits
•
Seizures
•
Neuropsychiatric manifestations

146!
Imaging Investigations 
•
Contrast head CT scan-demonstrates ring-enhancing lesions
•
Contrast brain MRI with diffusion weighted sequences (DWI)
•
CXR
Laboratory 
Investigations 
Toxoplasma serology (IgM) 
Non-pharmacological Treatment 
Similar to bacterial meningitis 
Pharmacological Treatment For 
acute infection give: 
D:sulfadiazine (PO) 1g 6hourly for 6weeks 
AND 
D: pyrimethamine (PO) 100mg loading dose then 50mg /day for 6weeks 
AND 
S: folinic acid (PO) 10mg /day for 6weeks. 
After six weeks of treatment give maintenance treatment with 
D: sulfadiazine (PO) 500mg 6hourly 
AND  
D: pyrimethamine (PO) 25-50mg /day 
AND 
S: folinic acid (PO) 10mg /day until CD4 counts is above 200cells/microlitre and/or 
undetectable viral load for 3-6months 
For those allergic to sulphur replace Sulfadiazine with 
S: clindamycin (PO) 450mg 6hourly for for 6weeks. 
8.1.4 Helminthic infections 
 Neurocysticercosis (NCC) 
NCC is a neurologic infection caused by the larval stage of the tapeworm Taenia solium. In the 
developing world NCC is the most common cause of new onset acquired epilepsy among the adult 
population. Humans are the definitive hosts for this parasite, and swine are the intermediate hosts. 
The mature tapeworm develops in humans after they ingest live cysticercus in undercooked pork. 
NCC develops when humans accidentally ingest eggs from fecal contaminated food.  
Clinical presentation 
•
Headache
•
Seizures
•
Focal neurological deficit
•
Features of increased intracranial
pressure
Imaging Investigations 
•
Contrast head CT scan-can demonstrate ring enhancing lesions, calcified lesions
•
Contrast brain MRI can demonstrate viable cystic lesions with scolices
Laboratory Investigations 
•
FBP, serum electrolytes
•
Enzyme-linked immunotransfer blot (EITB)
•
Liver function tests
Non-pharmacological Treatment 
•
If unconscious, airway and breathing management
•
Insert NGT for feeding
•
Insert urethral catheter

147!
Pharmacological Treatment 
Table 8.3: Pharmacological Management of NCC 
Condition 
Treatment 
Duration 
Antihelminthic 
treatment for single 
viable lesion 
A: albendazole (PO) 15mg/kg/day divided into two daily 
doses (maximum of 1200mg/day) 
2-4weeks
Anthelminthic treatment 
for multiple viable 
lesions 
A: albendazole (PO) 15mg/kg/day divided in two daily 
doses (maximum of 1200mg/day) 
        AND 
A: praziquantel (PO) (50mg/kg/day) 
2-4weeks
2weeks 
Seizures control 
C: phenytoin (IV) 15mg/kg loading dose infused at 
50mg/min followed by 100mg (IV/PO) 8hourly 
       OR 
A: carbamazepine (PO) 200mg 12hourly (can be adjusted 
based on individual response) 
        OR 
C: sodium valproate (PO) 250mg 12hourly 
(escalate dose as required based on response) 
Until seizure free 
for at least 6 
months 
Control of increased 
ICP 
D: dexamethasone (PO) 0.15mg/kg 6 hourly for 3-5days 
then taper down. 
       OR 
B: dexamethasone (IV) 0.15mg/kg 6 hourly for 3-5days 
then taper down 
2weeks 
Note 
Fundoscopic examination is mandatory for all patients before initiation of   anthelminthic therapy. 
Surgical management 
•
Refer all patients diagnosed with CNS cysticercosis associated with clinical or radiological
features of increased intracranial pressure from hydrocephalus for neurosurgical
evaluation directed at management of the associated hydrocephalus.
•
In patients with untreated hydrocephalus or diffuse cerebral edema, management of
elevated intracranial pressure should proceed anthelminthic treatment.
8.1.5 Viral infections 
Viral infections of the nervous system are mainly caused by Herpes simplex virus (HSV) and Human 
immunodeficiency virus (HIV). (Refer to section on viral infections and HIV) 
Herpes simplex encephalitis 
Most of cases in adults are caused by HSV-1, a small number are caused by HSV-2 usually in 
immunosuppressed states or in neonates. It should be suspected in all patients not responding to 
antibiotics/other treatments. 
Clinical presentation 
•
Early features are fever, headache & altered consciousness which may develop gradually
over days or rapidly over hours
•
The most common manifestations are personality change, dysphasia, behavioural
disturbance, and occasional psychotic features
•
Focal or generalized seizures
Investigations 
•
Lumbar puncture--CSF is under increased pressure and may appear normal or show a
mild-moderate lymphocytosis, a mild-moderate elevated protein levels and normal or
decreased glucose.
•
CSF PCR
•
HSV1+HSV2 CSF Rapid test
•
MRI—demonstrate predominant involvement of the limbic system structures, medial
temporal lobes, and insular cortex

148!
Pharmacological Treatment 
B: acyclovir (IV/PO) 10–15mg/kg 8hourly for 14–21days 
Non pharmacological treatment 
Provide supportive therapy as for unconscious patients 
8.2 Initial Management of Stroke 
8.2.1 Management of Acute Hemorrhagic Stroke 
Spontaneous, nontraumatic intracerebral hemorrhage (ICH) remains a significant cause of morbidity 
and mortality throughout the world. However, population-based studies indicate that most ICHs in 
most patients are survivable with good medical care thus emphasizing the importance of improved 
clinical care. in determining ICH outcome.  
Clinical presentation 
•
Severe headache, vomiting,
•
Focal neurological deficits
•
decreased level of consciousness
that may progress to coma
•
symptom progression over minutes
or hour
Investigations 
•
Rapid neuroimaging: plain CT to distinguish ischemic stroke from ICH
•
MRI with angiography-useful to evaluate for underlying structural lesions e.g., vascular
malformations and tumors in suspicious cases
Admit all patients with ICH in an ICUor dedicated stroke unit for initial management and 
monitoring. 
Pharmacological Treatment 
For elevated SBP (150-220mmHg), initiate BP lowering treatment, target at 140mmHg. Consider 
more aggressive reduction if SBP>220mmHg. 
C: labetalol (IV) at 1mg/min until target SBP is attained. 
Anticoagulation-related ICH: withhold anticoagulants and correct INR, if elevated, start on vitamin K 
and consider FFP transfusion 
B: phytomenadione (vitamin K) (IV) 1mg slow infusion over 60 minutes 
If increased ICP based on clinic radiological features, give 
C: mannitol (IV bolus) 0.25-1gm/kg 4-6hourly for 24-72hours 
OR 
C: hypertonic saline 3% (IV bolus) at 3-5ml/kg 4-6hourly for 24-72hours 
Monitor serum osmolarity and renal function when giving Mannitol or Hypertonic saline, stop if 
osmolarity goes >320mOsm/L 
Treat fever with antipyretic medications and/or external cooling methods 
D: paracetamol (IV) 1g 8hourly for 3-5days then when required 
Perform regular monitoring and control of blood glucose to prevent both hyperglycemia and 
hypoglycemia. 
Treat clinical or electrographic seizures associated with decreased loss of consciousness   
S: levetiracetam (PO/IV) 500mg 12hourly for 2weeks 
C: phenytoin (IV) 15mg/kg loading dose over 30min, then maintenance at 100mg 8hourly 
for 2weeks. 
Non-pharmacological Treatment 
•
Apply compressive stockings or intermittent pneumatic compression at admission to
prevent VTE
•
LMWH can be started later after cessation of bleeding in immobile patients.
•
Consider systemic anticoagulation or IVC filter only in patients with symptomatic deep
vein thrombosis or Pulmonary embolism.

149!
!
Surgical management 
• 
Consider neurosurgical evaluation for External Ventricular drainage (EVD) in patients 
with decreased level of consciousness from resultant hydrocephalus in the setting of 
intraventricular hemorrhage. 
• 
Refer for surgical evacuation of hematoma as soon as possible in patients with 
cerebellar hemorrhage who are deteriorating neurologically or who have brainstem 
compression and/or hydrocephalus from ventricular obstruction  
• 
For supratentorial hematomas, consider evacuation in deteriorating patients with or 
without decompressive craniectomy as a life-saving measure in selected cases, based on 
expert neurosurgical clinical judgement. 
• 
Consider minimally invasive clot evacuation via stereotactic or endoscopic aspiration with 
or without thrombolytic usage, based on expert clinical judgement and available resources.  
 
8.2.2 Initial Management of Acute Subarachnoid Hemorrhage from Ruptured 
Cerebral Aneurysm 
Subarachnoid haemorrhage (SAH) refers to presence of blood in the fluid-filled subarachnoid 
spaces around the brain and spinal cord. The most common presentation is sudden onset of severe 
novel headache. SAH from ruptured cerebral aneurysms is associated with high mortality and 
morbidity hence clinician’s high index of suspicion and proper initial management is crucial for 
patient’s survival and improved functional outcome.  
 
Clinical presentation 
• 
Severe headache (worst headache 
of life) 
• 
Altered mental status that may 
progress to coma 
• 
Focal neurological deficits 
• 
Seizures
 
Laboratory Investigations 
• 
CBC, PT/PTT/INR 
• 
Serial ABGs, electrolytes  
• 
serum and urine osmolality   
 
Imaging investigations 
• 
CT angiography 
• 
Four vessel catheter angiography/digital subtraction angiography (DSA) 
o 
Perform 4-vessel catheter angiography to determine source of bleeding  
o 
The timing of study takes into consideration the patient’s condition (unstable or 
premorbid patients are not candidates), the feasibility of early treatment, the 
likelihood of endovascular therapy (based on patient’s age and predicted 
aneurysm location as well as availability of required resources and expertise) 
• 
CXR—monitor for pulmonary edema if in hyperdynamic therapy 
 
Principles of initial management of aneurysmal SAH are focused on  
• 
Initial hemodynamic stabilization and life support of the patient 
• 
Prevention of rebleeding through timely coiling or surgical clipping 
• 
Prevention, identification, and early management of hydrocephalus  
• 
Prevention and management of delayed ischemic neurologic deficit (DIND) from 
vasospasm 
 
 
Admitting orders 
• 
Admit all aneurysmal SAH patients to ICU regardless of their initial GCS score 
• 
Document initial Hunt & Hess, WFNS clinical scores, and Fisher CT scan score 
• 
Bedrest with head of bed elevation at 30°.  
• 
Initiate SAH precautions (low level of external stimulation, restricted visitation, dim light, no 
loud noises) 
• 
Check neurological status every 1 hour. 
• 
Bed pan, indwelling Foley catheter if patient is lethargic, incontinent with strict Inputs & 
outputs measurements. 
• 
Keep Nil per Oral (if in preparation for surgery or endovascular intervention) 

150!
!
• 
Maintain SBP 120–160mmHg in unsecured (unclipped/uncoiled) aneurysm to minimise 
rebleeding risk, consider 
 
D: labetalol (IV) 1mg/min until target SBP is attained. 
 
• 
IV fluids: 0.9% NS + 20 mEq KCl/L at 2 ml/kg/hour maintenance fluid 
 
Prophylactic anticonvulsants:  
S: levetiracetam (PO/IV) 500mg 12 hourly while aneurysm is unsecured, continue for 
1week post clipping/endovascular intervention  
OR 
C: phenytoin (IV) 15mg/kg loading dose at 50mg/min rate then 100mg 8hourly for 2-4 
weeks 
 
Sedation (not over sedation):  
D: propofol (IV) (for intubated patients) at 25-75mcg/kg/minute 
 
Give  
B: dexamethasone (IV) 4mg 6 hourly for 3-5days to reduce neck pain  
AND 
S: fentanyl (IV) 25–100mcg (0.5–2 ml) every 1–2hours when required in ICU. 
 
Stool softener: Initiate  
C: lactulose (PO) 30mls 8hourly until aneurysm is secured. 
 
Anti-emetics:  
D: ondansetron (IV) 4mg over 2–5minutes, may repeat 8hourly for 1–2days.  
 
Prevention of vasospasm: Initiate  
S: nimodipine (PO/NGT) 60mg 4hourly, continue for 21days  
 
Stress ulcer prophylaxis: 
C: pantoprazole (IV) 40mg 24hourly for 1-2weeks  
 
Oxygenation goals (for intubated ventilated patients) 
o 
pO2 > 100mm Hg, O2 saturation 100% in patients at risk for vasospasm, aim for 92% 
saturation in all others.  
o 
To achieve above goals, increase FiO2 and mean airway pressure (PEEP) in 
ventilated patients 
o 
in non-intubated patient: Give O2 2L per nasal cannula PRN (based on ABG)  
• 
Strive for normocarbia, avoid prophylactic hyperventilation  
• 
Avoid arterial hyperoxia (paO2 > 300mm Hg)- to avoid risk of vasoconstriction 
• 
maintain normothermia and encourage other cooling measures to reduce and prevent fever. 
D: paracetamol (IV) 1g 8hourly for 3-5days then when required 
• 
Hemoglobin and hematocrit: Transfuse whole or PRBC when Hct drops < 40%) 
• 
Monitor serum glucose and maintain normoglycemia  
 
Surgical management 
Refer to a centre that can handle neurovascular cases for prompt neurosurgical evaluation and 
subsequent surgical clipping or endovascular intervention (coiling or embolization) to secure the 
ruptured cerebral aneurysm.  
 
8.2.3 Initial management of Acute Ischemic Stroke 
Acute ischemic stroke (AIS) is a leading cause of adult disability in the developed world.In AIS, a 
thrombus impairs cerebral blood flow, resulting in brain tissue infarction. Collateral blood flow gives 
rise to an area of hypoperfused tissue (ischemic penumbra) that is at risk of infarction if 
hypoperfusion persists. Prompt reopening of an occluded blood vessel to re-establish blood flow to 
the ischemic area (reperfusion) in eligible patients, can rescue the ischemic penumbra from death 
and spare the patient from serious long term disabilities.  
 
 

151!
Clinical presentation 
•
Severe headache
•
Focal neurological deficits
•
decreased level of consciousness
that may progress to coma
•
seizures
•
symptom progression over minutes
or hours
Investigations 
•
FBP, PT/PTT/INR,
•
Random blood glucose
•
serial ABGs, serum electrolytes
•
Non contrast CT scan to distinguish
AIS from ICH
•
CT 
angiogram 
in 
potential
candidates for reperfusion
•
CT/MR perfusion studies
•
MR 
angiography 
(MRA) 
with
•
DWI for selected patients. (contraindicated with cardiac pacemakers, metal implants)
•
Four-vessel catheter angiography
•
Baseline ECG and ECHO
Prehospital and lower level health facilities 
•
Provide initial airway management and hemodynamic stabilization
•
Exclude stroke mimics like hypoglycemia
•
International stroke guidelines recommend rapid identification of all fibrinolytic-eligible and
mechanical thrombectomy-eligible patients to facilitate initiation of treatment in the fastest
achievable onset-to-treatment time
•
Consider prompt referral to a centre that can handle stroke patients including rapid
neuroimaging and administration of reperfusion therapy.
Referral hospital and specialized centres 
•
Provide initial stabilization of the patient as per ABCDE protocol
•
Perform rapid careful neurological examination.
•
Order emergency brain imaging evaluation before initiating any stroke specific treatments.
•
Screen for reperfusion eligible patients and initiate appropriate treatment protocol.
•
In patients with AIS who awake with stroke symptoms or have unclear time of onset > 4.5
hours from last-known-well (LKW) state, perform brain MRI to identify diffusion-positive,
FLAIR-negative lesions to aid selecting those who can benefit from IV alteplase
administration.
•
In potential candidates for mechanical thrombectomy, consider imaging of the extracranial
carotid and vertebral arteries, in addition to the intracranial circulation, to provide useful
information on patient eligibility and endovascular procedural planning.
Reperfusion criteria: all must be met 
•
Onset of stroke or Last known well (LKW) state <4.5hours
•
No increased bleeding risk contraindications
•
Blood pressure controlled to <185/105mmHg target.
•
Non contrast brain CT has excluded intracranial hemorrhage and/or
•
established a hypodense zone or hyperdense vessel sign.
Non-pharmacological Treatment 
•
Oxygenation—support airway, maintain O2 saturation >94%
•
Monitor BP, if elevated, initiate BP lowering treatment to target BP<185/110 mmHg
•
For patients who are non-eligible for fibrinolysis aim to lower BP by 15% in the first 24
hours
•
Monitor body temperature and initiate treatment when >38°C
•
In immobile stroke patients without contraindications, offer compressive stockings, or
pneumatic compression devices for DVT prophylaxis.
•
Start on enteral diet (PO/NGT) within 7days of admission after AIS.

152!
Pharmacological treatment 
A: acetylsalicylic acid (PO) 325mg 24hourly for 4weeks 
AND 
C: labetalol (IV) 10-20mg infusion 1-2min, repeated until target BP is attained. 
AND 
D: paracetamol (IV) 1g 8hourly for 3-5days then when required. 
Note 
For those treated with alteplase, acetylsalicylic acid administration should be delayed until 24 hours 
later 
For seizure control 
C: phenytoin (IV) 15mg/kg loading dose over 30min, then 100mg 8hourly for 4weeks. 
OR 
S: levetiracetam (PO/IV) 500mg 12hourly for 2-4 weeks 
•
Initiate statins in eligible patients and continue statins in patients already taking statins at
the time of onset of AIS.
Reperfusion treatment: 
In patients qualified for intravenous thrombolysis, benefit of therapy is time dependent, and 
treatment should be initiated as quickly as possible. 
Admit the patient to an ICU or designated stroke unit for monitoring and initiate, 
         S: alteplase (IV) 0.9mg/kg maximum dose 90mg (given over 60minutes with initial 10% of dose 
given as bolus over 1 minute)  
Important precautions: 
•
Be prepared to treat potential emergent adverse effects, including bleeding complications
and angioedema in patients undergoing fibrinolytic therapy.
•
Maintain BP at <180/105mmHg for at least 24 hours following Alteplase infusion.
•
Obtain a follow-up CT or MRI scan at 24 h after IV alteplase before starting anticoagulants
or antiplatelet agents.
•
For management of intracranial hemorrhage complication within 24 hours following
thrombolysis:
o
Stop alteplase, obtain an emergent non contrast head CT.
o
Obtain hematology and neurosurgery consultations
o
Provide supportive care and initiate
C: tranexamic acid (IV) 1g infused over 10 minutes. 
AND 
D: cryoprecipitate (includes factor VIII): 10 U infused over 10–30 min 
•
In case of angioedema following Alteplase infusion, stop alteplase and provide
airway support as required. Give
D: methylprednisolone (IV) 125mg
AND 
A: chlorpheniramine (IV) 10mg stat 
If there is further increase in angioedema, administer 
A: adrenaline (S/C) (0.1%) 0.3 mL or by nebulizer 0.5 mL stat 
Non-pharmacological Treatment 
Mechanical thrombectomy 
•
Consider for selected patients who present between 6 and 16 hours of LKW with an
anterior-circulation large-vessel occlusion (ICA or proximal MCA) and meet other
specified eligibility criteria based on expert assessment, clinical judgement, and availability
of required resources.

153!
•
Consider decompressive craniectomy in patients ≤60 years of age who deteriorate
neurologically within 48 hours from brain swelling associated with unilateral MCA
infarctions despite appropriate medical therapy.
•
Consider external ventricular drainage (EVD) in the treatment of obstructive
hydrocephalus following cerebellar infarction.
•
Emergency carotid end arterectomy (CEA) in the acute stage is not well established hence
not recommended in initial management of AIS.
8.3 Management of Epilepsy 
Epilepsy is a common neurological disorder characterised by recurring seizures.  About two-thirds of 
people with active epilepsy have their epilepsy controlled satisfactorily with anti-epileptic drugs 
(AEDs). Other treatment approaches may include surgery and neuromodulation. Optimal 
management is required to improve patient’s health outcomes and minimise detrimental impacts on 
social, educational, and occupational activities.  
Clinical presentation 
Recurrent seizures 
Investigations 
•
Serum electrolytes
•
Serum antiepileptic drug levels
•
Electroencephalogram (EEG)
•
Brain CT scan
•
Brain MRI with epilepsy protocol
Classification of epileptic syndromes 
Classify epileptic seizures and epilepsy syndromes in all patients using a multi-axial diagnostic 
scheme (refer to ILAE classification) as failure to classify the epilepsy syndrome correctly can lead 
to inappropriate treatment and persistence of seizures.  
Pharmacological management 
•
Utilize a single AED (monotherapy) and increase dose until seizures are controlled or side
effects cannot be tolerated.
•
If the initial treatment is unsuccessful, initiate alternative monotherapy with different drugs
before resorting to drug combinations.
•
Combination therapy (adjunctive or 'add-on' therapy) should only be considered when
attempts at monotherapy with AEDs have not resulted in seizure freedom.
•
If trials of combination therapy do not bring about worthwhile benefits, revert treatment to
the initial monotherapy regimen that has proved most acceptable to the patient and
consider referral for expert evaluation.
For management of status epilepticus—refer to emergency and critical care chapter 
I.
Focal seizures
First Line: 
A: carbamazepine (PO) 10-20mg/kg 12hourly for 4weeks 
OR  
S: lamotrigine (PO) 1-5mg/kg 12hourly for 4weeks 
Second line: 
S: levetiracetam (PO) 10mg/kg 12hourly for 4weeks 
Add-on treatment: gabapentin or sodium valproate as adjunctive treatment if first-line treatments are 
ineffective or not tolerated.  
II.
Generalised tonic–clonic (GTC) seizures
C: sodium valproate (PO) 10-15mg/kg 12hourly for 4weeks
OR 
S: lamotrigine (PO) 1-5mg/kg 12hourly for 4weeks 
Add on treatment: offer levetiracetam as adjunctive treatment if first-line treatments are ineffective or 
not tolerated.  
Surgical management of AIS 

154!
First Line: 
C: sodium valproate (PO) 10-15mg/kg 12hourly for 4weeks 
Second line: consider levetiracetam 
Note 
DO NOT offer carbamazepine, phenytoin or pregabalin for absence seizures. 
IV.
Myoclonic seizures
First Line: 
C: sodium valproate (PO) 10-15mg/kg 12hourly for 4weeks 
Second line: 
S: levetiracetam (PO) 10mg/kg 12hourly for 4weeks 
V.
Lenox Gastaut syndrome (LGS)
First Line: 
C: sodium valproate(PO) 10-15mg/kg 12hourly for 4weeks 
Second line: 
S: lamotrigine (PO) 1-5mg/kg 12hourly as adjunctive treatment 
Note 
DO NOT offer carbamazepine or pregabalin. 
VI.
Idiopathic generalised epilepsy (IGE)
First Line: 
C: sodium valproate (PO) 10-15mg/kg 12hourly for 4weeks 
Second line: 
S: lamotrigine (PO) 1-5mg/kg 12hourly for 4weeks 
VII.
Juvenile Myoclonic epilepsy (JME)
First line: 
C: sodium valproate (PO) 10-15mg/kg 12hourly for 4weeks 
Second line: 
S: lamotrigine (PO) 1-5mg/kg 12hourly for 4weeks 
OR  
S: levetiracetam (PO) 10mg/kg 12hourly for 4weeks 
VIII.
Childhood absence epilepsy
First Line: 
C: sodium valproate (PO) 10-15mg/kg 12hourly for 4weeks 
Second line:  
S: lamotrigine (PO) 1-5mg/kg 12hourly for 4weeks 
Add-on treatment: consider clonazepam, levetiracetam if first-line treatments are ineffective or not 
tolerated. 
Management of epilepsy in pregnancy 
The use of antiepileptic drugs (AEDs) is associated with increased baseline risk of fetal 
malformations during pregnancy. Prescribe Folic acid to all women of childbearing age and girls on 
AEDs preconception.  Attempt to decrease pharmacological treatment to monotherapy and utilize 
the lowest possible effective dose of drugs that have shown minimal risk of maternal and fetal neural 
tube defects 
S: lamotrigine (PO) 1-5mg/kg 12hourly for 4weeks 
OR  
S: levetiracetam (PO) 10mg/kg 12hourly for 4weeks 
AND 
A: folic acid (PO) 5mg 24hourly for 3-6months 
In women who have not had a seizure for at least 2years, attempt complete withdrawal of AEDs. 
III.
Absence seizures

155!
Non-pharmacological Treatment 
•
Consider ketogenic diet—based on specialist assessment and expert opinion
•
Refer all medically refractory seizures for expert neurosurgical evaluation for epilepsy
surgeries
•
Consider evaluation for Vagus Nerve Stimulation (VNS) as an adjunctive treatment in
reducing the frequency of seizures in adults who are refractory to AEDs but who are not
suitable for resective surgery
8.4. Parkinson’s Disease 
Parkinson’s disease (PD) is a common chronic, progressive, neurodegenerative disorder in geriatric 
population, characterized by the loss of dopaminergic neurons from the substantia nigra that 
subsequently results in the loss of control of voluntary movement over time. 
Clinical presentation 
Motor symptoms: Tremors, rigidity, akinesia or bradykinesia, postural instability 
Non motor symptoms: drooling, dementia, depression, orthostatic hypotension 
Diagnosis is clinical based on United Kingdom Parkinson’s Disease Society Brain Bank (UKPDSBB) 
criteria 
Pharmacological management of motor symptoms 
First line:  
D: levodopa+carbidopa (FDC) (PO) 100/25mg 8 hourly (escalate dose based on individual 
response) for 4weeks 
Give adjunctive treatment for motor symptoms: MAO-B or COMT inhibitors in persistent motor 
symptoms despite adequate tolerable doses of Levodopa+carbidopa FDC treatment. 
S: selegiline (PO) 2.5-5mg 24hourly (maximum dose 10mg/day) 
Pharmacological management of non-motor symptoms 
Drooling: 
S: glycopyrrolate (PO) 0.5-1mg 8hourly for 2weeks 
Orthostatic hypotension: consider Levodopa dose reduction and give 
S: fludrocortisone (PO) 0.1mg 24hourly for 2 weeks 
Depression: Individualize therapy, consider 
S: fluoexetine (PO) 20mg 24hourly (maximum 60mg/day) for 4weeks 
OR  
A: amitriptyline (PO) 50mg 24hourly for 4-12 weeks 
Impulse control disorders: Consider modification of dopaminergic drug dosages. 
Non-pharmacological management 
•
Provide physiotherapy, occupational, speech and language therapies
•
Refer for expert neurosurgical evaluation for Deep Brain Stimulation (DBS) in patients
with advanced Parkinson's disease whose symptoms are not adequately controlled by best
medical therapy.
8.5 Congenital Pediatric Nervous System Diseases 
8.5.1 Pediatric Hydrocephalus 
Pediatric hydrocephalus (HDC) is a common surgically correctable neurological problem in children 
with estimated incidence of 1 in every 500 children. HDC can result from various congenital and 
acquired causes including aqueductal stenosis, Chiari malformations, intraventricular hemorrhage, 
trauma, tumors, and infection. There are effective surgical interventions that can preserve and 
improve quality of life in patients with HDC.  
Clinical presentation 
•
Abnormal increase in head size

156!
•
Delayed/regressed developmental
milestones
•
Headache and impaired vision
•
Seizure
Investigations 
•
Cranial Ultrasound
•
Non contrast head CT scan
•
MRI brain scan
Pharmacological management 
Management of associated seizures: 
A: phenobarbital (PO) 5mg/kg 12hourly for 4weeks 
OR 
C: sodium valproate (PO) 10-15mg/kg 12hourly for 4weeks 
Non pharmacological management 
•
Both CSF shunts and endoscopic third ventriculostomy (ETV) are options in the treatment
of pediatric hydrocephalus. Refer for expert neurosurgical evaluation.
•
Consider Endoscopic third ventriculostomy with choroid plexus coagulation (ETV+CPC)
as first line option in cases with clear obstruction to CSF flow.
•
Consider insertion of ventriculoperitoneal shunt (VP shunt) where ETV+CPC is not
available, has failed or is contraindicated. Other alternative CSF shunts include
ventriculoatrial (VA) or ventriculopleural shunts.
•
Prescribe preoperative antibiotics to prevent shunt infection in patients undergoing shunt
surgery.
Pharmacological management 
D: ceftriaxone+sulbactam (FDC) (IV) 100mg/kg stat during anesthesia induction 
8.5.2 Management of Pediatric CSF Shunt Infections 
Clinical presentation 
•
CSF leak, purulence, skin erosion,
•
Fever, meningismus, erythema,
•
exposed or protruding hardware
Lab investigations 
•
FBP, CRP
•
CSF analysis, C/S
•
Blood C/S
Pharmacological management 
Initiate empirical antibiotic treatment 
C: amoxicillin +clavulanate (FDC) (IV) 12hourly for 2weeks 
OR 
D: ceftriaxone+sulbactam (FDC) (IV) 100mg/kg 12hourly for 2weeks 
AND 
B: metronidazole (IV) 7.5mg/kg/day 8hourly for 2weeks 
Alternative regimen based on C/S results 
S: piperacillin+tazobactam (FDC) (IV) 300mg/kg/day (of piperacillin component) divided in 
4doses per day 
OR 
S: meropenem (IV )10mg/kg 8 hourly, (may increase up to 40mg/kg) for 10-14days 
Shift to organism’s specific regimen after CSF/hardware culture results 
For confirmed Staph spp. infections add  
S: vancomycin (IV) 10mg/kg 6hourly for 2weeks or more. 
Non-pharmacological management 
•
Consider partial (externalization) or complete infected shunt hardware removal.

157!
•
Insert External ventricular drain (EVD) as interim measure for intracranial pressure
monitoring and therapeutic diversion of CSF in the setting where an infected internal shunt
device has been removed.
8.5.3 Congenital Spina Bifida 
Spina Bifida (SB) is one of the commonest complex congenital birth defects in developing countries. 
Children with SB are faced with multiple medical and psychosocial issues that require a 
comprehensive multidisciplinary care plan. 
Clinical presentation 
•
Swelling on the back
•
CSF leak
•
Lower limb weakness
•
Lower limb deformities
Investigations 
Prenatal diagnosis 
•
Ultrasound in second trimester of pregnancy
•
Amniotic fluid analysis
Postnatal diagnosis 
•
Cranial Ultrasound—evaluate for associated hydrocephalus
•
Neuraxial MRI-is indicated in complex cases to plan surgical management and evaluate for
associated defects—Hydrocephalus, chiari malformations, tethered cord
•
Preoperative screening echocardiogram (ECHO)
Pharmacological Treatment 
Initiate antibiotics in children with open infected spinal bifida lesions 
B: ceftriaxone (IV) 100mg/kg 12hourly for 2 weeks 
OR 
B: amoxicillin +clavulanate (FDC) (PO) 15mg/kg 8hourly for 2weeks 
OR 
C: amoxicillin +clavulanate (FDC) (IV)15mg/kg 8hourly for 2weeks 
AND 
A: metronidazole (PO) 7.5mg/kg/day 8hourly for 2weeks 
OR 
B: metronidazole (IV) 7.5mg/kg/day 8hourly for 2weeks 
Non-pharmacological Treatment 
Surgical management of SB 
•
Refer for expert neurosurgical evaluation for surgical closure of the spinal defect and
subsequent evaluation for the need to treat associated hydrocephalus with CSF shunts or
ETV+CPC.
Supportive and preventive and measures 
•
Provide routine screenings and testing for specific secondary conditions (HDC, skeletal
limb deformities, UTIs) to minimize medical complication rates and help control cost of
care.
o
Provide lower limb orthoses (splints, calipers)
o
Provide wheelchair for ambulation
•
Track and counsel women about recurrence risk and prescribe 5mg of folic acid beginning
at least one month (preferably 3 months) before another conception and continue through
the first 3 months of pregnancy.
8.6 Cranial Nerve Disorders 
8.6.1 Trigeminal Neuralgia 
Trigeminal neuralgia (TN) is a syndrome characterized by chronic paroxysmal brief episodes of 
unilateral electric shock-like pains, in one or more divisions of the trigeminal nerve. TN is often 
mistaken as a dental problem leading to delayed correct diagnosis and appropriate treatment. 
The diagnosis is based on the characteristic clinical picture. 

158!
•
CT scan to exclude structural brain pathologies
•
MRI to assess the trigeminal nerve root entry zone (REZ)
Pharmacological Treatment 
First line treatment:  
A: carbamazepine (PO) 200mg 12hourly for 4-12weeks 
Non-pharmacological management 
Refer to neurosurgeon for procedures that involve controlled trigeminal ganglion ablation to alleviate 
pain 
•
Radiofrequency ablation
•
Gasserian ganglion baloon compression rhizotomy
•
Glycerol rhizolysis
•
Stereotactic radiosurgery rhizotomy
Surgical management 
Refer all patient with poor response to conservative management for expert neurosurgical 
evaluation for microvascular decompression (MVD), a surgical procedure undertaken to identify, 
isolate and separate a vascular loop abutting the trigeminal nerve at the root entry zone (REZ). 
8.6.2 Bell’s Palsy 
Bell's palsy, also referred to as idiopathic facial nerve palsy is unilateral paralysis of all the muscles 
of facial expression of suspected viral etiology. Inflammation and edema of the facial nerve likely 
play a role in pathogenesis. Reactivation of herpes simplex virus (HSV) is also thought to play an 
etiologic role. Most patients recover within a few weeks or months.  
Clinical presentation 
•
Unilateral facial paralysis (sudden
onset)
•
Inability to close the eye
•
Drooping at the affected corner of
the mouth
•
Decreased tearing
•
Hyperacusis
Investigations 
•
HIV testing
•
RBG
•
otoscopic exam
Pharmacological management 
A: prednisolone (PO) 60mg 24hourly for 5 days, then taper down to 50mg 24hourly for 
next 5days.  
AND 
B: acyclovir (PO/IV)800mg 4-8hourly for 7-14days. 
Non-pharmacological management 
•
Provide facial muscle massage and exercises
•
Provide eye patch for ocular protection during sleep.
•
Refer for ophthalmological evaluation in severe cases
8.7 Spinal Cord and Peripheral Nerve Disorders 
8.7.1 Acute Transverse Myelitis (TM) 
Acute onset, usually postinfectious, rapidly progressive neurologic syndrome caused by focal 
inflammation of the spinal cord. Thoracic spinal cord level is the most commonly involved. 
Clinical presentation 
•
Rapid progressive bilateral lower
limb weakness
•
Backache and neuropathic pain
•
Numbness and paresthesis
•
Bladder and bowel incontinence
Clinical presentation
Unilateral jaw pain exacerbated by cutaneous stimuli, 
e.g., chewing, brushing
Investigations 

159!
Investigations 
•
FBP, serum electrolytes
•
CSF analysis
•
Emergency MRI or CT/myelogram to rule out a compressive lesion.
•
Brain MRI—may be required to exclude multiple sclerosis
Perform baseline severity score such as American Spinal Injury Association (ASIA) impairment 
score to assist in clinical management decisions and monitor improvement. 
Pharmacological management 
Give high-dose steroids 
D: methylprednisolone (IV) 500-1000mg/day for 3–5days 
Consider cyclophosphamide in refractory cases (under the direction of an oncologist) 
S: cyclophosphamide (IV) 800-1000mg/m
2 pulse dose. 
Long term management 
Manage generalized pain with 
A: diclofenac (IM) 75mg 12hourly for 3-5days 
OR 
B: tramadol (PO) 50mg 8hourly for 7-14days. 
Manage neuropathic pain with 
D: pregabalin (PO) 75mg 12hourly (maximum dose 300mg) for 2-4weeks 
Manage spasticity with 
S: baclofen (PO) 10mg 8hourly, (maximum dose 120mg/day) for 2weeks 
OR 
S: tizanidine (PO) 2mg 8hourly, (maximum dose 36mg/day) for 2weeks 
Non-pharmacological management 
•
Monitor respiratory function, support ventilation where required
•
Catheterize bladder and offer stool softeners to aid bowel emptying
•
Provide manual position changes 2hourly to avoid pressure sores
•
Provide rehabilitation--exercises to assist ambulation
•
Offer assisted ambulation devices—e.g., high back wheelchairs
8.7.2 Guillan Barre Syndrome 
Guillain–Barré syndrome (GBS) is potentially fatal, immune-mediated acute-onset ascending 
sensorimotor neuropathy usually triggered by infections. Timely recognition, diagnosis, and prompt 
referral to a centre equipped to provide ventilatory support is essential to improve mortality and 
minimize long term morbidity. 
Clinical presentation 
•
Rapid ascending bilateral lower
limb weakness
•
Little or no sensory deficits
•
Evolving respiratory distress
•
Cardiac arrhythmias
•
Facial or bulbar palsy
Investigations 
•
FBP, serum electrolytes
•
CSF analysis-albuminocytologic dissociation (↑ protein without pleocytosis)
•
Emergency MRI to exclude acute spina cord inflammation or compression
Pharmacological management 
Admit to ICU and provide ventilatory support to all patients with evolving respiratory distress or 
severe autonomic cardiovascular dysfunction  
S: human immunoglobulin G (IV) 0.4g/kg 24hourly for 5days (started within 2weeks of 
disease onset) 

160!
For severe cases, consider 
S: plasma exchange 200-250ml plasma/kg body weight for 5sessions (started within 
4weeks of disease onset) 
Monitor respiratory function-patient is deemed at risk of respiratory failure if the vital capacity is 
<20ml/kg, the maximum inspiratory pressure is <30cmH2O or the maximum expiratory pressure is 
<40cmH2O 
Non-pharmacological management 
•
Provide rehabilitation-exercises to assist ambulation
•
Assisted ambulation devices—e.g., high back wheelchairs
8.7.3 Peripheral Neuropathy 
Peripheral neuropathies encompass disorders of peripheral nerve cells and fibers which manifest 
secondary to a wide range of pathologies that can affect motor, sensory, and autonomic fibers. 
Peripheral neuropathies can be classified as mononeuropathies, multifocal neuropathies, and poly-
neuropathies. Further sub classifications categorize peripheral neuropathies as axonal, 
demyelinating, or mixed types, which is essential for treatment and management purposes.  
Clinical presentation 
•
Numbness and paresthesis,
•
Neuropathic pain
•
Extremities weakness,
•
Loss of coordination
•
Orthostatic hypotension
•
Cold, pale feet
Investigations 
•
FBP
•
Renal function tests
•
RBG and HbA1c (Diabetes is a
common cause of neuropathy)
•
Testing for vitamin and mineral
deficiencies such as copper,
thiamine, pyridoxine, folate, B12.
•
Infectious workup for HIV, and
•
Thyroid function testing
•
Anti-body testing for specific
autoimmune diseases known to
cause peripheral neuropathies such
SLE and rheumatoid arthritis
•
Nerve conduction studies (NCS)
and needle
electromyography (EMG) to
differentiate axonal from
demyelinating neuropathies
•
MRI or CT scans in suspected
nerve compression
•
Urine Test for Bence-Jones
proteins
•
Genetic testing (for inherited
neuropathies)
•
Nerve biopsy in selected cases
where expertise and resources are
available
Table 8.5 Guide to clinical diagnosis of peripheral neuropathies 
Type 
Clinical features 
Common causes 
Distal 
Symmetric 
Polyneuropathy 
-Length-dependent:
diffuse 
involvement
-affects
distal 
segments 
first 
-Symptoms occur below the knees
prior to affecting fingertips
Most common cause: diabetes, Chronic 
Idiopathic axonal polyneuropathy, Alcohol, 
chemotherapy induced. 
Mononeuropath
y 
-Symptoms restricted to distribution of
single nerve, myotome, or dermatome
-Asymmetric reflexes
Entrapment neuropathies e.g., carpal tunnel, 
peroneal nerve entrapment. Post traumatic 
neuropathies, diabetes 
Mononeuropath
y multiplex 
-Occurrence of several concurrent
mononeuropathies
Autoimmune vasculitic etiologies 
Hereditary 
neuropathies 
-Distal calf atrophy, hammertoes, pes
cavus
-Motor deficits ≥ sensory deficits
-Diffuse areflexia
Genetic diseases 
Pharmacological management 
•
Focus on the management of the underlying disease process if identified.

161!
•
Ensure glucose control in diabetic neuropathy, alcohol cessation in alcoholic neuropathy
and correction of vitamin or mineral deficiencies in nutrition related peripheral
neuropathies.
•
For drug related neuropathies, stop the offending medicine and give a suitable substitute.
e.g., substitute stavudine or didanosine with tenofovir or lamivudine.
•
Initial management of symmetric polyneuropathies and postherpertic neuralgia
D: pregabalin (PO) 150mg 12hourly for 4-12weeks 
OR 
A: amitriptyline (PO) 50-100mg 12hourly for 4-12weeks 
AND 
B: vitamin B1, B6, and B12 (FDC) (PO) 12hourly for 4-12weeks 
•
If the initial treatment is not effective, consider one of the combination therapies.
(1)
Gabapentanoid+Tricyclic Antidepressant
D: pregabalin (PO) 150mg 12hourly for 4-12weeks 
AND 
A: amitriptyline (PO) 25-50mg 12hourly for 4-12weeks 
AND 
B: vitamin B1, B6, and B12 (FDC) (PO) 12hourly for 4-12weeks 
(2) Gabapentanoid +Selective Serotonin Reuptake Inhibitors
D: pregabalin (PO) 150mg 12hourly for 4-12weeks 
AND 
S: fluoxetine (PO) 20mg 24hourly for 7days then titrate 12hourly for 4-12weeks 
AND 
B: vitamin B1, B6, and B12 (FDC) (PO) 12hourly for 4-12weeks 
In chronic demyelinating polyneuropathies add steroids 
A: prednisolone (PO) 20-60mg 24hourly for 6weeks (taper down based on response) 
Offer rescue therapy if required, to patients undergoing long term treatment. 
B: tramadol (PO) 50mg 8hourly for 7-14 days 
For localized symptoms, consider topical agents as adjunctive treatment. 
D: lidocaine 5% patches apply for 60minutes. 
For patients on isoniazid related neuropathies, start on 
B: pyridoxine (PO) 25–50 mg 8hourly for 3weeks, then 25mg 24hourly until completion of 
TB dose. 
Non-pharmacological management 
•
Transcutaneous electrical nerve stimulation (TENS) for pain relief.
•
Educate patients on increased risk of injury and infection due to loss of sensation
•
Recommend wearing socks with closed-toed shoes to decrease the risk of infection.
•
Offer support on cessation to patients with alcohol-induced neuropathy

162!
CHAPTER NINE 
RESPIRATORY DISEASE CONDITIONS 
9.1 Acute Respiratory Infections (ARI) 
It is an infection affecting upper or lower respiratory tract. Commonly caused by bacteria or viruses, 
other microbes including rickettsia or fungi may be present. 
9.1.1 Pneumonia 
Pneumonia is the inflammation of the lung tissue. Pneumonia can either be primary (to the causing 
organism) or secondary to pathological damage in the respiratory system.  
Clinical presentation 
•
Fever (typically>380C)
•
Dry or productive cough
•
Central cyanosis
•
Respiratory distress
•
Chest pain and tachypnoea
Table 9.1: Tool used for assessing Adult Patient with Pneumonia 
CURB 65 
Clinical Feature 
Points 
C 
Confusion 
1 
U 
Urea>7mmol/L 
1 
R 
RR>30 
1 
B 
SBP<90mmHg or DBP,60mmHg 
1 
65 
Age >65 
1 
CURB-65 Score 
Risk group 
30-day mortality
Management 
0-1
1 
1.5% 
Low 
risk, 
consider 
home 
treatment 
2 
2 
9.2% 
Probable admission vs close 
outpatient management 
3-5
3 
22% 
Admission, manage as severe 
DBP = diastolic blood pressure; SBP = systolic blood pressure. a Defined as a Mental Test Score of 
≤8, or new disorientation in person, place or time. Predicted 30-day mortality 
Note 
•
For patients with pneumonia treatment should be instituted when they have FEVER, COUGH
AND CXR with findings suggestive of pneumonia.
•
Consider alternative diagnosis when a patient is not responding.
•
Pulmonary embolism should be investigated carefully for patient with shortness of breath and
not responding to treatment of pneumonia
9.1.1.1 Pneumonia in Children 
(For more details, refer to Integrated Management of Childhood Illness (IMCI) guidelines) 
Table 9.2: Important clinical presentation of pneumonia in under-fives 
Age 
Signs 
Classification 
Infants less than 
2 months 
Severe chest in-drawing or 
60 breaths per minute or more 
Severe pneumonia (all young infants with 
pneumonia are classified as severe) 
No severe chest in-drawing 
Less than 60 breaths per-minute 
No pneumonia: 
Cough or cold 
Children from 2 
months 
to 
1 
year 
Chest in-drawing 
Severe pneumonia 
No chest in-drawing 
50 breaths per minute or more 
Pneumonia 
No chest in-drawing 
Less than 50 breaths per minute 
No pneumonia 
Cough or cold 
Children from 1 
year to 5 year 
Chest in-drawing 
Severe pneumonia 
No chest in-drawing 
40 breaths per minute or more 
Pneumonia 
No chest in-drawing 
Less than 40 breaths per minute 
No pneumonia 
Cough or cold 

163!
Investigations 
•
Measure oxygen saturation
•
FBC (look for increased WBC, neutrophilia) CRP/ESR (increased), ABG (look for pH,
bicarbonate), Blood culture, Sputum culture and sensitivity, Serology for HIV test (if
Unknown)
•
CHEST X-ray-PA/LATERAL (look for consideration, tap effusion>5cm), Bronchoscopy
(Consider if immunosuppression, critically ill, fail to respond, suspected TB or PCP or
inadequate
•
CT Scan: if patient is not improving, suspicion of fungal, ILD
Non-pharmacological Treatment: 
•
Oxygen therapy if available
•
Supportive care
o
Remove clothes
o
If wheezing giving rapid-acting bronchodilator: Nebulized Salbutamol
o
Ensure that the child receives daily maintenance fluid appropriate for the child’s age
but avoid over-hydration refer to IMCI/ STG & Essential Medicines List for Children
Pharmacological Treatment 
Non-severe pneumonia 
A: amoxicillin (PO) 25mg/kg 8hourly for 5days 
AND 
A: paracetamol (PO) 15mg/kg 8hourly for 5days(if fever present) 
OR  
A: paracetamol (supp) 10–15mg/kg (if there is fever) 
OR 
A: ibuprofen (PO) 15mg/kg 12hourly for 5days 
Give the first dose at the clinic and teach the mother how to give the other doses at home. 
Encourage breasting and feeding. 
Severe Pneumonia 
A: benzyl penicillin (IV/IM) 50000 units/kg every 6hours for at least 3days 
THEN 
A: amoxicillin (PO) 40 mg/kg 8hourly for 7days. 
Alternatively  
A: ampicillin (IV/IM) 50 mg/kg every 6hourly for 5days 
AND 
A: gentamicin (IV/IM) 7.5 mg/kg 24hourly for 5days 
THEN  
A: amoxicillin (PO) 40 mg/kg 8hourly for 7days. 
Note 
•
For children above 5 years, atypical pneumonia should be considered e.g. mycoplasma
•
Consider alternative diagnosis after three visit /not responding, refer patient to a
pediatrician
9.1.1.2 Pneumonia in Adults 
Community Acquired Pneumonia 
CAP refers to a pneumonia that is acquired outside hospital commonly caused by Streptococcus 
pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, atypical bacteria (ie, Chlamydia 
pneumoniae, Mycoplasma pneumoniae, Legionella species) and viral respiratory pathogens (i.e 
rhinovirus and influenza) 
Clinical presentation 
•
Fever,
•
Cough dry or productive
with/without purulent sputum,
•
Dyspnea,
•
Pleuritic chest pain
•
Tachypnea
•
Crepitation/Rales heard over the
involved lobe or segment
•
Increased tactile fremitus, bronchial
breath sounds may be present if
consolidation has occurred.

164!
•
Decreased 
tactile 
fremitus 
and
dullness on chest percussion 
Investigations 
•
Measure oxygen saturation use pulse oximetry or Monitor
•
FBC (look for increased WBC, neutrophilia),
•
CRP/ESR (increased in bacterial infection)
•
ABG (look for pH, bicarbonate),
•
Serology for HIV test (if Unknown)
•
Sputum culture and sensitivity (are indicated for inpatients and those with severe disease
(ICU admission),
•
Blood culture (are not recommended for ambulatory patients
•
CHEST X-ray-PA/LATERAL (look for one or more focal pulmonary infiltrates,
consolidation, tap effusion>5cm),
•
Bronchoscopy (Consider if immunosuppression, critically ill, fail to respond, suspected
TB or PCP or inadequate
•
CT-CHEST Scan Or HRCT: if patient is not improving, suspicion of fungal, ILD etc.
Note 
Do not use CT chest to diagnose pneumonia 
Non-pharmacological Treatment 
•
Stop smoking if previously smoking
•
Vaccination when indicated, in specialized centre for patient >65yrs and below 5years
Pharmacological Treatment 
First line treatment 
Table 9.3: First Line Treatment of Typical Community Acquired Pneumonia 
Condition 
Treatment 
Duration 
Mild CAP (treated on out-patient 
basis) 
(common organism S pneumonia 
and 
these 
patients 
have 
no 
comorbidities) 
A: erythromycin (PO) 500mg 8hourly 
            OR 
B: ampicillin + cloxacillin (FDC)(PO) 500–1000mg 
8hourly 
5-7days
Mild to Moderate CAP (failed to 
respond to Initial treatment) 
A: doxycycline (PO) 100 mg 12hourly (culture guided) 
          OR 
B: azithromycin (PO) 500mg stat and then 250mg 
24hourly  
           OR 
C: clarithromycin (PO) 500mg 12hourly 
5-7days
MILD 
CAP 
in 
patients 
with 
comorbidities (i.e. chronic heart, 
lung, 
liver, 
or 
renal 
disease; 
diabetes 
mellitus; 
alcoholism; 
malignancy; 
asplenia; 
immunosuppression; prior antibiotics 
within 90 days 
B: 
amoxicillin 
+ 
clavulanic 
acid 
(FDC) 
(PO) 
500mg/125mg 8-12hourly or   875mg/125mg 12hourly 
          OR 
D: cefuroxime (PO) 500mg 12hourly 
          AND  
A: doxycycline (PO) 100mg 24hourly 
          OR 
C: clarithromycin (PO) 500mg 12hourly 
5-7 days
Severe 
pneumonia/Aspiration 
pneumonia (in-patient) 
D: ceftriaxone + sulbactam (FDC) (IV) 1.5g 12hourly 
If suspicion of anaerobes or Aspiration pneumonia 
Add: 
B: metronidazole (IV) 500mg 8hourly 
Do culture and imaging if nonresponse consider 
second line 
7–
10days 
Second line treatment 
If no response to first line further investigation is required. If patient is in respiratory distress, or no 
response after 3 days of first line treatment, or patient’s condition deteriorates, then investigate, start 
empiric treatment while wait for culture and sensitivity 
S: piperacillin + tazobactam (FDC) (IV) 4.5g 6hourly for 7days 

165!
Table 9.4: Treatment of Typical and Atypical Community Acquired Pneumonias Organism 
Specific 
Condition 
Treatment 
Duratio
n 
Atypical pneumonias 
(Bordetella pertussis, Mycoplasma pneumonia, 
Chlamydophila pneumonia) 
A: erythromycin (PO) 500mg 6hourly 
OR     
C: clarithromycin (PO) 500mg 12hourly 
7-
10days 
Pseudomonas pneumonia 
(Risk factors structural lung disease, COPD, 
and bronchiectasis) 
A:ciprofloxacin (PO) 500mg 12hourly 
If 
culture 
sputum-positive 
or 
HRCT 
suggestive 
S: piperacillin + tazobactam (FDC) (IV) 4.5g e 
6-8hourly
          OR 
S: cefepime (IV) 2g 8hourly 
           OR  
D: ceftazidime (IV) 2g 8hourly 
           OR  
S: meropenem (IV) 1g 8hourly 
7-
10days 
H. influenza
A: amoxicillin (PO) 500mg 8hourly 
            OR 
D: cefuroxime (PO) 250-500mg 8hourly 
(culture & sensitivity should be done in order to 
choose alternativeantibiotics) 
7-
10days 
Pneumocystis jirovecii Pneumonia (PJP) 
(Refer to Tanzania HIV Guideline for more 
details) 
A: co-trimoxazole (PO) 1920mg 8hourly 
          AND     
A: folic acid (PO) 5mg 24hourly (if cytopenic) 
In sulphur allergy:  
S: clindamycin (PO) 450–600mg 6hourly 
21days 
Staphylococcus aureus Pneumonia 
B: ampicillin + cloxacillin (FDC) (IV) 1g 6hourly 
         OR  
S: clindamycin (IV/PO) 600mg 6-8 hourly 
14days 
Klebsiella 
Pneumonia 
(due to high mortality observe the duration of 
antibiotic given not < 10days) 
B: chloramphenicol (IV) 500mg 6hourly 
       AND/OR 
A: gentamicin (IV) 4-5mg/kg 24hourly in 2 
divided doses 
10-
14days 
For critical ill patient and those with risk factors 
for 
MRSA 
include 
hemoptysis, 
recent, 
influenza, 
neutropenia, 
hemodialysis, 
and 
congestive heart failure) 
S: vancomycin (IV) 15mg/kg 12hourly 
5-7days
Note 
•
In severe Pneumocystis jirovecii pneumonia (PCP), add 30 – 40mg prednisolone for 14days
consider tapering down after recovery
•
Patients with pneumonia should be afebrile for 48-72hours and have improved clinically
before antibiotic therapy is stopped. The duration of therapy may need to be increased if the
initial empirical therapy has no activity against the specific pathogen or if the pneumonia is
complicated by extra pulmonary infection.
Alternative in Staphylococcal and Klebsiella Pneumonia: 
D: ceftazidime (IV/IM) 2g 8hourly for 7–14days 
9.1.1.3 Hospital Acquired Pneumonia/Nosocomial Pneumonia 
This is defined as pneumonia that occurs two days (48hrs) or more after hospitalization but that was 
not incubating at the time of hospital admission. 
Clinical Presentation 
•
Fever
•
Increase in respiratory rate
•
Shortness of breath

166!
Pharmacological Treatment 
Empirical treatment until bacteriology available 
C: ciprofloxacin (IV) 400mg 12hourly for 7days 
OR  
D: ceftriaxone + sulbactam (FDC) (IV) 1.5g 12hourly for 7days 
Note 
In specialized unit management of CAP/HAP can be changed with supportive culture and sensitivity 
done, this may necessitate use of other broader spectrum antibiotics 48-72hours until the results are 
obtained 
9.2 Obstructive Lung Diseases 
It’s a chronic airway disease which result in airway flow limitation can be either reversible or 
irreversible 
 Clinical presentation 
•
Wheezing
•
Difficulty in breathing or shortness
of breath
•
Chest tightness
•
Cough (dry or productive cough)
•
Finger clubbing
9.2.1 Asthma 
It is a chronic reversible obstructive inflammatory airways disease in which many cells and cellular 
element play a role by constriction of bronchial smooth muscle causing bronchospasm, oedema of 
bronchial mucous membrane and blockage of the smaller bronchi with plug of mucous. 
Clinical presentation 
•
wheeze,
•
shortness of breath,
•
chest tightness
•
cough This presentation particularly
at night or in the early morning
•
Tachypnea,
•
Tachycardia,
•
Diffuse musical wheezes,
•
Prolonged phase of exhalation,
•
Chest hyperinflation.
•
Use of Accessory muscle.
Investigations 
•
FBP (Look for eosinophilia)
•
Serum IgEa
•
ESR
•
ABG
•
CXR if highly suspicion of
pneumonia
•
Sputum for cytology 
a (look for
eosinophilia),
•
Lung function Test (e.g.: spirometry
with reversibility test, PEFR 
measurement with a peak flow 
meter), Exhaled NO should be 
done to asses evidence of variable 
expiratory airflow limitation 
aVery important test to establish diagnosis of asthma 
Non-pharmacological Treatment 
•
Avoid polluted environment (both
indoors and outdoors)
•
Avoid 
non-selective 
β-blockers,
which can trigger asthmatic attack
•
Avoid heavy exercise
•
Stop smoking
•
Avoid both overweight and
underweight
Note 
•
The management of asthma in children is like that in adult. Infants under 18 months, may not
respond well in bronchodilator
•
Uncertain in diagnosis should prompt early referral, because asthma-COPD overlap has worse
outcome.
•
Patient intolerant of NSAIDs or who exhibit any of the high-risk clinical features for intolerance to
these drugs (severe asthma, nasal polyps or chronic rhino sinusitis) should use NSAIDs only
under close medical supervision.

167!
Table 9.5: Assessment and Treatment of Asthma attack in Children ≥2years & Adults 
Attack 
Clinical 
Presentation 
Treatment (Children & Adults) 
MILD-
MODER
ATE 
ATTAC
K 
Able to talk in 
sentences or 
phrases 
Not agitated 
Pulse rate 100-
120bpm 
Sat 02(on air)-90-
95% 
PEF>50% 
predicted 
I.
Salbutamol inhalation (can be given by pMDI or spacer or
Nebulization)
2
Give: 4-10 puffs by pMDI/ spacer/ every 20minutes for 1
st hour
          A: salbutamol(nebulization) Adult: Salbutamol respules 5mg 6hrly 
(2-3cycles and reassess); Pediatric: 2.5mg 6hrly (2-3cycles and 
reassess). 
If symptoms completely subside observe for 1–4hours, give Salbutamol 
for 24–48hours (2-4 puffs every 4–6hours) for 3 days. If attack is only 
partially resolved give 2–4 puffs of Salbutamol every 3–4 hours if attack 
is mild; 6 puffs every 1–2 hours if the attack is moderate, until symptoms 
subside. When attack completely resolved proceed as above.  
II. Prednisolone
A: prednisolone (PO): Adult 40mg am 7/7; Pediatrics 1-2mg/kg max
40mg
Do tapering if exceed seven days.
III: Controlled oxygen (if available): target saturation 93-95% (children: 
94-98%)
Note: If symptoms worsen or do not improve, treat as SEVERE 
ATTACK 
SEVER
E 
ATTAC
K 
• Talks in words
i.e. cannot
complete a
sentence in 1
breath or too
breathless to
talk/ feed
• Sits hunched
forwards
• Agitated
• Respiratory rate
>30/min.
• Accessory
muscles being
used
• Pulse rate > 120
bpm
• O2 saturation (on
air): < 90%
• PEF ≤ 50%
predicted or best
I. Admit the patient, place in semi-sitting position
II. Oxygen continuously 5L/min (maintain O2 saturation for adult 93-95%
(children 94-98%)
III. Inhalation
           A: salbutamol (nebulization) 4-10puffs every 20-30min in children 
<5years, up to 20 puffs in children >5years and adults  
             Add 
         S: ipratropium bromide (inhalation)0.25-0.5mg 6-8hourly 
AND 
         A: hydrocortisone (IV) 5mg/kg in children, 100mg in adults 6hourly 
then switch to oral       
A: prednisolone (PO)1-2mg/kg 24hourly to complete 7days of treatment 
If attack is completely resolved continue with salbutamol inhalation 2–
4puffs every 4hours for 24-48hours and oral prednisolone 1-2mg/kg 
24hourly to complete 3–5days of treatment. 
If not improving or condition worsens, treat as LIFE-THREATENING 
ATTACK 
Use!a!spacer!to!increase!effectiveness.!If!conventional!spacer!not!available,!take!a!500ml!plastic!bottle,!insert!the!mouthpiece!of!the!
inhaler!into!a!hole!on!the!bottom!of!the!bottle!(the!seal!should!be!as!tight!as!possible).!The!child!breathes!from!the!mouth!of!the!
bottle!in!the!same!way!as!he!would!with!a!spacer!

168!
!
LIFE-
THREA
TENIN
G 
ATTAC
K 
Altered 
level 
of 
consciousness 
(drowsiness, 
confusion, coma) 
Exhaustion 
Silent chest 
Paradoxical 
thoracoabdominal 
movement 
Cyanosis 
Collapse 
Bradycardia 
in 
children 
or 
arrhythmia/ 
hypotension 
in 
adults 
O2 saturation<92% 
I. Admit the patient, place in semi-sitting position 
 
II. Oxygen continuously 5L/min (maintain O2 saturation between 94-98%) 
 
III. A: salbutamol (nebulization) 2.5mg for children <5years and in 
children >5years & adults 2.5-5mg every 20–30min then switches to 
salbutamol aerosol when clinical improvement is achieved. 
Add: 
     S: ipratropium bromide (inhalation) 0.25-0.5mg 6-8hourly. 
AND 
     A: hydrocortisone (IV) 5mg/kg in children, 100mg (IV) in adults every 
6hours then switch to  
     A: prednisolone (PO) 1-2mg/kg 24hourly to complete 7days of 
treatment 
In adult administer a single dose of  
     A: magnesium sulphate (Infusion of 1-2g in 0.9% Sodium Chloride 
over 20 minutes) 
 
In children use continuous nebulization rather than intermittent 
nebulisation. 
Patient with life threatening asthma should be managed in HDU/ICU. 
 
Note 
Patients who get night attacks should be advised to take their medication on going to bed 
 
9.2.2 Chronic Asthma in Adults 
The assessment of the frequency of daytime and nighttime symptoms and limitation of physical 
activity determines whether asthma is intermittent or persistent. There are 4 categories (see table 
9.5) 
Therapy is stepwise (Step 1–4) based on the category of asthma and consists of: 
• 
Preventing the inflammation leading to bronchospasm (controllers) 
• 
Relieving bronchospasm (relievers) 
 
Controller medicines in asthma 
• 
Inhaled corticosteroids (ICS) e.g. Beclomethasone, Budesonide, Fluticasone 
• 
Leukotriene modifiers: e.g. Montelukast can added from step 2 patient (should be 
administer when low ICS or ICS-LABA has failed to achieve desired outcome. 
• 
long acting muscarinic antagonist (LAMA) e.g tiotropium 
• 
Long acting β2 agonists (LABA) e.g. formoterol, salmeterol 
 
Reliever medicines in asthma 
• 
Short acting β2 agonists (SABA) e.g. Salbutamol 
• 
short acting muscarinic antagonist (SAMA) e.g. ipratropium bromide (should be used in 
acute asthma attack) 
 
Note 
• 
In specialized centre when low dose ICS alone fails to achieve good control for difficult to 
treat and severe asthma, the addition of LABA + ICS should be instituted.  
• 
The most common side effects of inhaled steroids are a sore throat, hoarseness of 
voice, and infections/fungal infections in the throat and mouth.  
Things you can do to avoid or reduce these side effects include: 
• 
Rinsing your mouth and gargling after taking an inhaled steroid 
• 
Using a spacer/holding chamber to reduce the amount of steroid landing in your mouth 
and throat (For children and elderly patient) 
 
 
 
 
 
 

169!
!
Table 9.6: Long-Term Treatment of Asthma According to Severity 
Categories 
Treatment 
STEP 1 
Intermittent asthma 
• 
Intermittent 
symptoms 
< 
once/week 
• 
Nighttime symptoms < 
twice/ month 
• 
Normal physical activity 
A: As needed low dose ICS 
OR  
S: ICS AND LABA  
B: budesonide (inhalation) 100-200µg 12hourly  
                OR  
B: budesonide (inhalation) 100-200µg 12hourly 
                 AND 
C: salmeterol 100- 200mcg 2puff   12hourly  
                OR 
Low dose ICS taken whenever SABA is taken 
STEP 2 
Mild persistent asthma 
• 
Symptoms > once/ week 
but < once/ day 
• 
Nighttime symptoms > 
twice/ month 
• 
Symptoms may affect 
activity 
Daily low dose ICS plus as needed SABA 
                 OR  
As needed low dose ICS+ salmeterol 
                  OR 
Low dose ICS taken whenever SABA is taken 
ICS  
Add: - 
LTRA;  
D: montelukast (PO) 4mg nocte (6month to 6years) or > 6years to 
15years (PO) 5mg nocte or >15years (PO) 10mg nocte 
(for period not less than 3/12) 
STEP 3 
Moderate persistent asthma 
• 
Daily symptoms 
• 
Symptoms affect activity 
• 
Nighttime 
symptoms 
>once/ week 
• 
Daily use of Salbutamol 
Refer these patients to physician/ respiratory physician/ pulmonologist 
low dose ICS+LABA 
           OR 
Medium dose ICS 
           OR  
Low dose ICS +LTRA 
 
LTRA; 
D: montelukast (PO) 4mg nocte (6month to 6years) or (PO) 5mg nocte > 
6-15years or (PO) 10mg nocte >15years 
(for period not less than 3/12) 
STEP 4 
Severe persistent asthma 
• 
Daily symptoms 
• 
Frequent 
nighttime 
symptoms 
• 
Physical activity limited 
by symptoms 
Refer this patient to Respiratory physician/Pulmonologist 
Medium dose ICS+LABA 
            OR 
High dose ICS 
Add  
S**: tiotropium Mist (inhalation) 6mcg 2puff 24hourly  
            OR 
Add on 
LTRA 
D: montelukast (PO) 4mg nocte (6month to 6years) or (PO) 5mg nocte 
>6years to 15years or (PO) 10mg nocte>15years 
(for period not less than 3/12) 
Add: 
S: tiotropium mist inhaler 6mcg 2puff 24hourly  
         OR  
S: ipratropium Bromide (Inhalation) 40 mcg 2puff 12hourly 
For patient with rhinitis and asthma add sublingual immunotherapy (SLIT) 
provided FEV1>70% predicted 
STEP 5 
Severe asthma 
• 
Symptoms 
throughout 
the day 
• 
Night symptoms seven 
times per weeks 
• 
Physical activity extreme 
limited by symptoms 
Refer 
to 
expert 
opinion 
(respiratory 
physician/pulmonologist 
for 
phenotypic investigation+/- add on treatment 
 
High dose ICS-LABA 
Low dose OCS but consider side effects 
S: tiotropium (inhalation) as step 4 
Biologics as indicated  
S: omalizumab (SC) 75-600mg every 2-4weeks;  
 
 
 
 

170!
!
Table 9.7 Low, Medium and High Dose Inhaled Corticosteroids Adults and Adolescents (≥12 
Years) 
Inhaled corticosteroid 
Total daily dose (mcg) 
Low 
Medium 
High 
Budesonide (DPI) 
200-400 
>400-800 
>800 
Fluticasone 
propionate 
(DPI 
OR 
HFA) 
100-250 
>250-500 
>500 
Mometasone furoate 
110-220 
>220-440 
>440 
Triamcinolone acetonide 
400-1000 
>1000-2000 
>2000 
 
DPI: Dry powder inhaler, HFA: hydrofluoroalkane, CFC: Chlorofluorocarbon propellant (included for 
comparison),  
 
Table 9.8 Low, Medium and High Dose Inhaled Corticosteroids Children 6–11 Years 
Inhaled corticosteroid 
Total daily dose (mcg) 
Low 
 Medium 
High 
Budesonide (DPI) 
100-200 
>200-400 
>400 
Budesonide (nebules) 
250-500 
>500-1000 
>1000 
Fluticasone propionate (DPI) 
100-200 
>200-400 
>400 
Fluticasone propionate (HFA) 
100-200 
>200-500 
>500 
Momentansone furoate 
110 
>220-≤440 
≥440 
Triamcinolone acetonide 
400-800 
>800-1200 
>1200 
 
9.3 Bronchitis 
9.3.1 Acute Bronchitis 
Acute bronchitis was defined as an acute self-limited lower respiratory tract infection manifested 
predominantly by cough with or without sputum production, lasting no more than 3 weeks with no 
clinical or any recent radiographic evidence to suggest an alternative explanation.In acute bronchitis 
some isolated virus (influenza A and B viruses, parainfluenza virus, respiratory syncytial virus, 
coronavirus, adenovirus, and rhinovirus) and bacteria (Bordetella pertussis, Chlamydophila 
(Chlamydia) pneumoniae, and Mycoplasma pneumonia) 
 Clinical presentation 
• 
Patients with acute bronchitis present with a cough lasting more than five days (typically 
one to three weeks), which may be associated with sputum production.  
• 
Cough in the absence of fever, tachycardia, and tachypnoea suggests bronchitis, 
• 
Acute bronchitis should be distinguished from chronic bronchitis (see below), it is not a 
form of COPD 
 
Note 
When the acute bronchitis persists or worsens, we suggest that the patient is advised to seek 
reassessment and do below   targeted investigation(s). 
 
Investigation in COPD (bronchitis and Emphysema) 
• 
FBP 
• 
ESR /CRP OR Procalcitonin 
• 
Serum alpha-1 antitrypsin levels 
• 
Chest radiography (if the patient is elderly or physical findings   suggest pneumonia) 
• 
Sputum cytology (if the cough is persistent) 
• 
Blood culture and microbial sensitivity (if bacterial super-infection is suspected) 
• 
Bronchoscopy (to exclude foreign body aspiration, tuberculosis, tumours, and other 
chronic diseases and patient with worsening symptoms) 
• 
Lung function Test (Spirometry and Peak expiratory flow rate) 
 
Note 
An exception, however, is cough in elderly patients; pneumonia in elderly patients is often 
characterized by an absence of distinctive signs and symptoms. 
 
 
 

171!
Symptomatic Treatment 
•
With non-steroidal anti-inflammatory drugs: paracetamol, acetyl salicylic acid
•
Cough management refer section 9.1.1
•
There is NO benefit from antibiotic use in acute bronchitis.
•
Discourage smoking and other irritating factors.
9.3.2 Chronic Bronchitis 
It defined by a chronic productive cough for three months in each of two successive years in a 
patient in whom other causes of chronic cough have been excluded. Patients may get secondary 
bacterial infection with development of fever and production of thick smelly sputum. 
Table 9.9: Risk Factor for Chronic Bronchitis 
Risk factor 
1.
Cigarette smoking
2.
Indoor air pollution
>Exposure from burning wood
>Exposure to biofuel mass exposure
>Heating in poorly vented dwellings
3.
Occupational exposure
Coal miners >Tunnel Workers >Hard-rock miners >Concrete manufacture 
>Livestock farming (i.e. to pesticides)
4.
Exposure to agricultural
5.
Use of domestic solid fuel
Investigation 
As in acute bronchitis 
Non-pharmacological Treatment 
•
Stop smoking (Reducing loss of lung function) and/or remove from hazardous environment
•
Prompt treatment of infective exacerbations
•
Controlled oxygen therapy
•
Physiotherapy
•
Pulmonary Rehabilitation (consist of education, lifestyle modification, regular physical
activities, physiotherapy and avoid indoor and outdoor pollutants)
•
Nutrition support
•
BIPAP in specialized center
•
Influenza vaccine in specialized center
Pharmacological Treatment 
•
Pharmacologic therapy for Chronic Bronchitis is directed towards 3 major goals
•
Relieving symptoms during stable disease
Mucoactive Agents-Reduced overproduction and hypersecretion, increases elimination 
For pharmaceutical management; refer to emergency and critical care chapter 
Hypertonic saline-stimulate productive cough and decreases sputum viscoelasticity, increases 
mucociliary clearance. 
7% hypertonic saline or 0.9% saline bd for PRN 
Bronchodilators (Beta-agonists)-Promotes mucus clearance by increasing airway luminal 
diameter and ciliary beat frequency, reduces hyperinflation, improve PEF 
A: SABA: Salbutamol (Inhalation) 100µg 2puff 6hourly 
OR 
LABA: 
salmeterol+fluticasone 
or 
in 
combination 
with 
steroids 
(salmeterol+fluticasone or budenoside fluticasone) 
OR 
Muscarinic antagonists -Decrease contractility of smooth muscle in the lung, inhibits 
bronchoconstriction and mucus secretion 
SAMA: S: ipratropium bromide (aerosol) 20–80mcg, 6–8 hourly 
LAMA: 
S: 
tiotropium 
(mist 
inhaler) 
6mcg 
2puff 
24hourly 
Preventing 
exacerbations  

172!
Mucoactive Agents-Refer cough section 
Macrolides- (As indicated) antibacterial effects; Immune-modulatory and anti-inflammatory effects 
(Azithromycin/clarithromycin) 
Note 
•
In specialized center they may use N-acetyl cysteine and carbocysteine as mucolytic agents
•
Macrolide should be given in consultation with respiratory physician/Pulmonologist to avoid
antimicrobial resistance (Azithromycin and clarithromycin may be used).
Avoid use of systemic glucocorticoids due to numerous adverse side effects 
9.4 Emphysema 
It is a destructive process in the gas-exchanging air spaces of the lung that results in perforations, 
obliteration of airspace walls, and coalescence of small distinct airspaces into much larger ones, 
leading to enlargement of the gas exchanging units of the lungs These changes cause loss of elastic 
recoil of the lungs and abnormal gas exchange. 
 Clinical presentation 
•
Shortness of breath
•
Cough, sometimes caused by the
production of mucus
•
Wheezing
•
Slow and prolonged expiration
•
Chest wall hyperinflation,
•
Limited diaphragmatic motion on
auscultation,
•
Distant breath sounds, and heart
sounds
•
Coarse early inspiratory crackles.
•
Use of accessory muscles
•
Pursed-lip breathing
•
Signs of cor pulmonale. (Raised
JVP, 
peripheral 
oedema,
hepatomegaly etc)
•
Cyanosis
•
Asterixis
Investigations 
•
Haematocrit(men>52%
and 
>47men) 
Or 
FBP 
(look 
at
haematocrit)
•
ABG(look for bicarbonate-metabolic
alkalosis)
•
CXR
•
Sputum 
culture 
and 
Microbial
sensitivity
•
Pulmonary function tests
•
Six minutes’ walk test
•
CT SCAN OF THE CHEST/HRCT
(for evaluation for Lung Volume
Reduction Surgery)
Non-pharmacological Treatment: 
•
Stop smoking
•
Give oxygen after evaluation
Pharmacological Treatment 
Inhaled bronchodilators relax and open the airways. They may be short-acting (albuterol, 
ipratropium) or long-acting (salmeterol, tiotropium,). These medicines may be available as inhalers 
("puffers") or as a solution. A nebulizer machine aerosolizes the bronchodilator solution, which is 
then breathed through a tube.  For more detail refer Treatment in section 9.2 above 
Table 9.10: COPD Staging and recommended Therapies 
GOLD 
FEV1Stage 
Exacerbation 
Per Year 
Mild symptoms 
Mod/Severe Symptoms 
I: ≥80% 
≤2 
GROUP A  
Bronchodilator 
(SABA-
PRN) 
GROUP B 
LAMA OR LABA 
II: 50-79% 
III: 30-49% 
≥2 
GROUP C 
LAMA+ LABA 
GROUP D 
LAMA or LAMA + LABA or ICS+ 
LABA 
IV: 30% 

173!
9.5 COPD Exacerbation 
Chronic Obstructive Pulmonary Disease (COPD) exacerbation is a worsening or “flares up” of your 
COPD symptoms, commonly caused by infection in the lungs but in some cases the cause is 
unknown. 
Clinical presentation 
•
Worsening of cough,
•
Increase in phlegm production,
•
Change in phlegm quality, and
increase in dyspnea
Table 9.11: COPD Exacerbation Management 
AGENT 
DOSE 
SAMA  
S: ipratropium bromide (aeresol) 
MDI 4-8 puffs every 1-2 hours 
Nebulizer 0.5mg every 1-2hours 
SABA 
A: salbutamol (inhalation) 
MDI 4-8 puffs every 1-2hours 
Nebulizer 2.5-5mg every 1-2hours 
Corticosteroids 
A: prednisone (PO) 
If severe 
A: hydrocortisone (IV) 
D: methylprednisolone (IV) 
40mg AM for 5days 
1-2mg/kg 6hourly
125mg 6hourly for 72hours
(Then switch oral)
Antibiotic (If infection Presents) (Penicillin/Macrolide/Fluoroquinolone) 
A: amoxicillin (PO) 
500mg 8hourly for 7days 
OR 
A: ciprofloxacin (PO) 
500mg 12hourly for 7days 
OR 
A: doxycycline (PO) 
100mg every 12hrs 7days 
OR 
C: clarithromycin (PO) 
500mg 12hourly for 7days 
If possible, do culture and sensitivity 
Noninvasive positive pressure ventilation 
Oxygenation if indicated 
9.6 Other Respiratory Infections 
9.6.1 Acute Laryngo-Tracheobronchitis 
Laryngo-tracheobronchitis (croup) is acute inflammation of the larynx, trachea and bronchi which 
occurs in young children (usually between 6 months to 3 years of age). It arises as a result of 
narrowing of the airway in the region of the larynx. The most common cause is viral infection 
(particularly parainfluenza viruses) but may also be due to bacterial infection. The obstruction is due 
to inflammation and oedema. 
Clinical presentation 
•
The symptoms include paroxysmal “barking” cough, inspiratory stridor, fever, wheezing,
hoarseness of voice and tachypnoea
•
Such symptoms usually occur at night
•
Respiratory failure and pneumonia are potentially fatal complications.
Non-pharmacological Treatment 
•
Prevent asphyxiation
•
Treat inflammatory oedema
•
Humidification of inhaled air
•
Hospitalization may be necessary

174!
Note 
•
No stridor at rest, give no antibiotics
•
Stridor at rest or chest in-drawing or fast breathing REFER IMMEDIATELY to hospital
Mild Croup 
•
Only stridor when upset, no
moderate/severe ARI
•
Likely of viral origin
•
Home care – steam inhalation
•
Antibiotics NOT required
Severe Croup 
•
Likely bacterial origin
•
Stridor in a calm child at rest
•
Chest in drawing
•
Antibiotics are NOT effective and
should not be given
Pharmacological Treatment 
Admit to hospital, give Oxygen therapy to all patients with chest in-drawing (using nasal prongs only, 
DO NOT use nasopharyngeal or nasal catheter) until the lower chest wall in-drawing is no longer 
present 
D: dexamethasone (PO) 0.6mg/kg 24hourly in 1–2 divided doses 
AND 
A: adrenaline (inhalation) 400mcg/kg 2hourly if effective; repeat after 30min if necessary. 
9.6.2 Laryngeal Diphtheria 
Is an infection caused by Corynebacterium diphtheria; it is directly transmitted from person to person 
by droplets. Children between 1–5 years of age are most susceptible although non-immune adults 
are also at risk.  Diphtheria is characterized by grayish-white membrane, composed of dead cells, 
fibrin, leucocytes and red blood cells as a result of inflammation due to multiplying bacteria. 
Non-pharmacological Treatment 
•
Isolate the child
•
Gently examine the child’s throat – can cause airway obstruction if not carefully done.
•
NGT for feeding if unable to swallow
•
Avoid oxygen unless there is incipient airway obstruction
•
May need tracheostomy if there is incipient airway obstruction
Pharmacological Treatment: 
Drug of choice  
A: phenoxymethylpenicillin (PO) 250mg 6hourly for 14days 
OR 
A: erythromycin (PO) 125–250mg 6hourly for 14days 
OR 
B: azithromycin (PO) 500mg 24hourly for 3days 
OR 
A: benzyl penicillin (IV) 25,000–50,000units/kg to a max. of 1.2MU 12hourly until the 
patient can take oral medicine 
AND 
A: diphtheria antitoxin (IM or slow IV) dose depends upon the site and severity of infection: 
•
First give a test dose of 0.1ml of 1 in 10 dilution of antitoxin in 0.9% Sodium Chloride
intradermal to detect hypersensitivity
•
It should be given immediately because delay can lead to increased mortality
•
The dose should be administered intravenously over 60minutes in order to inactivate toxin
rapidly
•
20,000–40,000 units for pharyngeal/laryngeal disease of <48 hours’ duration,
•
40,000–60,000 units for nasopharyngeal disease
•
80,000–120,000 units for >3days of illness or diffuse neck swelling "bull-neck"
Note 
Tracheostomy may be required for airway obstruction 
9.6.3 Whooping Cough 
It is a highly infectious childhood disease caused by Bordetella pertussis. It is most severe in young 
infants who have not yet been immunized.  

175!
Clinical presentation 
•
Paroxysmal cough associated with a whoop
•
Fever
•
Nasal discharge
Non-pharmacological Treatment 
•
Place the child head down and prone, or on the side, to prevent any inhaling of vomitus
and to aid expectoration of secretions.
•
Care for the airway but avoid, as far as possible, any procedure that could trigger
coughing, such as application of suction, throat examination
•
Do not give cough suppressants, sedatives, mucolytic agents or anti-histamines.
•
If the child has fever (>38.50C) give paracetamol.
•
Encourage breastfeeding or oral fluids
•
Whooping cough is preventable by immunization with pertussis vaccine contained in DPT-
HepB-Hib vaccine at week 6, 10 and 14.
Oxygen 
•
Give oxygen to children who have spells of apnoea or cyanosis, or severe paroxysms of
coughing.
•
Use nasal prongs, not a nasopharyngeal catheter or nasal catheter which can provoke
coughing.
Pharmacological Treatment 
A: erythromycin (PO) 12.5 mg/kg 6hourly for 10days.  
This does not shorten the illness but reduces the period of infectiousness 
•
If there is fever
In Children older than age 2 months:
A: trimethoprim + sulfamethoxazole (FDC) (PO) 8mg+40mg/kg 12hourly
9.6.4 Bronchiectasis 
Bronchiectasis is a progressive respiratory disease characterized by permanent dilatation of the 
bronchi and associated with a clinical syndrome of cough, sputum production and recurrent 
respiratory infections.  
Investigations  
FBP, ESR, Serum IgE and IgE to aspergillus, serum immunoglobulin (IgG, IgA, IgM) CXR, Sputum 
culture and sensitivity, CT-Chest (CT contrast if suspicion of PE/HRCT, bronchoscopy. 
Non-pharmacological Treatment 
•
Physiotherapy and postural drainage
•
Avoid smoking
•
Airways clearance technique
•
Pulmonary rehabilitation
•
Respiratory care during childhood measles helps prevent the development of
bronchiectasis in children
Pharmacological Treatment 
Consider antibiotics in patients with bronchiectasis with >3 exacerbations per year.  (empirical 
treatment while wait for culture and sensitivity) 
Adults: 
A: ciprofloxacin (PO) 500mg 12hourly for 10days 
AND 
A: metronidazole (PO) 400mg 8hourly for 10days 
Children: 
A: amoxicillin (PO) 40mg/kg in 2 divided doses for 7days 
AND  
A: metronidazole (PO) 7.5 mg/kg 8hourly for 5–7days 
If pseudomonas aeruginosa suspicion (should be culture guided) 
D: ceftazidime (IV) 2g 8hourly for 14days 
OR 

176!
S: piperacillin+tazobactam (FDC) (IV) 4.5mg 8hourly for 14days 
AND 
D: itraconazole (PO) 100mg-200mg 12hourly 
Prevention of infection 
A: ciprofloxacin 500mg (PO) 24hourly for 7–14days 
OR 
A: erythromycin (PO) 250–500mg 24hourly for 7–14days 
9.6.5 Lung Abscess 
Lung abscess is a cavity within the lung parenchyma filled with necrotic tissues, which occurs as a 
result of tissue-destroying infection.  
Clinical presentation  
It is characterized by high fever, breathlessness, cough productive of large amounts of foul-smelling 
sputum and haemoptysis. 
Investigation 
FBP, ESR, CXR, Sputum Analysis (Gram Stain, Cytology, Gene Xpert, Culture), Blood Culture, CT 
Chest, Bronchoscopy, Sputum for ova and parasite (if Parasitic cause is suspected). 
Non-pharmacological Treatment 
Postural drainage 
Pharmacological Treatment 
B: ampicillin + cloxacillin (FDC)(IV) 500–1000mg for 7days then (PO) 8hourly for 3–
6weeks (children 50mg/kg/dose)  
AND 
B: metronidazole (IV) 500mg 8hourly for 7days then (PO) 400mg 8hourly for 4–6weeks 
(children 7.5mg/kg) 
Note 
The duration of antibiotics therapy depends on the clinical and radiographic response of the 
patient, but completely healing, with radiographic normalization can be seen after two months. 
Refer patient to specialized unit ifLarge cavity size (ie, >6cm in diameter), persistent fever.  
D: ceftriaxone + sulbactam (FDC) (IV) 1.5-3g 6hourly 4-6weeks 
OR  
S: clindamycin (IV) 600mg 8hourly for 7days and then (PO) 300mg 8hourly 4-6weeks 
OR    
S: piperacillin + tazobactam (FDC) (IV) 4.5g 6hourly 4-6weeks 
OR 
S: meropenem (IV) 1g 8hourly for 4-6 weeks 
9.6.6 Aspergilosis 
Clinical presentation  
•
Cough
•
Fever
•
Chest pain.
•
Difficulty breathing
•
Hemoptysis ranging from mild to
severe.
•
Wheezing 
may 
be 
noted 
on
auscultation.
•
Mucous plugs upon coughing.
•
Tachypneic 
and 
have 
rapidly
progressive worsening
•
Hypoxemia.
Investigations 
•
Chest X-ray and CT, pulmonary aspergillosis classically manifests as a halo sign and later
an air crescent sign
•
Sputum Culture.
•
Bronchoscopy (BAL)

177!
Non-pharmacological Treatment 
•
Surgical treatment
•
Bronchial artery embolization (for life threatening hemoptysis)
Pharmacological Treatment 
D: itraconazole (PO) 100-200mg 24hourly 6-12weeks 
9.6.7 Pneumocystis Pneumonia (PCP) 
Clinical presentation  
•
Cough dry/productive
•
Exertional dyspnoea
•
Fever
•
Tachypnoea
•
Chest pain
•
There may be signs of AIDS such
as thrush, oral hairy leucoplakia or
Kaposi's sarcoma
•
Scattered crackles and wheeze
may be present, or rarely signs of
focal consolidation
•
Pulse oximetry may show low
SaO2 at rest
•
Extra-pulmonary 
disease 
may
manifest as hepatosplenomegaly,
lymphadenopathy or ocular disease
Investigations 
•
Elevated lactate dehydrogenase
•
ABG may show hypoxia.
•
The alveolar-arterial oxygen tension gradient may be increased.
•
Serum (1-->3) Beta-D-glucan levels (high in PCP) is currently being investigated as a
diagnostic test.
•
Chest X-ray
•
CT-CHEST (ground glass infiltrates but has low sensitivity and specificity.)
•
Gallium scanning is highly sensitive but with low and variable specificity.
•
PFT (Reduction in Vital capacity (VC) and the total lung capacity (TLC).
Management 
Refer table 9.4 
9.6.8 Silicosis  
Clinical presentation 
•
Asymptomatic
•
Chronic cough
•
Dyspnea on exertion
•
Fine/coarse crackles
•
Rhonchi and/or wheezes
•
Tachypnea
Investigations 
•
Cor pulmonale
•
Chest X-ray
•
CT Scan (if indicated)
•
PFT
•
Lung function tests
•
Lung biopsy (if indicated)
Non-pharmacological 
•
Avoid further exposure to respirable
silica
•
Smoking cessation
•
Bronchodilators (if indicated)
•
Vaccination against influenza and
pneumococcus
•
Oxygen therapy (if indicated)
•
Lung transplantation
9.6.9 Coal worker’s pneumoconiosis 
Clinical presentation 
•
Asymptomatic
•
Chronic cough
•
Dyspnea on exertion
•
Fine/coarse crackles

178!
•
Rhonchi and/or wheezes
•
Tachypnea
•
Cor pulmonale
Investigations 
•
Chest X-ray
•
CT Scan (if indicated)
•
Lung function tests
•
Lung biopsy (if indicated)
Non-pharmacological 
•
Avoid further exposure to coal dust
•
Smoking cessation
•
Bronchodilators (if indicated)
•
Vaccination against influenza and
pneumococcus
•
Oxygen therapy (if indicated)
•
Lung transplantation
9.6.10 Sarcoidosis 
Clinical presentation 
•
The 
common 
symptoms/signs
depend on which organ or system
is affected.
•
Rales/crepitations
•
Jaundice is rare
•
Macules, papules, and plaques
may arise as single isolated lesions
•
Skin lesions frequently leave Scars,
pits, and pale, depigmented areas
•
Nerve palsies, headache, ataxia,
cognitive dysfunction, weakness,
and seizures.
•
Anterior uveitis
•
Tachyarrhythmias
and 
bradyarrhythmias
•
Polyarthritis,
chronic 
arthritis
Investigations 
•
FBP
•
ESR
•
LFT
•
RFT
•
RF,
•
CPR, S/Electrolytes, LP,
•
Auto immune profile
•
Biopsy
•
Images:
•
CXR,
•
CT SCAN,
•
PETSCAN, FUNDOSCOPY.
Pharmacological Treatment 
A: prednisolone (PO) 1mg/kg/day 
Referral: Refer to Specialized center (specialist- physician /dermatologist /rheumatologist 
/pulmonologist) 
9.6.11 Obstructive Sleep Apnea Syndrome (OSA) 
Obstructive sleep apnea (OSA) is characterized by episodes of complete or partial collapse of the 
airway with an associated decrease in oxygen saturation or arousal from sleep. OSA is a sleep 
disorder that involves cessation or significant decrease in airflow in the presence of breathing effort. 
Clinical Presentation 
•
Daytime sleepiness
•
Restless sleep
•
Loud snoring
•
Morning headaches;
•
Insomnia;
•
Decreased sex drive;
•
Unexplained weight gain;
•
Increased urination and/or nocturia.
•
Heartburn or gastro esophageal
reflux disease; and heavy night
sweats
•
Trouble 
concentrating; 
mood 
changes such as irritability, anxiety 
and 
depression; 
Forgetfulness; 
Increased heart rate and/or blood 
pressure;  

179!
Investigations 
•
Nocturnal polysomnography
•
Thyrotropin test
•
Cysteine levels
•
Multiple Sleep Latency and
Maintenance of Wakefulness Tests
Non-pharmacological Treatment 
•
Lifestyle modification (avoid alcohol, sleeping pills, and other sedatives)
•
Continuous positive airway pressure (CPAP)
•
The oral appliance (e.g. a mandibular advancement splint)
Pharmacological Treatment 
C: acetazolamide (PO) 500mg-1g 24hourly for 3-5days 
Surgical intervention 
(Maxillomandibular advancement, Tonsillectomy) Uvulopalatopharyngoplasty) 
9.6.12 Cor Pulmonale 
Cor pulmonale is defined as an alteration in the structure (hypertrophy or dilation) and function of the 
right ventricle (RV) of the heart caused by a primary disorder of the respiratory system resulting in 
pulmonary hypertension. 
Clinical Presentation 
•
Fatigue
•
Tachypnea
•
Exertional dyspnea
•
Cough
•
Anginal chest pain
•
Syncope with exertion
•
lower limb edema
•
Raised JVP
•
Wheezes and crackles
•
Systolic 
murmur 
of 
tricuspid
regurgitation.
•
Shortness of breath
•
Wheezing
•
Chronic wet cough
•
Swelling of the abdomen with fluid
•
Swelling of the ankles and feet
•
Enlargement of the liver
•
Bluish discoloration of face
Investigations 
•
Electrocardiography (ECG)
•
Echocardiography
•
ABG
•
BNP
•
CXR
•
Chest 
computed 
tomography
(CT)+/-CTPA
•
Ventilation/perfusion 
(V/Q) 
scanning 
•
Cardiac 
magnetic 
resonance 
(CMR) (as indicated) 
•
Other test to rule out etiology
•
FBP/Hematocrit level
•
Serum alpha1-antitrypsin
•
Antinuclear antibody (ANA)
•
Anti-SCL-70 antibodies
•
Coagulations studies (serum levels
of proteins S and C, antithrombin
III, factor V Leyden, anticardiolipin
antibodies, homocysteine)
Non-pharmacological Management 
•
Oxygen therapy when PaO2 is less
55mmHg
•
Pulmonary embolectomy
•
Uvulopalatopharyngoplasty (UPPP)
•
Surgical embolectomy
•
Lung transplant
•
Pulmonary rehabilitation

180!
Pharmacological Treatment 
Treat Heart Failure (right sided heart failure) 
B: nifedipine ER (PO) 30mg 12hourly 
Pulmonary Hypertension management 
S: sildenafil (PO) 5mg -20mg 8hourly 
OR 
warfarin or rivaroxaban for indicated patient (For dosage refer to Pulmonary embolism management) 
9.6.13 Pleural Effusion 
Pleural effusion, is excessive collection of fluid in the pleural space, is rarely a primary disease 
process but is usually secondary to other diseases. 
Clinical presentation 
•
Progressive dyspnea
•
Cough
•
Pleuritic chest pain
When pleural fluid >300ml you will get these symptoms 
•
Dullness to percussion
•
Decreased tactile fremitus
•
Asymmetrical chest expansion
•
Pleural friction rub
•
Displacement of the trachea and mediastinum toward the side of the effusion
Investigations 
•
CXR
•
Full blood picture
•
Erythrocyte Sedimentation Rate (ESR)
•
Serum ADA
•
Point care bed side USS
•
Pleural fluid analysis: - (The pleural fluid analysis above will be requested as per indication
of suspected diagnosis.)
o
pleural fluid cytology
o
pleural fluid culture
o
pleural fluid Gene x pert, ADA, LDH, glucose, pH
o
pleural fluid cell count.
o
pleural fluid amylase
o
pleural fluid triglycerides and cholesterol
o
pleural fluid bilirubin
•
Tumour markers as indicated (e.g.
CA-15, CEA, CA-125etc).
•
Rheumatoid Factor (if indicated)
•
Autoimmune profile or single
marker (ANA, ACE etc)
•
Renal function (creatinine and
BUN)
•
Liver function and liver enzymes
(Albumin, bilirubin total, direct, PT,
PTT, INR ALT, AST, GGT, ALP)
•
ECHO
•
ECG
•
CT-Scan Chest with contrast
•
Thoracoscopy
•
Pleural Biopsy (when suggestive of
malignancy)
•
Bronchoscopy

181!
Table 9.12 Staging Pleural Infections and Recommending Drainage 
Effusion Stage 
Pleural Space Features 
Bacteriology 
Pleural Fluid 
Chemistry 
Thoracentesis/ 
Drainage 
I 
(uncomplicated 
parapneumonic) 
Minimal, 
free-flowing 
effusion (< 10 mm on 
lateral decubitus) 
Culture 
and 
Gram 
stain 
results unknown 
pH unknown 
No/No 
II (uncomplicated 
parapneumonic) 
Small-to-moderate 
free-
flowing effusion (> 10 mm 
and less than one-half 
hemithorax) 
Negative culture 
and Gram stain 
pH ≥ 7.20 or 
glucose ≥ 60 
mg/dL 
Yes/No 
III 
(complicated 
parapneumonic) 
Large, 
free-flowing 
effusion 
(one-half 
hemithorax 
or 
greater); 
loculated effusion; effusion 
with 
thickened 
parietal 
pleura 
Positive 
culture 
or Gram stain 
pH < 7.20 or 
glucose < 60 
mg/dL 
Yes/Yes 
IV (empyema) 
Pus 
Tests 
not 
indicated 
Yes/Yes 
Non-pharmacological Treatment 
•
Serial Thoracentesis-This approach may require an average of eight thoracenteses in 2 -
4weeks, this is for non-complicated pleural effusion.
•
Chest Tube Drainage-Chest tubes vary in size but can be classified as large-bore (24F to
34F) or smallbore (8F to 24F) viscous pleural pus, the surgical tradition recommends the
use of large-bore chest tubes (28F to 32F)
•
Fibrinolytic Therapy-use of streptokinase, urokinase, and rtPA, indicated for patients with
empyema and complicated parapneumonic pleural effusions.
•
Thoracoscopy-medical thoracoscopy and video-assisted thoracoscopic surgery
(VATS), indicated for patient with fibrinopurulent pleural infections and loculated effusion.
•
Thoracotomy, Decortication, and Open Drainage-Thoracotomy remains the main
salvage procedure after unsuccessful thoracoscopy, as defined by the failure of lung
expansion to the chest wall
Indication for thoracostomy/decortication 
•
Indicated for Patients with organized empyemas who cannot tolerate thoracotomy or have
trapped lungs can undergo rib resection with open drainage
•
Chronic empyemas with bronchopleural fistulas or chronic empyemas that are not
amenable to surgery
•
Critical ill and toxic patients with associated mediastinitis or bronchopleural fistulas who
require mediastinal drainage or fistula closure.
For Malignant Effusions 
Chest tube drainage, radiation, chemotherapy, surgical pleurectomy, pleuroperitoneal shunt, 
pleurodesis or decortication. 
Note 
•
Emergent thoracentesis and/or chest tube placement is necessary in patients with pleural
effusion with significant respiratory or cardiac decompensation
•
Do consultation with a pulmonologist, interventional radiologist, or thoracic surgeon,
depending on the location of the effusion and the clinical situation for patients not
responding to treatment.

182!
9.6.14 Respiratory Failure 
Respiratory failure is a clinical condition that happens when the respiratory system fails to maintain 
its main function, which is gas exchange, in which PaO2 lower than 60 mmHg and/or PaCO2 higher 
than 50 mmHg. Respiratory failure is classified according to blood gases abnormalities into type 1 
and type 2. 
Hypoxemic respiratory failure (type I): has a PaO2 < 60 mmHg with normal or subnormal PaCO2. 
In this type, the gas exchange is impaired at the level of alveoli-capillary membrane. Examples of 
type I respiratory failures are carcinogenic or non-cardiogenic pulmonary edema and severe 
pneumonia. 
Hypercapnic respiratory failure (type II): has a PaCO2 > 50 mmHg. Hypoxemia is common, and it 
is due to respiratory pump failure 
Investigations 
•
ABG
•
FBP
•
Creatine kinase
•
ECHO
•
ECG
•
Troponin-I
•
TSH
•
CXR
•
Electrolytes
•
Creatinine and BUN
•
AST/ALT/ALP/GGT, albumin and
bilirubin total, direct
•
PFT-if patient able to perform
Non-pharmacological Treatment 
Noninvasive Ventilatory Support: Patients with mild-to-moderate acute respiratory failure. 
Mechanical Ventilation 
Refer to management of cardiogenic pulmonary edema and acute exacerbations of chronic 
obstructive pulmonary disease (COPD) in obstructive lung disease  

183!
!
CHAPTER TEN 
GASTROINTESTINAL DISEASE CONDITIONS 
10.1 Infections of Gastrointestinal Tract 
10.1.1 Amoebiasis 
Amoebiasis is an infection caused by the protozoa organism Entamoeba histolytica, which can 
cause colitis and other extra-intestinal manifestations. The infection is primarily acquired through 
ingestion of contaminated food and water and occasionally can be acquired through oral-anal sexual 
practices. 
 
Clinical presentation 
• 
Bloody diarrhea 
• 
Crampy abdominal pain 
• 
Fever 
• 
Weight loss 
• 
Peritonitis in severe forms 
• 
Evidence of motile trophozoites or 
cysts on saline wet mount from a 
stool specimen 
Pharmacological Treatment 
A: metronidazole (PO) 400–800mg 8hourly for 5days 
OR 
B: tinidazole (PO) 2g 24 hourly for 3days   
 
10.1.2 Amoebic Liver Abscess 
It is the most frequent extra-intestinal manifestation of Entamoeba histolytica infection which results 
from the invasion of the portal venous system from the colon leading to inflammation and 
subsequently abscess formation particularly involving the right lobe of the liver. 
 
Clinical presentation 
• 
High grade fever, 39°C 
• 
Right upper quadrant pain, 
• 
Tender and enlarged liver 
• 
Positive imaging evidence of liver 
abscess   
• 
Serological evidence of E. 
histolytica antibodies or antigens. 
 
 
Pharmacological Treatment 
B: metronidazole (IV) 800mg 8hourly for 10days.  
OR  
B: tinidazole (PO) Adults: 2g once daily for 3days  
 
Note 
• 
Metronidazole and Tinidazole should not be given in the first trimester of pregnancy due to 
potential teratogenic effects.  
• 
Should not be taken with alcohol due to disulfiram like effects 
 
Surgery: 
Abscess cavity (size >5 cm in diameter) not regressing despite 7days treatment should be aspirated. 
 
10.1.3. Giardiasis 
It is the infestation of the upper small intestine caused by the flagellate protozoan Giardia lamblia (or 
G. intestinalis), cytopathic effects of which leads to malabsorption and diarrhea. It is more common 
in immune compromised individuals and is acquired through ingestion of contaminated water 
 
Clinical presentation 
• 
Crampy abdominal pain 
• 
Chronic diarrhoea  
• 
Steatorrhea  
• 
Weight loss  
 
 

184!
Investigations 
•
Evidence of Giardiaintestinalis trophozoites or cysts on serial 3 samples of stool
examination
•
Serological evidence of G. Intestinalis trophozoites antigen or antibody
•
Evidence of G. Intestinalis in duodenal aspirates or biopsy specimen.
Pharmacological Treatment 
A: metronidazole (PO) 400–800mg 8hourly for 5days 
OR 
B: tinidazole (PO) 2g once daily for 3days  
10.1.4 Ascariasis 
It is a small intestinal infestation caused by Ascaris lumbricoides which leads to malnutrition, iron 
deficiency anaemia, impaired growth and cognition in susceptible hosts. It is most common 
infestation in children, and it is acquired through ingestion of contaminated food and water. 
Clinical presentation 
•
Chronic Diarrhea
•
Steatorrhea
•
Malnutrition
•
Chronic Cough (Loffler’s syndrome)
•
Intestinal obstruction
•
Obstructive jaundice
Investigations 
•
Stool examination: evidence of ova or worms on wet mount
Pharmacological Treatment 
A: mebendazole (PO) 500mg stat or 100mg 12hourly for 3days.    
OR 
A: albendazole (PO) 400mg stat 
10.1.5 Ancylostomiasis 
It is a hookworm disease caused by infestation of the small intestine with Ancylostoma duodenale or 
Necator americanus leading to anaemia and malnutrition. 
Clinical presentation 
•
Abdominal pains
•
Chronic diarrhea
•
Melena stool
•
Weight loss
•
Chronic cough (Loffler’s syndrome) PLUS
•
Evidence of ova or worms on wet mount stool examination
•
Anaemia
Pharmacological Treatment 
A: mebendazole (PO) 500mg stat or 100mg 12hourly for 3days. 
OR 
A: albendazole (PO) 400mg stat 
Note 
If persistent, give second course after 4 weeks. Iron replacement and nutritional supplementation 
(protein and vitamins) should be part of the management strategy.  Albendazole is 
contraindicated in the first trimester of pregnancy 

185!
10.1.6 Strongyloidiasis 
Small intestinal infestation caused by Strongyloides stercoralis usually asymptomatic in immune 
competent adult but can lead to life-threatening infestation and disseminated strongyloidiasis in an 
immune-compromised host associated with high mortality rates 
Clinical presentation  
•
Pruritic papulo–vesicular rash at
the site of penetration or urticarial
rash involving the perennial region
extending to the buttocks, thighs
and abdomen
•
Chronic cough
•
Colicky abdominal pains
•
Chronic diarrhea and passage of
mucus
•
Weight loss
•
Hyper-infection syndrome
Investigations 
•
Evidence of rhabditiform larva in wet mount stool examination with Serological evidence
(ELISA) for anti-strongyloides antibody
Pharmacological Treatment 
A: albendazole (PO) 400mg 12hourly for 3days (Repeat after 4 weeks if still positive stool 
findings) 
OR 
A: ivermectin (PO) 200 µg /kg 24hourly for 2days 
Note 
Give treatment for 10 days in case of disseminated/super infestation 
10.1.7 Taeniasis 
Is a tapeworm disease acquired from eating raw or not-well cooked food? Can be due to Taenia 
saginata (beef tapeworm), Taenia solium (pork tapeworm), Diphyllobothrium latum (fish tapeworm) 
and Hymenolepsis nana (faecal oral contamination from human and dogs) leading to chronic 
malnutrition (Taeniasis) or multi-organ dissemination and dysfunction (Cysticercosis) 
Clinical presentation 
•
Taeniasis
•
Colicky abdominal pain
•
Body Weakness
•
Loss of or increased appetite
•
Constipation or diarrhea
•
Pruritus ani
•
Hyperexcitability
Investigations 
•
Evidence of characteristic ova, proglottids or scolex in the wet mount stool examination
Cysticercosis - The cysticerci are most often located in subcutaneous and intermuscular tissues, 
followed by the eye and then the brain. The CNS is involved in 60-90% of patients i.e. 
Neurocystercosis which may manifest as  
Convulsions and/or seizures: 
•
Intracranial hypertension: headache, nausea, vomiting, vertigo, and papilledema.
•
Personality and mental status changes (Neuropsychiatric changes)
•
Behavioral changes and learning disabilities more marked in children and
immunocompromised adults. PLUS
•
Head CT scan OR Brain MRI
Note 
Refer the patient to high centers for further investigation and expertise. 

186!
Pharmacological Treatment 
Taeniasis 
A: praziquantel (PO) 5–10mg/kg stat 
AND  
A: magnesium sulphate (PO) 5–10 g in a glass of water after 2hours 
Cysticercosis (NCC) 
A: praziquantel (PO) 50mg/kg 24hourly for 21days 
OR 
A: albendazole (PO) 15mg/kg 24hourly for 30days. 
AND 
B: dexamethasone (IV) 4mg 12hourly can be given up to 7days. 
AND 
A: carbamazepine (PO) initially 200 mg 12-24hourly, increased slowly to 0.8–1.2 g 
24hourly in divided doses 
Note 
Hydrocephalus should be treated with surgical shutting. Ocular manifestation cysticercosis, should 
be referred to eye specialist 
10.1.8 Echinococcosis 
It is a canine tape worm Echinococcus Granulosus which is transmitted by dogs, sheep and horses. 
Human infestation is through contamination of food or water causing visceral cysts (Hydatid Cyst 
Disease) particularly in the liver and lungs and is usually asymptomatic in susceptible host.  
Clinical presentation 
•
Upper abdominal discomfort and pain, poor appetite,
•
Upper abdominal mass swelling with enlarged liver.
•
Cough with features of acute hypersensitivity reaction. (for ruptured cysts)
•
Portal hypertension, biliary obstruction or Budd-Chiari syndrome (for complicated cases)
Pharmacological Treatment 
A: albendazole (PO) 400mg 12hourly for 3months  
OR   
A: mebendazole (PO) 500mg 12hourly for 3months  
Referral: For symptomatic/ complicated cases refer to higher centres with management and 
expertise. 
10.1.9 Schistosomiasis 
Parasitic disease caused by blood flukes (trematodes) of the genus Schistosoma. Common species 
found in Tanzania are S. haematobium responsible for urogenital schistosomisis and S. mansoni 
responsible for intestinal schistosomiasis as a result of immune mediated reaction which leads to 
progressive inflammation and fibrosis of the urinary bladder or portal venous system respectively. 
Clinical presentation 
Schistosoma mansoni 
•
Swimmer’s itch or katayama fevers
in acute infection phase.
•
Colicky abdominal pains
•
Diarrhoea and dysentery
•
Anemia
•
Hepatomegaly
•
Portal hypertension with bleeding
esophageal varices
•
Decompensated liver disease

187!
Schistosoma hematobium 
•
Dysuria and terminal hematuria
•
Hematospermia
•
Obstructive uropathy
(hydronephrosis, hydroureters)
•
Glomerulonephritis and amyloidosis
•
Bladder carcinoma
•
Chronic kidney failure
Investigations 
•
Laboratory evidence characteristic eggs in urine, (S. Hematobium) or in stool (S. manson,
S. japonicum) examined by kato katz thick smear procedure or PCR assays of both urine
and stool samples.
Pharmacological Treatment 
A: praziquantel (PO) 40mg/kg stat or in 2 divided doses 
10.1.10 Typhoid and Paratyphoid 
It is an acute systemic disease resulting from infection by Salmonella typhi and S. paratyphi, serovar 
group A and B respectively. Infection is acquired through ingestion of contaminated food and water. 
Clinical presentation 
•
Fever, severe headache, abdominal and muscle pains (myalgia)
•
Delirium, obtundation, intestinal hemorrhage, bowel perforation,
•
Sequela neuropsychiatric complications
Investigations 
•
Laboratory evidence of positive cultures from bone marrow aspirates; blood or stool done
within 1 week of acute infection OR
•
Salmonella stool antigen test
•
Indirect fluorescent Vi antibody, ELISA for immunoglobulin M (IgM) and IgG antibodies to
S. Typhi polysaccharide.
Pharmacological Treatment 
Uncomplicated typhoid fever 
A: ciprofloxacin (PO) 500mg 12 hourly for 10-14days 
OR 
B: azithromycin (PO) Adult 500mg 24hourly for 7days 
OR  
S: cefixime 400mg (PO) 24hourly for 7-14days 
For complicated typhoid fever 
C: ciprofloxacin (IV) 200-400 mg 12hourly daily 7days 
OR 
B: ceftriaxone (IV) 1-2gm 24hourly 4-7days 
10.1.11 Shigellosis 
Shigella organisms are a group of gram-negative, facultative intracellular bacteria pathogens. They 
are grouped into 4 species: Shigella dysenteriae, Shigella flexneri, Shigella boydii, and Shigella 
sonnei, also known as groups A, B, C, and D respectively. Shigellosis is spread by means of fecal-
oral, by ingestion by ingestion of contaminated food or water and leads to bacillary dysentery. 
Note 
Definitive treatment of typhoid (enteric fever) is based on susceptibility. For patients with severe or 
complicated disease (e.g. systemic toxicity, depressed consciousness, prolonged fever, organ 
system dysfunction or other features that prompt hospitalization), initial therapy with a parenteral 
agent is appropriate. 

188!
Clinical presentation 
•
Acute abdominal cramping, high-grade fever, emesis and large-volume watery diarrhea
•
Tenesmus, urgency, fecal incontinence, mucoid bloody diarrhea
•
Severe headache, lethargy, meningismus, delirium, and convulsions
•
Hemolytic uremic syndrome (HUS), microangiopathic hemolytic anemia,
thrombocytopenia, and renal failure
•
Profound dehydration and hypoglycemia
Investigations 
•
Laboratory evidence of microscopic isolation of the bacteria from stool or rectal swabs
specimens
•
Stool culture for suspected cases in early course of infection
•
An enzyme immunoassay (ELISA) for shiga toxin detection in stool for S. dysenteriae type
I.
Pharmacological Treatment 
A: ciprofloxacin (PO) 500mg 12hourly for 5days 
OR  
A: erythromycin (PO) 500mg 6hourly for 5days. 
10.1.12 Cholera 
For diagnostic criteria, investigations, prevention and treatment refer to under notifiable diseases. 
10.2. Disorders of Gastrointestinal Tract 
10.2.1 Peptic Ulcer Disease 
Refers to acid related peptic ulceration involving the lower esophagus; stomach and duodenum as a 
result of active inflammation induced by acid –pepsin leading to disruption of the mucosal integrity 
causing local defect or excavation 
10.2.1.1 Gastroesophageal Reflux Disease (GERD) 
It is a disorder resulting from gastric acid-pepsin activity and other gastric contents reflux into the 
esophagus due to incompetent barriers at the gastroesophageal junction leading to active 
inflammation of the distal third of the esophagus (prolonged contact with acid can evolve to stricture) 
Clinical presentation 
•
Heartburn and regurgitation are cardinal symptoms.
•
Odynophagia, dysphagia, weight loss and bleeding
•
Chronic cough, laryngitis, pharyngitis
•
Chronic bronchitis, asthma, COPD, pneumonia, chronic sinusitis and dental decay
Investigations 
•
Endoscopic evidence mucosal ulceration
•
Histological evidence of chronic active inflammation
•
Positive finding with a gold standard 24-hours esophageal pH testing.
Pharmacological Treatment 
Non-erosive, symptomatic 
A: omeprazole (PO) 20mg 24hourly for 8weeks 
OR 
S: esomeprazole (PO) 20mg-40mg 24hourly for 8weeks. 

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Erosive esophagitis 
C: pantoprazole (PO) 40mg 24hourly for 8-16weeks 
For refractory cases acid suppression therapy may require continuation up to 6 months. Lifestyle 
modification and avoidance of triggers is important including avoidance of smoking, alcohol and 
NSAID use.    
Referral: Refer to next level center with adequate expertise and facility for refractory cases or cases 
with alarming symptoms (red flags) such as bleeding, anemia, early satiety, progressive dysphagia 
or odynophagia, unexplained weight loss, recurrent vomiting or family history of gastrointestinal (GI) 
cancers, age ≥ 40 years. 
10.2.1.2 Gastroduodenal Ulcers (PUD) 
This is a disorder resulting from breakdown of mucosal defense mechanisms against hydrochloric 
acid and proteolytic enzymes, most commonly secondary to H. Pylori infection or NSAID use. 
Clinical presentation 
•
Burning epigastric abdominal pains,
usually relived by antacids.
•
Anorexia, early satiety, bloating,
•
Hematemesis or melena stools
•
Weight loss
Investigations 
•
Endoscopic evidence of gastric or duodenal mucosal ulceration
Pharmacological Treatment 
A: omeprazole (PO) 20mg 24hourly for 8weeks 
OR 
C: pantoprazole (PO) 40mg 24hourly for 8weeks 
OR 
S: esomeprazole (PO) 20mg 24hourly for 8weeks 
AND  
A: antiacid liquid (PO) 10-15ml 12hourly to 8hourly for 7-14days 
For bleeding PUD: refer to higher centers 
C: pantoprazole (IV) 80mg stat then 40mg 12hourly for 2-3days, then (PO) as above if 
bleeding stops 
OR 
S: esomeprazole (IV) 40mg 12hourly for 2-3days, then (PO) as above if bleeding stops 
10.2.1.3 Helicobacter Pylori Related Peptic Ulcer Disease 
Helicobacter pylori is a ubiquitous organism that is present in about 50% of the global population. 
Chronic infection with H pylori causes atrophic and even metaplastic changes in the stomach, and it 
has a known association with peptic ulcer disease. The most common route of H pylori infection is 
either oral-to-oral or fecal-to-oral contact. 
Clinical presentation 
•
As above in cap 10.2.1.1
Investigations 
•
Positive stool antigen test (Stop
PPI 2 weeks before testing)
•
Positive urease breath test
•
Positive urease test on endoscopic
biopsy sample
•
Identification of the pathogen by
histopathology examination
Pharmacological Treatment 
Triple therapy is indicated for complete eradication of the organism 

190!
A: omeprazole (PO) 20mg 12hourly for 10-14days 
AND 
A: amoxycillin (PO) 1000mg 12hourly 10-14days 
AND 
A: metronidazole (PO) 400mg 12hourly for 10–14days 
Alternatively  
C: lansoprazole (PO) 30mg 12hourly for 10-14days 
AND 
C: clarithromycin (PO) 500mg 12hourly 10-14days 
AND 
B: tinidazole (PO) 500mg 12hourly for 14days 
OR 
Concomitant Therapy (all for 7 days) 
A: omeprazole (PO) 20mg 12hourly 
AND  
A: amoxicillin (PO) 1000mg 12hourly 
AND  
A: metronidazole (PO) 400mg 12hourly 
AND  
C: clarithromycin (PO) 500mg 12hourly 
Treat with Bismuth-based therapy for H. pylori treatment failure 
C: pantoprazole (PO) 40mg 12 hourly 10-14days 
OR  
S: esomeprazole (PO) 40mg 12hourly 10-14days 
AND 
S: bismuth subsalicylate (PO) 525 mg 6hourly 10-14days 
AND 
A: metronidazole (PO) 250 mg 6 hourly or 500 mg 8hourly 10-14days 
AND 
S: tetracycline (PO) 500 mg 6hourly for 10-14days. 
Note 
H.pylori diagnostic tests should be repeated 5 weeks after the last dose of eradication therapy, and
the PPI should be stopped 2weeks before testing the H.pylori stool antigen test to confirm
eradication.
10.2.2 Ulcer Related Conditions 
10.2.2.1 Non-ulcer Dyspepsia (Functional Dyspepsia, Indigestion) 
It is a chronic recurrent dyspeptic disorder characterized by upper abdominal symptoms, discomfort, 
pain, fullness, early satiety, bloating, burning epigastric pain syndrome and post prandial distress 
syndrome without any organic, systemic or metabolic disease to explain its presence. 
Clinical presentation 
•
Dyspeptic symptoms present for
last 3 months and onset at least
months prior to diagnosis
•
Bothersome abdominal discomfort
post prandial fullness.
•
Early satiety
•
Epigastric pains
•
Epigastric burning
Investigations 
•
Lack of evidence of structural disease by upper endoscopic examination.
Pharmacological Treatment 
H. pylori eradication (see under H. pylori)
A: omeprazole (PO) 20mg 24hourly for 4-8weeks 
OR 

191!
C: pantoprazole (PO) 40mg 24hourly for 4-8weeks 
OR 
S: esomeprazole (PO) 40mg 24hourly for 4-8weeks 
AND 
C: metoclopramide (PO) 10mg 8hourly when required (bloating and nausea symptoms, 
delayed gastric emptying) 
OR 
D: domperidone (PO) 10mg 8hourly when required to alleviate bloating and nausea 
symptoms, delayed gastric emptying. 
AND 
A: amitriptyline (PO) 25mg at bedtime when required for refractory cases 
Note 
Presence of alarm features (see list above under GERD) warrant OGD. 
10.2.2.2 Gastritis 
This is an inflammatory mucosal response to injury from variety of agents and mechanisms including 
infections, drugs, alcohol, acute stress, radiation, allergy, acid and bile, ischemia or direct trauma. 
The inflammation may involve the entire stomach (pangastritis) or a region of the stomach (antral 
gastritis) while the severity of inflammation may be erosive or non-erosive. 
Clinical presentation 
•
Nausea, vomiting, loss of appetite, belching, and bloating
•
Acute abdominal pain or abdominal discomfort
•
Fever, chills, and hiccups also may be present
Investigations 
•
Endoscopic evidence of gastric mucosal inflammation
•
Histologic evidence of chronic active inflammation of biopsy specimen.
Non-pharmacological Treatment 
•
Reduce the use of drugs known to cause gastritis (e.g., NSAIDs, alcohol)
•
Stop smoking
•
Reduce fatty, spicy and deep-fried foods
Pharmacological Treatment 
Triple therapy for H. pylori eradication if confirmed present.  
Administer fluids and electrolytes as required, particularly if the patient is vomiting. 
C: pantoprazole (IV) 40mg 6hourly 2-3days 
OR 
S: esomeprazole (IV) 40mg 12hourly 2-3days 
AND 
C: metoclopramide (IM) 10mg 12hourly when required (for cases presenting with 
intractable vomiting) in order to relieve symptoms.  
Switch to oral PPI once patient can tolerate oral intake.  
Referral 
Refer to next level service with adequate expertise and facilities for complicated case with alarm 
features (anemia, vomiting blood and weight loss, see complete list under GERD above). 
10.2.3 Gastrointestinal (GI) Bleeding 
Intraluminal blood loss anywhere from the oropharynx to the anus. Classification: upper = above the 
ligament of Treitz; lower = below the ligament of Treitz “Severe” GIB: defined as having associated 
shock, orthostatic hypotension, fall in hematocrit by 6% (or decrease in Hb by 2 g/dL), or requiring 
transfusion ≥2U PRBCs. Requires hospitalization. 

192!
10.2.3.1 Upper GI Bleeding (UGIB) 
PUD caused by Helicobacter pyloriinfection or NSAID use is the most common cause of nonvariceal 
UGI bleeding. Characteristic findings are hematemesis, melena, or (infrequently) bright-red blood 
per rectum or a high serum BUN/creatinine ratio. Slow and/or chronic bleeding is suggested by iron 
deficiency and is typical of erosive disease, tumor, esophageal ulcer, portal hypertensive 
gastropathy, Cameron lesion (erosions found within large hiatal hernias), and angiodysplasia. 
Table 10.1: Differential Diagnosis of Upper GI Bleeding 
Presentation 
Diagnosis 
Dyspepsia, H. pylori infection, NSAID use, 
anticoagulation, severe medical illness 
Peptic ulcer disease 
Stigmata of chronic liver disease, evidence of portal 
hypertension or risk factors for cirrhosis (alcohol 
use, viral hepatitis) 
 Variceal bleeding 
History of heavy alcohol use and retching before 
hematemesis, hematemesis following weightlifting, 
or young woman with bulimia 
 Mallory-Weiss tear 
Heartburn, regurgitation, and dysphagia; usually 
small-volume or occult bleeding 
 Esophagitis 
Progressive dysphagia, weight loss, early satiety, 
or abdominal pain; usually small-volume or occult 
bleeding 
Esophageal or gastric cancer 
NSAID use, heavy alcohol intake, severe medical 
illness; usually small-volume or occult bleeding 
Gastroduodenal erosions 
Initial management 
Assess severity: vital signs including orthostatic changes, JVP. Tachycardia (can be masked by βB 
use) suggests 10% volume loss, orthostatic hypotension 20% loss, shock >30% loss. After the 
patient is stabilized, upper endoscopy is required to document the source of bleeding. If upper 
endoscopy shows an ulcer, test for H. pylori infection.  
Resuscitation: placement of 2 large-bore (18-gauge or larger) intravenous lines, volume 
replacement: NS or LR to achieve normal vital signs, urine output, and mental status. 
Pharmacological Treatment  
For variceal bleeding refer to (10.4.2.3 Bleeding Esophageal Varices) 
For bleeding peptic ulcer disease 
C: pantoprazole (IV) 40mg 12hourly for 2-3days 
OR 
S: esomeprazole (IV) 40mg 12hourly for 2-3days 
Laboratory Investigations 
•
FBP, LFT, RFT.
•
Abdominal ultrasound
•
Viral hepatitis screening
•
H. pylori stool antigen
10.2.3.2 Lower gastrointestinal (GI) Bleeding 
Acute, painless LGI bleeding in older adult patients is usually due to colonic diverticula or 
angiodysplasia. Ten percent of rapid rectal bleeding has an UGI source. 
Consider outpatient follow-up or early discharge when: 
Note 
•
Treat high-risk ulcers endoscopically (haemoclips, thermal therapy, or injection therapy)
and continuous IV PPI infusion for 72 hours. Blood transfusion to target haemoglobin level
of 7 g/dl Repeat endoscopic therapy for continued bleeding
•
Surgery or interventional radiology if endoscopic therapy unsuccessful

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•
patient age <60 years
•
no hemodynamic instability
•
no evidence of gross rectal bleeding
•
identification of an obvious anorectal source of bleeding
Table 10.2: Differential Diagnosis of Lower GI Bleeding 
Note 
•
According to expert opinion, the blood transfusion threshold for patients with colonic bleeding is a
haemoglobin value <9 g/dL (note this is different for the evidence-based threshold for UGI bleeding).
•
If the patient is hemodynamically unstable, resuscitate the patient before diagnostic studies are
performed. Most episodes of LGI bleeding resolve spontaneously.
•
Colonoscopy is recommended early, usually within the first 48 hours of admission, and endoscopic
therapy is used to control continued bleeding.
•
If colonoscopy does not identify a discrete lesion or endoscopic therapy does not control the bleeding,
interventional angiography or surgery may be indicated.
•
Patients with angiodysplasia in the setting of AS (Heyde Syndrome) may benefit from valve
replacement surgery.
10.2.3.3 Bleeding of Obscure Origin 
Obscure GI bleeding is recurrent blood loss without an identified source of bleeding despite upper 
endoscopy and colonoscopy.Patients aged ≤50 years are more likely to have tumors (leiomyomas, 
carcinoid, adenocarcinoma, or lymphoma), Dieulafoylesion, or Crohn’s disease. Older patients are 
more likely to have vascular lesions, such as angiodysplasia. Angiodysplasia is the most common 
cause of obscure GI bleeding overall (40% of all cases). Patients may present with either melena or 
hematochezia or positive fecal occult blood test (FOBT). The first step is to repeat upper endoscopy 
and/or colonoscopy, which is diagnostic in approximately 40% of cases. 
For patients with obscure activeGI bleeding 
•
nuclear studies (technetium 99m-labeled erythrocyte or sulfur colloid nuclear scan) first,
followed by angiography
•
if unrevealing, consider push enteroscopy or balloon-assisted enteroscopy (deep
enteroscopy)
Presentation 
Diagnosis 
Painless, self-limited, massive hematochezia 
Diverticular bleeding (most common overall cause) 
Chronic blood loss or acute painless hematochezia 
in an older adult patient 
Angiodysplasia 
Stool positive for occult blood in an asymptomatic 
patient 
Colonic polyp or cancer 
Risk factors for atherosclerosis and evidence of 
vascular disease in an older adult patient; typically, 
with LLQ abdominal pain 
Ischemic colitis 
Aortic stenosis 
Angiodysplasia (Heyde Syndrome) 
History of bloody diarrhea, tenesmus, abdominal 
pain, fever 
IBD 
Rapid UGI bleeding 
Dieulafoy lesion (large, tortuous, submucosal 
arteriole) 
Large hiatal hernia 
Cameron lesion (mucosal erosions) 
Recent liver or biliary procedure 
Hemobilia 
Necrotizing pancreatitis 
Hemosuccus pancreaticus (bleeding from 
pancreas) 
Aortic aneurysm repair 
Aortoenteric fistula 
Painless hematochezia in a young patient and 
normal upper endoscopy and colonoscopy 
Meckel diverticulum 
Mucocutaneous telangiectasias 
Hereditary hemorrhagic telangiectasia 

194!
•
surgery and intraoperative enteroscopy is a last diagnostic option
For patients with occult GI bleeding 
•
capsule endoscopy (first choice GIE 2015; 81:889) or deep enteroscopy
•
if unrevealing, repeat endoscopic examinations (upper endoscopy, colonoscopy, capsule
endoscopy), or deep enteroscopy
10.3 Diseases of the Intestine 
10.3.1 Inflammatory Bowel Diseases 
Inflammatory bowel disease (IBD) is an idiopathic disease involving an immune reaction of the body 
to its own intestinal tract. The 2 major types of IBD are ulcerative colitis (UC) and Crohn’s disease 
(CD). Pathologically, ulcerative colitis is limited to the colon while Crohn’s disease can involve any 
segment of the gastrointestinal (GI) tract from the mouth to the anus. 
10.3.1.1 Ulcerative Colitis (UC) 
Inflammatory condition that involves the rectum and extends proximally to affect a variable extent of 
the colon up to the caecum 
Clinical presentation 
•
Diarrhoea
•
Rectal bleeding
•
Tenesmus, passage of mucus
•
Crampy abdominal pain
•
Fevers and chills
Investigations 
•
Endoscopic evidence of diffuse and continuous colonic mucosal inflammation with friability
and loss of mucosal vascularity characteristic cobble stone appearance.
•
Histologic evidence of abnormal crypt architecture and superficial inflammation typical of
UC.
Pharmacological Treatment 
D: sulfasalazine (PO) 1000mg 6hourly a day for acute disease, reducing to 1000mg once 
daily for maintenance   
OR 
S: mesalazine (PO) 1.5g–4g/day in divided doses reduced to 0.75–2g g/day in divided 
doses for maintenance 
AND  
A: prednisolone (PO) 30–60mg 24hourly for severe, acute and extensive disease; tapering 
gradually after induction of remission within 8 weeks. 
For severe disease flares give IV corticosteroids, 
D: methylprednisolone (IV) 16-20mg 8hourly 5- 7days 
If irresponsive (i.e. fewer stools, less bleeding) to IV corticosteroids for 5-7days, or acute 
complications give the following; 
S: cyclosporine (IV) 2-4mg/kg 12hourly for 7days 
THEN change to  
S: azathioprine (PO) 1.5-2.5 mg/kg 24hourly for maintenance. 
OR  
S: infliximab (IV) 5 mg/kg at 0, 2, and 6weeks, then every 8weeks 
Note 
Complication of UC may present with massive haemorrhage, toxic mega colon, AND perforation with 
features of peritonitis necessitates hospitalization. Colonoscopy with random biopsy 8 years after 
diagnosis to evaluate for dysplasia, every 1-3 years thereafter based on risk factors. Use steroids only 
when the disease is confirmed and for induction of remission only. 

195!
10.3.1.2 Crohn’s Disease 
Crohn’s disease is an idiopathic, chronic, transmural inflammatory process of the bowel that often 
leads to fibrosis and obstructive symptoms and can affect any part of the gastrointestinal tract from 
the mouth to the anus. 
Clinical presentation 
•
Abdominal pain, diarrhea, weight
loss, anorexia and fever
•
Gross rectal bleeding or acute
hemorrhage is uncommon
•
Anemia due to illeal disease
involvement
•
Small bowel obstruction, due to
structuring
•
Perianal disease associated with
fistulization
•
Gastroduodenal ulceration
Investigations 
•
Endoscopic evidence of rectal sparing skip lesions, cobble stoning with linear ulceration
appearance with,
•
Histological evidence of transmural disease, aphthous ulcers, and non-caseating
granulomas
Pharmacological Treatment 
S: methotrexate (PO) 7.5–15mg weekly 
OR 
S: azathioprine (PO) 50mg 24hourly for maintenance of remission. 
AND  
A: prednisolone (PO) 1–2mg/kg for induction of remission only (Taper in 8 weeks) 
AND 
A: metronidazole (PO) 400mg 8hourly for 7–10days  
OR 
A: ciprofloxacin (PO) 500mg 12hourly for 7–10days – can be added in presence of 
perianal disease or evident septic complications. 
For severe disease flare or acute complications  
Patients who have had inadequate response to conventional therapy, also for reducing the number 
of draining enterocutaneous and rectovaginal fistulas and maintaining fistula closure in adult patients 
with fistulizing Crohn disease. 
S: infliximab (IV) 5 mg/kg at 0, 2, and 6 weeks, THEN every 8weeks thereafter 
AND  
S: azathioprine (PO) 1.5-2.5 mg/kg 24hourly 
Note 
Resuscitative and supportive management should be instituted as for UC section note above. 
10.3.2 Pseudomembranous Colitis 
This condition is caused by Clostridium difficile, a gram positive, anaerobic bacterium causing 
antibiotic associated diarrhoea as a result of altered bacterial flora and release of enterotoxins. 
Clinical presentation 
•
Bloody Diarrhea
•
Abdominal cramps and tenderness
•
Nausea, fever, dehydration
 

196!
•
Lower endoscopic pathognomonic findings of pseudomembranous yellowish plaques
overlying the ulcerated and friable rectal sigmoid colon mucosa
•
Laboratory evidence of C. difficile toxin A-B isolation from cultured stool samples (Toxin B)
OR ELISA assay (Toxin A)
Pharmacological Treatment 
Stop the causative antibiotics 
A: metronidazole (PO) 400mg 8hourly for 10-14days 
OR 
S: vancomycin (PO) Adults, 125mg–500mg 6hourly for 10-14days 
Note 
Resuscitative and supportive management should be instituted as for UC above. Refer to next level 
of care with adequate expertise and facilities for all suspected cases for initial evaluation and 
management and cases presenting with acute complications such as Toxic mega colon 
10.3.3 Radiation Proctitis 
Radiation proctopathy is defined as epithelial damage to the rectum due to radiation that is 
associated with minimal or no inflammation. Acute radiation proctitis occurs during or within six 
weeks of radiation therapy. Chronic radiation proctitis has a more delayed onset. The first symptoms 
often occur 9 to 14 months following radiation exposure but can occur any time post-irradiation up to 
30 years after exposure. 
Clinical presentation 
•
Symptoms of acute radiation proctitis include diarrhea, mucus discharge, urgency,
tenesmus, and, uncommonly, bleeding.
•
Patients with chronic radiation proctitis have similar symptoms as patients with acute
radiation proctitis, but bleeding is usually more severe. In addition, patients may have
symptoms of obstructed defecation due to strictures with constipation, rectal pain, urgency,
and, rarely, fecal incontinence due to overflow.
•
Concomitant injury to the genitourinary tract or small bowel may lead to fistulas, small
bowel obstruction, small intestinal bacterial overgrowth, urethral stenosis, and cystitis
•
Acute radiation proctitis should be suspected in patients with diarrhea, mucus discharge,
urgency, tenesmus, or bleeding during or within six weeks of radiation therapy. Chronic
radiation proctitis should be suspected in patients who develop these symptoms nine
months or more after pelvic radiation exposure.
Investigations  
•
Stool studies for C. difficile toxin, routine stool cultures (Salmonella, Shigella,
Campylobacter, and Yersinia), Escherichiacoli O157:H7. Microscopy for ova and parasites
(three samples)
•
Testing for STI, including C. trachomatis, N. gonorrhoeae, HSV, and Treponema pallidum,
•
Endoscopy (colonoscopy and biopsy)
•
Magnetic resonance imaging
Pharmacological Treatment 
D: sulfasalazine (PO) 3g 24hourly for 4weeks 
AND 
S: sucralfate enemas (rectal preparation) 2g 12hourly for 4weeks 
Note 
Refer to higher level facility with expertise and experience in the management complications such as 
bleeding. Endoscopic therapy — Argon plasma coagulation (APC) for bleeding. Surgery — Surgery 
should be reserved for patients who have. intractable symptoms such as a stricture, pain, bleeding, 
perforation, or a fistula 
Investigations

197!
10.3.4 Irritable Bowel Syndrome 
Irritable bowel syndrome (IBS) is a functional GI disorder characterized by abdominal pain and 
altered bowel habits in the absence of specific and unique organic pathology. 
Four bowel patterns may be seen with IBS; 
I.
IBS-D (diarrhea predominant)
II.
IBS-C (constipation predominant)
III.
IBS-M (mixed diarrhea and constipation)
IV.
IBS-U (unclassified; the symptoms cannot be categorized into one of the above three
subtypes)
Clinical presentation 
•
Recurrent abdominal pains or discomfort at least 3 days per month in the last 3 months
associated with two or more of the following
•
Improvement with defecation
•
Onset associated with a change in frequency of stools
•
Onset associated with a change in form of stool
•
Bloating or feeling of abdominal fullness
Non-pharmacological Treatment 
•
Counseling on compelling psycho –social factors, lifestyle modification, avoidance of
trigger factors, and reassurance are corner stone of long-term management strategy. Plus,
supportive therapies such as:
•
High fiber diet and eating a healthy diet.
Pharmacological Treatment 
A: hyoscine butyl bromide (PO) 10mg 6hourly when required 
OR    
D: mebeverine (PO) 135mg 8hourly when required 
AND  
A: amitriptyline (PO) 25mg nocte for one week then 50mg nocte week 2-4. 
AND 
C: lactulose (PO) 20mls 12hourly (when required for constipation) 
OR  
A: bisacodyl (PO) 5-15mg when required for constipation 
For diarrheal predominant IBS 
B: loperamide (PO) 4mg stat, for diarrhoea followed by 2mg 8hourly or after each 
unformed stool until diarrhoea is controlled. 
10.3.5 Diverticulosis 
Acquired herniations of colonic mucosa and submucosa in areas where vasa recta penetrate, 
thought to occur in setting of abnormal motility and increased intraluminal pressure. 
Clinical presentation 
Asymptomatic but 5–15% develop diverticular hemorrhage (see “GIB” above) and <5% diverticulitis 
10.3.6 Diverticulitis 
Retention of undigested food and bacteria in diverticulum leads to fecalith formation with obstruction 
which compromise diverticulum’s blood supply, infection, perforation 
Uncomplicated: microperforation leading to localized infection 
Complicated: macroperforation leading to abscess, peritonitis, fistula, obstruction 
Clinical presentation 
•
LLQ abdominal pain, fever, nausea, vomiting, constipation or diarrhea

198!
•
Physical findings range from LLQ tenderness and/or palpable mass to peritoneal signs and
septic shock
•
Differential diagnosis includes IBD, infectious colitis, PID, tubal pregnancy, cystitis,
colorectal cancer
Investigations 
•
Plain abdominal radiographs to rule out free air, ileus or obstruction
•
Abdominal CT scan with contrast, to assess complicated disease (abscess, fistula)
•
Colonoscopy contraindicated acutely as increases the risk of perforation; do 6–8 weeks
after to rule out neoplasm
Pharmacological Treatment   
Mild: outpatient indicated if patient has little comorbidity and can tolerate oral intake 
A: amoxicillin + clavulanate FDC (PO) 625mg 12hourly daily for 7–10days 
AND 
A: metronidazole (PO) 400mg 8hourly for 7–10days 
AND 
Liquid diet until clinical improvement 
Alternatively 
A: ciprofloxacin (PO) 500mg 12hourly daily for 7–10days 
OR 
A: metronidazole 400mg (PO) 8hourly for 7–10days 
AND 
Liquid diet until clinical improvement 
For severe cases 
B: ceftriaxone (IV) 1-2g 24hourly for 7-10days 
OR  
S: piperacillin + tazobactam (IV) 4.5gm 6-8hourly 7-10days (for severe/complicated cases) 
OR  
S: meropenem (IV) 1gm 8hourly 7-10days 
AND 
B: metronidazole (IV) 500mg 8hourly for 7-10days 
Note 
•
Abscesses >4 cm should be drained percutaneously or surgically.
•
Surgery: if progressions despite medical treatment, undrainable abscess, free perforation.
•
After source control, 4days antibiotics may be enough.
•
Resection for recurrent bouts of diverticulitis on a case-by-case basis.
10.3.7 Polyps and Adenomas 
Accumulation of mutations in colonic epithelial cell DNA affecting oncogenes and tumor suppressor 
genes which leads to tumor initiation (formation of adenoma) tumor progression (adenoma to 
carcinoma). 
Neoplastic polyps: adenomas (tubular, villous, tubulovillous dysplasia), sessile serrated 
adenomas/polyps (concern for interval CRC), carcinomas. 
Non-neoplastic polyps: hyperplastic, juvenile, Peutz-Jeghers, inflammatory. 
Investigations  
Colonoscopy is gold standard 
Note 
•
Colonoscopy in all patients starting at age 50 years, then typically every 10years unless
pathology found.
•
If positive family history, start age 40, or 10 years before age of diagnosis in youngest
family member, repeat every 5 years.

199!
10.3.8 Hemorrhoids 
Hemorrhoid disease is due to enlargement or thrombosis of the veins in the external or internal 
hemorrhoidal plexus. 
Clinical presentation 
•
Painless anal rectal piles
•
Painless bleeding –post defecation
•
Pain
•
Pruritus
•
Prolapse
Investigations  
•
Endoscopy (Anoscopy, or proctosigmoidoscopy) for evidence of characteristic anal recta
piles.
Treatment 
•
Depends on severity of the disease
•
Grade I hemorrhoids are treated with conservative medical therapy and avoidance of
nonsteroidal anti-inflammatory drugs (NSAIDs) and spicy or fatty foods
•
Grade II or III hemorrhoids are initially treated with nonsurgical procedures
(sclerotherapy, band ligation
•
Very symptomatic grade III and grade IV hemorrhoids are best treated with surgical
hemorrhoidectomy
Pharmacological Treatment 
A: benzyl benzoate 1.25%, bismuth oxide 0.875%, bismuth subgallate 2.25%, 
hydrocortisone acetate 0.25%, Peru balsam 1.875%, zinc oxide 10.75% (PR) suppository 
one or twice a day 
OR 
S: (Euphobia prostrate extract 100mg + Calcium dobesilate 500mg) (PO) 24hourly 
(chewable do not swallow) 
AND 
S: (Prednisolone hexanoate 1.3mg +Cinchocaine hydrochloride 1mg) Suppository 
24hourly 5-7days 
10.3.9 Anal Fissures 
These are painful linear ulcers in the anal canal. Young and middle-aged adults most affected. 
Primary fissure occurs in the posterior midline. It can also be secondary to Crohn’s disease, anal 
cancer, or infection such as syphilis, TB in which case they occur more lateral. Passage of hard 
stools is a common predisposition to primary fissures. 
Clinical presentation 
•
Severe sharp pain during and after defecation with/out bright red bleeding.
Investigations 
•
Evidence of linear anal rectal ulceration on proctoscopy examination
Non-Pharmacological Treatment 
•
Ensure high fluid intake
Pharmacological Treatment 
•
Topical anesthetics and frequent seat baths can reduce sphincter spasm (should be
offered before surgery)
•
Use non stimulant osmotic laxatives
Surgery: Surgical sphincterotomy is definitive treatment. 

200!
10.3.10 Fistula in Ano 
Is a chronic abnormal communication lined by degree of granulation tissues which runs outward 
from mucosal lumen. 
Risk factors 
•
Previous perianal abscess formation
•
Chhorn’s disease
•
Diabetes mellitus
•
Tuberculosis
•
Trauma
•
Radiotherapy
•
Immunosuppression-HIV, malignancy
Classifications of fistula in ano
I.
Intersphincteric
II.
Suprasphincteric
III.
Transphincteric
IV.
Extra sphincteric
Clinical presentation 
•
Purulent or bloody discharges
•
Pruritis ani
•
History of anorectal abscess
Investigations 
•
Fistulography
•
Endoanal USS
•
Pelvic MRI-gold standard
•
Surgical Treatment options
•
Fistulotomy, Fistulectomy, Seton,
Fibrin glue, anal fistula plug,
Advancement flap
10.3.11 Appendicitis 
 This is characterised by inflammation of the appendix, and usually requires urgent surgical 
intervention. 
Clinical presentation 
•
Sudden peri-umbilical pain often
migrating to the right iliac fossa.
•
Nausea and vomiting
•
Loss of appetite
•
Fever
•
Constipation or occasionally
diarrhea.
•
Bloated abdomen.
•
Rebound tenderness
•
guarding and rigidity.
•
Right iliac fossa tenderness.
•
Right iliac fossa rebound pain.
•
Severe persistent abdominal pain.
Investigations 
•
FBP
•
Urinalysis
•
Pregnancy test in females
•
LFT
•
Lipase/amylase excludes
pancreatitis
•
Abdominal USS
•
CT scan
Complications 
•
Perforation/peritonitis
•
Appendicular abscess
•
Appendicular mass
Pharmacological management 
B: ceftriaxone (IV) 1g 12hourly for 5-7days 
AND 
B: metronidazole (IV) 500mg 8hourly for 5-7days 
AND 
A: diclofenac (IM) 75mg 8hourly for 3days 

201!
!
10.4 Pancreatitis 
Pancreatitis is an inflammatory process in which pancreatic enzymes auto digest the pancreatic 
gland leading to functional and morphologic loss of the gland. 
 
10.4.1 Acute Pancreatitis 
It is due to sudden inflammation of the pancreas due to pancreatic enzymes auto digestion. 
Common risk factors which trigger the acute episode are presence of gallstones and alcohol intake.  
 
Clinical presentation 
• 
Severe, unremitting epigastric pain, 
radiating to the back  
• 
Nausea and vomiting 
• 
Signs of shock may be present 
• 
Ileus is also common 
• 
Local complications: inflammatory 
mass, obstructive jaundice, gastric 
outlet obstruction 
• 
Systemic 
complication: 
sepsis, 
acute 
respiratory 
distress 
syndrome, acute renal failure  
 
Investigations  
• 
Raised Serum levels for lipase and amylase greater than 3 times the upper limit of normal 
ULN (Lipase is more specific and sensitive than amylase). And,  
• 
Radiological (ultrasound, CT, MRI) evidence of inflamed and/or necrotizing pancreatitis. 
 
Treatment 
• 
Principles of management include supportive therapies.  
• 
Intravascular volume expansion (colloids/crystalloid) 
• 
Opiates analgesia usually required (follow WHO analgesic ladder) 
• 
Enteral feeding, (only in absence of illeus) start within 72 hours 
• 
Correction of electrolytes and metabolic deficit accordingly 
 
Pharmacological Treatment 
B: ceftriaxone (IV) 1g 12hourly for 7days 
OR  
C: ciprofloxacin (IV) 200-400mg 12hourly for 7days 
AND  
B: metronidazole (IV) 500mg 8hourly for 7days  
OR 
S: meropenem (IV) 1g 8hourly for 7days  
 
 
Note 
• 
Fever can be because of pancreatitis itself; antibiotics should be avoided before 7 days.  
Pancreatic necrosis: Nonviable pancreatic tissue. CT-guided FNA if infection suspected.  
Sterile necrosis: if asymptomatic, can be managed expectantly, no role for prophylactic 
antibiotics. 
Infected necrosis: high mortality. Treat with carbapenem or metronidazole plus 
fluoroquinolone 
• 
If stable, defer drainage to >4 weeks. If symptomatic or unstable, percutaneous drainage 
and minimally invasive surgical debridement or endoscopic necrosectomy superior to open 
necrosectomy. ERCP + Sphincterotomy may be needed.  
 
10.4.2 Chronic Pancreatitis 
Chronic pancreatitis is long-term (chronic) inflammation of the pancreas that leads to permanent loss 
of function and morphology of the gland.  
 
Clinical presentation 
• 
Chronic upper abdominal pain associated with nausea, vomiting and loss of appetite. 
• 
Malabsorption diarrhoea (exocrine pancreatic insufficiency (steatorrhea)) 

202!
•
Recurrent attacks of pancreatitis weight loss
•
Diabetes
Investigations  
•
Radiological (Abdominal Ultrasonography/CT scan) evidence pancreatic calcification and
atrophy.
Pharmacological Treatment   
Supportive therapies with analgesics in the following order; 
A: paracetamol (PO) 1g 8hourly daily when required 
OR  
B: tramadol (PO) 50mg 12hourly when required for chronic pain relief. 
OR  
C: morphine (PO) 5-10mls 6hourly when required 
If pain unresponsive to above medications 
ADD 
A: amitriptyline (PO) 25mg nocte when required for pain control 
OR 
D: pregabalin (PO) 75mg once daily when required for pain relief 
Manage complications   
Pancreatic enzymes deficiency and steatorrhea 
S: pancreatic (PO) 1–3tablet 24hourly to supplement digestive enzyme and improve food 
absorption. 
Diabetes mellitus  
Refer to metabolic and endocrine disease conditions chapter 
Note 
•
In patients with persistent or refractory pain look for a dilated pancreatic duct and
intraductal calcifications. These patients may benefit from endoscopic stenting, lithotripsy,
or surgical drainage (pancreatojejunostomy).
10.4   Disorders of The Liver and Biliary Tract 
10.4.1 Hepatitis 
This is the term referring to inflammation of the liver, which may result from various causes, both 
infectious (i.e. viral, bacterial, fungal, and parasitic organisms) and non-infectious e.g. alcohol, 
drugs, autoimmune and metabolic diseases; this section focuses on viral hepatitis and its sequels.  
10.4.1.1 Viral Hepatitis 
It is a systemic infection predominantly affecting the liver caused hepatotropic viral agents namely 
Hepatitis A virus (HAV), Hepatitis B virus (HBV), Hepatitis C virus (HCV), HBV – associated delta 
agent or Hepatitis D virus (HDV), and Hepatitis E virus (HEV); in most cases leads to a self-limiting 
disease but can take a fulminant course and lead to hepatic failure or progress to chronic liver 
disease (HBV, HBV-HDV and HCV) 
Note 
For comprehensive management of viral hepatitis refer to the National Guidelines for Prevention and 
Management of Viral Hepatitis 2020. 
Hepatitis A Virus (HAV) 
HAV is the RNA virus from piconaviridae family under genus hepatovirus. It primarily infects the 
liver. The disease occurs sporadically or in epidemics and has an incubation period of 14- 28 days. 
The group most affected is aged between 5-14 years and adults are often infected by spread from 
children.  

203!
Clinical presentation 
Mild flulike symptoms of anorexia, nausea and vomiting, fatigue, malaise, low-grade fever (usually < 
39.5°C), myalgia, and mild headache, dark urine appears first (bilirubinuria). Pale stool soon follows; 
Jaundice occurs in most adults. Abdominal pain itching (pruritus), Arthralgias and skin rash, (less 
frequent than the above symptoms). 
Investigations 
Specific diagnosis involves serological detection of Hepatitis A specific immunoglobulins IgM or   IgG 
antibodies in blood for acute and resolved infection respectively. Viral RNA detection   through PCR 
is definitive and confirmatory specialized laboratory test. Other tests include FBP, LFT, RFT and 
tests for other viral hepatitis viruses (HBV±HDV, HCV, and HEV). 
Treatment 
•
Supportive management such as hydration, adequate feeding and
avoidance of 
concomitant use of hepatotoxic medications including herbals is all that is required in mild 
infections. The disease resolves spontaneously in several weeks or months. 
•
Hospitalization is necessary in settings of acute liver failure. Therapy is aimed at
maintaining fluid replacement, balanced nutritional feeding, relief of pains and fever
including specific management for liver failure.
Hepatitis B Virus (HBV) 
New-onset hepatitis B infection that may or may not be icteric or symptomatic. Diagnosis is based 
on detection of hepatitis B surface antigen (HBsAg) and IgM antibodies to hepatitis B core antigen 
(anti-HBc). Recovery is accompanied by clearance of HBsAg with seroconversion to anti-HBs 
(antibodies to hepatitis B surface antigen), usually within 3 months. 
Clinical presentation 
•
Fever, anorexia, malaise, jaundice and abdominal pain
•
Enlarged   and tender liver
•
Altered consciousness, coma (hepatic encephalopathy), and bleeding stigmata (in
fulminant cases).
Investigations 
•
Serological evidence of specific viral antigen/ core antibody tests (HBc IgM or HBc IgG);
and biochemical alteration of liver transaminases (ALT, AST).
Treatment of Acute Viral Hepatitis B 
•
No specific antiviral treatment is required.
•
Offer supportive management and counselling.
•
Offer a follow up plan at 4 or 6 weeks’ intervals for a clinical and laboratory re assessment
for evidence of symptoms recovery and biochemical remission.
•
Re-test at 6 months to assess seroconversion status or progression to chronicity
Chronic Hepatitis B infection.  
Defined as persistence of hepatitis B surface antigen (HBsAg) for six months or more after acute 
infection with HBV. 
Clinical presentation 
•
Usually asymptomatic
•
Right upper quadrant abdominal pains.
•
Fatigue, malaise, anorexia, low grade fever; jaundice is frequent in severe disease.
•
Ascites, variceal bleeding, encephalopathy, coagulopathy, and hypersplenism.
•
Urticaria, arthritis, vasculitis, polyneuropathy, glomerulonephritis, thyroiditis

204!
•
HBsAg, HBsAb, HBeAg, HBeAb, HBV DNA PCR
•
LFT, RFT, FBP, HIV,
•
Alfa Feto Protein (AFP)
•
Colour Doppler ultrasonography or duplex Doppler ultrasonography or real time
ultrasonography.
•
CT scan
•
Fibroscan (if available)
Treatment of Chronic Hepatitis B infection 
Pre Treatment Considerations – Who to Treat: 
•
Patient in chronic active/ Reactivation phase characterized by elevated liver enzymes ALT
>2X ULN, HBeAg +ve, viral load >20,000.
•
ALT > 2X ULN, HBeAg –ve, HBeAb –ve, viral load>2000(mutant strain).
•
Patients with evidence of fibrosis development (APRI score >2)/cirrhosis should receive
treatment irrespective of age, and viral loads.
•
Adults aged > 30 years with three determinations of persistently abnormal   ALT levels
above ULN made at unspecific intervals during 6-12month period   with DNA viral load >
20,000 IU/ml irrespective of HBeAg status.
•
Patients co-infected with HIV
Pre Treatment Considerations – Who not treat: 
•
Treatment   should not be given to patients with persistently normal ALT levels and APRI
score < 2 regardless of age and HBeAg status.
•
Immunotolerant patients characterized by high viremia with normal liver chemistry, age
less than 30 years old   require no treatment. Re assess after 24weeks interval.
•
Patient in latent or inactive phase characterized by low viremia, normal liver chemistry with
or without HBeAg sero-conversion requires no treatment. Re assess after 2 weeks’
intervals.
Pharmacological Treatment 
(For eligible adults with no contraindications to tenofovir) 
A: tenofovir (TDF) (PO) 300mg 24hourly; for at least 48weeks; 
Note 
•
Re-asses at 24 weeks for evidence of biochemical and viral replication remission.
(Normalization of ALT, viral suppression to undetected level and seroconversion to anti-
HBe).
•
Offer a consolidated TDF therapy for extended 48 weeks for patients with evidence of
HBeAb sero-conversion and biochemical remission at the end of the first 48 weeks. For
patients still with detectable viral load and or not yet seroconverted to HBeAb, continue
with Tenofovir 300mg daily dose and reassess every 6 to 12 months for HBV DNA,
HBeAg/Ab status
•
Absolute Contraindications to Tenofovir in patients aged < 12 Years
OR 
S: entecavir in the following groups: Children and adolescents between age 2 to 18 years 
weighing between 10kg and 32kg 
Adults with renal insufficiency (CrCl<49ml/min 
Entecavir dose Considerations 
•
Children age 2 to 18 years weighing between 10kg and 32kg - 0.5mg (PO) 24hourly
•
Adults naive to nucleoside therapy (PO) 0.5mg 24hourly
•
Adults with Lamivudine resistance/previous exposure; and decompensated cirrhosis -
1mg (PO)
•
Adults with renal insufficiency (CrCl<49ml/min); dose should be adjusted according to
Investigations 
calculated GFR 

205!
A: Tenofovir (PO) 300mg 24hourly for   patients who have treatment failure with other 
Nucleotides analogues with low resistance barrier (i.e. Lamivudine) OR Interferon based 
therapy. 
Note 
•
Lamivudine should not be prioritized due to their low resistance barrier. Interferon based
therapy is not recommended in our setting due to undesirable side effects, route of
administration and high cost.
When to Stop Treatment 
•
Patient who has been put on Nucleotides analogues therapy without evidence of cirrhosis
or APRI< 2 should be given a follow up plan.
•
Patients who are HBeAb sero-converted after 48 weeks of consolidation therapy, with
persistently normal ALT and undetectable DNA levels should stop treatment and
monitored closely
•
Patients with evidence of HBsAb sero-conversion after completing consolidated therapy
regardless of their DNA and HBeAg status should stop treatment.
•
Treatment in patient with Liver cirrhosis or significant Fibrosis is indefinitely
Monitoring and evaluation of therapeutic response and toxicity. 
•
HBsAg, HBeAb, HBeAg, HBV DNA, AFP, ALT should be monitored pre, during, and post
treatment patients. PLUS (Fibrosis assessment by APRI scores) at 24/ 48weeks interval
•
Renal functions in adults and growth development in children should be monitored
annually   for renal toxicity for patient on Tenofovir and Entecavir respectively.
•
Abdominal Ultrasound (AUS) and Alpha Feto Protein (AFP) should be done at 24- 48
weeks’ interval for   HCC surveillance.
Note 
Screening all close contacts is important. All at risk individuals eg. Healthcare workers, men who 
have sex with men, patients on hemodialysis, prisoners, children born to mothers with HBV and 
patients requiring multiple transfusions, patients with non-B viral hepatitis should be tested for HBV 
and vaccinated if found negative for HBsAg and no evidence of natural immunity  to HBV. 
HBV in Pregnancy 
All Infants and Neonates should have mandatory vaccination according to the recommended 
National EPI schedule. Neonates born to mothers infected with HBV and HBeAg positive, should 
receive at birth dose of hepatitis B immunoglobulin (HBIG) and HBV Vaccine, and then follow up 
with EPI program schedule at 6weeks. During pregnancy, prevention of HBV transmission from 
mother to childshould follow similar protocols as per adults with HBV infection.HBsAg positive 
pregnant mothers with VL >200,000 IU/ml should receive TDF at 3rd trimester until 6months post-
natal period.  
Pharmacological Treatment 
•
First dose for the infant: Hepatitis B vaccine born to HBsAg-negative mothers
•
Medically stable infants weighing ≥2,000 grams: 0.5 ML (IM) within 24h of birth
•
Preterm infants weighing <2,000 g: 0.5 mL (IM) 1 month after birth or at hospital discharge
First dose for the infant: Hepatitis B vaccine born to HBsAg-positive mothers 
B: hepatitis B vaccine (HBV) (IM) 0.5 mL within 12hours of birth 

206!
AND       
S: hepatitis B immune globulin (HBIG) (IM) 0.5 mL within 12hours of birth 
For the HBV positive pregnant mother 
A: tenofovir (PO) 300mg 24hourly (from third trimester to 6 months post-delivery for the 
mother) 
Post exposure prophylaxis (PEP) 
HBIG and HBV vaccine should be given to individuals who are HBsAg negative exposed to HBsAg 
positive focus within 24hours followed by active standard schedule to complete 3 doses.  
S: hepatitis B immune globulin (HBIG) (IM) 0.06 mL/kg once 
AND 
B: hepatitis B vaccine (HBV) (IM) 1 mL (20 mcg) at 0, 1, and 6months 
10.4.2.3 Hepatitis C virus (HCV) 
Hepatitis C virus (HCV) is a small enveloped RNA virus and a member of the family Flaviviridae. 
HCV comprises six genotypes and hundreds of subtypes with variable geographical distribution and 
bears significance in determining the rate of liver disease progression, development of HCC and 
specific therapeutic responses. 
Clinical presentation 
•
Initial symptoms of HCV are often
extrahepatic, 
most 
commonly
involving the joints, muscle, and
skin.
•
Arthralgias,
•
Paresthesias,
•
Myalgias,
•
Pruritus,
•
Sicca syndrome.
•
Sensory neuropathy
Symptoms characteristic of complications from advanced or decompensated liver disease are 
related to synthetic dysfunction and portal hypertension, such as the following: 
•
Mental status changes (hepatic encephalopathy), Ankle edema and abdominal distention
(ascites), Hematemesis or melena (variceal bleeding)
Signs in patients with decompensated liver disease include the following: 
•
Hand signs: Palmar erythema, Dupuytren contracture, asterixis, leukonychia, clubbing
•
Head signs: Icteric sclera, temporal muscle wasting, enlarged parotid gland, cyanosis
•
Fetor hepaticus, Gynecomastia, small testes
•
Abdominal signs: Paraumbilical hernia, ascites, caput medusae, hepatosplenomegaly,
abdominal bruit, Ankle edema, Scant body hair, Skin signs: Spider nevi, petechiae,
excoriations due to pruritus
Other common extrahepatic manifestations include the following: 
•
Cryoglobulinemia, Membranoproliferative glomerulonephritis, Idiopathic thrombocytopenic
purpura, Lichen planus, Keratoconjunctivitis sicca, Raynaud syndrome, Sjögren syndrome
•
Porphyria cutanea tarda, Necrotizing cutaneous vasculitis
Note 
•
Mother's HBsAg status unknown: 0.5 mL IM within 12 hour of birth AND HBIG 0.5ml(IM); if
newborn wt <2 kg, determine mother's HBsAg status as soon as possible and, if she is
HBsAg-positive, also administer HBIG for infants weighing 2 kg or more (no later than age
1 week)
Note:  
•
HBIG and HBV Vaccine should be given at different intramuscular sites PEP should be
given in <24hours, may not be effective after 72hours of exposure.

207!
Investigations   
General baseline studies in patients with suspected HCV include the following: 
•
FBP, LFT, RFT TSH, T3
•
Screening tests for coinfection with HIV or HBV
•
Screening for alcohol abuse, drug abuse, or depression
•
Pregnancy testing
Tests for detecting HCV infection include the following: 
•
Hepatitis C antibody testing:
•
Qualitative and quantitative assays for HCV RNA PCR
•
HCV genotyping
•
Serologic testing (essential mixed cryoglobulinemia is a common finding)
Treatment 
Use pangenotypic drugs which are efficacious, safe and cost-effective. 
Who to treat 
•
Confirmed cases of Hepatitis C irrespective of clinical stage of the liver disease
•
Patients with HCC who are eligible for liver transplant if feasible.
•
Liver transplant patients if MELD score is < 18 (pre transplant) or >18 (post-transplant)
Who not to treat 
•
HCC patients who are not eligible for liver transplant.
•
Patient with limited life expectancy due to ESLD (by MELD score or Child-Pugh), or non-
hepatic related comorbidities.
Pharmacological Treatment 
All individuals diagnosed with HCV infection who are ≥ 12 years old are eligible for treatment 
children (<12 years old), the treatment should be deferred until they reach that age. 
S: ledipasvir (PO) 90mg 24hourly for 12-24weeks 
AND  
S: sofosbuvir (PO) 400mg 24hourly for 12-24weeks 
AND 
S: ribavirin (PO) given in two divided doses *<75kg of Body weight =1g/day; >75Kg of 
Body weight =1.2g/day for 12weeks (in treatment naive patients) OR for 24 weeks (in 
treatment experienced patients) for genotypes 1, 4, 5 & 6. 
OR 
S: sofosbuvir (PO) 400mg daily AND ledipasvir (PO) 90mg daily AND ribavirin if a patient 
has been previously exposed to other antivirals.       
Note 
•
Due to complexity and variability of HCV management, care and treatment should be done
at the tertiary level facility
•
Ribavirin is contraindicated in patients with anaemia (HB<8.5g/dL), and the dose should be
reduced if HB <10g/dL
Sofosbuvir is contraindicated if eGFR < 30ml/min/1.73m2 
When to stop medications 
•
Ribavirin regimen should be stopped if patients’ HB drops to < 8.5g/dl during follow up
schedules.
•
If there’s adverse drug reaction
•
When there are ALT flares or massively increased ALT (>10 X UNL)
•
If there’s evidence of drug to drug interactions- consider switching with medication with a
less interacting potential

208!
Clinical monitoring and follow up 
•
Assess treatment adherence, tolerance and toxicity at 4 weeks after treatment initiation.
•
Treatment toxicity
•
Stop Ribavirin if HB drops to <8.5
•
Stop all DAAs if ALT >10 X ULN and other causes have been ruled out
•
Stop Sofosbuvir if eGFR drops to < 30ml/min/1.73m2
10.4.2.4 Hepatitis D Virus 
Hepatitis D virus (HDV) is a defective RNA virus belonging to genus of delta virus that requires the 
helper function of Hepatitis B (HBV) for virion assembly, release and transmission, and therefore the 
infection does not occur in the absence of hepatitis B virus. The routes of HDV transmission are 
similar for HBV the most important being sexually, percutaneous or   parenteral exposure to blood or 
blood products. 
Investigations 
Serology assays for HDV immunoglobulin titres for IgM and IgG are diagnostic for acute and post 
exposure/chronic infections respectively. Real time PCR for HDV RNA is confirmatory. 
Treatment 
There is no specific treatment for acute or chronic HDV infection. 
Note 
The more risk population includes health care workers, transfusion recipients and haemophiliacs, 
PWID, and immigrants of endemic areas.  Nucleotide sequences of HDV obtained worldwide 
indicates the existence of eight genotypes, with genotype 1 being detected worldwide.  HDV 
Antiviral nucleotide analogues for HBV have no or limited effect on HDV replication and Pegylated 
interferon alpha is the only drug effective against HDV now and more than one year of therapy may 
be necessary as most of patients relapses after discontinuation of therapy. 
10.4.2.5 Hepatitis E Virus 
Hepatitis E virus (HEV) belongs is a RNA virus belonging from a family Hepadna viridae under 
Genus Hepevirus and acute liver infection. The virus has at least 4 different types: genotypes 1, 2, 3 
and 4. Genotypes 1 and 2 have been found only in humans. Genotype 3 and 4 viruses circulate in 
several animals (including pigs, wild boars, and deer) without causing any disease, and occasionally 
infect humans.  
Clinical presentation 
Prodromal-phase symptoms include the following: 
•
Myalgia, Arthralgia, Fever with mild temperature elevations
•
Anorexia, Nausea/vomiting, Weight loss. Dehydration, Right upper quadrant pain
Icteric-phase symptoms may last days to several weeks and include the following: 
• 
Jaundice, Dark urine, Light-colored stool, Pruritus
Other features include the following
•
Malaise (most common), Arthritis, Pancreatitis
•
Aplastic anemia, Thrombocytopenia
•
Neurologic symptoms of polyradiculopathy, Guillain–Barré syndrome, Bell palsy, peripheral
neuropathy, ataxia, and mental confusion
•
Membranoproliferative glomerulonephritis and membranous glomerulonephritis
Investigations 
Serology assays for HEV immunoglobulin titres for IgM and IgG are diagnostic for acute and post 
exposure/chronic infections respectively. Real time PCR for HEV RNA in serum and particularly in 
stool is confirmatory. 

209!
Treatment 
There is no specific treatment for cure or reversing the course of acute hepatitis E. The disease is 
usually self-limiting; hospitalization is generally not required except for patients with fulminant 
hepatitis or for symptomatic pregnant women where severity of infection is usually high and 
associated with high rates of fetal loss and mortality especially in third trimester. 
Note 
•
The virus is shed in the stools of infected persons and enters the human body through the
intestine. It is transmitted mainly through contaminated drinking water. Usually the infection
is self-limiting and resolves within 2–6 weeks. Rarely the infection can lead to fulminant
hepatitis with acute liver failure.
•
The virus causes sporadic cases and major epidemics of viral hepatitis and occurs in
resource poor population with unhygienic conditions and through ingestion of
contaminated water and food.
10.4.2 Portal Hypertension 
This is high blood pressure in the hepatic portal system which includes the portal veins and its 
branches which drains from most of the intestines to the liver. It is indicated when the hepatic 
venous pressure gradient exceeds 7mmHg, while liver cirrhosis remains the most common cause 
which in our local setting is commonly caused by chronic viral hepatitis followed by heavy alcohol 
intake. 
Clinical presentation 
•
Ascites, Splenomegaly
•
Esophageal varices, and hematemesis
•
Swollen veins of the anterior abdomen (caput medusa) and hemorrhoids
Investigations 
•
Radiological evidence of shrunken liver, with typical features of cirrhosis.
10.4.2.1 Ascites  
Ascites is the pathologic accumulation of fluid in the peritoneal cavity, and its most common cause is 
cirrhosis. 
Pharmacological Treatment 
C: spironolactone (PO) 50mg – 400mg 24hourly incrementally till ascites resolves 
OR  
S: eplerenone (PO) 50mg 24hourly 
AND 
B: furosemide (PO) 40mg–160 mg 24hourly or in divided doses incrementally till ascites 
resolves 
AND 
A: propranolol (PO) 40mg–160mg 12hourly daily incrementally target heart rate 55-60bpm. 
OR 
C: carvedilol (PO) 6.25mg 24hourly, increase to 6.25mg (PO) 12hourly unless persistent 
arterial hypertension, SBP should not decrease <90mmHg.   
AND 
S: albumin 25% (IV) – in refractory ascites and large volume paracentesis. Give 25g stat, 
repeat at 15–30min Interval at Max Dose of 250g/48hourly  
Note 
•
Consider discounting βB if SBP <90 or MAP ≤82 mmHg, serum Na <120 mEq/L, AKI,
HRS, SBP, sepsis, severe alcoholic hepatitis, poor follow-up.
•
Large-volume paracenteses (LVP; >5 L fluid removal): give 6–8g albumin per L fluid
removed (above 5 L) as colloid replacement is associated with decreased risk of post-
paracentesis circulatory dysfunction and possibly decreased mortality.

210!
10.4.2.2 Spontaneous Bacterial Peritonitis  
Spontaneous bacterial peritonitis is an acute bacterial infection of ascitic fluid in the absence of a 
contagious cause of infection (e.g., intestinal perforation or abscess) 
Clinical presentation 
•
Fever and chills
•
Abdominal pain or discomfort
•
Worsening or unexplained
encephalopathy
•
Diarrhea
•
Ascites that does not improve
following administration of diuretic
medication
•
Worsening or new-onset renal
failure
•
Ileus
Investigations  
Diagnosis of Spontaneous bacterial peritonitis is based on the demonstration of an absolute number 
of polymorphonuclear cells in ascitic fluid equal to or greater than 250/mm3
Pharmacological treatment 
Community Acquired Spontaneous bacterial peritonitis 
B: ceftriaxone (IV) 1g 12-24 hourly for 5- 10days 
OR 
B: amoxicillin-clavulanic acid (FDC) (IV) 1-2g 6-8hours for 5-10days 
OR 
C: ciprofloxacin (IV) 200mg 12hourly for 5–10days 
AND  
S: administration of albumin dose is 1.5 g/kg on day 1 and 1 g/kg on day 3 
Nosocomial Spontaneous bacterial peritonitis Treatment 
S: meropenem (IV) 1gm 8hourly for 5-7days 
Spontaneous bacterial peritonitis prophylaxis 
Prophylaxis should be continuous until the disappearance of ascites (i.e., patients with alcoholic 
hepatitis), death, or transplant. 
A: ciprofloxacin (PO) 400mg 24hourly for 10-14days 
OR  
A: co-trimoxazole (PO) 960mg 24hourly for 10-14days 
10.4.2.3 Bleeding Esophageal Varices 
Esophageal varices are collateral veins within the wall of the esophagus that project directly into the 
lumen. Acute variceal bleeding is a fatal complication in patients with liver cirrhosis. In patients with 
decompensated liver cirrhosis accompanied by ascites or hepatic encephalopathy, acute variceal 
bleeding is associated with a high mortality rate. 
Pharmacological Treatment 
S: octreotide (SC) 50–100µg 8hourly for 3days (infusion 50µg/hour for 72hours up to 
5days) 
OR  
S: terlipressin: Adult (body weight up to 50 kg): Initially 2 mg every 4 hours until bleeding 
controlled, then reduced to 1 mg every 4 hours if required, maximum duration 48 hours. 
Adult (body weight 50 kg and above): Initially 2 mg every 4 hours until bleeding controlled, 
reduced if not tolerated to 1 mg every 4 hours, maximum duration 48 hours 
AND 
Band ligation of beeding esophageal varices (EVL); 3 – 6 shoots per session. 
OR 
Sclerotherapy (Histo Acryl Glue Inj. 5 %;( mixed with Lipiodol at a ratio 1:1) Ethanolamine oleate 
5%); given 2 -5ml per varix up to 20ml per session. 

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AND 
B: ceftriaxone (IV) 1g 24hourly for 7days 
Note  
Blood transfusion (PRBC, PLT concentrates and FFP) when required. 
10.4.2.4 Hepatic Encephalopathy (HE) 
Hepatic encephalopathy (HE) is defined as “a condition which reflects a spectrum of 
neuropsychiatric abnormalities seen in patients with liver dysfunction after exclusion of other known 
brain disease.” 
Clinical presentation 
Stage 
Symptoms 
I 
Mild confusion, agitation, irritability, sleep disturbance, decreased attention 
II 
Lethargy, disorientation, inappropriate behavior, drowsiness 
III 
Somnolent but arousable, slurred speech, confused, aggressive 
IV 
Coma 
Pharmacological Treatment 
S: L-Ornithine L-Aspartate (IV) 10g 8hourly daily for 3-5days 
THEN 
S: L-Ornithine L-Aspartate (PO) 9g 24hourly in divided doses for 4–12weeks 
AND 
C: lactulose solution (PO) for bowel cleansing when required 
Episode of HE (grade 2 or higher)—enemas: 
A: 0.9% sodium chloride 300mL in 1000mL water 2hourly until there is clinical 
improvement 
Episode of HE (able to tolerate oral administration)—(PO): 45mL every hour until there is bowel 
movement and clinical improvement 
Outpatient therapy: 15-45mL 8-12hourly until there are 2-3 bowel movements per day 
AND 
A: metronidazole (PO) 400mg 8 hourly for 7days 
AND  
B: ceftriaxone (IV) 1g 12 hourly for 7days (if evidence of spontaneous bacterial peritonitis) 
Fluid deficit correction and electrolytes replacements as appropriate (screen for and correct all 
precipitants of HE as shown in the table below). 
Table 10.2: Precipitants of HE 
Hyponatremia 
Vomiting 
Gastrointestinal bleeding 
Diarrhea 
Infection 
Sedative drugs (narcotics, sleep aids, 
antihistaminics) 
Surgery 
Alkalosis 
Dehydration 
Azotemia 
Fluid restriction 
Hypokalemia 
Diuretics 
Excessive protein intake 
Excessive paracentesis 
Constipation 
10.4.2.5 Hepatorenal Syndrome  
Hepatorenal syndrome (HRS) is the development of renal failure in patients with advanced chronic 
liver disease and, occasionally, fulminant hepatitis, who have portal hypertension and ascites. 

212!
Table 10.3: Pharmacological treatment 
Vasoconstrictor 
Recommended Dosage 
S: terlipressin 
OR 
Bolus 
Initially 0.5 mg (IV) 4-6hourly. If no response by day 
3 can increase the dosage to 1mg 4-6hourly. 
Maximum dosage is 2mg 4-6hourly. Maximum 
duration 14days. 
Continuous 
infusion 
Initially 2mg/day. If no response by Day 3, can 
increase the dosage to 4mg/day. Maximum dosage 
is 12mg/day. Maximum duration 14days. 
S: norepinephrine 
Continuous 
infusion 
0.5-3mg/hour continuously to achieve an increase in 
mean arterial pressure of 10 mmHg. Treatment is to 
be continued until serum creatinine concentration is 
< 1.5mg/dL, or < 133µmol/L. 
S: Albumin must be given concomitantly with any of the vasoconstrictors at a dosage of 20-40 
g/day. 
10.4.3 Biliary Tract Diseases 
Cholestasis is a pathologic state of reduced bile formation or flow which can be hepatocellular 
(Intrahepatic), where an impairment of bile formation occurs or ductular (extra hepatic), where 
impedance to bile flow occurs after it is formed. Intrahepatic causes of cholestasis include viral 
hepatitis, alcohol, primary biliary cirrhosis, drug toxicity, Hodgkin’s lymphoma and pregnancy. 
Extrahepatic causes include choledocholithiasis, carcinoma, and ascariasis of the biliary tree.  
Clinical presentation 
•
Jaundice,
•
Dark urine,
•
Pale stools, and
•
Generalized body itching/pruritis.
Investigations 
•
Laboratory evidence of elevated serum levels of total bilirubin, direct bilirubin, alkaline
phosphatase, gamma-glutamyl transferase, and transaminases. WITH
•
Supporting radiological evidence of dilated intra or extra hepatic biliary radicles.
Pharmacological Treatment  
Definitive treatment:  
Identify and treat specific cause 
Supportive treatment: 
S: cholestyramine (PO) 4–16g/day 
OR 
S: ursodeoxycholic acid (PO) 20–30 mg/kg/day 
Note 
•
Surgical intervention is indicated for extra hepatic cholestasis.
10.4.3.1 Cholelithiasis 
Cholelithiasis involves the presence of gallstones which are concretions that form in the biliary tract, 
usually in the gallbladder. Choledocholithiasis refers to the presence of one or more gallstones in 
the common bile duct (CBD). Treatment of gallstones depends on the stage of disease. 
Clinical presentation 
•
Asymptomatic in majority of patients.
•
Biliary pain (episodic RUQ or epigastric pain), pain radiating to scapula;
•
Pain precipitated by fatty foods; nausea

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•
Physical exam: afebrile, and/or RUQ tenderness or epigastric pain
•
Nonspecific symptoms (eg, indigestion, dyspepsia, belching, or bloating)
Investigations 
•
Full Blood count
•
Liver function panel
•
Pancreatic enzymes (Amylase, Lipase)
•
Abdominal radiography (upright and supine) – to exclude other causes of abdominal pain
•
Ultrasonography
•
CT scan –superior for demonstrating stones in the distal CBD
•
MRI with MRCP
•
Scintigraphy (HIDA) scans
•
Endoscopic retrograde cholangiopancreatography (ERCP)
•
Percutaneous transhepatic cholangiography (PTC)
Complications 
•
Cholecystitis
•
Choledocholithiasis leading to cholangitis or gallstone pancreatitis
•
Mirizzi syndrome
•
Cholecystenteric fistula stone erodes through gallbladder into bowel
•
Gallstone ileus: SBO (usually at term ileum) due to stone in intestine that passed through
fistula
•
Gallbladder carcinoma
Non-pharmacological Treatment 
•
Asymptomatic gallstones – Expectant management
•
Symptomatic gallstones – definitive surgical intervention (cholecystectomy)
Pharmacological Treatment 
A: paracetamol (PO) 1g 8hourly for 5days 
OR   
A: ibuprofen (PO) 400mg 4-6hourly for 3-5days 
OR 
B:  tramadol (PO) 50mg 12hourly for 3-5days 
AND 
S: ursodeoxycholic acid 8-10mg/kg/day divided once to three times up to 6months 
Note 
 Cholecystectomy (open or laparoscopic) for asymptomatic gallstones may be indicated in the 
following: 
•
Those with large (>2 cm) gallstones
•
Nonfunctional or calcified (porcelain) gallbladder on imaging studies and at high risk of
gallbladder carcinoma
•
Those with spinal cord injuries or sensory neuropathies affecting the abdomen
•
Sickle cell anemia patients- difficult to distinguish between painful crisis and cholecystitis
•
Cholecystectomy, 
Cholecystectomy, 
Endoscopic 
sphincterotomy, 
Extracorporeal
shockwave lithotripsy
10.4.3.2 Choledocholithiasis 
Gallstone lodged in common bile duct (CBD). Occurs in some of patients with gallbladder stones; 
can form de novo in CBD. 
Clinical presentation 
•
Asymptomatic
•
RUQ pain,
•
Epigastric pain due to obstruction
of bile flow which leads to increase
in CBD pressure,
•
Jaundice,
•
Pruritus,
•
Nausea.

214!
Investigations 
•
LFT,
•
Amylase
•
Lipase.
•
Abdominal (RUQ) Ultrasound
•
ERCP, if ERCP unavailable or
unsuccessful
EUS/MRCP
Non-pharmacological Treatment 
ERCP & papillotomy w/ stone extraction (± lithotripsy) 
Cholecystectomy typically within 6 weeks unless contraindication 
Pharmacological Treatment 
S: cholestyramine (PO) 4-8g 12hourly when required for itching. 
Complications 
Cholangitis, cholecystitis, pancreatitis, stricture 
10.4.3.3 Cholecystitis 
Cholecystitis is inflammation of the gallbladder that occurs most commonly because of an 
obstruction of the cystic duct by gallstones (stone impaction in cystic duct leads to inflammation 
behind obstruction causing GB swelling and secondary infection of biliary fluid).  
Acalculous cholecystitis: Occurs in critically ill. GB stasis and ischemia (without cholelithiasis) 
leading to necroinflammation. 
Clinical presentation 
•
RUQ/epigastric pain, radiating to right shoulder/back, nausea, vomiting, fever
•
Signs of peritoneal irritation may be present
•
Patients with acalculous cholecystitis may present with fever and sepsis alone
•
RUQ tenderness, Murphy’s sign, palpable gallbladder, jaundice
•
The absence of physical findings does not rule out the diagnosis of cholecystitis.
Investigations 
•
FBP, LFT, amylase, lipase
•
Ultrasonography RUQ ultrasound: high Sensitivity and specificity for stones but need
specific signs of cholecystitis: GB wall thickening >4 mm, pericholecystic fluid and a
sonographic Murphy’s sign
•
Radiography
•
Computed tomography (CT)
•
Magnetic resonance imaging (MRI)
•
Hepatobiliary scintigraphy (HIDA)
•
Endoscopic retrograde cholangiopancreatography (ERCP)

215!
!
Pharmacological Treatment  
In acute cholecystitis, the initial treatment includes bowel rest, IV hydration, and correction of 
electrolyte abnormalities 
 
A: paracetamol (PO) 1g 8hourly daily ORD: paracetamol (IV) 1g 8 hourly daily (for 
analgesia 
AND 
C: metoclopramide (IV/PO) 10mg 12hourly daily (for intractable vomiting) 
 
 
 
AND  
S: piperacillin + tazobactam FDC (IV) 4.5g 6-8 hourly 7-10 days (for severe/complicated 
cases) 
 
 
 
OR  
B: ceftriaxone (IV) 1-2gm 24hourly for 7-10days  
 
 
 
OR  
C: ciprofloxacin (IV) 200-400mg 12hourly for 7-10days  
AND 
B: metronidazole (IV) 500mg 8hourly for 7-10days  
 
In cases of uncomplicated cholecystitis, outpatient treatment may be appropriate.  
A: ciprofloxacin (PO) 500mg 12hourly for 7days  
AND  
A: metronidazole (PO) 400mg 12hourly for 7days  
 
Note 
• 
Laparoscopic cholecystectomy (standard of care for surgical treatment of cholecystitis) 
others include ERCP. 
• 
Endoscopic ultrasound-guided transmural cholecystostomy, Endoscopic gallbladder 
drainage.  
 
10.4.3.4 Cholangitis 
Bile duct (BD) obstruction leads to infection proximal to the obstruction, etiologies include BD stone, 
malignant (biliary, pancreatic) or benign stricture, infection with fluke (Clonorchis sinensis, 
Opisthorchis viverrini) 
 
Clinical presentations  
• 
Charcot’s triad: RUQ pains, jaundice, fever/chills; present in three quarter of patients 
• 
Reynolds’ pentad: Charcot’s triad + shock and altered mental status; present in 15% of 
patients 
 
Investigations  
• 
Ultrasound, RUQ USS often demonstrates dilation 
• 
FBP, LFT, amylase, lipase  
• 
Blood cultures 
• 
ERCP; percutaneous transhepatic cholangiogram if ERCP unsuccessful 
 
Pharmacologic Treatment 
B: ceftriaxone (IV) 1-2g 24hourly for 7-10days  
OR 
S: piperacillin+tazobactam FDC (IV) 4.5g 6-8hourly for 7-10days (for severe/complicated 
cases) 
OR  
S: meropenem (IV) 1g 8 hourly for 7-10days  
 
 
AND  
C: metronidazole (IV) 500mg 8hourly for 7-10days  
Alternatively 
C: ciprofloxacin (IV) 200-400mg 12hourly for 7-10days  
 
 
AND 
B: metronidazole (IV) 500mg 8hourly for 7-10days  

216!
Note 
•
About 80% respond to conservative treatment and antibiotics then, 20% require urgent
biliary decompression via ERCP (papillotomy, stone extraction and/or stent insertion)
•
If sphincterotomy cannot be performed (larger stones), decompression by biliary stent or
nasobiliary catheter can be done; otherwise, percutaneous trans hepatic biliary drainage or
surgery

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CHAPTER ELEVEN 
OBSTETRICS, GYNECOLOGY AND CONTRACEPTION 
11.1 Bleeding in Pregnancy 
Bleeding during pregnancy is common, especially during the first trimester. Bleeding can sometimes 
be a sign of something serious, therefore it is important to know the possible causes and take 
adequate measures.  
11.1.1 Abortion 
It is a spontaneous loss of a fetus before it is viable (has the potential to survive outside the womb). 
The World Health Organization (WHO) defines it as expulsion or extraction of an embryo or fetus 
weighing 500mg or less, approximately at or less than 24 weeks of gestation. In Tanzania abortion 
is defined as loss of pregnancy before 28 weeks of gestations. Clinical features will depend on the 
types of abortion.  
11.1.1.1 Threatened Abortion 
Clinical presentation 
•
Mild vaginal bleeding
•
Mild/no lower abdominal pain
•
Cervix is closed on digital examination
Investigation 
Check Hb level 
Management of threatened abortion in Dispensary & Health Centre 
•
Adequate bed rest at home
•
Avoid strenuous activities and sexual intercourse until all the symptoms have subsided
•
Schedule a follow up within 7 days
•
Tell the woman to come immediately if;
o
Bleeding becomes heavy
o
Experiences offensive discharge
o
Severe abdominal pain
Referral 
Refer to higher-level health facility with adequate expertise and diagnostics if: 
•
Bleeding recurs
•
Experiences fever
•
Experiences offensive discharge
•
Experience severe abdominal pain
In higher level health facilities: 
•
Take thorough history and perform investigations to establish the causes
•
Perform ultrasound to confirm pregnancy, gestational age, foetal viability and potential
causes of abortion.
•
Admit the patient and manage appropriately
•
Encourage bed rest
•
For unexplained recurrent miscarriage (3 consecutive abortions) or PRL due to luteal
phase defect manage with
Pharmacological Treatment 
S: dydrogesterone (PO) 40mg stat then 10mg 24hourly until the bleeding stops for 
threatening abortion 
OR 10mg 24hourly from conception up to 20weeks for luteal phase defect. 
11.1.1. 2 Inevitable Abortion 
Abortion is said to be inevitable when it is not possible for the pregnancy to continue and the cervix 
is dilated, but all the products of conception are in situ. 
Clinical presentation 
•
Moderate or severe per vaginal bleeding
•
Moderate or severe lower abdominal pain

218!
•
Membranes may be intact or ruptured with leakage of
•
The uterine fundal height may correspond with gestational age
•
The cervix is dilated
Management of inevitable abortion in Dispensary & Health Centre (B-EMONC facilities) 
•
Apply Airway, Breathing, Circulation and Dehydration (ABCD) principles of resuscitation
A: compound sodium lactate (IV) OR 0.9% sodium chloride (IV) depending of amount of blood 
loss. 
•
Perform Manual Vacuum Aspiration (MVA) if gestation age is below 12 weeks
Augment the process by administering A: oxytocin 20 IU in 500mls RL/NS at 40–60
drops/minute if gestation age is above 12 weeks
•
Manage as incomplete abortion if after augmentation some products of conception remain
in the uterus
•
Manage as complete abortion if all products of conception are expelled
Referral: Refer to hospital if MVA is not possible and/or bleeding is persisting or severe to 
necessitate blood transfusion. 
Management of inevitable Abortion in the Hospital 
•
Apply Airway, Breathing, Circulation and Dehydration principles of resuscitation
•
Obtain blood samples for Hb, grouping and cross–matching
•
Give compound sodium lactate (IV)OR 0.9% sodium chloride aim at replacing 3 times the
amount of estimated blood loss.
•
Give blood transfusion if indicated
•
Perform Manual Vacuum Aspiration (MVA) if gestation age is below 12 weeks
•
Augment the process by administering oxytocin 20IU in 500mls RL/NS at 40–60
drops/minute if gestation age is above 12 weeks
•
Manage as incomplete abortion if after augmentation some products of conception remain
in the uterus
•
Manage as complete abortion if all products of conception are expelled
11.1.1.3 Incomplete Abortion 
Abortion is said to be incomplete when after expulsion some of the products of conception get 
retained in the uterine cavity. 
Clinical presentation 
•
Severe Cramping lower abdominal pain
•
moderate to severe PV bleeding
•
Fundus smaller than dates
•
The cervix is dilated and products of conception may be felt on or through the cervix on
digital examination
Management of incomplete abortion in dispensary & health centre (B-EMONC facilities) 
•
Apply Airway, Breathing, Circulation and Dehydration principles of resuscitation
•
Check hemoglobin level
A: compound sodium lactate (IV) OR 0.9% sodium chloride depending on amount of blood
loss
•
If feasible Perform digital evacuation of products of conception to miminize the PV bleeding
•
Perform MVA if gestation age is below 12 weeks
Pharmacological treatment in place 
In place where uterine evacuation is accessible give; 
A: oxytocin (IM) 10 IU 
OR 
A: misoprostol (sublingual) 600µg 
After evacuation give: 
A: erythromycin (PO) 500mg 8hourly for 5days 

219!
OR 
B: amoxicillin + clavulanic acid (FDC) (PO) 625mg 8 hourly for 5days 
AND 
A: metronidazole (PO) 400mg 8hourly for 5days 
AND 
A: paracetamol (PO) 1g 8hourly for 5 days 
Referral: Resuscitate the patient and to hospital level with an escort of a nurse if bleeding continues 
Management in a Hospital 
•
If patient is in shock, shout for help, mobilize resources
•
Apply ABCD principles of resuscitation
•
Obtain blood for HB, grouping and cross–matching
•
Blood transfusion if indicated
•
Give compound sodium lactate (IV) OR 0.9% sodium chloride aim at replacing 3times the
amount of estimated blood loss
•
Digital evacuation of products of conception if feasible to minimize the PV bleeding
•
MVA if gestation age is below 12 weeks
•
Evacuate uterus in theatre with sharp curette under general anesthesia if pregnancy was
more than 12 weeks
Pharmacological Treatment 
After evacuation give: 
A: erythomycin (PO) 500mg 8hourly for 5days 
OR 
B: amoxicillin + clavulanic acid (FDC) (PO) 625mg 8hourly for 5 days 
AND 
A: metronidazole (PO) 400mg 8hourly for 5 days 
AND 
A: paracetamol (PO) 1g 8hourly for 5days. 
AND 
A: ferrous sulfate + folic acid (FDC) (PO) 1 tab 24hourly for 4 weeks 
Patient education. 
•
Counsel and educate the patient on possible reasons for abortion and future fertility
•
Provide family planning counseling and give appropriate contraceptive method before the
patient leaves the facility premises.
•
Provide linkage to other reproductive and non reproductive health services depending on
patient needs
11.1.1.4 Complete Abortion 
Abortion is said to be complete when the Products of conception are completely expelled 
Clinical presentation 
•
Minimal or no PV bleeding
•
Uterus smaller than dates and often well contracted.
•
Cervix may or may not be closed
•
The patient may be in Shock due to severe bleeding
Pharmacological Treatment 
A: erythromycin (PO) 500mg 8hourly for 5days 
OR 
B: amoxicillin + clavulanic acid (FDC) (PO) 625mg 8hourly for 5days 
AND 
A: metronidazole (PO) 400mg 8hourly for 5days 
AND 
A: ferrous sulfate + folic acid (FDC) (PO) 1 tablet 24hourly for 4weeks 
If patient is in shock; 
•
Shout for help and mobilize resources
•
Apply ABCD principles of resuscitation

220!
!
• 
Give compound sodium lactate (IV) OR 0.9%sodium chloride (IV) 3litres or more in the first 
hour  
• 
Insert an indwelling urethral catheter  
• 
Give ampicillin (IV) 1g and metronidazole (IV) 500mg stat  
• 
Obtain blood for HB, 
 
Referral: Resuscitate the patient and referto hospital with an escort of a nurse 
 
Management in a hospital  
• 
If patient is stable continue as above; 
• 
If patient is in shock, perform as above and give blood transfusion if indicated  
 
Patient Education 
Provide counseling, education and FP services as in incomplete abortion above 
 
11.1.1.5 Septic Abortion 
Abortion is said to be septic when It is complicated by infections. 
Clinical presentation 
• 
Moderate to severe Abdominal pain following abortion  
• 
Fever may be present  
• 
Foul smelling PV discharge which may be mixed with blood. 
• 
May be in shock  
• 
Tender uterus with or without rebound tenderness  
• 
Cervix is usually open  
 
Management of septic abortion in dispensary & health centre 
• 
Apply ABCD principles of resuscitation  
• 
Give compound sodium lactate (IV) OR sodium chloride (IV) 0.9% in case of hypotension 
or shock. Avoid IV fluid in case of chronic anaemia. 
• 
Insert an indwelling urethral catheter  
• 
Obtain blood for Hb or FBC 
• 
Perform Ultrasound if feasible 
 
Pharmacological Treatment 
 
C: amoxycillin + clavulanic acid (FDC) (IV) 1.2g 8hourly for 24-48hours 
 
 
 
AND  
 
 
      B: metronidazole (IV) 500mg 8hourly for 24–48hours 
 
 
Referral: Resuscitate and immediatelyrefer the patient to hospital with an escort of a nurse.  
 
Management in the Hospital: 
• 
Full Blood Count (FBC) 
• 
Draw Blood for culture and susceptibility testing 
• 
Check abdominal pelvic ultrasound as appropriate 
• 
IV RL/NS depending on individual patient needs 
• 
Give blood transfusion if indicated  
• 
Evacuate the uterus with sharp wide curette under general anesthesia 
 
Pharmacological Treatment 
Treat as above and when the patient is stable continue with;  
 
  
B: amoxicillin+ clavulanic acid (FDC) (PO) 625mg 8hourly for 7days  
 
  
A: metronidazole (PO) 400mg 8hourly for 7days  
 
If no response with the above antibiotics within 3 days; adjust according to culture and sensitivity 
results or switch to  
 
  
D: ceftriaxone + sulbactam (FDC) (IV) 1.5g 12hourly for 5days  
 
  
 
AND 
 
  
B: metronidazole 500mg (IV) 8hourly for 5days 
 
AND 
A: ferrous sulfate +folic acid (FDC) (PO) 1tablet daily for 4weeks then reassess. 

221!
Patient Education 
•
Counsel educate and provide appropriate contraceptive method.
11.1.1.6 Molar Pregnancy 
A molar pregnancy is a gestational trophoblastic disease which grows into a mass in the uterus that 
has swollen chorionic villi. These villi grow in clusters that resemble bunches of grapes. Once 
diagnosed it should be treated right away. 
Clinical presentation 
•
Vaginal bleeding
•
Uterus that is bigger than gestational age.
•
Exaggerated pregnancy symptoms (Severe nausea and vomiting)
•
Vaginal discharge of tissue that resemble grapes
•
Heavy PV bleeding when the mole abort spontaneously
Management of Molar pregnancy at the dispensary and Health centers 
•
Apply Airway, Breathing, Circulation and Dehydration principles of resuscitation
•
Check hemoglobin level
•
If the patient is actively bleeding, catheterize, Establish Iv line and Give IV RL/NS 2lts at a
rapid rate
Referral: Resuscitate and refer the patient to higher level facility with a nurse escort for appropriate 
management 
Management of molar pregnancy at the Hospital 
•
Apply Airway, Breathing, Circulation and Dehydration principles of resuscitation
•
If the patient is patient is actively bleeding or in shock shout for help and mobilize
resources
•
Cheek HB, Blood grouping and Cross matching
•
Perform quantitative serum Beta Human Chorionic Gonadotropin (bHCG)
•
Check abdominal pelvic Ultrasound to confirm the diagnosis (Snowstorm appearance)
•
Infuse compound sodium lactate (IV) OR 0.9% sodium chloride (IV) as needed
•
Initiate blood transfusion if indicated
•
Perform suction curettage in operating theatre
•
Perform other investigations as appropriate (chest X ray, RFT, LFT, Chemistry panel)
Follow up for Molar pregnancy after Molar Evacuation 
•
Check weekly bHCG until when it becomes normal(5-10mIU/ml) for 3 weeks consecutively
•
Then check monthly bHCG and pelvic ultrasound for 12 months
•
Advice the patient to use effective contraception during follow up (preferably COCs)
11.1.1.7 Missed Abortion 
This happens when a Fetus less than 24weeks die in utero, but it’s not expelled out 
Clinical presentation 
•
History of amenorrhea
•
Regression of the pregnancy symptoms
•
Uterine size smaller than dates
•
Mild of no PV bleeding
Management of a missed abortion at the dispensary and Health center 
Referral: Referto higher level health facility with adequate expertise and diagnostics/equipment 
Management of missed abortion at the hospital 
Investigations 
•
Abdominal pelvic ultrasound
•
Full blood count, Blood Grouping and cross matching
•
Clotting indices (PT, APTT, INR)

222!
Pharmacological Treatment 
Induce abortion with misoprostol if it is more than 12 weeks 
 
A: misoprostol (PV) 100mcg 8hourly to max. 400mcg followed by sharp curettage in case of 
incomplete abortion 
Evacuate by Dilatation and Curettage (D&C) if the GA is less than 12weeks  
Note 
Avoid misoprostol in case of previous uterine scar 
After evacuation give 
A: metronidazole (PO) 400mg 8 hourly for 7days 
AND 
B: amoxicillin+ clavulanic acid (FDC) (PO) 625mg 8hourly for 7days 
Patient education. 
Counsel and provide appropriate contraception. 
11.2 Ectopic Pregnancy 
Ectopic pregnancy (EP) is defined as a pregnancy in which the implantation of the embryo occurs 
outside the uterine cavity, most frequently in one of the two fallopian tubes or, rarely, in the 
abdominal cavity. 
11.2.1 Un-ruptured Ectopic Pregnancy 
Clinical presentation 
•
History of amenorrhea
•
PV Sport bleeding in early pregnancy
•
Unilateral Abdominopelvic pain. Unilateral(localized) abdominal tenderness
Management of Un-ruptured ectopic pregnancy 
Referral: Patients should be referred to higher level facilities with equipment and expertise 
•
At higher level facilities un-ruptured EP may be managed surgically or pharmacologically
depending GA and available expertise
Pharmacological Treatment 
S: methotrexate (IV) 50mg/M2 single dose 
OR 
S: methotrexate 2.5mg (PO) 24hourly for 5days (in case IV methotrexate is not available) 
Perform weekly pelvic ultrasound to ensure regression of Gestation sac 
Note 
Contraindications of methotrexate include a ruptured ectopic, ectopic mass greater than 3.5 cm, fetal 
cardiac activity, high level hCG value (10,000 IU), breastfeeding and immunodeficiency 
11.2.2 Ruptured Ectopic Pregnancy 
Clinical presentation  
•
History of amenorrhea
•
Acute generalized abdominal-pelvic pain
•
Hypotension
•
Fast and weak pulse
•
Abdominal distension and tenderness with rebound tenderness
Management of ruptured ectopic at the dispensary and Health Center (B-MONC facilities) 
•
Apply ABCD principles of resuscitation
•
Perform abdominal pelvic ultrasound if available
•
Check Hb
•
Start compound sodium lactate (IV) OR 0.9% sodium chloride (IV) infuse at a rate of
500mls per hour

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Referral:  Ectopic pregnancy is an obstetric emergency, resuscitate and refer the patient 
immediately, with an escort by skilled attendant. 
Management of Ectopic pregnancy at the Hospital (C-EMONC facilities) 
•
Perform abdominal pelvic/Transvaginal ultrasonography
•
Hb level
•
Grouping and cross-matching
•
compound sodium lactate (IV) OR 0.9% sodium chloride (IV) depending on amount of blood
loss
•
Blood transfusion if indicated depending on the blood loss
•
Perform Emergency laparotomy
11.3 Antepartum Hemorrhage 
It is the bleeding from the birth canal after the 28th week of gestation but before the onset of labour. 
The main forms are placenta praevia and abruption placenta. Other rare cause may include VASA 
previa, heavy show and gynecological malignancies (cervical cancer) 
11.3.1 Placenta Praevia 
•
It is an obstetric complication in which the placenta embeds itself partially or wholly in the
lower segment of the uterus. It is an obstetric emergency which should be managed in a
facility offering CEMONC services
Clinical presentation 
•
Sudden onset of bright red fresh painless bleeding after 28weeks of gestation
Management 
•
If partial PP and asymptomatic – Bed rest at home and follow up every 2weeks
•
If complete placenta praevia
o
Admit for close monitoring and observation
o
Perform ultrasound to localize the placenta
o
Perform FBP, Coagulation tests, Blood grouping and cross matching.  Keep at least 2
units of blood ready in the bank for transfusion in case of acute bleeding
o
Consider Blood transfusion if indicated
o
Avoid vaginal digital examination
o
If ˃34weeks and no PV bleeding or contraction, expectant management
o
Deliver by Cesarean section preferably at 37–38 weeks of gestation
o
Deliver by caesarean section by C/S any time incase of onset of labour or severe Pv
bleedingc
o
Partial or marginal placenta praevia: Carefully perform amniotomy for vaginal delivery
if the head is engaged.
Pharmacological management 
 
D:  dexamethasone (PO) 6mg 12hourly for 48 hours if pregnancy is ˂34weeks for fetal lung 
maturation 
B:  nifedipine (PO) 20mg 8hourly until labour symptoms subside 
11.3.2. Placental Abruption 
It is PV bleeding due to premature separation of a normally situated placenta in pregnancy after 28 
weeks of gestation.  
Clinical presentation 
•
Vaginal bleeding of dark colored blood or clots. Sometimes bleeding can be concealed
•
Abdominal pain is moderate to severe but may be absent in revealed AP
•
The uterus may be enlarged and very tender
•
Fetal demise or fetal distress may be present
Management of Abruptio Placenta at Dispensary and Health centre. 
•
Apply the ABCD principles of resuscitation

224!
•
Insert large bore cannula IV line, start rapid infusion with RL/NS
•
Insert Urethral catheter
Refer: resuscitate and referimmediately to the hospital with an escort of a skilled health attendant 
Management of Abruption Placenta at the hospital 
Investigations  
•
Ultrasound: Fetal wellbeing, placenta localization and evidence of retro placental clot
•
Full blood count and cross–match
•
Renal function test, Liver function test and electrolytes
•
Fibrinogen tests if available, D-dimer, PT, PTT, INR
Note 
The diagnosis of placental abruption is mainly clinical 
Maternal resuscitation 
•
Apply the ABCD principles of resuscitation
•
Insert two (2) large bore IV lines and give Normal Saline/Ringers Lactate. Replete
crystalloids at ratio of 1 unit of blood loss: 3 unit of crystalloids
•
Blood Transfusion is usually necessary
•
Give oxygen supplementation at a flow of 6L/min
•
Insert a urinary catheter to monitor input/output
•
If Disseminated Intravascular Coagulation: Give fresh frozen Plasma 1 Unit/hour, give
whole blood 2–4 units
•
Monitor blood pressure, pulse, bleeding, hourly, full blood count, clotting profile every 2
hours
Obstetrical Management 
•
If the foetus is alive and viable: emergency Caesarean section
•
If the foetus is dead: Normal vaginal delivery is preferable if no contraindication for vaginal
delivery (eg uterine scar)
•
Perform artificial rupture of membrane,
If no spontaneous labour: induce with Oxytocin infusion 5IU in 500 ml NS beginning with 10
drops/min increase the rate after every 20min until optimal contractions are achieved.
•
Do active management of third stage of labour and uterine massage
•
Emergency Caesarean section should be considered if:
o
Worsening of maternal condition
o
Failure/Non progressing vaginal delivery
Prophylactic antibiotics 
C: amoxycillin + clavulinic acid (FDC) (IV) 1.2gstat 
AND  
B: metronidazole (IV) 500mg stat. 
11.4 Obstructed Labour 
Also known as labour dystocia, is when despite adequate uterine contractions the baby does not exit 
the pelvis during due to being physically blocked. Obstructed may commonly be caused by; big 
baby, narrow maternal pelvis, malpresentation and malpositions. 
Clinical presentations 
•
Prolonged 
labour 
(˃8hours 
of
active labour)
•
Delayed second stage of labour
(˃1hour)
•
Fetal distress
•
Severe moulding (3+)
•
Severe caput succedaneum
•
Maternal dehydration (neglected
obstructed labour)
•
Bundl’s ring (sign of neglected
obstructed labour)
Management of obstructed labour at B-EMONC facilities 
•
Insert IV line with and start RL/ DNS infusion 2L
•
Insert urethral catheter
•
Check Hb

225!
!
• 
Encourage the patient to lay in left lateral position 
Management of Obstructed labour at the C-EMONC facilities 
• 
Optimize hydration by RL/NS 2lt before caesarean section 
• 
Ensure the patient is catheterized,  
• 
Perform Hb estimation 
• 
Perform emergency caesarean section. 
Pharmacological treatment 
A: compound sodium lactate (IV)/sodium chloride (IV) 0.9%to ensure adequate hydration 
OR 
 
A: ampicillin (IV) 2g within 30m before CS, continue 2g 24hourly for 3days 
 
 
 
OR 
B: ceftriaxone (IV) 1g stat within 30min before CS, continue 1 g 24hourly for 3days 
 
 
OR 
C: amoxycillin + Clavulinic acid (FDC) (IV) 1.2g within 30min before CS, continue 1.2g 
8hourly for 3days 
 
 
AND 
B: metronidazole (IV) 500mg within 30min before CS, continue 500mg 8hourly for 3days.  
 
11.5 Postpartum Hemorrhage (PPH) 
It is abnormal uterine bleeding following delivery through 6 weeks (42 days). It is sub classified in to 
Primary and Secondary PPH 
 
Primary PPH 
It is typically loss of more than 500 ml of blood from the genital tract after vaginal delivery or more 
than 1000 ml after Caesarean section in the first 24 hours. OR it is any amount of blood loss after 
delivery that would result in to haemodynamic instability. 
 
Management of PPH at Dispensary and Health centre 
 
• 
Insert 2 large bore cannula IV line, start rapid infusion with compound sodium lactate or 
sodium chloride 
• 
Start oxytocin (IV) 20IU in 500mls NS at a rate for 20drops per minute 
• 
Ensure no retained placental tissues 
• 
Clamp or ligate bleeding perineal tears if any. 
• 
Massage the uterus 
• 
Insert Urethral catheter 
 
Referral: If bleeding continues, immediately refer the patient to the hospital an escort of a skilled 
health attendant.  Maintain IV infusion during transfer. 
 
Management of PPH at the hospital 
• 
Shout for help and mobilize resources 
• 
Obtain blood samples for Hb, blood grouping and cross matching 
• 
Insert 2 large bore cannulas and start infusing compound sodium chloride or sodium 
chloride (IV) rapidly 
• 
Blood Transfusion depending on amount of blood loss 
• 
Start oxytocin (IV) 20IU in 500mls compound sodium lactate/0.9% sodium chloride (IV) 
titrate at 20 drops per minute OR misoprostol (PO) 1000mcg or per rectal 
• 
Perform other manoeuvres (balloon tamponade, TAH, Illiac artery ligation, B-Lych suture) 
including surgical interventions depending on patient condition and available expertise. 
 
Prevention of PPH –Active management of Third Stage of Labour (AMSTL) 
Ensure no remaining second twin 
A: oxytocin (IM)10IU  
OR  
A: misoprostol (PO) 600mcg  
 

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Controlled cord traction (CCT) is recommended for vaginal births. Sustained uterine massage is not 
recommended as an intervention to prevent PPH in women who have received prophylactic 
oxytocin. 
Prevention of PPH in Caesarean sections 
A: oxytocin (IV/IM) 10IU is the recommended uterotonic drug for the prevention of PPH in 
Caesarean section 
Cord traction is the recommended method for the removal of the placenta in Caesarean 
section 
11.6 Prelabour Rupture of Membranes (PROM) 
It is the rupture of membranes (breakage of the amniotic sac) before the onset of labor. If rupture 
occurs before 37weeks it is called preterm prelabour rupture of membranes (PPROM). Prolonged 
PROM is a case of premature rupture of membranes in which more than 24 hours have passed 
between the rupture and the onset of labour. Prolonged PROM for more than 18 hours is a risk of 
ascending infection which can lead to chorioamnionitis (infection of chorion, amnion and amniotic 
fluid. 
Clinical presentation 
Leakage of watery fluid per vagina confirmed by performing a sterile speculum examination. 
Management of PROM at the dispensary and health center 
Give the following antibiotics for prophylaxis against chorioamnionitis 
A: erythromycin (PO) 500mg 8hourly for 7days 
AND 
A: metronidazole (PO) 400mg 8hourly for 7days 
Referral: Referto the hospital for further evaluation and management 
Management of PROM at the hospital 
 Investigations 
•
Ultrasound for fetal wellbeing, amount of liquor and gestation age.
•
Perform a sterile speculum examination to confirm leakage
•
Perform HVS for culture and susceptibility testing
•
Urinalysis
General Management 
If PROM at term: Delivery within 24 hours 
Assess Bishop’s Score and Induce Labour accordingly with 
A: misoprostol (PO) 25mcg 8hourly (Max 3doses) if unfavorable cervix.   
OR  
A: oxytocin (IV) 5IU in 500ml of D5% titrate beginning with 10dpm if favourable cervix 
Monitor FHR vigilantly during the process of IOL. Deliver by C/S if vaginal delivery is 
contraindicated, fetal distress or failed induction of labour. 
For Preterm PROM: 
If no sign of infection, wait for foetal maturity and give
B: dexamethasone (IM) 6mg 12hourly for 48 hours if pregnancy is ˂34weeks for fetal lung 
maturation 
AND
B: nifedipine (PO) 20mg 8hourly for 7 days for tocolysis 
Monitor for infection (FBP, RCP, Pulse, Fever) and fetal wellbeing (fetal movement, FHR, obstetric 
ultrasound)
Administer prophylactic antibiotics
A: metronidazole (PO) 400mg 8hourly 10days. 
AND 
A: erythromycin (PO) 500mg 8hourly for 10days 

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!
 
 
OR 
B: amoxicillin + clavulanic acid (FDC) (PO) 625mg 8hourly for 10days  
 
 
 
Deliver irrespective of gestation age in case of infection 
 
If there are signs of infections-pyrexia, foul smelling liquor (chorioamnionitis) 
 
A: metronidazole (PO) 400mg 8hourly for 5-7 days  
AND 
C: amoxycillin + clavulanic acid (FDC) (IV) 1.2g 8hourly for 5-7days  
OR  
D: ceftriaxone + sulbactam (FDC) (IV) 1.5g 12hourly for 5-7 days  
11.7 Antenatal Care 
11.7.1 Anaemia in Pregnancy 
It is hemoglobin levels less than 11 g/dl in early pregnancy and less than 10.5 g/dl in the 2nd and 
3rd trimester of pregnancy. Mild anemia– hemoglobin: 8–11g/dl; Severe anemia– hemoglobin<7g/dl. 
Iron deficiency anemia during pregnancy has been associated with an increased risk of low birth 
weight, preterm delivery and perinatal mortality.  
 
 
 
Clinical presentation 
• 
Tiredness, weakness, palpitations and dyspnea  
• 
Exercise intolerance  
• 
Pallor of skin and mucous membranes  
• 
Dizziness, faintness, headache  
• 
Intermittent claudication (ache, cramp, numbness or sense of fatigue)  
 
Note 
Some patients with anaemia in pregnancy may be asymptomatic 
 
Investigations  
• 
Full blood count and blood cross-match - red cell morphology 
• 
Red blood cell electrophoresis if haemoglobinopathies suspected 
• 
Blood smear for malaria  
• 
Stool and urine analysis  
• 
HIV test 
 
Non-pharmacological Treatment  
• 
Iron rich diet (fish, eggs, fruits and vegetables etc.)  
• 
Prevent and early treatment of malaria  
• 
Investigate and treat associated worm infestations  
 
Pharmacological Treatment  
 
Prophylaxis in Antenatal Care 
A: ferrous sulfate(PO) 200mg 8-12hourly 
AND  
 
A: folic acid (PO) 5mg 24hourly 
 
Note: 
• 
Ferrous sulfate should be taken in a full stomach and avoid taking it with tea/coffee 
• 
Where vomiting is experienced reduce dosage to tolerable level 
 
If Hb is <7g/dl in 1st and second trimester give:   
A: ferrous sulphate + folic acid (FDC) (PO) 1 tab 12hourly for 4 weeks. 
AND  
A: vitamin B (PO) 12hourly for 4 weeks  
 
If HB is ˂7g/dl in 3rd trimester or in case of signs for severe anaemia (features of heart failure)  
• 
Refer/admit the patient for blood transfusion at least 2 units of Packed RBCs 

228!
•
Continue with ferrous and folic acid as above after blood transfusion
11.7.2 Hypertensive Disorders in Pregnancy 
Hypertension is blood pressure (BP) 140/90 mmHg or greater, measured on two occasions at least 
four hours apart or elevated systolic BP >30mmHg, or diastolic BP 15mmHg from the baseline.  
Chronic Hypertension 
This is hypertension that is present at the booking visit or before 20 weeks or if the woman is already 
hypertensive before conception. Most women with chronic hypertension are asymptomatic. New 
onset chronic hypertension should have further evaluation to find underlying cause e.g. renal artery 
stenosis, chronic renal disease, Cushing syndrome etc. 
Pharmacological Treatment 
A: methyldopa (PO) 250–500mg 8hourly 
AND 
B: nifedipine (PO) 20mg 12hourly 
Pregnancy induced hypertension (gestation hypertension) 
Gestational hypertension or pregnancy-induced hypertension (PIH) is the development of new 
hypertension in a pregnant woman after 20 weeks of gestation without the presence of protein in the 
urine or other signs of preeclampsia. Usually disappears within 12 weeks postpartum  
Non-pharmacological Treatment 
•
Adequate rest at home and avoid strenuous activities
•
Eat a normal balanced diet and plenty of oral fluids
•
Schedule antenatal visits every 2 weeks up to 32 weeks and every week thereafter
•
Recommend to deliver in the hospital and should be delivered at 37 completed weeks of
gestation
Pharmacological Treatment 
For mild hypertension 140–159 mmHg systolic and/or 90–109 mmHg diastolic. 
A: methyldopa (PO) 250–500mg 8hourly 
OR 
B: nifedipine (PO) 20mg 12hourly 
OR 
C: labetalol (PO) 100mg 12hourly a day 
Severe hypertension 
Severe hypertension is Blood Pressure (BP) of 160/110 mmHg or higher. Admit the patient to 
hospital  
A: methyldopa (PO) 500mg 8hourly 
AND 
C: hydralazine 10mg (slow IV) stat (over 4-5 minutes); recheck the BP after 20 minutes if 
DBP is more/equal to 110mmHg give another dose of hydralazine (IV slowly) 5–10mg. 
AND 
B: nifedipine (PO) 20mg 12hourly 
OR 
C: labetalol (PO)100mg 12hourly 
Note 
Ensure slow administration and monitor closely for hypotension if using hydralazine. 
Referral: Refer to the next level facility in case there is no improvement 
11.7.3 Pre-eclampsia 
Is diagnosed when blood pressure is ≥ 140/90 mmHg after 20 weeks of pregnancy plus proteinuria 
of 300 mg per 24 hours or >2+ on urine dipstick. Or elevation of BP in pregnancy with features of 
end organ damage (eg pulmonary edema, renal or liver damage)  

229!
Diagnostic Criteria 
•
Most patients are asymptomatic, but symptoms may include headaches, dizziness, blurred
vision, and epigastric pain.
•
Blood pressure of ≥ 140/90 mmHg
•
Proteinuria (≥ 300mg per 24 hours)
•
Generalized edema may be present (not a necessary criteria)
Investigations 
•
Urine for Proteinuria (qualitative/quantitative 24-hour urine collection)
•
Obstetric Ultrasound and biophysical profile
•
Urea, creatinine, electrolytes, liver function test and uric acid
•
FBP and clotting profile
•
Fundoscopy
Non-pharmacological Management 
Pregnancy < 37 weeks of gestation  
•
Hospitalization and close monitoring
•
Bed rest
•
Monitoring BP, urine output, proteinuria, fetal movement and fetal heart beats (every day)
•
˂34weeks
Pregnancy >37 weeks of gestation: admit and deliver accordingly. 
Pre-eclampsia with Severe Features: 
This is diagnosed when BP ≥ 160/110 mmHg (especially diastolic ≥110 mmHg), or BP of 
≥140/90mmHg with features of end organ damage eg severe headache, epigastric pain, blurring of 
vision +/_vomiting, pulmonary oedema, renal or liver damage, features of haemolysis and low 
platelets 
Pharmacological Treatment 
C: hydralazine (IV) 5mg in 10ml sterile water over 4minutes’ initial dose. Followed by 
boluses 5–10mg as needed every 20 minutes until when the diastolic BP is less than 
110mmHg) 
AND 
A: methyldopa (PO) 500mg 8hourly 
AND 
A: nifedipine (PO) 20mg 8hourly until BP is stabilized 
OR 
if hypertension is refractory to hydralazine 
C: labetalol (IV bolus)10–20mg stat repeat each 10–20 minutes, with doubling doses not 
exceeding 80mg in any single dose for maximum total cumulative dose of 300 mg.  
Antenatal corticosteroids (dexamethasone Inj. 6mg 12hourly for 48hours) if pregnancy 
Prophylaxis for Seizures 
Anti-convulsion treatment of choice is magnesium sulfate. 
A: Magnesium sulfate (IV) 1g hourly in 250mils of RL (OR 5g of 50% MgSO4 4 hourly or 
alternate buttock) for 24 hours if GA is ≤34 weeks or until 24 hours post-delivery if GA 
is≥34 weeks (Refer to eclampsia section) 
Obstetrical Management  
If at term deliver immediately when stable, preferably vaginal delivery 
11.7.4 HELLP syndrome 
It is a life-threatening complications of pre-eclampsia characterized by Haemolysis, Elevated Liver 
enzymes and Low Platelets 
Diagnostic criteria 
•
Haemolysis
o
Abnormal peripheral smear
o
Total bilirubin > 1.2 mg/dL

230!
o
Lactic dehydrogenase > 600 U/L
•
Elevated Liver Functions
o
Serum glutamic oxaloacetic transaminase > 70 U/L
o
Lactic dehydrogenase > 600 U/L
•
Low Platelets
o
Platelets < 1,000,000/mm3
Management of HELLP syndrome 
The management is the same as for severe pre-eclampsia 
11.7.5 Eclampsia 
Eclampsia is a condition peculiar to pregnancy and post-partum periods, characterized by elevated 
BP and tonic-clonic convulsions which are not caused by epilepsy, severe malaria, meningitis, 
hypoglycemia or other causes of convulsions.  Majority (50%) occur preterm. Eclampsia may occur 
without prior elevation of BP. 
Diagnostic Criteria 
•
Signs of severe pre-eclampsia (BP > 160/110mm Hg)
•
Loss of consciousness
•
Tonic-clonic seizures, coma
Investigations 
•
Full blood count and crossmatch
•
Ultrasound for GA and fetal viability
•
Urea and creatinine + electrolytes
•
Liver enzymes tests
•
24h urine collection for proteinuria
•
Clotting profile
•
Blood smear to exclude malaria
•
Blood sugar estimation to exclude
hypoglycemia.
•
Lamber puncture may be indicated
to exclude meningitis
Pharmacological Treatment 
Manage with antihypertensive as in pre-eclampsia with severe features AND 
A:magnesium sulfate (IV) 
Loading dose: magnesium sulfate (IV) 4g of 20% (MgSO4) slowly over 5minutes.  
If having 50% MgSO4 dilute it to make it 20% MgSO4 by Drawing 8mls of 50% MgSO4 and adding 
12mls water for injection to make it 20mls of 20% of MgSO4 and  
OR 
Draw 10mls (5gms) of 50% MgSO4 into each syringe 1ml of A: 2% lignocaine in each syringe then 
give deep IM into each buttock. Continue with maintenance dose until 24hours post-delivery or since 
the last episode of convulsion: With MgSO4 infusion 1g per hour (in 200–300 ml of Ringer’s Lactate), 
or MgSO4 5g undiluted 50% of MgSO4 injection (add 1ml of lignocaine 2%) apply deep intra-
muscular (IM) injection into each buttock every 4hrs for about 24 hours after delivery or the last 
seizure whichever come last.16 
Note 
The magnesium sulfate infusion should only be given if patellar reflexes are present, respiration rate 
is ≥ 12 per minute, and urine output is >100mls in 4 hours. 
If convulsions recur within 15 minutes give; 
A: magnesium sulfate 2g. Draw 4mls of 50% of MgSO4 (2gm), add 6mls of water for 
injection to make it 10mls of 20% MgSO4 then give IV slowly over 5 minutes 
Features of Magnesium Sulphate toxicity 
•
Respiratory depression (˂16cycles/min
•
Reduced urine output(˂30mls/hour)
•
Loss of deep tendon reflexes
In case of   magnesium sulphate toxicity 
•
Stop magnesium sulphate administration
•
A: calcium gluconate (IV) 1g slow bolus in 2 to 3 minutes

231!
Obstetrical management 
Patients with eclampsia should be delivered within 12hours after the onset of seizures, even if the 
foetus is premature. Expectant management is contraindicated. If not in labour, and no 
contraindications, induce labour with misoprostol 50µg (PO) ,4hourly or 25µg vaginally and repeat 
8hourly up to a total of four doses maximum  
•
If failure of induction or contraindication to vaginal delivery, immediate Caesarean section
is indicated
Prevention of pre-eclampsia and eclampsia 
•
Ensure effective antenatal care
•
Calcium supplementation calcium supplementation at doses of 1.5–2.0g elemental
calcium/day) for those at high risk of developing pre-eclampsia.
•
Low-dose acetylsalicylic acid (aspirin, 75 mg) is recommended for the prevention of pre-
eclampsia in women at high risk of developing pre-eclampsia.
11.7.6 Antiphospholipid Syndrome (APS) in Pregnancy 
It is an autoimmune disease characterized by the presence in maternal circulation of one or more 
auto antibodies against membrane phospholipids. It is an acquired condition. Antiphospholipid 
syndrome (APS) is characterized by venous or arterial thrombosis and/or an adverse pregnancy 
outcome. APS occurs either as a primary condition or in the setting of an underlying disease, usually 
systemic lupus erythematosus (SLE). 
Clinical presentation 
•
Recurrent
pregnancy 
adverse 
outcome 
e.g.
(miscarriages) recurrent 
miscarriage, intrauterine growth restriction, early severe pre-eclampsia and preterm birth. 
•
Unexplained venous thrombosis (DVT) or arterial thrombosis (Stoke) or myocardial
infarction
•
thrombocytopenia (common finding but among the clinical classification criteria)
Classification with APS requires one clinical and one laboratory manifestation: 
Clinical 
•
A documented episode of arterial, venous, or small vessel thrombosis
•
1 or more unexplained deaths of a morphologically normal fetus ≥ 10-week GA
•
3 or more unexplained consecutive spontaneous abortions before the 10th weeks of GA
with anatomic, hormonal or chromosomal causes excluded
•
Eclampsia or severe pre-eclampsia according to standard definitions, or recognized
features of placental insufficiency
Laboratory: 
•
Anti-cardiolipin IgG and/or IgM measured on 2 or more occasions, not less than 12 weeks
apart;
•
Anti-β2 glycoprotein I IgG and/or IgM measured on 2 or more occasions, not less than 12
weeks apart
•
Lupus anticoagulant detected on 2 occasions not less than 12 weeks apart.
Pharmacological Treatment 
A: acetyl salicylic acid (PO) 75-120mg 24hourly beginning as soon as the pregnancy is 
confirmed throughout pregnancy 
AND 
C: unfractionated heparin (SC) 5000–10000 
OR 
S: low molecular weight heparin (SC) 30–40mg 24hourly 
Patients with Thrombosis such as stroke or pulmonary embolism need therapeutic 
anticoagulation.  
C: unfractionated heparin (SC) 5,000 bolus and subsequent 15,000–20,000 doses at 
12hourly intervals 

232!
OR   
S: low molecular weight heparin (SC) 1mg/kg 12hourly 
Note 
•
Warfarin should be avoided in pregnancy due the risk of teratogenicity
•
The aPTT needs to be checked and is best done midway between the 12hourly doses,
24hourly.
•
A target of 1.5–2.5 times the control should be aimed
Referral 
Refer immediately to a level where expertise and monitoring for treatment through laboratory testing 
is available. 
11.7.7 Deep Vein Thrombosis in Pregnancy 
Deep vein thrombosis (DVT) and acute pulmonary embolism (PE) are two manifestations of venous 
thromboembolism (VTE. The risk of VTE is increased in pregnancy by about five timesbecause of a 
more hyper-coagulable state. VTE contributes to significant maternal morbidity and mortality. The 
mainstay of therapy for DVT is anticoagulation, provided there is no contraindication 
Clinical presentation 
•
Pain on the affected limb
•
Swelling or redness of the calf or thigh
•
Homan’s sign (pain in the calf in response to dorsiflexion of the foot)
Investigations 
•
Venous doppler ultrasound
•
Venography (CT MRI)
•
Fibrin degradation product (FDP) or D-dimer
Prevention of DVT 
•
Early passive and active ambulation in women undergoing major obstetric surgery
•
Compressive stockings in women ≥100kg undergoing obstetric surgery
•
LMWH prophylaxis 5000IU within 1-hour post-surgery to at risk women.
Pharmacological Treatment 
B: unfractionated heparin (SC) 5,000 bolus and subsequent 15,000–20,000 doses at 
12hourly intervals (under supervision of a specialist) 
OR   
S: low molecular weight heparin (SC) 1mg/kg 12hourly 
OR 
C: warfarin (PO) 5mg 24hourly (in delivered women) consider bridging warfarin with 
Heparin for 5days as it takes longer to act. Warfarin to be continued up to 6weeks 
postpartum 
Note 
Check PTT every 4hours and PTT should be maintained at 1.5–2.5 X control. Once steady state has 
been achieved measure PTT levels daily. Change heparin to SC route after 5–10days 
Referral: Immediate referral to a hospital with expertise and monitoring of the treatment through 
laboratory testing is recommended. 
11.7.8 Pulmonary Embolism in Pregnancy 
It is a blockage, usually a blood clot that prevents oxygen from reaching the tissues of the lungs; it 
can be life-threatening 
Diagnostic Criteria 
•
Acute onset of shortness of breath
(dyspnea)
•
Pleuritic chest pain
•
Cough and/or hemoptysis
•
Low grade fever
•
Tachypnea
•
Diminished oxygen saturation
•
Diminished breath sounds

233!
!
 
Investigations 
• 
Venous Doppler ultrasound 
• 
Pulmonary angiography 
• 
CT scan, MRI  
• 
D-dimer 
 
Non-pharmacological Treatment 
Respiratory support and Oxygen supplementation 
 
Pharmacological Treatment 
B:    unfractionated heparin (UFH) is the treatment of choice 
Loading dose 150 U/kg (or minimum of 5000 U) followed by  
Initial infusion 15–25 U/kg/hour (or minimum of 1000U/hourly) 
 
Note 
Check PTT every 4 hours and adjust infusion to maintained PTT at 1.5–2.5 x control. Once steady 
state has been achieved measure PTT levels daily. Change heparin to SC route after 5–10 days to 
avoid formation of hematoma. 
 
Referral 
Immediate referral to a health facility where expertise and monitoring of the treatment through 
laboratory tests is available is recommended. 
 
11.7.9 Vomiting in Pregnancy and Hyperemesis Gravidarum 
It is excessive nausea and vomiting in early pregnancy requiring hospital admission and rehydration. 
 
Clinical presentation 
 
• 
Weight loss 
• 
Excessive Nausea and vomiting 
typically in early pregnancy  
• 
Dehydration 
• 
Altered general status (fast pulse, 
restlessness)  
 
Investigations  
• 
Full blood count 
• 
Blood for urea, electrolytes and 
serum creatinine 
• 
Urinalysis, micro urine and culture, 
ketonuria 
• 
Liver function tests 
• 
Thyroid function tests 
• 
Obstetric ultrasound to exclude 
multiple pregnancy and GTD 
 
Non-pharmacological Treatment  
• 
Nil per oral (nothing by mouth) for 
24–48 hrs. 
• 
Input/output monitoring for 24–48 
hrs. 
• 
Monitor electrolytes for 24hrs  
• 
Counselling and Reassurance 
• 
Emotional support 
• 
Rest and Lifestyle adjustment 
• 
Ensure adequate hydration and 
Frequent small carbohydrate meal 
 
Pharmacological Treatment 
A: compound sodium lactate with 5% dextrose and 0.9%sodium chloride according to daily 
needs and severity.  
AND 
C: vitamin B1 (IV)100mg 24hourly mix in intravenous rehydration solution 
 
 
AND 
C: metoclopramide (IM) 5–10 mg 8hourly till vomiting stops.  
OR 
A: promethazine (IM) 12.5 mg 12hourly a day 
 
 
OR 
B: pyridoxine + doxylamine (FDC) (PO) 10mg/10mg 8hourly till vomiting stops 
 
Referral: Depends on the status of the patient, refer to a hospital if vomiting is intractable and if 
there is a need for high volume replacement. 
 

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11.7.10 Heartburn in Pregnancy 
Heartburn (also called acid indigestion or acid reflux) is a burning sensation that often extends from 
the bottom of the breastbone to the lower throat. It is caused by some of the hormonal and physical 
changes in pregnant women. 
Non-pharmacological Treatment  
Pregnant women should avoid: 
•
Food and beverages that cause gastrointestinal distress
•
Tobacco and alcohol
•
Do not eat big meals, instead eat several small meals throughout the day
•
Drinking large quantities of fluids during meals
•
Do not eat close to bedtime, they should give themselves 2–3 hours to digest food before
they lie down
•
Sleep propped up with several pillows or a wedge.
Pharmacological Treatment 
A: compound magnesium trisilicate (PO) as needed until when the heartburn subsides. 
OR 
A: omeprazole (PO) 20–40mg 24hourly 
OR  
C:pantoprazole (PO) 40mg 24hourly 
11.7.11 Other Medical Disorders in Pregnancy 
Other medical disorders in pregnancy/other gynecological disorders include diabetes mellitus, 
glucose intolerance, malaria, HIV/AIDs complications, Pelvic Inflammatory Diseases (PID) etc. All 
these complications are discussed under specific disease chapters. 
11.7.12 Stimulation of Labour and Myometrial Relaxation 
Myometrium stimulants should be used with great care before delivery especially in porous women. 
Use in obstructed labour should be avoided. 
Oxytocic’s are indicated for: – 
•
Augmentation of labour
•
Induction of labour
•
Active management of third stage
of labour.
•
Uterine stimulation after delivery for
management of PPH due to uterine
atony
Induction of Labour 
Indications/Contraindications 
•
The indication for induction must be documented, and discussion should include reason for
induction, method of induction, and risks, including failure to achieve labour and possible
increased risk of Caesarean section5
•
If induction of labour is unsuccessful, the indication and method of induction should be re-
evaluated.
Pre-induction assessment 
•
Health care providers should assess the cervix (using the Bishop score) to determine the
likelihood of success and to select the appropriate method of induction.
•
The Bishop score should be documented.
•
Care providers need to consider that induction of women with an unfavorable cervix is
associated with a higher failure rate and increased rate of operative deliveries.
Post-dates induction 
•
Women should be offered induction of labour between 41+0 and 42+0 weeks as this
intervention may reduce perinatal mortality and meconium aspiration syndrome without
increasing the Caesarean section rate
•
Women who chose to delay induction >41+0 weeks should undergo twice-weekly
assessment for fetal wellbeing

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Options for Cervical Ripening/Induction: Unfavorable Cervix 
•
Intracervical Foley catheters are acceptable agents that are safe both in the setting of a
vaginal birth after Caesarean section and in the outpatient setting
•
Double lumen catheters may be considered a second-line alternative
Pharmacological Treatment 
A: misoprostol (PO) 25µg 2 hourly for 24hours or Misoprostol (PV) 25µg 6hourly for 
24hours can be considered a safe and   effective agent for labour induction with intact 
membranes and on an inpatient basis. 
OR 
S: dinoprostone (PV) 3mg 6hourly a total of 2doses 
Note 
•
Misoprostol should not be used in the setting of vaginal birth after Caesarean section due to
the increased risk of uterine rupture.
•
Oxytocin should be started no earlier than 4hours after the last dose of misoprostol.
Options for induction with a favourable cervix 
•
Amniotomy should be reserved for women with a favorable cervix. Care should be given in
the case of unengaged presentation because there is a risk of cord prolapse.
•
After amniotomy, oxytocin should be commenced early in order to establish labour.
•
In the setting of ruptured membranes at term, oxytocin should be considered before
expectant management.
•
Women positive for group B streptococcus (GBS) should be started on oxytocin as early
as possible after ruptured membranes in order to establish labour within 24 hours.
•
Both high- and low-dose oxytocin may be considered within a hospital protocol.
•
Because of the various concentrations, oxytocin infusion rates should always be recorded
in mU/min rather than mL/hr.
•
Oxytocin induction maybe considered in the hospital setting of vaginal birth after
Caesarean section.
•
For induction of labour use: Oxytocin IV, the dose will depend on parity.
Primigravida 
A: oxytocin (IV) 5IU in 500mls of 0.9% sodium chloride the initial dose should be 
8-10drops/Minute, the titration may be gradually increased at intervals not shorter
than 20 minutes and increments of not more than 5drops/minute, until a
contraction pattern similar to that of normal labour is established. The
recommended maximum rate is 40d/m.
Multiparous 
A: oxytocin (IV) start with low dose e.g., 2.5IU in 500mls of fluid titrate as above. 
Regulate the dose according to response. 
Note 
•
Induction of labour with uterotonic drugs requires vigilant monitoring
•
Induction of labour should only be attempted at hospitals with capacity to perform Caesarea
section
Augmentation of Labour 
If labour progress is not optimum labour augmentation is necessary. Can be achieved by: 
A: oxytocin as above 
OR 
Artificial rupture of membranes (ARM) and oxytocin. If membranes are already ruptured and no 
labour progress the steps above should be followed; rule out obstruction before augmenting labour 
with oxytocin. 
Myometrial stimulation after delivery 
A: oxytocin (IM) 10IU after delivery of the infant; when no response give oxytocin (IV 
infusion) 20 units in 500mls of NS running at 10–20 drops per minute. 
OR 
C: ergometrine (IM) 0.25–0.5mg after delivery of the infant, in the absence of myometrium 

236!
contraction and to prevent postpartum hemorrhage. 
OR 
A: misoprostol (PO/PV) 800–1000µg 
Note 
Use Ergometrine cautiously in cardiac and hypertensive disease patients 
Myometrium relaxation (Tocolysis) 
It is done to relax the uterus in order to: 
•
Relieve fetal distress immediately
prior to Caesarian section
•
Stop 
uterine 
contractions 
in
premature labour
•
Prevent uterine rupture
•
Perform external cephalic version
Pharmacological Treatment 
B: nifedipine (PO) 20 mg stat, followed by 10–20mg 6–8hourly 
OR 
B: salbutamol (PO) 4mg stat, when required (maximum daily dose 32mg) 
Note 
•
β -stimulants should never be used if the patient had an antepartum hemorrhage
•
β -stimulants are contra-indicated for cardiac disease and severe anemia in
pregnancy
11.7.13 Rhesus Incompatibility 
Incompatibility between an infant’s blood type and that of its mother, resulting in destruction of the 
infant’s red blood cells (hemolytic anemia) during pregnancy and after birth by antibodies from its 
mother’s blood circulation. 
Investigations 
•
Maternal Blood group+ Rhesus factor
•
Paternal blood group+ Rhesus factor
•
Infant Cord blood at delivery for grouping, FBC, Coombs test to detect maternal antibodies
and Total Billirubin
Prevention of Rhesus isoimmunisation 
If the mother is Rhesus negative give 
C: anti D immunoglobin 300microgram within 72hours of delivery 
Antepartum 
C: anti D immunoglobulin (IM)at 28-32weeks of gestation 
Abortion in Rhesus negative mother give 
C: anti D immunoglobulin 100microgram (IM) within 72hours of abortion 
Note 
For the management of other medical conditions in pregnancy e.g. Malaria, Peripartum 
cardiomyopathy, Diabetes and Renal disease in pregnancy refer to specific chapters in this 
guideline. 
11.8 Postpartum Care 
11.8.1 Mastitis                                                                          
It is the inflammation of the breast usually associated with breastfeeding. 
Clinical Presentation  
•
May develop rapidly,
•
Breast becomes red and swollen, tenderness, warmth and burning sensation
•
Fever

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!
Non-pharmacological Treatment  
• 
Drinking plenty of liquids and resting 
• 
Feed the baby more frequently and ensure adequate emptying.   
• 
Expressing the milk more often in non-breastfeeding mothers.  
 
Pharmacological Treatment 
 
 
C: flucloxacillin + amoxycillin (FDC) (PO) 500mg 12hourly for 5-7days 
 
 
 
OR 
 
 
B: amoxycilling + clavulic acid (FDC)(PO) 625mg 12hourly for 5-7days 
 
 
 
AND 
 
 
A: ibuprofen (PO) 500mg 8hourly for 5days 
 
 
 
OR  
 
 
A: paracetamol (PO) 500–1000mg 8hourly for 5days 
 
11.8.2 Puerperal Sepsis 
It is the infection of the uterus and surrounding tissues within 6 weeks postpartum manifesting as 
postpartum metritis, postpartum endometritis parametritis, peritonitis or septicaemia.   
Clinical presentation 
• 
Fever 
• 
Foul smelling lochia 
• 
Lower abdominal pain or generalized abdominal pain and tenderness 
• 
Delayed involution 
Investigations  
• 
Full blood picture and Cross Matching 
• 
Check LFT, RFT, Electrolytes 
• 
Blood culture in case of suspected septicaemia 
• 
Abdominal pelvic ultrasound 
Management of Puerperal sepsis at Dispensary and Health Center 
A: Establish IV line and give compound sodium lactate/0.9% sodium chloride 2l 
then continue as required 
 
AND 
B: amoxicillin + Clavulanic acid (FDC) (PO) 625 12hourly for 5days 
 
AND 
A: metronidazole (PO) 400mg hourly for 5days 
 
AND 
A: gentamycin (IV) 80mg 12hourly for 24-48hours. 
 
Referral: resuscitate and refer immediately to hospital for further investigations and management. 
Management of puerperal sepsis at the hospital 
• 
Blood transfusion in anaemic 
• 
Plan interventions eg (laparotomy, uterine evacuation etc) appropriately. 
• 
Continue with the above antibiotic for 5-7 days 
• 
Adjust drugs depending on the Culture and susceptibility results or if not available and 
there is no improvement after 3 days of treatment with above antibiotics switch to:  
 
B: metronidazole (IV) 500mg 8hourly for 5-7days 
AND 
D: ceftriaxone + sulbactam (FDC) (IV) 1.5g 12hourly for 5-7 days 
 
OR 
S: piperacillin + tazobactam (FDC) (IV) 4.5g 12hourly for 5-7days  

238!
Prevent Puerperal infections by 
Observation of aseptic technique when performing all obstetric procedures including Pelvic 
examinations during labour. Administration of prophylactic antibiotics within 1hour before performing 
a caesarean section or manual removal of Placenta. 
C: amoxycillin + clavulanic acid (FDC)(IV) 1.2g stat 
OR 
D: ceftriaxone + sulbactam (FDC) (IV)1.5g stat 
AND 
B: metronidazole (IV) 500mg stat 
11.8.3 Abnormal Uterine Bleeding (AUB) 
It is the uterine bleeding after menopause, in between menstrual periods or abnormally heavy and or 
prolonged menstrual bleeding. Abnormal uterine bleeding (AUB) is a common condition affecting 
women that has significant social and economic impact.  
The causes of AUB are classified and summarized into an Acronym; PALM-COEIN 
•
P-Polyps
•
A-Adenomyosis
•
L-Leiomyosma
•
M-Malignancy
•
C-Coagulopathy
•
O-Ovulatory dysfunction
•
E-endometrial causes
•
I-Iatrogenic
•
N-Not yet Classified
Clinical presentation 
Polyps 
•
Contact vaginal bleeding
•
Abdominal discharge
•
Pelvic pain or heaviness
Adenomyosis 
•
Premenstrual uterine cramps
•
Dysmenorrhea
•
Heavy menstrual bleeding
Leiomyoma 
•
Abdominal mass and distension
•
Heavy or prolonged menstrual
bleeding
•
Lower abdominal pain and
discomfort
Malignancy 
•
Presentation depend on type of
malignant
•
Abnormal intermenstrual or
postmenopausal contact bleeding
(cervical cancer)
•
Foul smelling bloody or mucoid
Vaginal discharge
•
Wight loss, loss of appetite, early
satiety
Coagulopathy 
•
History of bleeding tendencies
•
Heavy and or prolonged
menstruation
Anovulatory dysfunction 
•
Irregular bleeding, often heavy
•
Infertility or subfertility
Endometrial causes 
•
Heavy or prolonged menstruation
•
Irregular menstruation associated with endometrial hyperplasia

239!
Investigations 
•
Investigate 
according 
to 
the
possible cause of AUB basing on
clinical suspicion
•
A complete blood count (CBC)
•
Pregnancy test in reproductive age
to exclude pregnancy
•
Examination 
under 
anaesthesia
and biopsy in case of malignancy
•
Cervical and vaginal swab
•
Abdominal pelvic Ultrasound, CT
scan, MRI, Xray as indicated
•
LFT, RFT, Electrolytes
•
Hysteroscopy, 
Cystoscopy,
Proctoscopy in case of suspected
malignancy
•
Biopsy 
in 
case 
of 
suspected
malignancy
•
Specific Tumor markers in certain
suspected 
malignancies 
e.g.
ovarian tumors.
•
Testing for coagulation disorders
should 
be 
considered 
only 
in
women who have a history of
heavy 
menstrual 
bleeding
beginning at menarche or who
have a personal or family history of
abnormal bleeding
Pharmacological Treatment 
The treatment will depend of the causative factor. 
C: tranexamic acid (PO) 500 –1000mg 6–8hourly as required until the bleeding is 
controlled 
OR 
A: combined oral contraceptives (PO) Useful for anovulatory bleeding. 
OR 
A: medroxyprogesterone acetate (PO) 5–10mg 24hourly for 10–14days initially and 
repeated for 10days each month thereafter 
OR 
C: norethisterone (PO) 5mg 24hourly for 10days. Then 5mg 12hourly from days 19 to 26 of 
the two subsequent cycles, should be given to prevent recurrence of the condition. 
Surgical management 
AUB due to organic causes may be amenable to surgical intervention. The decision regarding the 
approach and the timing for surgical intervention should depend on final diagnosis, expertise and 
other resources.  
Referral 
Immediately refer to the next level facility with capable for appropriate evaluation and 
managementrecommend 
11.8.4 Dysmenorrhea 
It is a painful menstruation preventing normal activities and requires medication. There are 2 types 
of dysmenorrhea: 
Primary (no organic cause). Typically, pain occurs on the first day of menses, usually about the 
time the flow begins. 
Secondary (pathological cause) e.g., usually the pain is due to other underlying causes eg PID, 
endometriosis, etc. 
Pharmacological Treatment 
A: ibuprofen (PO) 200–600mg 8hourly (maximum 2.4 g/day) 
OR 
A: acetylsalicylic acid (PO) 300–600mg 4hourly 
OR 
A: diclofenac (PO) 50–100mg 8–12hourly 
OR 
B: mefenamic acid (PO) 500mg 8hourly 
AND 
A: hyoscine butyl bromide (PO) 20mg 8hourly for 5days 
Women with regular complaints can easily detect length of use during their periods (2–3days usually 
enough). Treat the underlying condition if known 

240!
!
 
 
Note 
For primary dysmenorrhea patients may be advised to start taking ibuprofen one or two days 
before menses and continue 
for three to four days during menses to minimize painful menstruation  
 
11.8.5 Endometriosis 
It is the presence of endometrial glands and stroma in locations other than the uterine endometrium 
and musculature. The common locations of endometriosis include the pelvis, small intestines, 
bowels, appendix, anterior abdominal wall and incision scars 
 
Clinical presentation 
• 
Chronic pelvic pain, lower back 
pain and rectal pain 
• 
Dysmenorrhea 
• 
Dyspareunia 
• 
Dysfunctional uterine bleeding 
• 
Infertility 
 
Management at Dispensary and Heath center 
 
A: ibuprofen (PO) 200–600mg 8hourly (maximum 2.4 g/day) 
 
OR 
A: acetylsalicylic (PO) acid 300–600mg 4hourly 
 
  
OR 
 
A: diclofenac (PO) 50–100mg 8–12hourly 
OR 
B: mefenamic acid (PO) 500mg 8hourly 
OR 
A: hyoscine butyl bromide (PO) 20mg 8hourly for 5days 
 
Referral: Refer the patient with endometriosis to hospital for further investigations and management. 
 
Management of endometriosis at Hospital 
Investigations 
• 
Abdominal 
pelvic/transvaginal 
ultrasound 
• 
CT scan 
• 
MRI 
• 
Laparoscopy 
 
Pharmacological treatment of endometriosis 
A: combined oral contraceptive pills (PO) 1 tab 24hourly for 3months 
 
 
 
OR 
 
A: medroxyprogesterone acetate (IM) 300mg monthly for 6months. 
 
 
 
OR 
 
S: danazol (PO) 200-400mg 12hourly depending on the severity. Continue RX to maintain 
amenorrhea. 
 
 
 
OR 
 
S: Goserelin (IM) 3.6mg monthly for 4-6months 
 
11.9 Contraception 
11.9.1 Short term Contraceptive Methods 
Short-term hormonal contraceptives 
Before initiating hormonal contraceptives: 
• 
Check blood pressure 
• 
Perform vaginal examination (to check normal size of uterus) 
• 
Check for contraindications like deep vein thrombosis 
 
Follow up: 
• 
Instruct women always to inform the doctor or nurse that they are on contraceptives while 
attending clinic or hospital. 

241!
!
• 
Women on oral contraceptives need regular physical check-ups including blood pressure 
measurement every six months  
• 
Need to withdraw Contraceptives in: 
o 
Pregnancy 
o 
Severe headaches especially associated with visual disturbances 
o 
Numbness or paresis of extremities 
o 
Unexplained chest pain or shortness of breath 
o 
Severe leg pains etc 
o 
Deep vein thrombosis.  
 
The recommended short-term hormonal contraceptives are: 
A: ethinyloestradiol+norgestrel (FDC) (PO) 0.03mg/0.3mg 24hourly   
 
 
 
OR 
 
A: ethinyloestradiol+levonogestrel (FDC) (PO) 0.03mg/0.15mg 24hourly  
 
 
 
OR 
 
A: ethinyloestradiol+desogestrell (FDC) (PO) 0.03mg/0.15mg) 24hourly 
 
 
 
OR 
 
A: medroxyprogesterone acetate (IM) 150mg every three months 
 
 
 
OR 
 
A: levonorgestrel (PO).0.03mg 24hourly  
 
Note 
• 
Take the first pill on the 5th day of menstruation and then continue every day without 
any interruptions 
• 
Check blood sugar and hypertension after every 6 months  
• 
Avoid use in women with severe hypertension and women without proven fertility 
 
Post-coital contraception 
The method is applicable mostly after rape and unprotected sexual intercourse where pregnancy is 
not desired. Within 3 days (72 hours) of unprotected sexual intercourse, give: 
A: levonorgestrel (PO) 1.5mg stat 
OR 
A: levonorgestrel (PO) 0.75mg 12hourly. 2 doses 
 
 
 
OR 
B:CuT380A Intrauterine Contraception Device (IUCD) may also be used. 
 
Note 
Emergency contraception should not be used as a routine method of contraception. Clients should 
be advised to use regular effective contraceptive methods of their choice. 
 
Barrier methods (condoms) 
 
A: Male Condoms 
 
A: Female Condoms 
 A correct use of both male and female condoms is required with every act of sexual intercourse for 
greatest effectiveness.   
 
Note 
Condoms are the only contraceptives that can protect against both pregnancy and STIs 
 
11.9.2 Long-term Contraceptive methods 
Implant Contraceptives 
Implants are contraindicated to: 
• 
Severe hypertension 
• 
Thromboembolism 
• 
Active liver disease 
• 
Sickle cell anaemia 
• 
Genital bleeding 
• 
Severe headaches 
 
The following are the recommended implants: 
A: etonogestrel 68mg in single silastic capsule with applicator is implanted in the left upper 
arm with local anesthesia. Is effective for 3 years 
OR 
A: levonorgestrel 75mg in two silastic capsules implanted subdermal in the left upper arm 

242!
!
with local anesthesia. Is effective for 5 years and is recommended for women who have 
completed their family or not ready for sterilization or those not able to take estrogen 
containing contraceptives. 
 
Note 
Implants may be inserted during the immediate postpartum period, or after 4 weeks postpartum 
 
Intrauterine Contraceptive Device 
It is the devise containing copper or Levonorgestrel that is inserted in the uterus to prevent 
pregnancy 
 
B: CuT380A Intrauterine Contraception Device (IUCD) may also be used 
 
It can be inserted during the immediate postpartum period, within 48hours postpartum or after 4 
weeks postpartum  
 
The contraindication to postpartum IUD includes
• 
Active postpartum haemorrhage 
• 
Puerperal sepsis/chorioamnionitis, 
active PID 
• 
Allergy to copper 
• 
Period within 48 hours and 4we 
 
 
 
 
 
 
Note 
Use the WHO Medical eligibility criteria (MEC) wheel on providing FP methods 
 
11.9.3 Permanent (surgical) Contraceptive Methods 
The available permanent contraceptive options include; 
• 
Bilateral tubal ligation (female sterilization) for women who will not want more children 
• 
Vasectomy for men who will not wat more children 
11.8.4 Infertility 
Infertility is a condition of the reproductive system defined by the failure to achieve a clinical 
pregnancy after 12 months or more of regular unprotected sexual intercourse. 
A detailed history taking, and physical examination are invaluable for the diagnosis for causes of 
infertility 
 
Investigation: Not every fertility test will be done for every case. 
 
WOMEN: For women, fertility testing may include basic gynaecologic examination 
• 
VDRL tests 
• 
Urine routine and microscopic 
• 
Cervical mucus examination 
• 
Abdominal pelvic/Transvaginal USS 
• 
HSG (hysterosalpingogram)for tubal patency  
• 
Hysteroscopy- 
• 
Diagnostic laparoscopy- This test is only done when symptoms point to possible 
endometriosis, as part of treatment for blocked fallopian tubes, or in some cases of 
unexplained infertility. 
• 
Hormonal profile- FSH, LH, TSH, AMH, T3 & T4, Testosterone, prolactin, estradiol and 
progesterone.

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!
MEN: Perform the following 
• 
Semen analysis 
• 
VDRL tests 
• 
Hormonal profile-FSH, Testosterone, but sometimes also LH, estradiol, or prolactin 
 
Treatment will depend on the underlying cause 
 
Non-pharmacological Treatment 
• 
Weight reduction in obese clients. 
• 
Educate the couple on the importance of having sexual intercourse during the fertile 
window 
• 
Try to avoid smoking/excessive drinking 
 
Pharmacological Treatment 
Ovulation stimulation; 
C: clomiphene citrate (PO) 50mg 24hourly for 5days from the 2nd–5th day of 
menstruation. (maximum 6 cycles) 
 
Polycystic Ovarian Syndrome (PCOS) 
A: metformin (PO) 500mg 8hourly is used for PCOS treatment, alone or along with fertility 
drugs 
 
Hyperprolactinemia 
C: bromocriptine (PO) 2.5–5mg 24hourly until the prolactin level is within the normal range 
OR 
S: cabergoline (PO) 0.25–0.5mg once or twice weekly initially then the dose is gradually 
increased monthly until prolactin levels normalize. Doses of less than 3mg per week are 
usually enough to achieve this goal 
 
Surgeries: 
• 
Tubal surgery for Tubal blockage 
• 
Myomectomy for uterine fibroids 
• 
Ovarian drilling is a possible surgical treatment for PCOS–related infertility 
 
Referral 
Refer all patients with infertility to a gynecologist. 
 
 
 
 
 

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!
CHAPTER TWELVE 
SEXUALLY TRANSMITTED INFECTIONS 
 
Sexually transmitted infections (STIs) — are generally acquired by sexual contact with a person who 
has an STI. The organisms (bacteria, viruses or parasites) that cause sexually transmitted diseases 
may pass from person to person in blood, semen, or vaginal and other bodily fluids. Reproductive 
tract infections (RTIs) occur in the genital tract and affect both women and men. Some RTIs, such 
as syphilis and gonorrhea, are sexually transmitted, but many are not. In women, overgrowth of 
endogenous microorganisms normally found in the vagina may cause RTIs (yeast infection, 
bacterial vaginosis).  
Clinical Presentation
• 
Sores or bumps on the genitals or 
in the oral or rectal area. 
• 
Painful or burning urination. 
• 
Discharge from the penis. 
• 
Vaginal discharge that is abnormal 
in 
colour, 
odour, 
amount 
or 
consistency. 
• 
Itching or irritation of the vulva or 
vagina. 
• 
Unusual vaginal bleeding. 
• 
Pain during sex. 
• 
Lower abdominal pain 
• 
Genital ulcers, sores or blisters 
• 
Swelling, lumps or ulcer in the groin 
area 
 
12.1 STIs/RTIs Management Approaches 
Management of STIs/RTIs can be done in either of the following approaches: 
• 
Aetiological laboratory approach: By identification of causative agents through 
laboratory methods and sensitivity pattern to the medicine to used, followed by disease-
specific treatment. 
 
• 
Aetiological clinical approach: By targeting disease treatment based on suspected 
causative agents diagnosed clinically. This is not appropriate at any health facility because 
of its demands on the clinical acumen of the service provider and the danger of incorrect 
diagnosis and, hence, insufficient treatment. 
 
• 
Syndromic approach: This identifies clinical syndromes (symptoms and signs) followed 
by syndrome-specific treatment that targets causative agents which cause the syndrome. 
 
Management of STIs/RTIs using Aetiological Laboratory Approach 
It identifies causative agents through laboratory methods, followed by disease-specific treatment. 
This is the best approach to be used at a Health Facility (HF) which has a Laboratory capable of 
doing the Laboratory Investigation and producing timely result(s) so as to enable the clinician to 
prescribe medicine (s) according to the causative agent(s) and sensitivity pattern.  
 
Management of STIs/RTIs using Syndromic Approach 
This approach is recommended if the HF is not able to conduct appropriate Laboratory 
Investigation(s) and producing timely result(s) to enable the clinician to prescribe the medicine in 
accordance with causative agent(s).  
Syndromic management of STIs is based on the diagnosis of defined symptoms and easily 
recognizable clinical signs. Each syndrome can be caused by several different causative agents. For 
each syndrome, a well-defined standard treatment which has been proven to be effective against 
most endemic causative agents for the syndrome are used. 
 
Syndromic approach of managing STIs/RTIs entails the service provider to follow laid down steps in 
a flow chart which guides him/her in making rational management decisions for treating the client. 
These are therefore known as treatment flow-charts. They may also be known as treatment 
algorithms, treatment protocols or treatment decision trees. They guide the provider through a series 
of decisions and actions that need to be made. Each decision or action is enclosed in a box, with 
one or two routes leading out of it to another box, with another decision or action. Upon learning a 
patient’s symptoms and signs, the service provider turns to the flow chart for the relevant syndrome 

245!
!
and works through the decisions and suggestions it guides to manage the client accordingly. Each 
flow chart is made up of a series of three steps. These are: 
• 
The clinical problem (the patients presenting symptoms and signs), 
• 
The decision that needs to be taken, 
• 
The action that needs to be carried out. 
12.2 Urethral Discharge Syndrome (UDS) 
UDS refers to the presence of abnormal secretions in the distal portion of the urethra.  
Causes 
• 
Neisseria gonorrhoeae and  
• 
Chlamydia trachomatis.  
 
 
Clinical Presentation 
• 
Urethral discharge,  
• 
Burning or painful micturition,  
• 
Itchy urethra and increased frequency and urgency of micturition. 
 
Note 
• 
Persistent or recurrent symptoms of urethritis may be due to drug resistance, poor 
compliance or re-infection. In some cases, there may be infection with Trichomonas 
vaginalis (TV). 
• 
Male patients complaining of urethral discharge and/or dysuria should be examined for 
evidence of discharge. If none is seen per inspection, the urethra should be gently milked 
from the ventral part of the penis towards the meatus. 
• 
Delayed or inadequate treatment may result into orchitis, epididymitis, urethral stricture 
and/or infertility. 
 
Investigation(s) if the HF has a Laboratory capable of doing:  
• 
Culture and Sensitivity 
• 
Gram stain 
• 
ELISA 
• 
Quantitative or qualitative PCR 
• 
Genetic sequencing 
 
Management and Treatment of UDS (seeflow chart 12.1)  
12.3 Vaginal Discharge Syndrome (VDS) 
VDS refers to change of colour, odour and/or amount of vaginal secretions.  
Causes 
• 
T. vaginalis,  
• 
C. albicans 
• 
Bacterial Vaginosis  
• 
Neisseria gonorrhoeae 
• 
Chlamydia trachomatis 
 
Clinical Presentation 
• 
Abnormal vaginal discharge,  
• 
Burning or painful micturition,  
• 
Itchy vulva,  
• 
Increased frequency and urgency 
of micturition and/or painful coitus. 
 
Note 
• 
A spontaneous complaint of abnormal vaginal discharge is most commonly due to a vaginal 
infection.  
• 
T. vaginalis, C. albicans and Bacterial Vaginosis are the commonest causes of vaginal 
infection while  
• 
Neisseria gonorrhoeae and Chlamydia trachomatis cause cervical infection.  
• 
The clinical detection of cervical infection is difficult because a large proportion of women with 
gonococcal or chlamydia infections are asymptomatic. 
• 
vaginal discharge is therefore highly indicative of vaginal infection, but poorly predictive for 
cervical infection 
• 
Due to the high prevalence of gonorrhea and chlamydia, all women presenting with VDS 
should receive treatment for both vaginal and cervical infections. 

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!
• 
Delayed or inadequate treatment of VDS may result to endometritis, salpingitis, oophoritis or 
ectopic pregnancy.  
• 
Gonococcal or chlamydial cervical infection may be asymptomatic 
 
Investigation(s) if the HF has a Laboratory capable of doing:  
• 
Wet preparation 
• 
Gram stain 
• 
Culture and Sensitivity 
• 
Fluorescent Microscopy 
• 
Pap test (Papanicolau test) 
• 
ELISA 
• 
Quantitative or qualitative PCR  
• 
NB starts simple to complex 
 
Management and Treatment of VDS (see flow chart 12.2) 
12.4 Lower Abdominal Pain Syndrome or Pelvic Inflammatory Disease (PID) 
PID is defined as the inflammation of the uterus, fallopian tubes, ovaries and pelvic peritoneum. It is 
also known as lower abdominal pain syndrome. It commonly occurs as a result of infection 
ascending from the cervix. It can also occur as a result of trans-cervical procedure. 
Causes 
• 
Neisseria gonorrhoeae,  
• 
Chlamydia trachomatis and  
• 
Anaerobic 
bacteria
 
Clinical Presentation 
• 
Lower 
abdominal 
pain 
and 
tenderness,  
• 
Painful micturition,  
• 
Painful coitus,  
• 
Abnormal vaginal discharge,  
• 
Menometrorrhagia,  
• 
Fever and sometime  
• 
Nausea 
and 
vomiting.
 
Note 
• 
Delayed or inadequately treated PID may lead to chronic lower abdominal pain,  
• 
Pelvic abscess,  
• 
Ectopic pregnancy,  
• 
Dysmenorrhea and infertility. 
 
Investigation(s) if the HF has a Laboratory capable of doing: 
• 
Wet preparation 
• 
Gram stain 
• 
Culture and Sensitivity 
• 
Fluorescent Microscopy 
• 
Pap test (Papanicolaou’s test) 
• 
ELISA 
• 
Quantitative or qualitative PCR  
 
Management and Treatment of PID (see flow chart 12.3) 
 
In-patient treatment of PID 
All patients with PID who have fever or body temperature ≥ 380C should be admitted for closer care. 
The recommended in-patient treatment options for PID are as follows: 
Regimen 1: 
A: cefixime (PO) 400mg 12hourly for 7-14days 
AND 
A: doxycycline (PO) 100mg 12hourly for 7-14days 
AND 
A: metronidazole (PO) 400mg 8-12hourly for 7-14days 
OR 
B: metronidazole (IV) 500mg 8-12hourly for 7-14days 
Regimen 2: 
A: ceftriaxone (IM) 1gm 24hourly for 5-7days 
AND 
A: doxycycline (PO) 100mg 12hourly for 7-14days 
AND 
A: metronidazole, (PO) 400mg 8-12hourly 7-14days 
OR 
A: metronidazole (IV) 500mg 8-12hourly 7-14days 

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Regimen 3: 
S: clindamycin (IV) 900mg 8hourly for 7-14days 
AND 
A: gentamicin (IV) 1.5 mg/kg 6-8hourly 7-14days 
 
Note 
For all three regimens, therapy should be continued for two days after the patient has improved 
and then be followed by doxycycline (PO) 100 mg 12hourly for 14days. 
• 
Patients taking metronidazole should be cautioned to avoid alcohol. 
• 
Doxycycline is contraindicated in pregnancy. 
 
12.5 Painful Scrotal Swelling (PSS) 
PSS is the inflammation of the epididymis and testis, often accompanied with scrotal pain, swelling 
and tenderness. It is also known as epididymorchitis. 
Causes 
• 
Neisseria gonorrhoea and  
• 
Chlamydia trachomatis 
 
Clinical Presentation 
• 
Scrotal pain,  
• 
Scrotal swelling and tenderness,  
• 
Scrotal oedema  
• 
Fever
 
 
Note 
Among the common complications of painful scrotal swelling include infertility and scrotal abscess. 
 
Investigation(s) if the HF has a Laboratory capable of doing:  
• 
Gram stain  
• 
Culture and Sensitivity 
• 
ELISA 
• 
 Quantitative or qualitative PCR  
• 
Genetic sequencing 
 
Management and Treatment of PSS (see flow chart 12.4) 
12.6 Ano-rectal Syndrome (ARS) 
Is defined as soreness, burning, itching or other irritation of the rectum together with redness in the 
area of anus. Sometimes it is accompanied by diarrhea and it may occur as a toxic side effect of oral 
administration of certain broad-spectrum antibiotics. 
Causes 
• 
Neisseria gonorrhoeae,  
• 
Chlamydia trachomatis,   
• 
Treponema pallidum  
• 
Herpes Simplex Virus.  
• 
Shigella spp., or  
• 
Entamoeba histolytica 
Clinical presentation 
• 
Purulent rectal discharge 
• 
Mucous rectal discharge 
• 
Watery rectal discharge 
• 
Soreness, burning, itching or other irritation of the rectum together with redness in the area 
of anus 
• 
There may also be ineffectual straining to defecate (“tenesmus”), sometimes mistakenly 
described as “constipation” by patients.  
• 
The anus and rectum may be intensely painful, with external and internal ulceration 
• 
Abdominal pain or cramping, abdominal swelling, distention or bloating;  
• 
Bloody stool (blood may be red, black, or tarry in texture),  
• 
Burning feeling,  
• 
Change in bowel habits, constipation, diarrhea;  
• 
Fecal incontinence (inability to control stools),  
• 
Flatulence; pain, which may be severe, in the abdomen, pelvis, or lower back,  

248!
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• 
Urgent need to pass stool and watery diarrhea including multiple episodes. 
• 
A proctoscopic examination (which should be done, if feasible) will reveal rectal pus, 
bleeding or ulceration.  
 
Note 
• 
Proctitis may be caused by Salmonella spp., Shigella spp., or Entamoeba histolytica as a 
part of gastroenteritis, which may manifest as diarrhoea with fever, anorexia, and 
abdominal cramps.  
• 
Antibiotics that destroy normal intestinal bacteria and allow other bacteria to grow in their 
place may also cause proctitis. 
• 
Herpes proctitis may be mistaken for the rectal manifestation of ulcerative colitis or 
Crohn’s disease.  
• 
Proctitis typically causes painless bleeding or the passage of mucus (sometimes 
mistaken for diarrhoea) from the rectum.  
• 
All cases of proctitis in MSM should be treated for gonorrhoea and chlamydia infections.  
• 
Symptoms of diarrhoea, bloody stools, abdominal cramping, nausea, and/or bloating 
may indicate Giardia spp infection or amoebic dysentery. 
 
Other non-STI causes of ARS include: 
Anal fissure, Fecal impaction, Food intolerance, Gastroenteritis (bacterial and viral), Inflammatory 
bowel disease (includes Crohn’s disease and ulcerative colitis), Neurological damage, and Perirectal 
or perianal abscess. 
 
Other symptoms might occur with rectal discharge includes gastrointestinal symptoms which vary 
depending on the underlying disease, disorder or condition. These may include: 
• 
Abdominal pain or cramping, abdominal swelling, distention or bloating; bloody stool (blood 
may be red, black, or tarry in texture), burning feeling, change in bowel habits, 
constipation, diarrhea; fecal incontinence (inability to control stools), flatulence; pain, which 
may be severe, in the abdomen, pelvis, or lower back, urgent need to pass stool and 
watery diarrhea including multiple episodes. 
 
 
Investigation(s) if the HF has a Laboratory capable of doing:  
• 
Wet preparation 
• 
Gram stain 
• 
Pap test (Papanicolaou’s test) 
• 
Culture and Sensitivity 
• 
Rapid Plasma Reagin (RPR) 
• 
Treponema 
palladium 
particle 
agglutination (TPPA) 
• 
ELISA 
• 
 Quantitative or qualitative PCR  
• 
Genetic sequencing 
• 
Fluorescent Microscopy 
 
Management and Treatment of ARS(see flow chart 12.5.) 
 
12.7 Oropharyngeal Syndrome 
Oral sex can lead to oropharyngeal STIs (infections of mouth and throat). 
Causes 
• 
Human Papilloma Virus,  
• 
Herpes Simplex Virus,  
• 
N. gonorrhoea  
• 
Chlamydia spp 
• 
Treponema pallidum 
 
Clinical presentation 
• 
Pharyngitis,  
• 
History of unprotected oral sex  
 
Investigation(s) if the HF has a Laboratory capable of doing:  
• 
Wet preparation 
• 
Gram stain 
• 
Pap test (Papanicolaou’s test) 
• 
Culture and Sensitivity 
• 
Rapid Plasma Reagin (RPR) 
• 
Treponema 
pallidum 
particle 
agglutination (TPPA) 
• 
ELISA 
• 
 Quantitative or qualitative PCR  
• 
Genetic sequencing 

249!
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• 
Fluorescent Microscopy 
 
Management and Treatment of Oropharyngeal syndrome(see flow chart 12.6.) 
 
12.8 Genital Ulcer Disease (GUD) 
GUD is a loss of continuity of skin or mucous membrane producing one or more lesions in the 
genital area.  
Causes 
• 
Treponema pallidum,  
• 
Haemophilus ducreyi,  
• 
Chlamydia trachomatis,  
• 
Herpes simplex virus type 2 (HSV) 
• 
Calymmatobacterium granulomatis. 
 
Clinical presentation 
• 
Ulcer 
• 
Sore 
• 
Vesicle 
 
Investigation(s) if the HF has a Laboratory capable of doing:  
• 
Wet preparation 
• 
Gram stain  
• 
Culture and Sensitivity 
• 
 Fluorescent Microscopy 
• 
Treponema 
palladium 
particle 
agglutination (TPPA) 
• 
Rapid Plasma Reagin (RPR) 
• 
ELISA 
• 
Quantitative or qualitative PCR  
• 
Genetic sequencing 
 
Management and Treatment of GUD (see flow chart 12.7)  
12.9 Neonatal Conjunctivitis (Ophthalmia Neonatorum) 
Ophthalmia Neonatorum (ON) means inflammation of the conjunctiva of a newborn baby of less 
than 1 month of age.  
Is a potentially sight threatening condition. If the baby is older, the cause is unlikely to be an STI. 
Causes 
• 
Neisseria gonorrhoeae   
• 
Chlamydia trachomatis. 
• 
Other non-STI causes of neonatal conjunctivitis include:  
o 
Staphylococcus aureus,  
o 
Streptococcus pneumoniae,  
o 
Haemophilus and Pseudomonas spp,  
o 
Viral, chemical and physical irritation. 
Presentation 
• 
Reddish conjunctiva,  
• 
Oedema/swelling of the eyelids  
• 
Purulent eye discharge 
 
Prevention and control measures 
• 
Screening of pregnant women,  
• 
Early treatment of VDS in pregnant women 
• 
Routine eye chemoprophylaxis in the newborn by providing  
A: 1% oxytetracycline eye ointment to all newborns.  
 
Note 
Examine the neonate and exclude other congenital diseases 
 
Management and Treatment of Neonatal conjunctivitis (see flow chart 12.8) 
12.10 Inguinal Bubo (IB) 
Inguinal and femoral bubos are localized enlargements of the lymph nodes in the groin area, which 
are painful and may be fluctuant.  
They are frequently associated with lymphogranuloma venereum and chancroid  
Causes 
• 
Chlamydia trachomatis  

250!
!
• 
Haemophilus ducreyi 
 
Clinical presentation 
• 
Localized 
enlargements 
of 
the 
lymph nodes in the groin area,  
• 
Painful and may be fluctuant.  
• 
Pain,  
• 
Fever  
• 
Tenderness. 
 
Note 
• 
In many cases of chancroid an associated genital ulcer is visible, but occasionally may not 
be.  
• 
Non-sexually transmitted local and systemic infections (e.g. infections of the lower limb) can 
also cause swelling of inguinal lymph nodes. These should therefore be ruled out. 
 
 
Investigation(s) if the HF has a Laboratory capable of doing:  
• 
Culture and Sensitivity  
• 
ELISA 
• 
Quantitative or qualitative PCR  
• 
Direct Fluorescent Antibody (DFA) 
 
Management and Treatment of Inguinal BUBO (see flow chart 12.9) 
 
12.11STI/RTI flow charts 
Steps in using the flow charts: 
• 
Start by asking the patient for his/her symptoms.  
• 
Find the appropriate flow chart, stated in the clinical problem box with “Patient Complaints 
of.” 
• 
The clinical problem box usually leads to an action box, which asks you to examine the 
patient and/or take the history. 
• 
Next, move to the decision box. After taking the history and examining the patient you 
should have the necessary information to choose Yes or No accurately. 
• 
Depending on your choice, there may be further decision boxes and action boxes. 
 
Note 
For the appropriate management of STIs/RTIs syndrome, drugs in the watch group (azithromycin, 
cefixime and ceftriaxone) are the standard recommended for use as a first line treatment for the 
most STIs/RTIs starting at the Dispensary level, therefore, should be used only for STIs/RTIs at 
Primary HFs) 

251!
!
 
Flow Chart 12.1: Management of Urethral Discharge Syndrome (UDS) 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

252!
!
Flow Chart 12.2: Management Of Vaginal Discharge Syndrome (VDS) 
 

253!
!
 
 
Flow Chart 12.3: Management Of Lower Abdominal Pain Syndrome (PID) 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 

254!
!
Flow Chart 12.4: MANAGEMENT OF PAINFUL SCROTAL SWELLING (PSS) 
 
 
 
 
 
 

255!
!
Flow Chart 12.5: MANAGEMENT OF ANORECTAL SYNDROME (ARS) 
 
 
 
 
 
 
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!
!
!
!
!
!
1st!Visit!
Patient!complains!of!anorectal!discharge!or!pain!and!discomfort!in!
the!perianal!area!
Take!history!
Examine,!the!perianal!area!and!do!a!proctoscopy!if!available!to!identify!discharge!!
History!of!anal!sex!
No!history!of!anal!sex!
Other!STI(s)!found!
Treat!for!Gonorrhoea!and!Chlamydia!
!
A:!Cefixime!400!mg!PO!stat!!
A:!Azithromycin!1g!PO!start!!
• 
Provide!health!education!!
• 
Partner!management!!
• 
Promote!and!provide!condoms!!
• 
Offer!HIV!counseling!and!testing!
 
 
Use!appropriate!
Flow!Chart(s) 
• 
Find!other!cause!of!anorectal!discharge,!pain!
or!discomfort!and!treat!accordingly!such!as!!
anogenital!warts!and!herpes!simples!!!!
• 
Provide!health!education!
• 
Counsel!on!risk!reduction!
Incontinence,!prolapse,!etc!
Refer!to!Surgeon!
Appointment!in!7!days!
2nd!
Visit!
• 
Take!history!to!assess!treatment!compliance!&!possible!
re-infection.!
• 
Examine!
Anorectal!discharge!or!pain/!discomfort!in!the!
perianal!area!confirmed!
Persistent!Anorectal!discharge!or!pain/!
discomfort!in!the!perianal!
No!dischargeor!pain/!
discomfort!in!the!perianal!
Other!STI(s)!
Use!appropriate!
Flow!Chart(s) 
!
Cured,!Discharge!from!clinic!
Provide!prolonged!Chlamydia!treatment!and!2nd!line!for!
gonorhoea:!
A:!Doxycyline!100mg!PO!12!hourly!for!7!days!
A:!Metronizadole!2!g!PO!stat!!
A:!Inj.!Ceftriaxone!1gm!IM!stat!
!

256!
FLOW CHART 12.6: MANAGEMENT OF OROPHARYNGEAL SYNDROME 

257!
Flow Chart 12.7: MANAGEMENT OF GENITAL ULCER DISEASE (GUD) 
!
!
!
!
1st!Visit!
Patient!complains!of!genital!sore!or!ulcer!
•
Take!history!
•
Examine
Ulcer/Sore!found!
Only!Vesicles!present!
Other!STI(s)!found!
Treat!for!Syphilis,!Chancroid,!LGV&(HSV-2!if!!history!
of!vesicles)!
A:! Benz.! Penicillin! 2.4! MU! i.m! stat! 1/2! in! each!
buttock!
A:!Azithromycin!1g!PO!start!
B:!Acyclovir!400!mg!PO!8!hourly!for!7!days!
Use!appropriate!
Flow!Chart(s)!
Treat!for!HSV-2!
•
Keep!clean!and!dry!
B:!Acyclovir!tabs!400!mg!8!hourly!for!7!days
B:!Acyclovir!cream!
•
Ensure!Compliance!
•
Provide!health!Education!
•
Counsel!on!risk!reduction
•
Partner!management
•
Promote!and!provide!condoms
•
Offer!HIV!counseling!and!testing
•
Offer!follow!up!date!
•
Reassure!
•
Provide!health!education!
•
Counsel!on!risk!reduction
No!ulcer/sore!
No!vesicle!
No!other!STI!
No!Improvement!
Cured!
Other!STI(s)!
Use!appropriate!
Flow!Chart(s)!
2ndVisit!
Appointment!in!7!days!
Take!History!and!Examine!
Treat!with!2nd!line!drug:!
A:!Ceftriaxone!1gm!IM!stat!
Discharge!from!clinic!!
1.
Patients!allergic!to!penicillin!substitute!with!Erythromycin!!500mg!PO!6!hourly!for!!15!days!
2.
Do!not!give!Acyclovir!during!pregnancy!and!breast!feeding.!

258!
Flow Chart 12.8: MANAGEMENT OF NEONATAL CONJUCTIVITIS 

259!
!
FLOW CHART12.9: MANAGEMENT OF INGUINAL BUBOS (IB) 
 
 
 
 
 
 
 
 

260!
Table 12.1 Management of Mixed Infections 
Mixed 
Sexually 
Transmitted 
Infections 
Drug treatment (new episode) 
UDS + SSS 
Ceftriaxone (IM) 250mg stat AND Azithromycin (PO) 1g per week for 
2weeks AND Metronidazole (PO) 2g stat AND Supportive therapy: to 
reduce pain advice bed rest, scrotal elevation with a scrotal support (T-
bandage) and analgesics. 
UDS + Balanitis 
Cefixime (PO) 400mg stat OR Ceftriaxone (IM) 250mg stat AND 
Azithromycin (PO) 1g stat OR Doxycycline (PO) 100mg 12hourly for 
7days AND Metronidazole (PO) 2g stat AND Clotrimazole cream, local 
application 12hourly for 7days 
UDS + GUS 
Cefixime (PO) 400mg stat OR Ceftriaxone (IM) 250mg stat AND Acyclovir 
(PO) 400mg 8hourly for 7days AND Benzathine Penicillin* (IM) 2.4MU 
stat AND Azithromycin (PO) 1g stat OR Doxycycline* (PO)100mg 
12hourly for 7days AND Metronidazole (PO) 2g stat 
VDS + LAP 
Ceftriaxone (IM) 250mg stat AND Azithromycin (PO) 1g per week for 
2weeks AND Metronidazole (PO) 400mg 12hourly for 7–14days. 
Clotrimazole pessary to be added, if vulva oedema, itching, excoriations 
or curd-like discharge present 
VDS + GUS (non-
pregnant) 
Cefixime 400mg stat OR Ceftriaxone (IM) 250mg stat AND Metronidazole 
(PO) 2g stat AND Benzathine Penicillin* (IM) 2.4 MU stat AND 
Azithromycin (PO) 1g stat OR Doxycycline* (PO) 100mg 12hourly for 
7days AND Acyclovir (PO) 400mg 8 hourly for 7 days. Clotrimazole 
pessary to be added, if vulva oedema, itching, excoriations or curd-like 
discharge present 
VDS 
+
GUS
(pregnant, 
breastfeeding) 
Cefixime 400mg stat OR Ceftriaxone (IM) 250mg stat AND Metronidazole 
(PO) 2g stat AND Benzathine Penicillin* (IM) 2.4 MU stat AND 
Azithromycin (PO) 1g stat OR Erythromycin* (PO) 500mg 6hourly for 
7days AND Acyclovir (PO) 400mg 8hourly for 7days. Clotrimazole 
pessary to be added, if vulva oedema, itching, excoriations or curd-like 
discharge present 
LAP + GUS 
Ceftriaxone (IM) 250mg stat AND Metronidazole (PO) 400 mg 12hourly 
for 7–14days AND Benzathine Penicillin* (IM) 2.4MU stat AND 
Azithromycin (PO) 1g per week for 2weeks OR Doxycycline* (PO) 100 mg 
12hourly for 7–14days AND Acyclovir (PO) 400 mg 8hourly for 7days 
SSS + GUS 
Ceftriaxone (IM) 250mg stat AND Benzathine Penicillin* (IM) 2.4MU stat 
AND Azithromycin (PO) 1g per week for 2weeks OR Doxycycline* (PO) 
100mg 12hourly for 7–14days AND Acyclovir (PO) 400mg 8hourly for 
7days 
Note 
In Penicillin-allergic patients: Give Doxycycline (non-pregnant women/men) or Erythromycin 
(pregnant women) for 14days instead of 7days 
12.8   Management of Other Common STI Conditions 
Late Syphilis 
This refers to Syphilis infection of more than 2years. 
A: benzathine benzylpenicillin (IM) 2.4MU once weekly for 3 consecutive weeks. 
AND 
A: azithromycin (PO) 2g stat. 
Syphilis in Pregnancy 
Pregnant women should be regarded as a separate group requiring close surveillance to detect 
possible re-infection after treatment has been given. It is also important to treat the sexual 
partner(s). 

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A: benzathine benzylpenicillin (IM) 2.4MU, as a single dose 
In case of late syphilis 3 doses of benzathine benzylpenicillin should be provided. 
 
Congenital Syphilis 
All infants born to sero-positive mothers should be treated with a single intramuscular dose of 
benzathine benzylpenicillin,  
50000IU/kg whether the mothers were treated during pregnancy (with or without penicillin).  
 
Treatment regimens for early congenital syphilis (up to 2 years of age), and Infants with abnormal 
cerebrospinal fluid: 
A: benzyl penicillin (IV) 100000–150000IU/kg/day administered as 50000IU/kg/dose 
12hourly, for the first 7days and every 8hourly thereafter for a total of 10days 
 
For congenital syphilis in children 2 or more years 
A: benzyl penicillin (IV or IM) 200000 – 300000IU/kg/day administered as 50000IU/kg 
every 4–6hourly for 10–14days 
 
The alternative regimen for penicillin allergic patients, after the first month of life 
A: erythromycin (PO) 7.5–12.5 mg/kg 6hourly for 30days. 
 
Syphilis and HIV Infection 
All patients with syphilis should be encouraged to undergo testing for HIV because of the high 
frequency of dual infection and its implications for clinical assessment and management. 
 
Genital Warts (Venereal Warts) 
Human papilloma virus (HPV) is a common sexually transmitted pathogen. Genital warts are 
painless but may lead to serious complications. The removal of the lesion does not mean cure of the 
infection. No treatment is completely satisfactory. Recommended regimens for venereal warts are as 
follows: 
 
Chemical Treatment (High level Health Facility Management) 
D: Podophyllin 10–25% in compound tincture of benzoin, applied carefully to the warts, 
avoiding normal tissue. External genital and perianal warts should be washed 
thoroughly 4–6 hourly after the application of podophyllin. Podophyllin applied to warts 
on vaginal or anal epithelial surfaces should be allowed to dry before removing the 
speculum or anoscope. Treatment should be repeated at weekly intervals. 
 
Other treatment approaches (Available at higher centres) 
Cryotherapy with liquid nitrogen, solid carbon dioxide, or a cryoprobe. Repeat applications 
every 1-2 weeks 
OR 
Electrosurgery 
OR 
Surgical removal 
 
Treatment for Vaginal Warts 
Recommended regimens for treatment of vaginal warts are: 
D: cryotherapy (with liquid nitrogen) 
OR 
D: podophyllin 10–25% (allow to dry before removing speculum) 
 
Treatment for Cervical Warts 
Treatment of cervical warts should not be started until the results from a cervical smear test are 
known 
 
Management of Meatal and Urethral Wart 
D: Cryotherapy 
OR 
D: podophyllin 10–25% 
Note 
Urethroscopy is necessary to diagnose intra-urethral warts, but they should be suspected in men 
with recurrent meatal warts. 

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CHAPTER THIRTEEN 
SKIN DISEASES AND ALLERGIC REACTIONS 
 
13.1 Bacterial Skin Infections 
Bacterial skin infections can range fromimpetigo, folliculitis, furunculosis, erysipelas, cellulitis to 
recurrent boils. All these skin conditions are caused by either Staphylococcus aureus alone or 
together with streptococcus, but rarely streptococcus alone.  
13.1.1 Impetigo 
Is a contagious primary infection of the skin involving the stratum corneum of epidermis. It is 
particularly common in children and people in disadvantaged areas.  
 
Clinical presentation 
• 
Polycyclic vesicles or blisters, which can contain pus 
• 
Early lesions are isolated or confluent Erosions and yellowish crusts (“honey-colored”) 
 
Fig 13.1 Impetigo 
 
Note 
Impetigo is a clinical diagnosis and the typical location in children is around orifices, especially 
the mouth and nose. 
 
Non-pharmacological Treatment 
• 
Improve personal hygiene 
• 
Hand washing 
• 
Wash lesions with soap and water 
• 
Remove crust 
 
Pharmacological Treatments   
A: Wet dressing with weak potassium permanganate (PP) soaks, 1:40000 (0.025%) 
solution 12hourly for 3–4days. Each session to last for 15 to 20minutes 
A: gentian violet paint (topical) 0.5% 12hourly for 5days 
OR 
C: mupirocin (topical) 2% 12hourly for 5–7days  
OR 
C: fusidic acid (topical) 12hourly for 5–7days 
 
If severe or systemic symptoms are present (e.g. pyrexia) add an oral antibiotic: 
A: phenoxymethylpenicillin (PO): Adult 500mg; paediatric 25mg/kg given 6hourly for 7days 
 
 
 
OR 
A: erythromycin (PO): Adult 500mg; paediatric 25—50mg/kg 8hourly for 10days 
OR 
B: amoxicillin + clavulanic acid 625mg (PO) 8hourly for 5days  
 
13.1.2 Folliculitis 
 
Folliculitis is an infection of the hair follicles commonly due to Staphylococcus aureus, and Gram-
negative bacteria such as Pseudomonas and Candida albicans. 
 
Clinical presentation 
Clinical features depend on risk factors, which may result into Pseudo-folliculitis, Carbuncles 
aggregation and Furuncle (boil). The following are some of the clinical features: 
• 
Scattered or extensive follicular 
pustules  

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•
Macular or papulo-erythematous
lesions, mainly located on thighs,
buttocks, back and bearded area
•
Papules and pustules
•
Post-inflammatory
hyperpigmentation
•
Necrosis 
and 
suppuration 
with
discharge of necrotic core
•
Permanent 
scars 
or 
scarring
alopecia
•
Firm, 
broad 
swollen, 
painful,
fluctuant deep nodules
•
Multiple drainage tracts
•
Fever and general body malaise
Non-pharmacological Treatment 
•
Suspected irritants should be avoided
•
In Pseudo-folliculitis (infection of the follicular opening) of the bearded area, shaving
should be stopped for several weeks until improvement occurs. Hair should be left to grow
to at least 1 mm long.
•
Shaving with electric razors is preferred over manual razors for beard folliculitis. Cleaning
with water and soap
Pharmacological Treatment 
A: potassium permanganate soaks, 1:40000 (0.025%) solution 12hourly for 3–4days. Each 
session for 15 to 20minutes 
Apply:  
A: gentian violet paint (topical) 0.5% 12hourly for 5days 
OR 
C: mupirocin (topical) 2% 12hourly for 7-14days 
OR  
C: fusidic acid (topical) 2% 12hourly for 7-14days 
Note 
If severe, or systemic symptoms are present (e.g. pyrexia) add an oral antibiotic as above in 
impetigo. 
Fungal folliculitis 
A: clotrimazole cream (topical) 12hourly for 4weeks 
OR  
C: miconazole cream (topical) 12hourly for 4weeks 
13.1.3 Abscess 
Abscess is a collection of pus caused by Staphylococcus aureus. 
Clinical presentation 
•
Painful pus-filled nodule
•
Inflammatory erythematous plaque.
•
Fluctuant palpable swelling
•
Fever is rare
•
Lymphangitis and satellite nodes
may be experienced
Non-pharmacological Treatment 
•
By placing hot compresses over the swelling until it breaks
Surgical Treatment 
•
Incision and drainage
Pharmacological Treatment 
Indicated in immunosuppressed patient, involvement of the face. 
A: erythromycin (PO): Adult 500mg; paediatric 25–50mg/kg 8hourly for 7–10days 
OR 
C: flucloxacillin + amoxicillin (FDC) (P0): Adult 500mg; paediatric 25mg/kg 6hourlyfor 7–
10days 

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13.1.4 Erysipelas and Cellulitis 
Erysipelas is an acute superficial spreading infection commonly caused by Streptococci without pus 
formation. Could also be due to Gram negative bacilli. 
Clinical presentation 
A prodrome of fever, chills, and malaise 
•
Locally, a large erythematous, swelling, well-demarcated, and usually raised lesion
•
Regional adenopathy is frequent
•
Superficial blistering secondary to edema,
•
Superficial hemorrhage, may be sometimes be observed
Non-pharmacological Treatment 
•
Bed rest
•
Elevation of the affected part
•
Venous compression is recommended during the acute phase and subsequent weeks to
reduce the risk of lymphedema
•
Prophylaxis of deep venous thrombosis (DVT) should be considered depending on
presence of other risk factors
Pharmacological Treatment
A: Weak potassium permanganate soaks, 1:40000 (0.025%) solution 12hourly for 3–
4days, with each session lasting for 15–20minutes 
AND 
A: silver sulfadiazine cream (topical) 12hourly 24hourly 
OR 
C: mupirocin (topical) 2% 12hourly for 5–7days 
OR  
C: fusidic Acid (topical) 2% 12hourly for 5–7days 
AND  
A: phenoxymethylpenicillin (PO): Adult 250–500mg; paediatric25mg/kg 6hourly for 5–
7days 
OR 
C: flucloxacillin + amoxicillin (FDC) (PO): Adult 500mg; paediatric 25–50/kg 6hourly for 5–
7days 
AND 
A: ibuprofen 400mg (OP) 6hourly for 5days 
Referral: Referif there are local or general signs of severity of developing necrotizing fasciitis. 
13.1.5 Paronychia 
Paronychia is a painful infection that usually occurs at the nail fold. It may occur after injury or minor 
trauma and is caused by Staphylococcus aureus. It may also occur as a result of fungal infection. 
Clinical presentation 
•
Painful nail
•
Redness
•
Swelling
Pharmacological Treatment 
Acute Paronychia 
B: amoxicillin with clavulanic acid (PO) 625mg 8hourly for 14days. 
AND 
C: mupirocin cream (topical) 12hourly for 14days 
OR 
S: clindamycin (PO) 300mg 12hourly for 14days 
Chronic Paronychia (commonly due to fungal infection) 
A: clotrimazole cream (topical) 1%, apply 12hourly for 14days 
AND 
A: fluconazole (PO) 200mg 24hourly for 14days 
OR 
D: itraconazole tablets (PO) 200mg 24hourly for 14days 

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Note 
For acute paronychia incision and drainage may be needed 
 
13.2 Fungal Skin Infections 
13.2.1 Tinea Corporis (Body Ringworm) 
Tinea corporis is a superficial fungal infection (dermatophytosis), commonly on the arms and legs, 
but may occur on any part of the body 
.  
Clinical presentation 
• 
Enlarging raised annular lesions with a central area of clearing  
• 
Fine scales may be present 
• 
Hair loss in areas of infection 
 
 
Tinea corporis- before treatment 
 
 
Tinea corporis- after treatment 
Investigation  
Scraping edge of lesion for KOH  
 
Pharmacological Treatment 
A: benzoic acid compound ointment (topical) 12hourly up to 2weeks. 
OR 
C: miconazole cream (topical) 2%, apply thinly 12hourly a day. Continue for 5-7days after 
clearing of lesions. 
 
 
OR  
C: terbinafine cream (topical) 12hourly for 2weeks 
 
If extensive, use 
                 C: terbinafine (PO) 250mg 24hourly for 2weeks 
 
13.2.2 Tinea Capitis 
Is a superficial fungal infection (dermatophytosis), on the scalp. It is quite common in children. 
 
Clinical features 
• 
Enlarging raised annular lesions with a central area of clearing  
• 
Fine scales may be present 
• 
Hair loss in areas of infection 
 
Pharmacological Treatment 
C: miconazole cream (topical) 2%, apply thinly 12hourly for 2weeks. Continue for 5-7days 
after clearing of lesions 
AND 
 
A: griseofulvin (PO): Adult 500 mg; Paediatric 10-20mg/kg 24hourly for 6-8weeks 
OR  
C: terbinafine (PO): Adult 250mg 24hourly 6-8weeks; paediatric 62.5mg/ 10-20kg 24 
hourly; 125mg/ 21-40 kg 24 hourly; 250mg/ 41kg 24hourly 
 
13.2.3 Pityriasis Versicolor 
It is a common fungal infection caused by yeast.  

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Clinical presentation 
• 
Hypo/Hyper pigmented macules and confluent patches 
• 
Lesions have fine scales 
• 
Commonly occurs on the chest, back, arms and occasionally neck and face 
Investigation  
• 
KOH 
 
Pharmacological Treatment 
A: clotrimazole cream (topical) 12hourly for 2weeks 
OR 
C: miconazole nitrate cream (topical) 2% 12hourly for 2weeks 
OR 
C: ketoconazole shampoo 3times per week for 4weeks (if extensive) 
AND  
A: fluconazole (PO) 300mg stat 
OR 
D: itraconazole (PO)200mg 24hourly for 2weeks 
13.2.4 Tinea Pedis (Athlete’s Foot) and Tinea Cruris 
It is a common fungal infection of the toes and is often the source of infection at other sites 
especially groin. 
 
Clinical presentation  
• 
Tinea pedis presents with erythema and maceration between the toes, sometimes 
accompanied by painful vesicles. 
• 
The chronic form is characterized by scaling, peeling on the soles. 
• 
Tinea cruris-Itching and patches in the groin. Check for interdigital maceration for all with 
tinea cruris. 
 
Prevention and Non-Pharmacological Treatment 
• 
Frequent change of socks/footwear, underwear. 
• 
Use of cotton socks, underwear. 
• 
Keep as dry as possible the spaces between toes after bathing always. Separating the 
opposing skin surfaces (e.g. with a piece of gauze) will help speeding healing. 
 
Pharmacological Treatment 
A: clotrimazole cream (topical) 1% apply 12hourly for 2weeks 
OR 
C: miconazole cream (topical) 2%apply 12hourly for 2weeks 
OR 
C: terbinafine cream (topical) 24hourly for 14days 
AND 
A: gentian violet 24hourly for 14days for bacterial super infection 
Alternatively 
C: terbinafine (PO) 250mg 24hourly for 2- 4weeks  
OR 
D: itraconazole (PO) 200mg 24hourly for 2-4weeks 
 
13.2.5 Candidiasis 
It is a fungal infection mainly caused by yeast, Candida albicans. Candidiasis is usually precipitated 
by prolonged use of contraceptive pills, AIDS, pregnancy,diabetes, prolonged use of antibiotics, 
corticosteroid use, and being on immunosuppressive treatment 
 
Clinical presentation (depending on the site of infection) 
• 
Erythematous, moist exudate in the skin folds and accompanying satellite pustules 
• 
Nail affection leads to painful swelling of the nail bed and folds, with pus discharge and is 
made worse by contact with water  
• 
Oral lesions are characterized by white, adherent mucosal plaques in buccal cavity 
including the tongue  

267!
•
Vaginal candidiasis is characterized by itchy, curd-like whitish vaginal discharge, dysuria
and dyspareunia
•
Gastrointestinal candidiasis may be associated with painful swallowing (odynophagia).
Characteristic lesions are seen on endoscopy.
Pharmacological Treatment 
Cutaneous candidiasis 
A: clotrimazole cream (topical) 1% apply 12hourly for 2weeks 
OR 
C: miconazole cream (topical) 2% apply 12hourly for 2weeks 
OR 
Oral candidiasis 
A: nystatin oral suspension - gurgle and swallow 6hourly a day 
•
Newborns: 200,000–400,000 Units for 24 hours
•
<2 years old 400,000–1,000,000 Units for 24 hours
>2 years old 1,000,000–2,000,000 Units for 24 hours
OR 
C: miconazole 2 % oral gel apply every 8hourly for 7days 
Vaginal candidiasis 
A: clotrimazole vaginal pessaries; insert one at night for 6days 
OR 
C: miconazole vaginal pessaries insert one at night for 3day 
AND (if severe) 
A: fluconazole (PO) 150mg stat 
Gastrointestinal Tract (GIT) candidiasis 
A: fluconazole (PO) 150mg 24hourly for 14days 
13.2.6 Onychomycosis 
It is defined as infection of the nail plate by fungus. Patients with diabetes or peripheral neuropathy 
may be at a higher risk. 
Clinical presentation 
•
Yellowish discoloration of the nail
•
Subungual hyperkeratosis
•
Over time lesions become more prominent and spread until the entire nail is affected
Investigations 
•
LFT before starting treatment and monitoring monthly.
Pharmacological Treatment 
A: fluconazole (PO) 150-300mg once weekly for 6–12months 
OR 
C: terbinafine (PO) 250mg 24hourly for 6-8weeks. For toe nails the duration of treatment is 
generally 12–16weeks. 
OR 
D: itraconazole (PO) 200mg 12hourly for 7days is given as pulsed dosing, of each month 
for 6months 
Note 
terbinafine and itraconazole should not be used in pregnancy and while breastfeeding 
13.2.7 Chromoblastomycosis 
Chronic infection involving inoculated after minor trauma e.g. thorn prick. 
Clinical presentation 
•
Nodule that progressively increases in into verrucous plaque

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D: itraconazole (PO) 200mg 24hourly for 6-9months 
13.2.8 Mycetoma (Madura Foot) 
Is a chronic infection of skin and subcutaneous tissue? It can be caused infection by fungi or 
bacteria. Once tests have established the etiology, the term Actinomycetoma is used for bacterial 
form, while Eumycetoma is used for the fungal form. Clinical presentation depends on the affected 
site and the disease can last for months to years.  
Clinical presentation 
•
First lesion: nodule
•
Localization: feet, legs, arms, buttocks, scalp, trunk
•
Discharging sinuses where grains may be visible usually white yellow for Actinomycetoma
or black for Eumycetoma
•
Pain before rupture of discharging sinus
Investigations 
•
KOH
•
Biopsy
•
Local Xray to rule infiltration of
underlying bone.
Treatment of Actinomycetoma (bacteria form) 
Pharmacological Treatment 
A: co-trimoxazole (PO) 480mg–960mg 12hourly for 5weeks 
AND 
S: amikacin 7.5mg/kg 12hourly for 5weeks 
Alternatively  
A: co-trimoxazole (PO) 480mg–960 mg 12hourly for 5weeks 
AND 
S: dapsone (PO): adult 100mg 24hourly for 2–4months; Paediatric 25–50mg 24hourly for 
5weeks 
Treatment of Eumycetoma (Fungi 
form) Non-pharmacological Treatment 
•
Surgery where indicated
•
Footwear and protective clothing in at-risk populations e.g. cattle herders
Pharmacological Treatment 
D: itraconazole (PO) 200mg 12hourly for 5weeks or longer (up to a year).  
Referral to surgeon 
•
Radical surgery for some cases.
13.3 Parasitic Infestations 
13.3.1 Scabies 
Scabies is an intensely pruritic and highly contagious infestation of the skin caused by mite 
Sarcoptes scabies.  
Clinical presentation 
•
Itchy vesicles and papules. Itching worse at night.
•
Papules in between finger spaces, wrists, penis and scrotum.
•
Someone else in the family is itching.
Non-pharmacological Treatment 
•
Treat all members of the household at the same time to prevent reinfection, regardless of
presence or absence of itching.
•
Advise patients to bath and dress regularly and changing bed linen at the same time of
treatment.
Pharmacological Treatment 
A: benzyl benzoate emulsion, BBE (25% for adults, 12.5% for children) 
Adults and children over 2 years: Apply with fingers, from neck down to cover the whole-
Pharmacological Treatment 

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!
body surface, while paying attention to all skin folds. Leave emulsion in place for 6-8 hours 
overnight.  
Repeat the application after 7 days. 
OR 
C: lindane lotion (1%) to be applied as BBE above (do not use in children less than 1 year) 
AND  
C: betamethasone valerate cream (topical) 12hourly for the itch 
AND 
A: cetirizine (PO) 10mg 12hourly for 3- 4weeks  
OR (if extensive, Norwegian scabies) 
A: ivermectin (PO) 200microgram/kg stat then repeat after 1week 
 
Should be in combination with the topical above  
 
13.4 Viral Infections 
13.4.1 Herpes Simplex 
It is an acute viral infection caused by Herpes simplex virus hominis (types HSV1, HSV2 acquired by 
close contact with an infected individual 
 
Clinical presentation 
• 
Preceding tingling sensation, discomfort and itching,  
• 
Grouped vesicles forming on the skin, and mucous membranes, particularly the 
buccal area, genitalia, conjunctivae, and cornea,  
• 
Eczema herpeticum –herpes simplex infection in Atopic Eczema patients. 
 
Pharmacological Treatment 
B: acyclovir cream (topical) applied 4hourly for 7–10days 
OR (especially if severe) 
B: acyclovir (PO) 200mg 6hourly for 7–10days 
 
For recurrent cases  
B: acyclovir (PO) 400mg 12hourly for 6months up to 1year. 
 
Note 
Benefit of systemic acyclovir is optimum when given within the first 72hours of onset of symptoms 
 
13.4.2 Chickenpox 
It is a highly infectious disease caused by Varicella zoster virus (VZV) 
 
Clinical presentation 
• 
Red macular rash with a 
central vesicle (blister) on the 
trunk, oral mucosa and scalp 
• 
Pustules and crusting 
• 
Intense pruritus  
• 
Occasional 
regional 
lymphadenopathy 
 
Pharmacological Treatment  
B: acyclovir (PO) 800mg 6hourly for 7days 
AND 
A: paracetamol (PO)1g 8 hourly for 4–5days 
AND  
A: calamine lotion (topical) 1% phenol, apply over the whole body 12hourly for 7days. 
 
13.4.3 Herpes Zoster (Shingles) 
It is due to resurgence or reactivation of the Varicella zoster virus infection which also causes 
chickenpox.  
 
Clinical presentation 
• 
Severe burning pain  

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•
Grouped vesicles overlying erythematous skin following a dermatomal distribution;
typically, lesions do not cross the midline
Pharmacological Treatment 
B: acyclovir (PO) 800mg 6hourly for 7–10days 
Wound care 
A: potassium permanganate soaks (1:4000) 12hourly for 3–4days 
For Secondary infection (bacterial) apply 
A: silver sulfadiazine cream (topical) applied 12hourly for 5days 
OR 
C: mupirocin 2% cream 12hourly for 5days 
13.4.4 Post-herpetic Neuralgia 
A complication of shingles (herpes zoster). 
Clinical presentation 
Intense pain described as burning, stabbing, or gnawing. 
Pharmacological Treatment 
A: amitriptyline (PO) 25mg at night, may be increased to 150mg at nightfor 4 weeks 
OR 
D: pregabalin (PO) 75-150mg 24hourly or divided doses for 2-4weeks 
Referral: Refer immediately to Ophthalmologist in case of herpes zoster ophthalmicus for 
atropinization 
13.4.5 Molluscum Contagiosum 
It is viral infection common in children and immunocompromised individuals. 
Clinical presentation 
•
Skin coloured umbilicated papules
•
It usually clears without treatment in 12-18months.
Molluscum contagiosum
Pharmacological Treatment: 
A: benzoyl peroxide 24hourly for 4weeks 
OR 
S: tretinoin cream (topical) 2.5 % 24hourly for 4weeks 

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Surgical treatment 
C: Cryotherapy 
D: Curatage 
13.4.6 Viral Warts 
Infection due to Human Papilloma Virusinclude; common warts, planar warts, and plantar warts, oral 
warts. 
Clinical presentation 
•
Verrucous papules on the body, palms, soles, genital and oral mucosa.
•
Painful on applying pressure for warts on palms and soles.
Pharmacological Treatment 
C: silver nitrate pencil 3times per week for 4weeks for plantar, common warts. 
OR 
S: tretinoin cream (topical) 2.5% 12hourly for 4weeks for planar warts. 
Surgical treatment 
C: Cryotherapy  
D: Curatage 
D: Excision of large warts 
Note 
For treatment of Genital warts refer to Sexually Transmitted Infections chapter 12 
13.5 Eczema (Dermatitis) Conditions 
13.5.1 Contact Dermatitis 
It is a delayed hypersensitivity reaction following skin meeting a chemical. This may be a dye, 
perfume, rubber, nickel, drugs, skin preparations containing lanolin, iodine, antihistamines, 
neomycin etc. 
Clinical presentation 
•
Red papulo-vesicular rash with
ill-defined margins 
•
Itching, which may be severe
•
Dry, cracked, scaly skin, if
•
Blisters, 
draining 
fluid
(weeping) and crusting, with 
severe dermatitis
•
Swelling, 
burning
or 
tenderness
chronic 
Investigations 
Patch test 
Non-pharmacological Treatment 
Avoid contact with allergen 
Pharmacological Treatment 
A: potassium permanganate soaks, 1:4000 solutions 12hourly for 5days each session 
lasting 15-20minutes (For weeping lesions weak) 
AND (for mild cases) 
B: betamethasone valerate 0.1% cream/ointment 12hourly for 4weeks 
OR(for moderate cases) 
S: mometasone furoate cream/ointment (topical) 12hourly for 4weeks 
OR (IF severe cases) 
D: clobetasol propionate 0.05% cream/ointment (topical) 12hourly for 4weeks 
Note 
A single application with occlusion at night is often more effective than multiple daytime 
applications. 

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13.5.2 Atopic Eczema 
It is a dermatitis/Eczema on a background of atopy. Hence there is often a personal or family history 
of atopic disease (asthma, hay fever or atopic dermatitis).  
 
Clinical presentation 
• 
Pruritus- face in children, flexures, 
nape  
• 
Chronic or chronic recurrent course 
• 
Positive personal or family history 
of atopy 
• 
Acute forms are weepy, chronic 
forms are lichenified, scaly 
 
 
 
Acute atopic eczema 
 
 
atopic dermatitis-lichenified and scaly 
 
Investigations 
FBP, prick test, patch test, Ig E levels 
 
Non-pharmacological Treatment  
• 
Education about chronicity of problems  
• 
Remove any obvious precipitant e.g. skin irritants or allergens (avoid irritants e.g. 
medicated soap, wool and extremes of temperature). 
• 
Generous use of emulsifiers (skin moisturizers) 
• 
Bath oils/soap substitutes  
 
Pharmacological Treatment 
A: promethazine (PO) 25mg at bedtime increased to 50mg if necessary, for 2weeks 
 
 
OR 
A: cetirizine (PO) 10mg 24hourly for 2weeks  
 
 
OR 
 
 
C: loratadine (PO) 10mg 24hourly for 2weeks 
 
 
 
AND 
A: hydrocortisone 1% ointment (topical) 12hourly (if mild disease, or on face) 
 
 
OR 
C: betamethasone valerate cream/ointment (topical) 0.1% or 0.25% 12hourly for other 
parts of the body.  
OR (in severe cases) 
D: clobetasol propionate cream/ointment (topical) 0.05% 12hourly for up to 8weeks 
OR 
S: tacrolimus ointment (topical) 0.03%/ 0.1% 12hourly not less than 1month 
 
In case of skin atrophy on the face and in children >1 year 
D: prednicarbate cream (topical) 0.1 % 24hourly for 
 
For severe cases- Erythroderma 
Extensive involvement of the whole body 
• 
Patient needs admission  
• 
Oral antibiotics as in impetigo 
• 
Short course of systemic steroid therapy-  
 
A: prednisolone (PO) 0.5 -1mg/ kg 24hourly for 1-2weeks then taper.  
 
• 
For recalcitrant cases 
S: methotrexate (PO) 7.5- 20mg weekly for not less than 3months 
OR  

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S: cyclosporine 3-5mg/kg/day up to 3months 
•
Phototherapy
Treat any infection (usually bacterial, but occasionally viral- eczema herpeticum).  
Choice of skin preparations depends on whether lesions are wet (exudative) or dry/lichenified 
(thickened skin with increased skin markings). 
o
If eczema is “weepy”, use saline baths or bathe in:
A: Potassium permanganate 1:4000 (0.025%) solution 24 hourly for 2-4 days until dry. 
Where large areas are involved give a course of antibiotics for 5-10 days (as for impetigo) 
o
After the lesions have dried, apply an aqueous cream for a soothing effect.
Start with mild topical steroid cream for wet lesions and use ointment for dry skin lesions.  
If the skin starts scaling (condition becomes chronic), add/apply an emollient such as: emulsifying 
ointment or liquid paraffin. 
Note 
Potent topical corticosteroids may cause harmful cutaneous and systemic side effects especially if the 
use is prolonged or involves extensive body surface. Striae, acne, hyperpigmentation and 
hypopigmentation, hirsutism and atrophy may result. Therefore, avoid long term use; don’t use on 
weepy or infected skin. Advise patients NOT to use them as cosmetics (eg for skin lightening purposes) 
Example of Classes of Topical steroids; 
Very Potent (0.05% clobetasol propionate), Potent (0.1% betamethasone valerate Mometasone 
furoate), Moderately Potent (0.05% clobetasol butyrate), Mild (1% hydrocortisone) 
13.5.3 Seborrheic Dermatitis 
Chronic recurring inflammatory skin disorder associated with Malassezia species. 
Clinical presentation 
•
Erythematous
macules, 
plaques
•
Pruritus
•
Scalp, face, chest, back axilla
and groin
Pharmacological Treatment 
A: clotrimazole cream (topical) 12 hourly for 4-16weeks 
OR 
C: miconazole cream (topical) 12 hourly for 4-16weeks 
AND 
A: hydrocortisone cream (topical) 0.5% 12 hourly for 4-16weeks 
OR 
C: ketoconazole shampoo 3 times per week for not less than 3 months 
13.6 Anaphylaxis 
It is an acute and often life-threatening immunologic reaction, frequently heralded by scalp pruritus, 
diffuse erythema, urticaria, or angioedema. Bronchospasm, laryngeal edema, hyperperistalsis, 
hypotension, and cardiac arrhythmia may occur. Antibiotics (especially penicillins), other drugs, and 
radiographic contrast agents are the most common causes of serious anaphylactic reactions.  
Prevention and Non-Pharmacological Treatment 
•
If acute (existing for less than 3 months), exclude drug reactions (e.g. penicillin), or
infection
•
Avoid precipitants
For management refer to emergency and critical care chapter. 
13.7 Papulosquamous Disorder 
13.7.1. Psoriasis 
It is an inherited inflammatory condition of the skin 

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Clinical presentation 
•
Thick, silvery white scaly plaques affecting mainly scalp, sacral region and extensor
body surfaces
•
Usually symmetrically distributed, with a chronic relapsing course.
•
Can involve joints
Note 
Exclude precipitating factors e.g. alcohol, deficiencies of B12 or folate, stress, streptococcal 
infections. 
Non-pharmacological Treatment 
Sun exposure to the lesions for half an hour or one hour daily may be of benefit 
Pharmacological Treatment 
C: crude coal tar 5% in Vaseline in the morning for not less than 3months 
AND 
C: salicylic acid 5% in Vaseline to de-scale, apply at night for not less than 3months 
AND 
C: betamethasone valerate ointment (topical) 0.25% 12hourly for not less than 12weeks. 
OR 
C: betamethasone dipropionate+ salicylic ointment (topical) 12hourly for not less than 
4months 
In severe disease 
D: clobetasol propionate cream/ointment (topical) 0.05% 12hourly for not less than 
4months 
For extensive involvement > 20% body surface area and involvement of joints 
ADD 
S: methotrexate (PO) 7.5-20mg weekly for not less than 6months 
Note 
Systemic steroids should not be used in psoriasis due to their rebound effect. 
13.7.2. Lichen Planus 
It is an extremely pruritic chronic inflammatory skin condition. 
Clinical presentation 
•
Primary lesions are violaceous, shiny flat-topped papules
•
Coalesce and evolve into scaly plaques
•
Distributed over inner wrists, arms and thighs as well as sacral area.
•
Post inflammatory hyperpigmentation is common.
•
Scarring alopecia may result from lichen planopilaris (severe)
Pharmacological Treatment 
C: loratadine (PO) 10mg 24hourly for 2-4weeks 
AND 
C: betamethasone valerate ointment (topical) 0.1% 12hrly for 2–4 weeks 
OR 
D: clobetasol propionate ointment (topical) 0.05%–0.1% twice daily for 2–4weeks 
AND 
for extensive involvement 
A: prednisolone (PO) 0.5-1 mg/kg 24hourly for 3-4weeks then taper 
For recalcitrant cases 
S: methotrexate (PO) 7.5- 20mg weekly for not less than 6months 

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13.7.3 Acne 
Acne is a multifactorial disease primarily of teenagers with follicular plugging and inflammation. 
Clinical presentation 
•
Open and closed comedones
•
Pustules, papules
•
Nodular and cystic lesions involving the face, chest, shoulder and the back
Non-pharmacological Treatment 
•
Avoid underlying precipitating factor e.g. stress, nuts, chocolate, overuse of ointments
on skin, steroids, anticonvulsant drugs etc.
•
Encourage a healthy lifestyle – exercise, sunshine exposure, etc.
•
Use ordinary soap (harsh antibacterial cleansers or iodine-containing preparations
may aggravate the acne)
•
Do not manipulate pustules and nodules
Pharmacological Treatment 
Mild to moderate acne without scarring 
Apply 
A: benzoyl peroxide 2.5%–5% once nocte 
  OR 
S: tretinoic acid cream (topical) 0.05% once nocte 
Moderate acne with scarring- 
A: doxycycline (PO) 100mg 24 hourly for 1–3 month 
     OR 
A: erythromycin (PO) 250mg 6 hourly for 1–3 month 
    AND 
A: benzoyl peroxide or topical retinoid as above. 
Nodulocystic and/or conglobate acne 
S: isotretinoin (PO) 0.025–0.5mg/kg 24hourly for at least 3–6months 
AND 
S: triamcinolone (intralesional) 40mg/ml for cysts stat 
Acne fulminans 
S: isotretinoin (PO) 0.025–0.5mg/kg 24 hourly for at least 4–6 months 
AND 
A: prednisolone (PO) 45mg stat then 5mg reduction daily up to 0mg. 
Note 
Isotretinoin is contraindicated in pregnant women. 
13.8 Drug Reactions 
Drug reactions can be classified in many ways. One useful approach is to separate predictable 
reactions occurring in normal patients from unpredictable reactions occurring in susceptible patients. 
Predictable adverse reactions; 
•
Over dosage (wrong dosage or defect in drug metabolism)
•
Side effects (sleepiness from antihistamines)
•
Indirect effects (antibiotics changing normal flora)
•
Drug interactions (altered metabolism of drugs; most commonly involving the cytochrome
P-450 enzymes)
Unpredictable adverse reactions 
•
Allergic reaction (drug allergy or hypersensitivity; immunologic reaction to drug;
requires previous exposure or cross-reaction)

276!
•
Pseudo allergic reaction (non-immunologic activation of mast cells).
•
Idiosyncratic reaction (unexplained reaction, not related to mechanism of action,
without known or suspected immunologic mechanism).
Note 
•
80% of allergic and pseudo allergic drug reactions are caused by Beta-lactam antibiotics,
aspirin, NSAIDs, andSulfonamides
13.8.1 Fixed Drug Eruption (FDE) 
It is a cutaneous drug reaction that recurs at the same site with repeated exposure to the agent. 
Clinical presentation 
•
Typically, red-brown patch or plaque
•
Occasionally may be bullous
•
common sites are genitalia, palms, and soles, as well as mucosa
•
Often multiple. Starts with edematous papule or plaque later becomes darker
•
Resolves with post-inflammatory hyperpigmentation
Note 
•
When confronted with hyper pigmented macule on genitalia, always think of Fixed Drug
Eruption
Non-pharmacological Treatment 
•
Avoidance of triggering drug;
Pharmacological Treatment 
A:  hydrocortisone (IV) 200mg 12hourly for 24hours 
AND 
B: betamethasone valerate cream (topical) 12hourly for 2weeks 
OR 
D: clobetasol propionate cream/ointment (topical) 0.05% 12hourly for 2- 4weeks 
13.8.3 Stevens Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) 
It is a life-threatening condition caused by reaction to drugs e.g. sulphur containing drugs. It causes 
the skin to blister and peel off. Less than 10% of body surface area involved. Is referred to as SJS. 
SJS progresses to Toxic Epidermal Necrolysis (TEN) with involvement of more than 2 mucosal 
surfaces. 
Clinical presentation 
•
Patients usually have prodromal with fever, malaise, and arthralgia’s
•
Erosions, hemorrhage and crusts on lips, and erosions in mouth covered by necrotic white
pseudo membrane
•
Involvement of the eyes: Erosive conjunctivitis, can lead to scarring
•
Involvement of genitalia with painful erosions
•
Sudden appearance of diffuse macules or diffuse erythema,
•
Early sites of cutaneous involvement are the presternal region of the trunk and the face,
but also the palms and soles.
•
Then prompt progression with widespread erythema and peeling of skin; skin lies in sheets
and folds on the bedding.
Pharmacological Treatment 
•
Identify and discontinue potential offending medications/drugs.
•
Transfer patient to intensive care unit or critical care unit or burn unit.
•
Wound care
•
Keep warm
•
Monitor fluid input and output –urine output 0.5-ml/kg/hour. Monitor electrolytes.
•
Consultations – Ophthalmologist, Physician, Dermatologist

277!
SCORTEN SCORE for determining prognosis of patient 
•
Age >40years
•
Malignancy
•
Total body surface area affected
>10%
•
Heart rate >120 beats/ min
•
Blood urea nitrogen >28mg/dl
•
Serum glucose >250 mg/dl
•
Serum bicarbonate <20mEq per 1
Calculate SCORTEN on days 1 & 3 of hospital 
stay Pharmacological Treatment 
A: hydrocortisone (IV) 200mg 12hourly for 48hours 
AND 
A: prednisolone (PO) 1–2mg/kg 24hourly for 5–7days 
Antibiotics in case of infection (as for treatment of sepsis) 
Note 
•
Topical sulfur containing medications should be avoided.
•
Systemic corticosteroids, if employed, should be used early to attempt to abort the immunologic
reaction (first 24 hours).
13.10 Pellagra 
Is a disease caused by deficiency of nicotinic acid? Cardinal signs: diarrhea, dermatitis (sites 
exposed to sun) and dementia. 
Clinical presentation 
•
Casal’s necklace; hyper-pigmented scaling involving the neck region
•
Hyper-pigmented scaly lesions on sun exposed areas
Pharmacological Treatment 
Treat both adults and children 
A: vitamin B complex (PO) 12hourly for 2months  
C: nicotinamide (PO) 500mg 24hourly for 4weeks or until healing is complete;In children: 
5mg/kg 24hourly for 4weeks or until healing is complete. 
Note 
The diet should be rich in deficient nutrients i.e. protein (meat, groundnuts, and beans) 
13.11 Vitiligo 
Is a condition presenting with patchy depigmentation of skin? 
Clinical presentation 
•
Depigmented patches commonly on the face, neck, trunk and extremities
•
Mucosal surfaces particularly oral and genital areas can also be depigmented
Pharmacological Treatment 
There is no cure for vitiligo, but there are several treatments that can improve the condition. 
C: betamethasone valerate ointment 0.1% 12hourly for 2–4 months 
OR 
S: tacrolimus 0.1% ointment 12hourly for facial lesions and children 
AND 
D: clobetasol propionate cream (topical) 0.05% 12hourly 
OR  
S: PUVA+ sun exposure 
Note 
Counsel the patient about the condition. 

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13.12 Pruritic Papular Eruption (PPE) 
A skin condition characterized by itchy papular eruptions on the extensor area of the upper and 
lower limbs which is associated with HIV infection. 
Clinical presentation 
•
Papular 
lesions 
on 
the
extensor areas
•
Extremely itchy
•
Excoriation
•
Lesions 
heal 
with 
hyperpigmented scars 
Pharmacological Treatment 
C: betamethasone valerate cream (topical) 0.025% 12hourly for 3–4weeks 
AND 
A: cetirizine (PO) 10mg 12hourly for not less than 4weeks 
OR 
S: dapsone (PO) 100 mg 24hourly for not less than 4weeks 
13.13 Oculo-cutaneous Albinism and Xeroderma Pigmentosum 
These are recessive inherited oculo-cutaneous conditions. 
Albinism characterized by the complete or partial absence of pigment (melanin) in the skin, hair and 
eyes. 
Clinical presentation 
•
Eye problems-photophobia, nystagmus, impaired vision
•
Loss of pigment on skin and hair
•
Freckles
Xeroderma Pigmentosum 
Genetic disorder in which there is a decreased ability to repair DNA damage such as that caused by 
ultraviolet light. 
Clinical presentation  
•
Freckling in sun exposed areas
•
Dry skin
•
Changes in skin pigmentation
•
Extreme photophobia
Non-pharmacological Treatment 
•
Counseling of parents that are genetic diseases
•
People with Xeroderma pigmentosum should avoid sunlight as much as
possible.
•
Patients are strongly advised to wear sun protective clothing (long sleeved shirt,
blouse, skirt and trousers and wide brimmed hats to prevent skin cancers)
•
Sun protective glasses with special ultraviolet B (UVB) filters
•
Advice on indoor income generating activities
•
Cryotherapy of early lesions
Pharmacological Treatment 
C: Sunscreen applications of SPF 30+ or above, applied twice a day at 8am and noon 
AND 
S: 5 Fluoro-uracil topical application of early lesions 
  Surgical treatment 
•
Excision of lesions
•
Refer to oncologist in extensive involvements

279!
Note 
Sunscreen lotions and creams contain physical and chemical products that absorb or scatter 
ultraviolet rays that would otherwise cause damage to skin. 
Uses of sunscreen; 
•
Albinism and xeroderma pigmentosum to prevent sunburn, and reduce risk of squamous
cell carcinoma, B cell carcinoma and melanoma.
•
Skin conditions e.g. Lupus Erythematosus, dermatomyositis whereby ultraviolet light
exacerbates these conditions
•
Normal use to prevent photoaging of the skin
13.14 Urticaria and Angioedema 
Chronic recurrent whealing of the skin, with or without angioedema. Associated with atopy. 
Clinical presentation 
•
Wheals which disappear within 24 hours
•
With or without Swelling of tongue or lips
•
Maybe precipitated by spices, food, food colourants, drugs.
Investigations 
•
FBP and ESR
•
Stool for ova and parasite
•
Autoantibodies-ANA
•
Thyroid function test
•
Prick and patch tests
Non-pharmacological Treatment 
•
Avoid precipitating factors e.g. NSAIDs, food, spices
•
Treat any infection appropriately fungal, viral if suspect H pylori investigate and treat as per
gastrointestinal section.
•
Deworm
Pharmacological Treatment   
Antihistamine can be increased to maximum dose for not less than 12weeks 
A: cetirizine 10mg 12hourly 4weeks can be increased up to 4 folds 
OR 
C: loratadine 10mg 24 hourly dose can be increased up to 4 folds 
OR 
S: desloratadine 5mg 24 hourly for not less than 16weeks 
AND 
D: montelukast 10mg 24hourly for not less than 16weeks 
13.15 Connective Tissue Diseases 
Are autoimmune diseases of unknown etiology that affects the skin, blood vessels and internal 
organs. 
Clinical presentation 
Scleroderma 
•
Localized scleroderma- shiny plaques on the extremities, scalp, hands
•
Systemic scleroderma- skin involvement, Raynaud phenomena, internal organ
involvement
Lupus erythematosus 
•
Discoid Lupus Erythematosus- hypo/depigmented plaques, follicular plugging on the
face mostly
•
Systemic Lupus - malar rash, discoid rash, photosensitivity, oral ulcers, arthritis, serositis,
renal disease
Dermatomyositis 
•
cutaneous-gottrons papules, heliotrope rash
•
proximal muscle weakness- inability to comb hair
•
inability to rise when squats

280!
Investigations 
•
FBP and ESR
•
LFTS
•
RFTS
•
Urinalysis
•
Autoantibodies- 
ANA, 
anti-dsDNA, 
anti-centromere, 
anti-scleroderma 
70, 
Anti- 
phospholipids, Anti- SM
•
Creatine kinase levels
•
Biopsy
•
Monitoring liver, renal and blood count 3 monthly
•
RBG every 3 months for patients on corticosteroids for long
Non-pharmacology Treatment 
•
Ophthalmology review before starting hydroxychloroquine and every 6 months after.
•
Monitor blood pressure
•
Use of sun protective factor (SPF) lotion and clothing especially for dermatomyositis and
Lupus.
•
Keep extremities warm
•
Physiotherapy
•
Involve physician
Pharmacological Treatment 
Deworm- Albendazole 400mg stat 
Localized scleroderma: 
D: clobetasol propionate cream / ointment (topical) 0.05% 12hourly 
Systemic scleroderma 
A: prednisolone (PO) 0.5-1mg /kg 24hourly for stabilizing then taper slowly 
AND  
S: methotrexate (PO) 7.5- 20mg weekly 
Discoid Lupus Erythematosus 
D: clobetasol propionate cream/ointment (topical) 0.05% 12hourly 
 AND       
S: hydroxychloroquine (PO) 200mg 24hourly for not less 3months 
Systemic Scleroderma 
D: clobetasol propionate cream/ointment (topical) 0.05% 12hourly 
AND 
A: prednisolone (PO) 0.5- 1 mg 24hourly for 4weeks then taper to lowest level that is 
effective.  
AND 
S: methotrexate (PO) 7.5- 20mg weekly 
AND 
A: omeprazole (PO)20mg 24hourly when needed for patients with gastritis, peptic ulcer 
disease. 
Dermatomyositis 
A: prednisolone (PO) 1mg/ kg 24hourly for 12weeks till improvement then start tapering to 
lowest effective dose 
AND 
S: methotrexate (PO) 7.5-20mg weekly for at least 6months 

281!
13:16 Autoimmune Blistering Disease 
Conditions in which autoantibodies target components of the skin and mucous membranes, leading 
to blister and bullae formation. These include pemphigus vulgaris, foliaceous, vegetans, Bullous 
pemphigoid, Dermatitis herpetiformis, Linear IgA. 
Clinical presentation 
•
Tense or flaccid Vesicles and bullae on the skin and mucus membranes
•
Vegetative plaques in axillae or groin
Linear IgA 
Investigations 
•
Biopsy
•
Immunofluorescence studies
•
FBP, LFT, RFT
Pharmacological Treatment 
C: betamethasone cream/ointment (topical) 12hourly till improves 
OR  
D: clobetasol propionate cream/ointment (topical) 0.05% 12hourly till improves 
 AND  
A: prednisolone (PO) 0.5-1mg/kg 24hourly for 2months then taper slowly to lowest 
effective dose 
AND in extensive involvement 
S: methotrexate (PO) 7.5 – 20mg weekly for not less than 4months 
  Treatment of Dermatitis Herpetiformis /pemphigus foliaceous 
S: dapsone (PO)100mg 24hourly for not less than 2months 
13.17 Keloids 
Excessive connective proliferation following an injury or spontaneously. 
Clinical presentation 
•
Skin coloured nodules, plaques extending beyond the scar line commonly on
earlobes.
Pharmacological Treatment 
S: triamcinolone (intralesional) 2.5-5mg/ml monthly for 4-6months for small – medium 
sized keloids.  
Surgical treatment 
S: total excision or debulking of keloids Inj Triamcinolone 20mg intraoperatively and post 
operatively for 3 months. 
13.18 Folliculitis Decalvans 
Characterized by pustules, papules, keloids and scarring alopecia on the nape of the scalp. 

282!
Pharmacological Treatment 
A: doxycycline (PO) 100mg 12hourly for 2-4weeks 
OR 
S: clindamycin (PO) 300mg 12hourly for 3months 
AND 
D: clobetasol propionate cream/gel (topical) 0.05% 12hourly for not less than 16weeks 
ANDin recalcitrant cases 
S: dapsone (PO) 100mg 24hourly for 6months 
13.19 Infantile Haemangioma 
Benign vascular tumor which appears at birth and continues growing till 9 months then starts 
involuting. 
Clinical presentation 
•
Red macule at birth
•
Grows progressively
•
regresses from 9-12 months
•
May be part of PHACES syndrome;
Posterior 
fossa 
malformation,
haemangiomas 
(mainly 
facial), 
arterial, cardiac, eye, and sternal 
anomalies 
Indications for treatment 
•
If interferes with feeding
•
If interferes with breathing
•
If interferes with vision
Investigations 
•
FBG before initiating treatment and
serially after
•
ECG
•
Record 
heart 
rate 
and 
blood
pressure before treatment
Pharmacological Treatment 
A: propranolol (PO) 1mg/kg divided into 3doses given 8hourly in 24hours. 
Monitor heart rate and blood pressure 2hourly for 3days if tolerated 
Increase the above-mentioned medication to 2mg/kg/day in 3divided doses till lesion regresses 
Adjust with change in weight. 
Note 
Request your pharmacist to prepare the syrup. 
13.20 Cysts 
Slow growing cystic structures. 
Include- Epidermoid cysts, Trichilemmal cysts, dermoid cyst 
Treatment 
•
Excision
13.21 Skin Lightening 
Skin lightening or skin bleaching is a cosmetic process that aims at lightening the dark areas of skin. 
Some of the products used are strong topical corticosteroids e.g. clobetasol propionate, 
hydroquinone, glutathione, lightening soaps, local concoctions etc. Melasma is a skin condition 
whereby medical treatment is to lighten dark patches. However, in most situations women and men 
desiring to have fairer skin go into great lengths to achieve this and end up with some reversible and 
irreversible changes. 

283!
Reversible conditions 
•
Tinea incognito – refer to treatment
of tinea
•
Steroid acne – refer to acne
treatment
•
Scabies – refer to scabies
treatment
•
Perioral dermatitis- Tacrolimus
ointment
Irreversible conditions 
•
Stria
•
Telangiectasia
•
Atrophy
•
Hirsutism
•
Ochronosis
•
Poor wound healing
Health Education 
•
Users should stop before they get
permanent irreversible changes.
•
Use sunscreen lotion to protect
from ultraviolet damage.

284!
CHAPTER FOURTEEN 
EYE DISEASES AND CONDITIONS 
14.1 Major Blinding Eye Diseases 
Eye Diseases are conditions affecting the eye. Diseases of most important are those leading to 
blindness or visual impairment. Blindness is defined as a presenting visual acuity of less than 3/60 
or central visual field of less than 10º in the better eye. The definition of blindness in children and 
infantsis the same as that in adults though there are different methods for testing vision in young 
children until when they are at preschool age when normal visual acuity chart can be used.The 
common causes of blindness and visual impairment among adults are Cataract, Glaucoma, 
Cicatricial Trachoma, Vitamin A deficiency (discussed under nutrition chapter) and other corneal 
opacities, diseases of the Retina, uncorrected Refractive Errors and Low Vision. These are diseases 
that affect both eyes however, they may be asymmetrical in their course. There are other eye 
diseases that do not lead into blindness or visual impairment, these are also addressed in this 
section. Patients presenting to eye clinic with uniocular eye complaint must have basic examination 
of the fellow eye as well.  
14.1.1 Cataract 
Cataract is clouding of the lens of the eye which prevents clear vision. It may be as a result of 
ageing process or secondary to trauma or inflammatory diseases. Children may be born with 
cataract or develop cataract in the early ages of life. 
Clinical Presentation 
•
Various 
degrees 
of 
vision
impairment unilateral or bilateral
•
History of trauma with a sharp
object for traumatic cataract
•
History of red eye for secondary
cataract.
•
Glare and haloes around light
•
Cloudiness in the lens seen as a
white mark behind the pupil and iris
seen with slit lamp microscope
•
Conjunctiva and cornea are clear
and the whole iris can be seen
clearly
•
Obscured red reflex
Note 
•
Cataract may present in all age groups, blindness due to cataract is reversible
•
Treatment is only by surgery
•
Early treatment in children is mandatory
•
White pupil in children may be a tumor in the eye, late referral may lead to permanent
loss of vision, squint, loss of eye or loss of life
Investigations 
•
Visual acuity
•
Slit Lamp Bimicroscopy
•
Refraction 
depending 
on 
the
density of cataract
•
Dilated Fundoscopy
•
B Scan if no fundal view
•
A Scan
•
Biometry 
for 
Intraocular 
(IOL)
calculation
For congenital cataract, the following 
additional 
investigations 
may 
be 
ordered 
with 
Paediatrician 
consultation  
•
ECG
•
Echocardiogram
•
Haemoglobin
•
Full blood picture
•
Chest X Ray
•
Blood 
grouping 
and 
Cross-
matching
Surgical Treatment 
The only treatment available for Cataract is surgery. There are different cataract surgical procedures 
depending on the causes of cataract, age of the patient and surgeons’ skills and equipment 
availability.  

285!
Pharmacological Treatment 
Preoperative Treatment 
A: amethocaine hydrochloride 1% Eye drops 
OR 
C: tetracaine 0.5% Eye drops 
AND 
C: tropicamide 1% +phenylephrine 2.5% (FDC) Eye drops 
Alternatively 
C: tropicamide 1% Eye drops 
AND  
A: iodine 2.5 – 5% Eye Drops 
AND  
A: lignocaine hydrochloride with adrenaline 2%, combined with hyaluronidase 1500IU, 5 
mL, retrobulbar or Subtenon injection stat,  
OR 
A: lignocaine hydrochloride, combined with hyaluronidase 1500IU, 5mL, retrobulbar or 
subtenon injection stat,  
Intraoperative Treatment 
A: adrenaline 0.5mL infusion in 500mL compound sodium lactate intracameral in during 
the surgery     
AND 
C: trypan blue 0.06% injection, 0.4mL intracameral, stat 
AND 
S: sodium hyaluronate 1% Intracameral and topical stat 
AND 
S: acetylcholine chloride 1% Injection, 0.5ml intracameral stat 
AND 
B: dexamethasone phosphate 1.25mg intracameral injection stat 
AND 
A: gentamycin 1.25mg intracameral and subtenon injection stat 
OR 
B: ceftriaxone 5mg intracameral and subtenon injection, stat 
In addition to the above intraoperative medicines, in children and patients with preoperative 
ocular inflammatory conditions, use 
S: triamcinolone acetone 20mg injection, Sub tenon, stat 
OR 
D: methylprednisolone 20mg injection, Sub tenon, stat 
Postoperative Treatment 
C:dexamethasone + chloramphenicol 0.1 – 0.5%, 1 -2 Drops in the operated eye, 2hourly 
for 7days then 4hourly for days 
OR 
C: dexamethasone + gentamicin 0.1 - 0.3%, 1 – 2 Drops in the operated eye, 2hourly for 
7days then 4hourly for 7days   
AND 
C: cyclopentolate 1%, 1 – 2 Drops in the operated eye, 12hourly for 14days 
OR 
B: atropine 1%, 1- 2 Drops in the operate eye, 24hourly for 14days 
AND 
C: acetazolamide (PO) 500mg, stat 
AND 
A: paracetamol (PO) 1 gm, 8hourly for 3days 
THEN: 

286!
D: prednisolone 0.5%, 1 – 2 Drops, 6hourly for 4weeks 
Note 
•
Atropine is given to patients where excessive inflammation is anticipated such as cataract
surgeries in children, traumatic cataract and secondary cataract.
•
Children may require longer term and more frequent topical steroids depending on their
postoperative response
Referral: Refer all cases to eye surgeon for cataract surgery, available at some of the Districts, 
Regional, Zonal and National Hospitals. Children should be referred immediately to a Tertiary Health 
Facility with capacity to operate children’s eyes safely. 
14.1.2 Glaucoma 
Glaucoma is a syndrome characterized by optic nerve damage and peripheral visual field loss which 
may be associated with raised intraocular pressure. The main classes of glaucoma are open angle 
glaucoma and angle closure glaucoma.  
Note 
Glaucoma may be congenital, primary or secondary to other secondary to ocular conditions 
14.1.2.1 Primary Open Angle Glaucoma 
Clinical presentation 
•
Painless loss of peripheral vision leading to absolute glaucoma as the end stage
•
Affects mainly adults of 40 years of age and above
•
Cornea and conjunctiva are clear
•
Pupil in the affected eye does not react with direct light in advanced stage
•
The optic nerve is always damaged, this can be seen through fundoscopy
•
One eye may be affected more than the other
•
First degree relatives of glaucoma patients are at increased risk
Note 
•
Primary Open Angle Glaucoma does not have symptoms in early stages, hence routine
intraocular pressure checkup and fundus examinations should be done in all people of 40
years and above by some qualified eye care personnel on annual basis.
•
All suspected cases of glaucoma should be referred to qualified eye care personnel for
confirmation of diagnosis and commencement of treatment plan
•
Surgical treatment is usually preceded by medical treatment
•
Refilling of antiglaucoma may be prescribed by a middle cadre eye worker but annual
monitoring should be done at a centre where there is an Ophthalmologist
•
For advanced and complicated Glaucoma, patients should be referred to a health facility
where there are Glaucoma Specialists
Investigations: 
•
Visual Acuity
•
Slit Lamp bimicroscopy
•
Fundoscopy
•
Tonometry
•
Gonioscopy
•
Refraction
•
Visual Field Analysis
•
Fundus Photography
•
Pachymetry test
•
Optical Coherent Tomography
Pharmacological Treatment 
This is initiated after a diagnosis is reached by an ophthalmologist, refill of some medicines can be 
done by Assistant Medical Officers in ophthalmology but with regular reviews at a health facility with 
eye specialist. Medical treatment should be lifelong unless there are conditions necessitating other 
interventions 
C: timolol 0.25% or 0.5%, one drop in the affected eye, instill 12hourly. 
OR 

287!
D: betaxolol 0.25% or 0.5%, one drop in the affected eye, instill 12hourly. Use lower 
strength in mild disease and those at risk of complications. 
In patients who comply to treatment and there is no good response 
ADD 
D: latanoprost 0.005% one drop, 2hourly in the affected eye. 
OR 
D: prostamide bimatoprost 0.03%, one drop, 24hourly in the affected eye. 
•
These may be used as first-line in patients with contraindication of beta-blockers.
•
They can be used as a second-line drug in patients on beta-blockers if the target IOP
reduction has not been reached.
In patients who are intolerant to prostaglandin analogue or are not responding give: 
D: brimonidine tartrate 0.15–0.2%, one drop, 12hourly, in the affected eye. 
OR 
S: dorzolamide 20mg/mL, one drop, 8hourly in the affected eye 
Failure to respond give: 
C: pilocarpine hydrochloride 2% or 4%, instill one drop in the affected eye 6 hourly. 
Note 
Pilocarpine causes long-standing pupil constriction so it should not be used unless a patient is 
prepared for glaucoma 
surgery or as an alternative topical treatment for patients who are contraindicated for Timolol use. 
Consult a specialist 
before using it. 
In severe cases or while waiting for surgery, use: 
C: acetazolamide (PO) 250mg 6hourly 
Note 
•
β-blockers are contraindicated to people who are known to have overt asthma as this
group of medication may cause an acute asthmatic attack within a short time following
instillation into the eye
•
Brimonidine is contraindicated in children below 12years
Laser Treatment 
•
It may be indicated in addition to or instead of eye drops or surgery.
•
Laser trabeculoplasty (Argon Laser Trabeculoplasty, Selective Laser Trabeculoplasty) or
cyclophotocoagulation are different options among others
Surgical Treatment 
It is done in all patients with poor compliance and when medical treatment is not useful. There are 
different surgical techniques depending on the age of the patients, patients’ response to surgical 
treatment, surgeons’ surgical skills and availability of equipment. It is recommended that all 
surgeries are done by Ophthalmologists after thorough assessment of the patients. 
14.1.2.2 Angle Closure Glaucoma 
This is also known as Congestive glaucoma and commonly affect people aged 40 years and above. 
It affects more females than males. 
Clinical Presentation 
•
Acute sudden onset of painful red
eye in the affected eye
•
Severe headache and cloudiness
of the cornea
•
Shallow anterior chamber
•
Fixed and semi-dilated pupil

288!
•
Severe
elevated 
intraocular 
pressure.
•
There is usually dramatic visual
impairment and vomiting may be
present
•
It may be asymptomatic if IOP
raises slowly
Note: 
•
Primary acute Angle Closure Glaucoma is an Ophthalmological Emergency
•
Refer all patients with Congestive glaucoma to eye specialist after initial medical treatment
to lower Intraocular pressure
Investigations: 
•
Visual Acuity
•
Slit Lamp bimicroscopy
•
Fundoscopy when cornea clear up
•
Tonometry
•
Gonioscopy when cornea clear up
•
Visual Field Analysis for chronic
disease
Pharmacological Treatment 
Institute therapy and then refer the patient to eye specialist at the Regional, Zonal or National 
Hospital for investigations and proper management. 
Try to achieve immediate IOP reduction  
First-Line Treatment 
C: acetazolamide (PO), 500mg immediately as a single dose followed by 250mg 6hourly 
AND 
C: timolol 0.25–0.5% eye drops, instill one drop 12hourly in the affected eye 
Use the above combined treatment until you have achieved your target IOP reduction, then continue 
with only Timolol eye drops for life unless patient has received surgical intervention and the IOP is 
reduced to normal level. 
Note 
Manage the associated pain and vomiting 
Second-Line Treatment 
If the above measures fail, use as a short-term treatment, givesystemic osmotic agents: 
C: mannitol 15–20% (IV)1.5–2mg/kg body weight to run slowly over 30–60minutes 
These medicines have diuretic effects, so they are only used as a single dose. They are also used in 
emergencies to prepare patients with high intraocular pressure for surgery as they lower intraocular 
pressure rapidly. 
Note 
Acetazolamide is a Sulphur containing medicine, do not use in patients allergic to Sulphur. 
Surgical Treatment 
This is done at a centre with Eye Specialists and necessary diagnostic and treatment equipment. 
Surgical or Later Peripheral Iridectomy will create a passage for the aqueous fluid from posterior 
chamber to the drainage angle.  
Referral: Management of advanced angle closure glaucoma is done by eye specialist. All patients 
with Angle Closure Glaucoma should be referred to eye specialist for other management modalities. 
14.1.2.3 Childhood Glaucoma 
•
Presents from birth to 5 years.
•
It is a syndrome whereby the intraocular pressure is raised and cause abnormality of the
eyeball and visual disturbances including blindness.

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Clinical Presentation 
•
Patients presents with eyes bigger
than normal for age (buphthalmos)
•
Photophobia
•
Tearing
•
Cloudy cornea,
•
Red conjunctiva though not severe.
•
Decrease in visual acuity
Investigations 
For children, examination is done under General Anaesthesia 
•
Tonometry
•
Cornea Diameters
•
Slit lamp examination
•
Fundoscopy
•
Gonioscopy depending on corneal
visibility
Surgical Treatment 
Treatment for congenital glaucoma is usually surgery, which is done by Pediatric Ophthalmologist or 
Glaucoma specialist. 
Referral: Refer any child who has the above-mentioned signs and you suspect that he/she is having 
congenital glaucoma to a specialist at the National Hospital or Zonal Referral Hospitals where there 
is Paediatric Eye team. 
14.1.2.4 Secondary Glaucoma 
This presents as a complication of other eye diseases such as uveitis, hypermature cataract, trauma 
and retinal diseases. It may also be due to prolonged use of steroids. 
Clinical Presentation 
•
Poor vision in the affected eye
associated with
•
High intraocular pressure
•
Optic nerve damage
•
New vessels on the iris if the cause
is retinal diseases
Investigations 
•
Visual Acuity
•
Slit Lamp bimicroscopy
•
Fundoscopy
•
Tonometry
•
Gonioscopy
•
Refraction
•
Visual Field Analysis
•
Fundus Photography
•
Pachymetrytest
•
Optical Coherent Tomography
Pharmacological Treatment  
Management of these patients depends on the cause, but it includes medical, surgical and laser. 
Institute these treatment as you refer these patients: - 
C: acetazolamide (PO) 500mg immediately stat followed by 250mg 6hourly 
AND 
C: timolol 0.25–0.5% eye drops, instill one drop 12hourly in the affected eye. 
Treatment of the preexisting eye disease is highly recommended. 
Referral: Refer all patients suspected to have secondary glaucoma to a qualified eye specialist 
available at the Regional, Zonal or National Hospital for proper assessment and definitive 
management. 
14.1.3 Trachoma 
It is a chronic conjunctivitis caused by infection with Chlamydia trachomatis (bacteria). It is one of 
the commonest causes of blindness worldwide. There is a chronic inflammation of the conjunctiva 
leading to scarring of the upper eyelid tarsal plate, entropion and in turn of eyelashes.  

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Clinical presentation 
•
Photophobia in early stages or re-
infection
•
More than 5 Follicles in the upper
tarsal plate seen as round and
white nodules in active diagnostic.
•
In late stages, in-turned eyelashes
rub on the cornea leading to
corneal ulcers
•
Loss of vision due to corneal
scarring.
Clinical Stages according to World Health Organization 
•
Trachomatous Inflammation Follicular (TF) - Presence of at least 5 follicles on the upper
tarsal plate
•
Trachomatous Inflammation Intense (TI) – There is intense inflammation, the conjunctival
blood vessels cannot be seen.
•
Trachomatous Scarring (TS) – Presence of white scars in the upper tarsal plate
•
Trachomatous Trichiasis (TT) – Presence of some eye lashes rubbing against the cornea
•
Corneal Opacity (CO) – Presence of corneal opacity (scar) affecting the central cornea
Investigations 
• Visual acuity
• Slit lamp bimicroscopy
• Conjunctival swab for dipstick test and or PCR
Non-pharmacological Treatment 
•
Face washing and total body hygiene to prevent transmission of disease from one person
to the other
•
Environmental improvement/hygiene
Pharmacological Treatment 
A: oxytetracycline eye ointment 3% 24hourly for 6weeks 
OR 
B: azithromycin (PO)1g stat- for preventive chemotherapy in mass treatment 
campaign 
Table 14.1: Dosage of Azithromycin in Children 
Weight (kg) 
I-day regimen
< 15 
20mg/kg 24hourly 
15 – 25 
400mg 24hourly 
26 – 35 
600mg 24hourly 
36-45
800mg 24hourly 
> 45
Dose as per adults 
Note 
Preventive chemotherapy in mass treatment campaign is conducted only once a year 
Surgery 
Surgical correction of entropion in TT patients. This procedure can be done at a Dispensary or 
Health Centre and community level by a trained health worker. 
Referral: Refer all patients with recurrent TT or lower Eyelid TT to Oculoplastic Surgeon at Regional 
Referral or Zonal Referral Hospital for proper assessment and surgical management. 
14.1.4 Diseases of the Retina 
Main diseases of the retina that cause blindness are Diabetic Retinopathy, Diabetic Macular Edema, 
Retinal Detachment and Age-related Macular Degeneration. 
14.1.4.1 Diabetic Retinopathy 
•
It is a complication of diabetes mellitus in the eyes

291!
•
It is a chronic progressive sight-threatening disease of the retinal blood vessels associated
with the prolonged hyperglycemia and other conditions linked to diabetic mellitus such as
hypertension
Clinical Presentation 
•
Loss of vision in advanced stages, when there is retinal haemorrhage or cataract
•
In early stages it may be asymptomatic
•
Regular and annual screening at Diabetic or Eye Clinic is recommended for early
diagnosis.
Diabetic retinopathy is mainly grouped into three stages/presentations: 
•
Background diabetic retinopathy
•
Diabetic maculopathy
•
Proliferative diabetic retinopathy
Investigations 
•
Visual acuity with and without
pinhole
•
Tonometry
•
Dilated 
fundoscopy 
(Direct 
or
indirect ophthalmoscopy with or
without biomicroscopy)
•
Fundus photography
•
Fluorescein Angiography
•
Optical 
Coherence 
Tomography
Note 
Dilate the pupils with combined 
         C: Tropicamide 1%/Phenylephrine 2.5% eye drops 
OR 
C: tropicamide 1% with  
C: cyclopentolate 1% eye drops to screen 
Table14.2 below gives a summary of the Stages of Diabetic Retinopathy at Eye Clinic, treatment 
options and Follow up schedule. Treatment is done in consultation with Diabetologist and Physician 
to ensure a good glycaemic and blood pressure control 
Table 14.2: Treatment options for various grades of DR 
Grade 
Treatment Options 
Follow-up 
No retinopathy 
a.
Patient counseling
b.
Strict control of blood sugar,
pressure and lipids
9 -12monthly 
Mild or Moderate Non-Proliferative 
Diabetic Retinopathy (NPDR) 
a.
No active treatment required
b.
Patient counseling
c.
Control of blood sugar, pressure
and lipids
6-9monthly
Pre-proliferative DR 
Severe NPDR * 
Close follow up for dilated fundoscopy 
2-3monthly
Very severe NPDR * 
Partial scatter PRP therapy (maximum 
LASER burns 800 spots) 
3monthly 
 Mild Proliferative DR** 
(NVD/ NVE 
No 
pre-retinal 
or 
vitreous 
hemorrhage 
No Fibrovascular membrane <FVM>) 
Full scatter PRP minimum 1200 shots in 
one sitting or/ and 
Anti-VEGF injection*** 
2monthly 
Moderate PDR ** 
(NVD/NVE, Moderate to severe 
Vitreous hemorrhage with visible 
fundus details for PRP, Pre-retinal 
Hemorrhage 
No FVM) 
Full scatter PRP up to Ora-serrata sparing 
the macula and away from the FVM *** 
3monthly 

292!
Severe PDR ** 
(NVD/NVE, Severe Vitreous 
hemorrhage obscuring fundus 
details/not visible for PRP, 
Extensive FVM, Tractional Retinal 
Detachment <TRD> 
Macular traction) 
REFER To VR clinic 
* LASER treatment should also be considered in our settings in patients with severe and very severe
NPDR with the following situations as it has shown to reduce the rate of vision loss by half: -
i.
Older type 2 diabetics
ii.
Difficult retinal view
iii.
Prior to cataract surgery
iv.
Only eye situation where the first eye was lost due to PDR
v.
Regular attendance to clinic for follow up is likely to be poor
vi.
Difficult to examine patient due to other reasons.
** Monthly intra-vitreal anti-VEGF injections has been found to be effective on treatment for PDR 
*** Mild and moderate PDR should be treated with full scatter PRP (minimum 1200 shots in one 
sitting) or intravitreal anti-VEGF injection whichever is available, accessible and affordable. If both 
are available and affordable then anti-VEGF injection is the treatment of choice provided the patient: 
i.
Is able to come for follow up at regular intervals- every month for 3 months and
then every 2 months for 3 months and then 3monthly
ii.
Can afford the injections which may total up to 6 injections in the first year
iii.
Has no contraindications to the injections?
If any one of the above does not apply, then the patient should have PRP done. 
Treatment options for DME 
Management of DME depends on the clinical stage of DME and treatment options available at the 
facility where the patient has been attended. 
Primary tests are required to be performed in order to grade the DME. Macula OCT for all diabetic 
patients should be the baseline test to determine presence or absence of DME. Macular thickness of 
equal or more than 400 microns should be considered as DME. Those facilities without this tool, the 
clinical assessment will be the baseline test where the best corrected visual acuity will be the key 
point for grading which will be matched with the clinical findings. Therefore, VA of less than 6/12 
should be considered as DME case. It is important to exclude other causes of visual impairment 
before concluding the presence of DME. Use of anti-VEGF has been found to be effective in the 
treatment of DME.  
Table14.3: Treatment options for various grades of DME 
Grade 
Treatment option 
Follow up period 
No DME 
Close observation 
review after 6 to 
12months 
Non-Centre 
involving DME 
Focal or Grid LASER 
3-6months
Centre involving 
DME 
3 intravitreal anti VEGF injections at monthly interval 
followed by 3 more injections at 6 weekly intervals.  
After 6 injections, refer patient to VR clinic if 
a. VA is not improving
b. There is clinically persistent DME
If anti VEGF injection is not available: 
i.
Grid LASER should be given for diffuse,
Exudative or edematous macular edema
ii.
Focal LASER to areas of focal Exudative edema
Every 1 month 

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Pharmacological Treatment  
For glycemic control give antioxidant in non-proliferative diabetic retinopathy 
C: multivitamin +carotenoids (PO) 24hourly to a maximum of 3months 
For intravitreal anti Vascular Endothelial Growth Factor (VEGF) in Proliferative Disease 
S: bevacizumab, 1.25mg per 0.05ml, intravitreal injection, stat. 
OR  
S: ranibizumab, 0.5mg per 0.05ml, intravitreal injection stat. 
Repeat after every month to a maximum of 3 months then 6weekly to complete 6 injections. Re-
assess on 3 monthly basis if there are signs of disease progression, restart treatment if any, with 
close follow up. 
AND 
S: triamcinolone acetonide, 0.05ml, intravitreal injection, stat. Repeat after 3months if it is 
necessary. This is indicated in Diabetic Macula Edema. 
Surgical Treatment 
•
This is done in the proliferative stage
•
It involves removal of vitreous and or blood, peeling of formed fibrovascular tissue and
reattachment of retina if the retina is detached
•
It is combined with retinal photocoagulation
•
The vitreous cavity may be filled with tamponade liquid such as silicon oil or expansile gas
like sulfur perfluoropropane or sulphur hexafluoride depending on the level of complication
•
It may also be combined with pharmacological treatment (Anti VEGF) mentioned above
Laser Treatment 
Laser photocoagulation: Extent and type of this treatment depending on the stage of the disease 
•
Focal Laser
•
Grid Laser
•
Pan Retinal Photocoagulation for
advanced disease
Note 
•
Ophthalmologists should work together with Physicians to holistically treat the diabetic
patient.
•
Poorly controlled diabetes mellitus and diabetic retinopathy can lead to blindness
•
All patients with diabetes mellitus regardless of their eye conditions, should have a
thorough eye examination by available eye care personnel or an eye specialist at least
once a year.
•
Dilated eye examination and direct viewing of the retina by an ophthalmologist or
qualified eye care personnel is mandatory at initial diagnosis of Diabetes Mellitus and
as per recommended schedule by the attending clinician.
•
Urgent referral of all diabetic patients with sudden loss of vision to eye specialist
14.1.4.2 Age Related Macular Degeneration 
It is a disease condition characterized by progressive macular changes that are associated with 
increase in age. 
Clinical Presentation 
•
Drusens around macula area (yellowish excrescence in the retina)
•
Affects elderly over 60 years
•
Poor central vision, later can lead to blindness
Investigations 
•
Visual Acuity
•
Refraction
•
Tonometry
•
Fundoscopy through a well-dilated
pupil,
•
Fundus photography

294!
•
Optical 
Coherence 
Tomography
and or
•
Fluorescein angiography.
Pharmacological Treatment 
•
This depends on clinical presentation.
•
Intravitreal injection in the affected eye
S: bevacizumab 1.25mg per 0.05ml stat
OR
S: ranibizumab 0.5mg per 0.05ml stat.
Give Antioxidant in non-proliferative Diabetic Retinopathy 
C: multivitamin + Beta-carotenoids, Zinc Sulfate and Lutein, 1 tablet once daily to a 
maximum of 3 months 
Surgical Treatment 
Type of surgery depends on the presentation/ stage of the disease. 
Referral: Refer patients with Age Related Macular Degeneration to Vitreo-retinal Surgeons for 
proper management 
14.1.5 Refractive Errors 
This is a condition where one presents with poor vision either at near or distance at any age. There 
are mainly 4 types of refractive errors namely presbyopia, myopia, astigmatism and hyperopia. A 
patient may have more than one type of refractive error. 
14.1.5.1 Presbyopia 
This is a disorder of refractive status commonly occurring in older people. 
Clinical presentation 
•
It usually starts after the age of 40 years
•
The main complaint is difficulty in reading/writing or doing near works
•
Diagnosis is only through refraction. Attendance to heath facility is also a good opportunity
for screening of glaucoma and diabetic retinopathy
Investigations 
•
Visual acuity
•
Tonometry
•
Fundoscopy
•
Refraction
•
Stereopsis test
•
Colour
vision 
test
Non-pharmacological Treatment 
Convex lens spectacles for near vision. 
14.1.5.2 Myopia (Short sightedness) 
Thisis a condition whereby patient has difficulty seeing far objects. 
Clinical presentation 
•
It is common in young age between
5–25 years
•
The condition persists throughout
life
•
If not treated early, it may progress
rapidly 
and 
lead 
to 
retinal
complications
•
It is diagnosed through refraction.
Investigations 
•
Visual acuity
•
Refraction
•
Fundoscopy
•
Stereopsis test
•
Colour
•
Strabismus 
assessment 
in 
all
children
Non-pharmacological Treatment 
Concave lens spectacles for constant wear. 

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14.1.5.3 Hypermetropia (Long sightedness) 
This is a condition where patients have difficulty in seeing near objects. It is less manifested in 
children as they have a high accommodative power.  
Clinical presentation 
•
Ocular strain
•
Diagnosis in children should be reached after refraction through a pupil that is dilated
Investigations 
•
Visual acuity
•
Refraction
•
Fundoscopy
•
Stereopsis test
•
Colour
•
Strabismus 
assessment 
in 
all
children
Non-pharmacological Treatment 
Convex lens spectacles for constant wear 
Note  
Spectacles should be given to: - 
•
Children who have only significant hypermetropia (more than +3.00 Diopter of Sphere both
eyes), all children who present with squint and have significant hypermetropia and children
with anisometropia
•
Elderly who present with signs of ocular strain
14.1.5.4 Astigmatism 
This is a condition where the cornea and sometimes the lens have different radius of curvature in all 
meridians (different focus in different planes). Some myopic and hyperopic patients may have 
astigmatism.  
Clinical Presentation 
•
Poor vision at distance,
•
Photophobia
•
Headache (sometimes).
•
Diagnosis 
is 
reached 
through
refraction
Investigations 
•
Visual acuity
•
Refraction
•
Fundoscopy
•
Stereopsis test
•
Colour
•
Strabismus 
assessment 
in 
all
children
Non-pharmacological Treatment  
Cylindrical lenses spectacles for constant wear. 
14.1.6 Low Vision 
Low vision is irreversible visual loss that cannot be corrected with surgeries or spectacles resulting 
in reduced ability to perform many daily activities. They have visual impairment even with treatment 
and or standard refractive correction and  
Note: 
•
Reassessment for all types of refractive errors is done annually and change the spectacles
of there are significant variation and improvement with new correction.
•
All children with rapid progression of refractive errors need to be seen by Paediatric
Optometrist and Paediatric Ophthalmologist for further assessment

296!
Clinical presentation 
Inability to 
•
Recognizing people in the streets,
•
Reading black boards,
•
Writing at the same speed as peers
and
•
Playing with friends.
•
Visual acuity from less than 6/18 to
perception of light and a reduced
central visual field.
Investigations 
•
Visual acuity
•
Refraction
•
Tonometry
•
Fundoscopy
•
Low vision assessment
•
Orthoptic Assessment
Non-pharmacological Treatment 
•
Assessment of the patients’ visual function
•
Accurate refraction and provision of spectacles if indicated
•
Low vision devices such as optical devices (magnifiers, telescopes) and or non-optical
devices (reading stands and or reading slits) as per assessment results.
•
Surgical intervention is indicated e.g. if a patient has cataract
Referral: All children with low vision should be referred to high level health facility for proofer 
assessment and management by a paediatric Eye Team 
14.2 Painful Red Eyes 
The eye conditions shown on Table 14.4 presents with an acute onset of red eyes: ocular trauma, 
corneal ulcer, uveitis and conjunctivitis. The Table also summarizes the diagnostics of red eyes. 
Table 14.4: Summary on diagnosis of Red Eyes 
Disease 
Condition 
Visual 
Acuity 
Affected 
Eye 
Cornea 
Pupil 
Pain 
Discharge 
Allergic/ 
viral 
Conjunctivitis 
Good 
Both 
Clear 
Normal 
No 
Watery/mucoid 
Bacterial 
Conjunctivitis 
Good 
Both 
Clear 
Normal 
No 
Purulent 
Ophthalmia 
neonatorum 
Poor +/- 
One/both 
Cloudy 
+/- 
Normal +/- 
Yes 
Copious 
purulent 
Cornea ulcer 
Poor 
One/ both 
Gray 
spot 
Normal 
Yes 
Watery/purulent 
Uveitis 
Poor 
One/ both 
Clear or 
cloudy 
Small 
& 
Irregular 
Yes 
Watery 
Acute glaucoma 
Poor 
One 
Cloudy 
Mid 
dilated 
Yes 
Watery 
14.2.1 Ocular Trauma 
These are eye injuries that may result from blunt or sharp objects or from chemical substances.The 
management of these injuries is guided by history from the patient and ocular findings by the 
clinicians. Classes of ocular trauma are as follows: - 
14.2.1.1 Blunt Trauma/Perforating Eye Injury/Foreign Body  
Establish the cause to determine the type of injury and whether there is penetration. 
Clinical presentation 
•
Corneal abrasion/laceration with or without an imbedded foreign body.
•
Eye lids may also be involved.

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Investigations 
This is done after the first aid measures 
•
Visual acuity
•
Examine the injured eye with slit
lamp or magnifier
•
Fluorescein 
staining 
to 
reveal
foreign body or corneal laceration
•
Tonometry in blunt injury
•
Fundoscopy in blunt injury or
embedded foreign body
•
B scan in embedded foreign body
•
CT Scan in suspected metal foreign
body
Non-pharmacological Treatment 
•
Provide first aid measures to the patients as per presentation
•
If no penetration, irrigate the eye with clean water or Ringers Lactate to reduce chemical
substance in the eye
•
Remove foreign body if visible with a cotton bud or surgical blade if shallow.
Pharmacological Treatment 
At the primary care: 
Corneal Abrasion: 
A: chloramphenicol eye ointment 1%, 8hourly to the injured eye until no 
fluorescein staining  
Steps Guiding Management of Complicated Blunt Trauma 
Complicated blunt trauma is a trauma where the vision is poor, patient’s experiences pain and there 
is hyphaema. It is best managed by eye specialist as surgery may be required in the management.  
Table 14.5: Steps guiding management of complicated blunt trauma 
Findings 
Action to be taken 
No hyphema, normal vision 
Observe 
Hyphema, no pain 
Refer 
No hyphema, normal vision, pain 
Paracetamol, observe for 2 days, refer if pain persist 
Poor vision and pain 
Paracetamol, refer urgently 
Hyphema, pain, poor vision 
Paracetamol, refer urgently 
14.2.1.2 Deep Corneal or Scleral Injuries 
These are corneal or scleral injuries caused by sharp objects. 
Clinical presentation 
•
History of injury with a sharp object such as knife or wire
•
Swollen eye
•
Eye discharge
Investigations 
•
Visual acuity
•
Examine the injured eye with slit
lamp or magnifier
•
Fluorescein 
staining 
to 
reveal
foreign body or corneal laceration
•
Fundoscopy
Non-pharmacological Treatment 
•
Apply an eye shield or pad with no pressure and refer immediately
While waiting for referral, use the following in the affected eye: 
Pharmacological Treatment 
A: chloramphenicol 1% eye drop, 2 drops stat 
OR  
A: chloramphenicol 1% ointment, stat 
AND 

298!
B: atropine 1%, 1–2 drops stat 
AND 
A: tetanus toxoid (IM) 0.5ml stat as prophylaxis 
AND 
A: paracetamol (PO)1gm 4–6hourly to a maximum of 4 doses in 24hours, for 3days in 
adults, the dosage in children is 10–14mg/kg 4–6hourly for 3days. 
Referralindicated if 
•
Intraocular foreign body is suspected
•
There is globe or intraocular penetration evidenced by:
o
Poor vision,
o
Distorted pupil
o
Ocular contents of foreign body is seen
o
Circumferential subconjunctival hemorrhage
o
Hyphaema with or without raised intraocular pressure
•
Conjunctival laceration requiring suturing (>1 cm)
•
Laceration/perforation or diffuse damage to the cornea and sclera
•
Chemical and thermal injuries
•
Damage to ocular adnexa including eyelids
•
Limited ocular movements
Surgical Treatment 
This is done by a well-trained eye specialist at the District, Regional, Zonal and National hospitals. It 
should be done within 48 hours of injury. Post-operative care should be monitored regularly for any 
signs of endophthalmitis. 
Note: 
•
Eye ointment should be applied very gently and in the lower fornix (behind the lower
eyelid).
•
Do not apply pressure on the eye in perforating injuries of the eyeball
Delay in surgical management of the injury may cause irreversible blindness or may necessitate 
removal of an eye 
Referral: Immediately refer the patient to a health facility with eye surgeon at the District, Regional, 
Zonal or National hospital depending on the staff availability. 
14.2.1.3 Chemical Injuries/Burn 
This is an Ophthalmological emergency. It occurs when chemicals such as acid or alkali (e.g. 
household detergents, bleaching agents), snake spit, insect bite, traditional eye medicine, cement or 
lime cause a damage to the eye.  
Clinical presentation 
•
Diagnosis 
relies 
mostly 
with
patients’ history
•
Patients 
may 
present 
with
photophobia
•
Inability to open the eyes
•
Excessive tearing/watery eye
•
Cloudiness of cornea with blurred
vision
•
Loss of conjunctival blood vessels
•
Traces of chemical substance such
as cement or herbs and blisters or
loss of eyelid skin in open flame
injuries.
Investigations 
•
Visual acuity
•
Slit lamp bimicroscopy
•
Fluorescein staining
Non-pharmacological Treatment 
If a patient gives you history of being in contact with the items mentioned above, the following 
should be done: 

299!
•
Irrigate the eye with clean water or Ringers lactate continually for a minimum of 20–30
minutes to reduce chemical substances. Irrigate longer for severe alkali burn.
•
Test the patients’ vision and examine the patient’s eye
Pharmacological Treatment 
C: tetracaine 0.5% eye drops, instill 2 drops in the affected eye. Repeat irrigation if 
possible. Evert the eye lids and remove the debris 
AND 
A: chloramphenicol 1% eye ointment, apply 6hourly to prevent infection for 3days. 
AND 
A: paracetamol (PO)1gm 4–6hourly to a maximum of 4 doses in 24hours, for 3days in 
adults, the dosage in children is 10–14mg/kg 4–6hourly for 3days 
Referral: Refer all cases within 12hours to eye specialist at high level health facilities for more care 
14.2.2 Herpes Simplex Keratitis 
It is an inflammatory condition of the cornea caused by Herpes Simplex Virus. 
Clinical presentation 
•
Acute unilateral painful eye
•
Blurring of vision
•
Reduced corneal sensation
•
Dendritic corneal ulcer seen on staining with fluorescein
Investigations 
•
Visual acuity
•
Slit lamp bimicroscopy
•
Fluorescein staining
Pharmacological Treatment 
C: acyclovir 3%, ophthalmic ointment inserted in the lower conjunctival sac, 4hourly. 
Continue for 3days after ulcer has been healed. 
AND 
B: acyclovir, (PO), 400mg 8–4hourly a day for 7–10days depending on initial response as 
well as the extent of the ulcer. 
Note 
Topical corticosteroids are contraindicated in the treatment of dendritic ulcers 
14.2.3 Corneal Ulcer 
This is a painful red eye condition resulting from a raw discontinuity to the corneal epithelium. It may 
be caused by infection (bacterial, viral e.g. Herpes simplex virus and measles, fungal, trauma 
(physical or chemical) and nutritional (Vitamin A deficiency). 
Clinical presentation 
•
Painful and red eye of acute onset
•
Excessive tearing
•
Severe photophobia
•
Poor vision
•
Gray/white spot on the cornea
staining with fluorescein
•
Hypopyon (Pus or white cells in
anterior 
chamber)
Investigations 
•
Visual acuity
•
Slit Lamp bimicroscope
•
Corneal scrapping for Gram Stain and
•
Corneal scrapping for Potassium Hydroxide staining
•
Fluorescein sodium drops or a drop of local anesthetic on a fluorescein strip to assess the
pattern of the ulcer and measure the size of corneal defect.

300!
Pharmacological Treatment 
While waiting for laboratory results, give: 
C: ciprofloxacin 0.3%, ophthalmic drops, instill 1–2drops 1–2hourly for 3days then reduce 
to 3–4hourly. 
OR 
D: ofloxacin 0.3%, ophthalmic drops, instill 1 drop 1–2hourly for 3days then reduce to 3–
4hourly 
Give antifungal, if fungal infection is suspected or confirmed 
S: natamycin 5%, ophthalmic drops, instill 1 drop 1–2hourly for 3–4days (specialist use 
only). Then reduce to 1 drop 3-4hourly. Continue for 14–21days until resolution of infection 
OR 
S: econazole 2%, ophthalmic drops, instill 1 drop 1–2hourly for 3–4days (specialist use 
only). Then reduce to 1 drop 3–4hourly. Continue for 14–21days until resolution of infection 
OR 
S: chlorhexidine 0.2%, ophthalmic drops, instill 1 drop 1–2hourly for 3–4days (specialist 
use only). Then reduce to 1 drop 3–4hourly. Continue for 14–21days until resolution of 
infection 
Give antiviral if viral causes are suspected after the examination of the eye 
C: acyclovir 3% eye ointment 5hourly a day until there is no corneal stain, then continue 
with treatment 8hourly a day for a maximum of 10–14days 
Note 
Treatment may be changed depending on corneal scrapping results 
Referral: Refer to the next level of care where there is an eye specialist when there is hypopyon 
(white cells in anterior chamber) 
14.2.4 Uveitis 
This isInflammation of the uveal tissue (Iris, choroid and ciliary body) and its adjacent structures. 
Majority of the cases are idiopathic whereby other cases are due to autoimmune diseases e.g. 
Rheumatoid Arthritis, Viraland systemic diseases like Tuberculosis, Leprosy, and Syphilis. 
Clinical presentation 
It has three main clinical presentations namely acute, chronic and acute on chronic. The commonest 
form is anterior uveitis. In acute type, patients present with: - 
•
Painful red eye
•
Excessive tearing
•
Severe photophobia
•
Loss of vision
•
Cells in anterior chamber
•
Irregular pupil with synechiae
Investigations 
•
Visual acuity
•
Slit lamp bimicroscopic examination
anterior chamber
•
Tonometry
•
B scan
•
Urinalysis
Laboratory blood tests for bilateral and 
granulomatous uveitis: - 
•
FBC
•
ESR
•
Antinuclear Antibody
•
VDRL
•
HIV Testing
Imaging: Chest X-Rays if Tuberculosis and Sarcoidosis are suspected. 
Pharmacological Treatment 
Treatment for uveitis is mainly steroids and specific treatment according to the cause. This should 
be initiated in a facility where workup and close monitoring can be done. 
Give: 
Steroidal Anti-inflammatory medicines 
D: dexamethasone 1% eye drops, 1–3hourly in the affected eye for 6weeks 
OR 

301!
D: prednisolone 0.5% or 1 % eye drops, 1–3hourly in the affected eye for 6weeks 
AND 
A: prednisolone (PO) 1mg/kg body weight, given in a tapering manner to maximum of 4–
6weeks 
AND 
D: triamcinolone (subtenon) 20mg stat, it can be repeated after 4 weeks if need arise. 
AND 
Pupil dilating eye drops 
B: atropine eye drops or ointment 1% 12hourly in the affected eye 
OR 
C: cyclopentolate 1 % eye drops, 1–2drops 8hourly in the affected eye. 
Treatment for uveitis is to be continued for a maximum of 6weeks 
Note 
•
Treatment of uveitis must involve various specialists
•
Acute uveitis is a serious problem and the patient should be referred urgently for specialist
treatment
•
Recurrences may occur or acute disease may end up becoming a chronic uveitis
14.2.5 Conjunctivitis 
This is an inflammation of the conjunctivae and one of the most common causes of red eyes. The 
cause of conjunctivitis may be bacterial, viral or allergy. Clinical features and treatment guideline 
depend on the type and cause of conjunctivitis. 
Note 
•
If conjunctivitis is due to an infection, counsel on the importance of frequent hand washing,
use separate linen, towels and wash towels and avoid direct contact with infected materials
or individuals
•
Contacts lenses should not be worn in patients with conjunctivitis until the condition has
resolved
14.2.5.1 Allergic Conjunctivitis 
Clinical presentation 
•
Patients present with history of itching of eyes, sand sensation, and sometimes mucoid
discharge
•
When examined,
o
the eyes may be normal or slightly red,
o
Conjunctival swelling in severe cases,
o
Limbal hyperpigmentation and papillae of the upper tarsal conjunctiva.
o
Normal iris, pupil and visual acuity.
o
Corneal complications in very advanced stages
Investigations 
•
Visual acuity
•
Slit lamp bimicroscopy
•
Full blood picture
•
Skin Allergic test
Non-pharmacological Treatment  
Treatment of allergic conjunctivitis depends on the severity of the condition and age of the patient. In 
mild cases where the eyes are white, 
•
Avoid allergens
•
Cold water compresses for 10 minutes four times a day

302!
Pharmacological Treatment 
Adults and children > 6 years of age: 
C: oxymetazoline 0.025% drops 6hourly a maximum of 7days 
If no response within 7days, use mast cell stabilizers such as: 
C: sodium cromoglycate 2% eye drops, instill 6hourly per day (Doctor initiated) 
Use may be seasonal (1–3 months) or long term. 
Children 2–6 years of age: 
A: chlorpheniramine (PO) 0.1 mg/kg/dose 6–8hourly 
If no response within 7days use 
C: sodium cromoglycate 2% eye drops, instill 6hourly per day (doctor initiated) 
o
Use may be seasonal (1–3 months) or long term for the prevention of further
attack, depending on the patient’s exposure to the allergen.
Persistent allergic Conjunctivitis in adults and children of >2 years of age: 
For long term use: 
Children 2–6years 
A: cetirizine (PO) Adult; 10mg. Children below 6year 5mg 24hourly 
o
Use may be seasonal (1–3 months) or long term
Note 
Do not give antihistamine to children under 2 years of age as its effectiveness at this age group has 
not been proven. 
Referral: Refer to eye specialist for further specialized care in case of the following: 
•
Moderate to severe allergic conjunctivitis
•
No response
•
Persons wearing contact lenses
•
Children <2 years of age
At the specialized centre, the following treatment may be added depending on the patient’s 
presentation: 
Short term steroid eye drops (in severe cases with involvement of the cornea, apart from mast cell 
stabilizers, give  
D: dexamethasone 0.1%, 6hourly for a maximum of 14days. 
OR  
D: prednisolone 0.5%, 6hourly for a maximum of 14days. 
In very severe form of allergic conjunctivitis, give steroid injection 
D: triamcinolone acetonide (subtenon) 20mg stat 
OR  
D: methylprednisolone sodium acetate (subtenon) 20mg stat 
14.2.5.2 Viral Conjunctivitis 
The commonest causative organism is adenovirus. It may be unilateral but usually bilateral 
Clinical presentation 
•
It may be associated with upper respiratory tract infection
•
Presents with morning crusting and watery eye discharge
•
A burning, sandy or gritty feeling in the eyes
•
Diffuse pink or red conjunctiva due to subconjunctival hemorrhages
•
Photophobia if the cornea is involved
•
Normal visual acuity
•
Preauricular lymphadenopathy
•
It appears in epidemics so there will be history of contact with patients with similar eye
condition
•
It is usually is self-limiting, but the irritation and discharge get worse on 3 – 5 days before
getting better and symptoms can persist for 2–3 weeks.

303!
Non-pharmacological Treatment 
•
Advise on correct cleansing or rinsing of eyes with clean water
•
Cold compresses for symptomatic relief
Pharmacological Treatment 
Children > 6 years and adults 
C: oxymetazoline 0.025% eye drops, instill 1–2drops 6hourly for a maximum of 7days. 
AND 
A: paracetamol (PO) Adult; 1g. Pediatric 10–15 mg/kg/dose 6hourly when required. 
Note: Viral conjunctivitis is very contagious so patients and members of the family should be 
alerted 
Referral: Refer all patients to a centre with eye specialist if there is 
•
No response after 5 days
•
Unilateral red eye for more than one day
•
Suspected herpes conjunctivitis
•
Loss of vision
•
Irregular pupil
•
Haziness of cornea
•
Persistent painful eye
14.2.5.3 Bacterial Conjunctivitis 
 Purulent conjunctival inflammation caused by bacterial infection 
Clinical presentation 
It is characterized by: 
•
Mucopurulent discharge from one
or both eyes
•
Sore, gritty or scratch eyes and
swollen lids
•
Conjunctiva redness more at the
fornices
•
Eyelids may be swollen
•
Matting of eye lashes in the
morning with eyelids stuck shut
Non-pharmacological Treatment 
•
Educate patient on personal hygiene to prevent spread
•
Educate patient correct application of ophthalmic ointment
o
To wash hands thoroughly before applying ophthalmic ointment
o
Not to share the ophthalmic ointment and drops
•
Eye swabs for Gram stain and for culture and sensitivity may be needed to tailor down
treatment.
Pharmacological Treatment 
A: chloramphenicol 1%, ophthalmic ointment, applied 8hourly for 5days. 
OR 
C: ciprofloxacin 0.3%, ophthalmic drops, instill 1drop, 4hourly for 2days. Then reduce 
frequency to 1 drop 6hourly for 5days 
OR 
D: ofloxacin 0.3%, ophthalmic drops, instill 1 drop 4hourly for 2days. Then reduce the 
frequency to 1drop 6hourly for 5days 
AND 
A: paracetamol (PO) Adult 1g. Children 10–15 mg/kg/dose 6hourly when required. Adults: 
Referral: Refer to eye specialist if no improvement after 2days of treatment 
14.2.5.4 Ophthalmia Neonatorum/Neonatal Conjunctivitis 
This is acute bacterial infection of the eyes that affect newborn baby during the first 28days of life. 
The infection is acquired from mother’s birth canal secretions. It is characterized by inflammation of 

304!
the conjunctivae, sticky eyes to abundant purulent discharge and eyelids oedema. Causative 
organisms are Neisseria Gonorrhea, Chlamydia spp and Staphylococcus spp.  
Clinical presentation 
•
Patients present with massive edema and redness of eyelids and with purulent and
copious discharge from the eyes, clinical presentation ranges from mild (small amount of
sticky exudates) to severe form (profuse pus and swollen eye lids) depending on the
causative organism
•
There is usually rapid ulceration and perforation of corneal which eventually leads to
blindness if treatment is delayed
•
It usually presents 3–4days of life
•
Late and mild presentation is due to Staphylococcus or undefined
•
Treat parents of a neonate with purulent discharge appropriately
Investigations 
•
Pus swab for Gram Stain
•
Pus for Culture and sensitivity
•
Vaginal swab for Gram stain and culture and sensitivity
Non-pharmacological Treatment 
Cleanse or wipe eyes of all newborn babies with a clean cloth, cotton wool or swab, taking care not 
to touch or injure the eye  
Pharmacological Treatment  
Screen women in the antenatal clinics and treat both parents for Sexually Transmitted Diseases. In 
Ophthalmia neonatorum, prevention is better than cure. 
A: Apply chloramphenicol 1% eye ointment, both eyes, to all newborn babies as 
soon as possible after birth. 
OR 
A: povidone iodine 2.5 % Eye Drops, both eyes 
Sticky eye(s) without purulent discharge: 
A: chloramphenicol 1% eye ointment, apply 6hourly for 7days 
Purulent discharge 
Mild discharge without swollen eyelids and no corneal haziness: 
A: compound sodium lactate eye wash, immediately then 2–3hourly until 
discharge clears 
AND 
B: ceftriaxone (IM) 50mg/kg immediately stat 
Given at District Hospital (Treatment to be initiated by Clinical Eye Care Professional eg. Assistant 
Medical Officer in Ophthalmology) 
Abundant purulent discharge and/or swollen eyelids and /or corneal haziness: 
A: compound sodium lactate eye wash, immediately then hourly until referral 
AND 
B: ceftriaxone (IM) 50mg/kg immediately stat 
Referral: To high level health facilities for proper management. 
Note 
•
Ceftriaxone should not be used in neonates that are seriously ill or are jaundiced
•
Ceftriaxone should not be administered if calcium containing intravenous infusion e.g
Compound Sodium Lactate is given or is expected to be given
Treat both parents of newborns who develop purulent conjunctivitis after 24 hours of birth for N-
gonorrhea and Chlamydia with 

305!
B: ceftriaxone (IM) 250mg stat 
(For ceftriaxone IM injection: Dissolve Ceftriaxone 250mg in 0.9 mL Lidocaine 
1% without adrenaline) 
AND 
B: azithromycin (PO) 1g stat 
Note: 
For more details on prevention and treatment see the “Neonatal Conjunctivitis (NC) Flow chart 
number 12.7 under the Sexual Transmitted disease chapter 
Referral: Urgently 
•
Neonates with abundant purulent discharge and/or swollen eyelids and/or corneal
haziness and
•
Neonates unresponsive to treatment within 2days.
14.3 Structural Abnormalities of the Eye 
These includes: 
•
Squint: eyes are looking in different directions; one eye appears to be turned in or out, in
children or in adult. Refer urgently all children who present with squint to Paediatric Eye
Tertiary Centre
•
Ocular surface disease: The most common ocular surface diseases are pterygium and
Squamous cell carcinoma of the conjunctiva.
•
Eyelids abnormalities: eyelashes rubbing on cornea (trichiasis), inturned eyelids
(entropion), eyelids bent out too much (ectropion), drooping eyelids (ptosis), inability to
close the eyes (lagophthalmos)
Referral: Refer all patients to health facilities with eye specialist for surgical intervention 
Note: Abnormal tissues excised from eye patients should be subjected to pathology examination for 
proper diagnosis 
14.4 Ocular Oncology 
14.4.1 Retinoblastoma 
It is the commonest childhood malignant tumor of the eyes. It is diagnosed between the first 1–
3years of life. It has a lower survival rate after diagnosis hence, monthly screening of all under-five 
children is important for timely referral and management. 
Clinical presentation 
•
White pupil reflex (leukocoria)
•
Squint
•
Rarely vitreous hemorrhage
•
Hyphema
•
Ocular/periocular inflammation
•
Secondary glaucoma
•
In 
late 
stages 
proptosis 
and
hypopyon
          Investigations 
•
Visual acuity
•
Tonometry
•
Fundoscopy
•
B Scan
•
CT Scan of the head
•
Examination
under 
anaesthesia
•
Histology of an enucleated
eye in advanced disease
•
Cerebral Spinal Fluid analysis
in advanced disease
Non-pharmacological Treatment 
Staging and treatment is done in specialized centres in consultation with Pediatrician and 
Oncologist. The following are treatment modalities:  
•
Enucleation of the affected eye and the eye is taken for histology
•
External beam radiotherapy
•
Plaque radiotherapy
•
Cryotherapy and laser photoablation

306!
Table 14.6: Classification of Retinoblastoma and recommended treatment options according 
the classification of Retinoblastoma (ICRB) 
Group 
Clinical features 
Recommended Treatment options 
A 
All small tumors (3 mm or less) 
that are only in the retina and are 
not near important structures such 
as the optic disc or the foveolar 
i.e. Not less than 3 mm from the
foveolar and 1.5mmfrom the optic
disc.
-
Focal therapy (cryotherapy or Transpupillary
thermotherapy (TTT).
-
TTT is indicated for posterior located tumors.
TTT use Diode Laser (810nm) or 1064nm or
532nm. Tumor is heated until it turns slightly
gray. Complete tumor regression can be
achieved by using 3-4sessions
-
Do not exceed 5 minutes per session to avoid
complication such as Cataract.
-
Cryotherapy is done to a small tumor at
equatorial and peripheral retina. Under GA
place the probe precisely on the sclera, directly
behind the intraocular focus of the tumor. apply
triple freeze/thaw at 3week intervals until
complete tumor regression.
Note: Administer cryotherapy or TTT 3-6 hours prior 
to chemotherapy if systemic treatment is indicated.  
Focal 
therapy 
synergistically 
increases 
drug 
penetration to the tumor 
B 
Tumor of > 3mm, close to the 
optic disc or foveola 
No subretinal fluid 
-
6cycles of standard dose chemotherapy are
indicated to allow adequate tumor reduction.
Note: Standard dose is a combination of Carboplatin, 
Vincristine and Etoposide (VEC). 
Do not perform focal therapy if tumors are located in 
the macular and juxtapupillary areas.  
-
If focal therapy is indicated chemotherapy
should be given within 6hr of focal therapy to
increase drug penetration to the eye and tumor
C 
Well-defined tumors 
with small amounts of subretinal 
or  
vitreous seeding (tumor cells 
floating within the vitreous cavity) 
NOTE: Vitreous seeding is one of 
the most challenging situations 
for eye-preservation therapy and 
is 
the 
primary 
reason 
for treatment failure 
following 
conservative management 
of 
retinoblastoma. 
-
6cycle of standard dose Chemotherapy is
indicated.
-
Chemotherapy should be given within 6 hours
of focal therapy (cryotherapy or TTT or
Subtenon Carboplatin)depending on site and
response to treatment.
-
Chemotherapy cycles are given at 3 weeks
intervals, every cycle is preceded by EUA and
focal therapy.
Note: Do not perform focal therapy if tumors are 
located in the macular and juxtapupillary areas 
-
vitreous seeding can be managed by
plaque radiotherapy (need license), External
beam Radiotherapy, Enucleation or intravitreal
chemotherapy (Melphalan). Melphalan salvage
about 60% of eyeball with vitreous seeding (8-
10µg is safe dose)
D 
Large or poorly defined tumors 
occupying up to 50% of the globe 
with 
widespread 
vitreous 
or 
subretinal seeding.  
There is retinal detachment up to 
50% of the globe 
-
If unilateral Enucleate.
-
If bilateral Start 3 cycles of chemotherapy
-
If no response and no visual potential enucleate
the worse eye.
-
If there is response complete 6cycles of
systemic chemotherapy.
-
Local radiation for persistent vitreous seeds
may be indicated (plaque therapy or Intravitreal
Melphalan)
Note: Focal therapy should be given prior to 
chemotherapy for every cycle. 
-
Chemotherapy should be given within 6 hours
of focal therapy to increase drug penetration to
the eye and tumor
E 
The tumor is very large with one 
or more of the following features: 
- 
Enucleation with minimal manipulation is indicated for 
-
All group E with no visual potential,
-
If all known effective treatment has failed

307!
•
No visual potential
•
Tumor 
in 
the 
anterior
segment
•
Tumor in or on the ciliary
body
•
Neovascular glaucoma
•
When there is no direct
visualization of an active
tumor 
(Vitreous
hemorrhage, 
cataract 
or 
hyphema) 
•
Phthisical or pre-phthisical
eye
•
Orbital 
cellulitis-like
presentation
•
Total RD of more than 50%
Note: Optic nerve length should not be less than 
17mm to minimize the chances of leaving tumor at 
surgical site. Also, when performing enucleation: - 
•
Take care not to perforate the globe
•
Use primary orbital implant to achieve excellent
cosmetic appearance
•
If histopathology results are positive for high risk
factors, 6cycles of Chemotherapy is indicated as
for Group D above.
Histopathological features in retinoblastoma are 
considered 
high-risk 
factors 
(HRF) 
for 
tumor 
progression and metastasis, thus their presence 
becomes an indication for adjuvant chemotherapy 
(HRF) includes:  
i) Scleral extension
ii) Post-laminar optic nerve invasion
iii) Disease at the cut margin of optic nerve
iv) Massive choroidal invasion of more than 3mm
v) Anterior chamber extension
•
If no HRF no need of chemotherapy.
•
Prosthesis and protective glasses are indicated
for all children who have been enucleated
EOE 
 Orbital RB 
•
3–6 cycles of high dose chemotherapy- followed
by enucleation if tumor regressed significantly
•
External 
Beam 
Radiotherapy 
and 
adjuvant
chemotherapy for a total of up to 12 cycles
NOTE: Exenteration is not encouraged at this stage 
since aim of treatment is for palliation. 
Distance 
metastasis 
CNS involvement RB- where 
Ct/MRI proved CNS extension or 
cerebral-spinal fluid is positive for 
RB cells 
Palliative care according to the National Palliative 
Care Guideline 
Metastatic 
RB 
where 
bone 
marrow biopsy is positive 
Palliative care according to the National Palliative 
Care Guideline 
Pharmacological Treatment 
Systemic chemotherapy is instituted by Oncologists and or paediatrician. Ophthalmologist institute 
intravitreal chemotherapy if need be.  
Referral: Refer to Oncology Section in this document for details of Chemotherapy in Retinoblastoma 
treatment. 
Note 
 Close follow up is very important due to the following: - 
•
There is a chance of developing retinoblastoma in the fellow eye
•
The risk is diminished with increase in age
•
Also watch for secondary tumors like osteosarcoma
Referral: Refer all children presenting with a white pupillary reflex, squint or acute painful red eye to 
some qualified eye care personnel/ophthalmologist. 
14.4.2 Squamous Cell Carcinoma of Conjunctiva 
Invasive squamous cell carcinoma of conjunctiva is the major and most common ocular malignancy 
of the eye. The tumor typically occurs on the bulbar conjunctiva, originating at the limbus, and often 
spreads onto the cornea, globe, orbit and nasolacrimal system. The cancer is a slow growing tumor 
of middle-aged to elderly people.  
Clinical presentation 
•
It manifests usually as a fleshy vascularized mass at the limbus. (temporal or nasally)
•
In advanced stage, it may intrude the eyeball and extend to other ocular adnexa structures

308!
•
Definitive diagnosis is by histopathological assessment of excised tissue
Investigations 
•
Visual acuity
•
Slit lamp Bimicroscopy
•
Tonometry
•
Fundoscopy
•
Histology 
examination 
of 
the
excised mass
Non-pharmacological Treatment 
•
Check for HIV status of the patient as recurrences occurs most frequently in HIV positive
patients
•
Close follow up of patients for at least the first 12 months postoperatively to look for
residual or recurrent tumors
Pharmacological Treatment 
D: 5-fluorouracil (5FU) 50mg/mL, on a sponge, on the surgical bed for about 2.5minutes 
then wash off with compound sodium lactate solution.  
OR  
D: mitomycin C 0.2mg/mL, on a sponge, on the surgical bed for about 2.5minutes then 
wash off with compound sodium lactate solution. 
AND 
C: dexamethasone + chloramphenicol eye drops, 0.1%–0.5 %, 6hourly, for 3–4weeks 
OR 
C: dexamethasone + gentamicin eye drops, 0.1–0.3%, 6hourly, for 3–4 weeks 
(These are post operatively until the wound is healed) 
THEN 
D: 5-fluorouracil (5FU) 1% eye drops, 4times daily for 2–3weeks 
Note 
•
5-fluorouracil (5FU) is used after the excision wound has healed
•
5 FU eye drops may cause watery eye, discomfort or eye inflammation, manage
accordingly
Surgical Treatment 
•
It depends on the tumor size, location, focality, and invasiveness
•
Surgical excision of the mass with clear margin of 4 mm without touching the tumor is
recommended, followed with topical adjunctive cryotherapy and or chemotherapy to the
residual conjunctival and scleral bed
o
Double - four freeze-thaw cycles of cryotherapy to the remaining
conjunctival margins, bed and limbus.
o
For tumors that are adherent to the sclera, perform a superficial sclerectomy
and use cryotherapy to the base.
•
A large or multicentric squamous conjunctival mass should be managed by a surgeon
experienced in treating such lesions
•
Removal of the eyeball and adnexa may be indicated for advanced stage
•
Radiotherapy if required, for palliation after removal of the eye.
Referral: 
•
All suspicious cases of Squamous Cell Carcinoma of Conjunctiva must be referred to
eye specialist for proper evaluation and management.
•
Refer all patients with advanced Squamous Cell Carcinoma of the conjunctiva to
Oncologist
14.5 Dry Eye 
It occurs when there is inadequate tear volume or function. 
Clinical presentation 
•
Feelings of dryness, grittiness, burning and foreign body sensation, usually worse during
the day

309!
•
Stringy discharge, redness and transient blurring of vision are also common. Exclude
allergic conjunctivitis
Investigations 
•
Visual acuity
•
Slit lamp bimicroscopy
•
Schirmer Test
•
Tear break up test
Non-pharmacological Treatment 
•
Control symptoms since the condition is not curable
•
Educate patients to avoid unprescribed eye medications which may worsen the dryness
and control their environmental factors by e.g. blinking frequently during visual attentive
tasks, avoid air conditioners
Pharmacological Treatment 
Tear substitutes give: 
C: hydroxypropyl methylcellulose 0.7%, ophthalmic drops, 1drop, 6hourly. 
14.6 Herpes Zoster Ophthalmicus 
Occurs when Varicella Zoster Virus reactivates in the trigeminal ganglion and passes down the 
ophthalmic division of the trigeminal nerve 
Clinical presentation 
•
Presents with painful vesicular rash in the trigeminal V1 area–vesicles on the tip of the
nose indicate nasociliary branch involvement and increases the risk of ocular involvement
•
Some patients develop conjunctivitis, keratitis, uveitis, retinitis and cranial nerve
involvement (oculomotor and optic nerves)
•
Later, chronic ocular inflammation, loss of vision, post herpetic neuralgia
•
All patients should be offered HIV testing
Investigations 
•
Visual acuity
•
Slit lamp bimicroscopy
•
Corneal sensation test
•
Fluorescein staining
•
HIV Testing
Pharmacological Treatment 
B: acyclovir (PO) 800mg 4hourly for 7–10days 
AND  
A: amitriptyline (PO) 25mg at night for 3months. 
Note: 
•
Treatment should be initiated within 3 days of the onset of symptoms, except in HIV infected
patients who should be treated if there are active skin lesions
•
Management of Herpes Zoster is Multidisciplinary so consult physician for proper management
of the patient.
Referral 
Refer to eye specialist in case of: - 
•
Vesicles on the tip of the nose
•
Fluorescein staining of the cornea shows corneal ulceration
•
Decreased vision
•
Red eye (uveitis or keratitis)
•
Cranial nerve palsies
14.7 Endophthalmitis 
It is an infection of the ocular cavity. It is an ophthalmic emergency that can cause blindness that 
may occur secondary to bacteraemia (endogenous infection) or following penetrating eye injury of 
surgery 

310!
Clinical presentation 
•
Loss of vision, may be associated with pain in the affected eye
•
Blood culture should be done to identify the source and how it can be treated (for
bacteraemia)
•
In post injury or surgery, culture of specimens of aqueous or vitreous humour should be
done
Investigations 
•
Visual acuity
•
Slit lamp bimicroscopy
•
Tonometry
•
Refraction
•
B Scan
•
Vitreous 
Tap 
for 
Gram 
stain,
Culture and sensitivity
Pharmacological Treatment 
Refer immediately to an ophthalmologist for treatment 
Endogenous Endophthalmitis 
Specialist initiated; vitrectomy often required 
B: ceftriaxone (IV) 2g 24hourly for 7days 
Adjust antibiotics according to culture and sensitivity 
AND 
D: ceftazidime (intravitreal) 2.25mg stat repeat after 16–24hours 
AND 
S: vancomycin (intravitreal) 1mg stat repeat after 72hours 
Administer using separate 1 ml tuberculin or Insulin syringes 
Post-Surgical endophthalmitis 
Specialist initiated; vitrectomy often required 
D: ceftazidime (intravitreal) 2.25mg stat repeat after 16 – 24hours 
AND 
D: vancomycin (intravitreal)1mg stat repeat after 72hours 
Administer using separate tuberculin on Insulin syringes 
In addition, if there is soft tissue involvement or as a prophylaxis after a penetrating injury: 
A: ciprofloxacin (PO) 750mg 12hourly for 7days. 
14.8 Retinitis 
It is seen in advanced HIV infection with CD4 count of less 100 cells/mm3. Management of these 
patients is done in consultation with treating physicians. 
Diagnostic Criteria 
•
Presents with characteristic retinal appearance of necrosis (white exudates and
haemorrhages at the edge of the exudates
•
Visual loss is irreversible
Pharmacological Treatment 
S: ganciclovir (intravitreal) 2mg once a week 
Once immune function has been restored with antiretroviral therapy, (CD4 > 100) and the features of 
active retinitis has been cleared, maintenance Ganciclovir can be stopped but monitor for 
recurrence. 
Referral: Refer to Ophthalmologist for confirmation of diagnosis and treatment. 
14.9 Orbital Cellulitis 
Orbital cellulitis is an infection of the soft tissues of the orbit posterior to the orbital septum. It may be 
a continuum of preseptal cellulitis, which is an infection of the soft tissue of the eyelids and 

311!
periocular region anterior to the orbital septum. Orbital cellulitis may result from an extension of an 
infection from the paranasal sinuses or other periorbital structures such as the face, globe, or 
lacrimal sac, direct inoculation of the orbit from trauma or surgery or as a haematogenous spread 
from bacteremia 
Clinical presentation 
•
Fever, malaise, and a history of
recent sinusitis or upper respiratory
tract infection
•
Proptosis and ophthalmoplegia are
the 
cardinal 
signs 
of 
orbital
cellulitis.
•
Conjunctival 
chemosis, 
dyschromatopsia, 
and 
relative 
afferent pupillary defect 
•
Decreased vision
•
Elevated intraocular pressure
•
Pain on eye movement
•
Orbital pain and tenderness are
present early
•
Swollen 
eyelids, 
chemosis, 
hyperemia of the conjunctiva, and 
resistance to retropulsion of the 
globe may be present  
•
Purulent nasal discharge may be
present
•
For very ill children, vision may
difficult to evaluate in very ill
children with marked edema
Investigations 
•
Visual acuity
•
Slit lamp bimicroscopy
•
Tonometry
•
Fundoscopy
•
Full Blood Count and ESR
•
Blood culture
•
Assessment 
of 
purulent 
nasal
discharge or from the abscess
(Swab for Gram Stain)
•
CT 
Scan 
of 
the 
orbits 
and
paranasal sinuses with Contrast
and
•
MRI will help differentiating it with
other diseases but also identifying
the source or extension of the
disease
Non-pharmacological Treatment 
•
Patients must be hospitalized
•
Adequate hydration
•
Lower the temperature
•
Daily evaluation and monitor the vital signs
•
Management of orbital cellulitis is done with consultation from other medical team
(Neurosurgical (if brain extension is seen), ENT (for involvement of sinuses), Paediatrician
(for paediatric patients) and Physicians
Pharmacological Treatment 
The antibiotic will be tailored when the laboratory results are out 
Adults, give:  
B: ampicillin + cloxacillin (FDC) (IV) 1g stat then 500mg 6hourly for 2weeks 
AND 
A: gentamicin (IV) 160mg 24hourly for 7days 
AND 
B: metronidazole (IV) 500mg 8hourly for 7days 
AND 
S: vancomycin (IV) 15–20 mg/kg 8–12hourly 
Children more than one-month old give: 
B: ampicillin + cloxacillin (FDC) (IV) 50 mg /kg 8hourly for 7–14days 
AND 
A: gentamicin (IV) 7.5mg/kg, 24hourly for 5 -7days 
AND 
B: metronidazole (IV) 7.5–15mg/kg 6hourly for 7–10days 
AND 
S: vancomycin (IV) 10mg/kg 6hourly for 7–10day 

312!
Note: Individual dose not to exceed 1g 
Children less or equal to one-month old give: 
B: ampicillin + cloxacillin (FDC) (IV) 25–50mg/kg 8hourly for 7–14days 
AND 
A: gentamicin (IV) 5mg/kg 24hourly for 5–7days 
Steroidal anti – inflammatory medicines  
To be given after 48 hours of antibiotic therapy. Give: 
A: prednisolone (PO) 1–2mg/kg 24hourly to be tapered slowly. 
AND 
Adults: 
A: ibuprofen (PO) 400–800mg 6–8hourly; not to exceed 3.2 g 24hourly 
OR 
A: paracetamol (PO) 1g 4–6hourly to a maximum of 4 doses 24hourly, for 
 3days 
Children: 
A: ibuprofen (PO) 30–40mg/kg per day in 3–4doses 
OR 
A: paracetamol 10–14 mg/kg for 3days 
Note 
Do not use ibuprofen in patients with bleeding disorders or peptic ulcers 
Surgical Treatment 
Surgical drainage is only indicated when there is: 
•
A decrease in vision
•
Development of an afferent pupillary defect
•
Progression of Proptosis despite appropriate antibiotic therapy
•
The size of the abscess does not reduce on CT scan within 48–72hours after appropriate
antibiotics have been administered
•
If brain abscesses develop and do not respond to antibiotic therapy, then craniotomy is
indicated
•
Presence of a drainable fluid collection is evident on CT scan in patients older than
16years
14.10 Visual Problems 
Visual problems may be due to refractive errors, damage to the eye or optic nerve. This may be an 
indication of underlying diseases such as diabetes or hypertension. 
Investigations 
•
Assess ocular alignment
•
Determine visual acuity accurately in both eyes by Snellen chart
•
If vision is diminished, (less than 6/12), perform the following: -
Pin hole test
o
Make a hole of about 1mm wide in a piece of dark/black paper – you can push a
hole in a paper or card with a pen tip
o
Ask the patient to look through this hole at the Snellen chart
o
If vision improves, this means that the patient has a refractive error
Red Reflex Test 
The patient looks past the examiners head focusing on a distant target. 
o
With the ophthalmoscope at 0 (zero) the examiner keeps close to his eye and
then focuses the beam of light so that it falls on the pupillary area of the cornea
o
The examiner stands about 60cm away from the patient.

313!
o
In normal individuals, the examiner should be able to see a red or pink colour
(reflex) through the pupil which comes from the retina.
Significance of absent red reflex  
If there is history of trauma or diabetes, the absence of a red reflex is probably due to: 
•
Retinal detachment
•
A vitreous hemorrhage
•
Mature cataract
If there are cataracts, one usually sees: 
•
Black shadows against the red reflex in immature cataract, or
•
Absence of red reflex in mature cataracts
In a >50years of age with no history of trauma, diabetes or previous eye disease, an absent red 
reflex is often due to cataract formation, especially with decreased visual acuity. 
Fundoscopy 
Note 
Associated diabetes or hypertension should be adequately managed with referral, as surgery can 
only be considered with appropriately managed systemic disease 
Referral 
Urgent within 12–24 hours 
•
Sudden loss of vision in one or both eyes
•
Pain or redness in one eye only especially with visual and pupillary abnormalities
•
Recent proptosis of one or both eyes or enlargement of the eye (buphthalmos) in children
•
Hazy cornea in children
•
Unilateral watery eye
Within days 
•
Squint of recent onset
•
Suspected or previously diagnosed glaucoma
•
Double vision following recent injury might indicate orbital fracture
•
Leukocoria (white reflex from the pupil) especially in children
•
Squint at an age if not previously investigated by ophthalmologist
•
Visual loss in patients with systemic disease such as diabetes
Non-urgent referral 
•
Cataracts in adults
•
Refractive errors in teenage and adults
•
Longstanding blindness–first visit to health facility
14.11 Onchocerciasis (River Blindness) 
Onchocerciasis is a tissue parasitic infestation caused by a filarial worm, Onchocerca volvulus. The 
microfilariae invade lymphatic system, subcutaneous and deep tissues producing acute 
inflammation and chronic inflammation at a later stage. 
Clinical presentation 
•
Skin inflammation with papules
•
Subcutaneous nodules
•
Atypical 
skin 
lesions 
(scarred,
saggy, hanging areas of skin,
leopard skin)
•
Skin 
nodules 
under 
the 
bony
prominent areas
•
Microfilaria in anterior chamber
•
Scleritis and Keratitis leading to
Impaired 
vision 
as 
well 
as
blindness.
Investigations 
•
Visual acuity
•
Rapid diagnostic test (OV-16 - Onchocerciasis IgG)

314!
•
Skin snip for microscopic examination
•
Slit lamp eye examination.
•
B Scan
Pharmacological Treatment 
Treatment is done in consultation with dermatologists and infectious disease specialists. 
Apart from WHO recommended mass treatment campaign to community at risk with annual 
preventive chemotherapy which polarize/paralyze the worm, treatment depends on individual patient 
presentation. 
A: ivermectin (PO) 0.15mg/kg once every 12months for 12–15years 
Note: 
•
Patients with heavy ocular infestation require retreatment every 3 to 6 months.
•
Treatment will only arrest progression of the clinical features but not reverse them.
Dosage guidelines based on body weight 
Weight 
Dosage 
15-25kg
3mg 
26-44 kg
6mg 
45 -64 kg 
9mg 
65- 84 kg
12mg 
85kg or more 
0.15mg/kg 
Surgical treatment 
Nodulectomy: It is done mostly for nodules located in the scalp to minimize the ocular complications. 

315!
CHAPTER FIFTEEN 
EAR, NOSE AND THROAT DISEASES 
Ear, Nose and Throat (ENT) is a specialty in medicine that deals with medical and surgical 
management of disorders affecting the ear, nose, throat, and the neck. Symptoms and diseases 
affecting this area are common and commonly lead to patients seeking medical care. 
15.1 Ear Condition 
15.1.1 Circumscript otitis Externa (Furunculosis) 
This is a localized infection of the hair follicle on the outer one-third of the external auditory canal. It 
is caused by Staphylococcus aureus. 
Clinical presentation 
•
Ear pain that is severe and disproportional to the visible lesion
•
Reduced hearing
•
Localized swelling on the external auditory canal
•
There may be a purulent discharge if the swelling ruptures
Non-pharmacological management 
•
Aural toilet if there is otorrhea (ear suctioning under direct vision).
•
Instruct the patient to keep the ear dry and avoiding scratching
Pharmacological management 
B: ampicillin+cloxacillin (FDC) (PO) Adults: 500mg 8hourly for 7 to 10days. Children: 
15mg/kg hourly for 7 to 10days  
OR 
C: amoxycillin + clavulanic acid (FDC) (PO) Adults: 625mg to 1g 12hourly for 7 to 10days. 
Children ≤ 3 months: 30mg/kg/day in 2 divided doses for 7-10 days. Children >3 months: 
25mg/kg/day in 2 divided doses for 7 to 10 days. 
AND 
A: paracetamol (PO) Adults: 500mg to 1g 4 to 8hourly as needed. Children ≤ 10kg: 
10mg/kg 4 to 8 hourly as needed. Children >10kg: 15mg/kg    4 to 8 hourly as needed 
OR 
A: ibuprofen (PO) Adults: 200 mg to 400mg 4 to 8hourly as needed. Children ≥ 6 months: 
5mg to 10mg/kg 4 to 8hourly as needed OR combined ibuprofen and paracetamol 
Surgical management 
•
Incision and drainage
15.1.2 Diffusewer Otitis Externa (Swimmer’s ear) 
This is an inflammation of the entire external auditory canal. It can be caused by bacteria, fungus or 
both. 
Clinical presentation 
•
Itchy, dry and scaly ear canal and painful ear
•
There may be a water or purulent discharge, debris and reduced hearing
Pain may become extreme when the ear canal becomes completely occluded with edematous skin 
and debris. 
Non-pharmacological management 
•
Aural toilet at least once a week (ear suctioning under direct vision using microscope or
endoscope).
•
Instruct the patient to keep the ear dry and avoiding scratching.

316!
C: ciprofloxacin ear drops 2 to 4drops each ear 6 to 8hourly for 14days. 
OR 
C: cream with combination of gentamicin or Neomycin+ Clobetasol or betamethasone or 
beclometasone + miconazole or clotrimazole. Dosage: Apply pea size in external auditory 
canal once per week for 4 to 6weeks. 
OR 
D: chloramphenicol+beclomethasone dipropionate+ clotrimazole + lignocaine ear drops 
(FDC) 
2 to 3drops each ear 6 to 8hourly for 14days. 
AND 
A: ciprofloxacin (PO) 500mg Adults and children above 12 years 12 hourly 7 to 14 day 
OR 
B: amoxycillin +clavulanate (FDC) (PO) Adult 625mg to 1g 12hourly: Paediatric ≤ 3 month 
30mg/kg/day in 2 divided doses. Paediatric˃ 25mg/kg/day in 2 divided doses for 7-14days 
AND 
A: paracetamol (PO) Adult 1g: Pediatric ≤ 10kg 10mg/kg 4. Paediatric >15mg/kg 6 to 8 
hourly as needed. 
OR 
A: ibuprofen (PO) 200 mg to 400mg 8 hourly as needed. Paediatric ≥ 6 months: 5mg to 
10mg/kg    4 to 8hourly as needed 
OR 
D: diclofenac+ paracetamol (PO)(FDC)Adults: 50mg diclofenac and 500mg paracetamol    
4 to 8hourly as needed.     
15.1.3 Necrotizing Otitis Externa 
This is a life-threatening infection that affects the external auditory canal and base of the skull. It is 
common to elderly diabetic patients and other immunosuppressive conditions. Most common 
causative 
organism 
is 
Pseumonas 
aureginosa. 
Controlling 
the 
underlying 
cause 
of 
immunosuppression is of paramount importance.  
Clinical presentation 
•
Ear pain, discharge, fullness and hearing impairment
•
May present with facial nerve paralysis or other cranial nerves palsy.
•
Presence of granulation tissues at the junction between the bony and cartilaginous parts of
external auditory canal
•
Necrosis of external auditory canal
Non-pharmacological management 
•
Aural toilet at least once a week (ear suctioning under direct vision using microscope or
endoscope).
•
Instruct the patient to keep the ear dry and avoiding scratching
Investigations 
•
culture and sensitivity of discharge
Pharmacological management 
C: ciprofloxacin ear drops 2 to 4 drops each ear 6 to 8hourly for 14days 
AND 
B: ceftriaxone (IV) 1 to 2 g 12hourly for 7days. 
For Children:  
B: ceftriaxone (IV) 50 to 100mg/kg 24hourly for 7 day 
OR 
C: ciprofloxacin (IV) 400mg for 5 to 7days THEN 500mg (PO) 12hourly for 4 to 6weeks 
days. 
OR 
S: meropenem (IV) (culture and sensitivity test is required) 500mg to 2g 8 hourly for 7 
to 14days. 
For Children ≥ 3 months: 
Pharmacological management 

317!
S: meropenem (IV) (culture and sensitivity test is required) 10mg/kg 8 hourly for 7 to 
14days. 
AND 
A: paracetamol (IV) 500mg to 1g 4 to 8hourly as needed. 
For Children ≤ 10kg: 
A: paracetamol (IV) 10mg/kg 4 to 8hourly as needed. 
ForChildren >10kg:  
A: paracetamol (IV) 15mg/kg 4 to 8hourly as needed. 
OR 
A: ibuprofen (PO) 200 to 400mg 4 to 8hourly as needed. 
For Children ≥ 6 months:  
A: ibuprofen (PO) 5mg to 10mg/kg 4 to 8hourly as needed 
OR 
C: diclofenac+ paracetamol (PO) 50mg diclofenac and 500mg paracetamol 4 to 8hourly as 
needed 
Surgical management 
Serial surgical debridement under local anesthesia(LA) or general anesthesia (GA). 
Note: Necrotizing otitis externa is an emergency therefore treatment should be vigorous including 
the treatment of underlaying immunodeficiency. Consider referral to tertiary facility for specialized 
care. 
15.1.4 Herpes Zoster Oticus (Ramsay Hunt syndrome) 
This is a viral infection of external, middle and inner ear caused by reactivation of Varicella Zoster 
virus in the geniculate ganglion.  
Clinical presentation 
•
Vesicular rash of the ear
•
Facial nerve paralysis
•
Ear pain
•
Ear discharge
Non-pharmacological management 
Instruct the patient to keep the ear dry and avoiding scratching 
Pharmacological management 
A: prednisolone (PO) 60mg 24hourly for 5days then taper down to 50mg 24hourly for next 
5days. Children: 1mg/kg 24hourly for 5days then taper down by half for the next 5days. 
AND 
B: acyclovir (PO) 800mg 4-8hourly for 7-14days. 
For Children birth to 3 months:  
B: acyclovir (IV) 10-20mg/kg 8hourly for 7-14days 
For Children from 3 months to 12 years:  
B: acyclovir (PO) 40-80mg/kg 6hourly for 7-14days 
For Children more than 12 years 
B: acyclovir (PO) 40-80mg/kg 6hourly for 7-14days 
AND 
B: acyclovir 5% cream.: Apply on the lesions 12 hourly. 
AND 
B: ampicilin+cloxacilin (FDC) (PO) 500mg 8hourly for 10-14 days. 
For Children:  
B: ampicilin+cloxacilin (FDC) (PO) 15mg/kg 6 hourly for 7-14 days 
OR 
B: amoxycillin+clavulanate (FDC) (PO) 625mg to 1g 12 hourly for 7-14 days. 
ForChildren ≤ 3 months:  
B: amoxycillin+clavulanate (FDC) (PO) 30mg/kg/day in 2 divided doses for 7-14 days. 
For Children >3 months:  
B: amoxycillin+clavulanate (FDC) (PO) 25mg/kg/day in 2 divided doses for 7 to 14 days 
OR 
A: paracetamol (PO) 500mg to 1g 4 to 8 hourly as needed. 
ForChildren ≤ 10kg:  
B: amoxycillin+clavulanate (FDC) (PO) 10mg/kg 4 to 8 hourly as needed. 

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For Children >10kg: 
B: amoxycillin+clavulanate (FDC) (PO) 15mg/kg 4 to 8 hourly as needed 
OR 
A: ibuprofen (PO) 200 to 400mg 4 to 8hourly as needed. 
For Children ≥ 6 months: 
A: ibuprofen (PO) 5mg to 10mg/kg 4 to 8hourly as needed 
OR 
C: diclofenac (PO) 50 mg 4 to 8hourly as needed.75 mg (IM) 8hourly as needed 
OR 
A: paracetamol + ibuprofen (PO) 400mg ibuprofen and 325mg paracetamol 4 to 8hourly as 
needed. 
For Children:  
A: paracetamol + ibuprofen (PO) 100mg ibuprofen and 162.5mg paracetamol 4 to 8hourly 
as needed 
15.1.5 Pre-auricular Sinus Tract Infection 
This is an infection of the pre-auricular sinus tract. May present with pre-auricular abscesses. Most 
common causative organism is Staphylococcus aureus.  
Clinical presentation 
•
Ear pain, sinus discharge
•
Pre-auricular Swelling
•
Fever, headache
Pharmacological management. 
B: ampincillin+cloxacillin (FDC) (PO) 500mg 8hourly for 7-10days. 
For Children:  
B: ampincillin+cloxacillin (FDC) (PO) 15mg/kg 6 hourly for 7-10days 
OR 
B: amoxycillin+clavulanate (FDC) (PO) 625mg to 1g 12hourly for 7-10days 
For Children ≤ 3 months: 
B: amoxycillin+clavulanate (FDC) (PO): 30mg/kg/day in 2divided doses for 7-10days 
For Children >3 months:  
B: amoxycillin+clavulanate(FDC)(PO) 25mg/kg/day in 2divided doses for 7-14days 
AND 
A: paracetamol (PO) 500mg to 1g 4-8hourly as needed. 
For Children ≤ 10kg: 
A: paracetamol (PO) 10mg/kg 4-8hourly as needed. 
For Children >10kg:  
A: paracetamol (PO) 15mg/kg 4-8hourly as needed 
OR 
A: ibuprofen (PO) 200 mg to 400mg 4-8hourly as needed. 
For Children ≥ 6 months:  
A: ibuprofen (PO) 5mg to 10mg/kg    4-8hourly as needed 
OR 
C: diclofenac (PO) 50 mg 4 to 4-8hourly as needed. THEN 75 mg (IM) 4-8hourly as 
needed 
OR 
C: diclofenac+ paracetamol (FDC) (PO) 50mg diclofenac and 500mg paracetamol 4-
8hourly as needed 
Surgical management 
•
Incision and drainage of the abscess
•
Excision of the sinus tract two to three weeks after incision and drainage i.e. when the
sinus tract is dry.

319!
15.2 Trauma of the Pinna 
15.2.1 Hematoma of the Pinna 
Clinical presentation 
•
History of trauma
•
Fluctuant, tender pinna swelling
Pharmacological Treatment: 
B: ampicilin+cloxacillin (FDC) (PO) 500mg 8hourly for 7-10days 
Children: B: ampicilin+cloxacillin (FDC) (PO) 15mg/kg 6hours for 7-14days 
OR 
B: azithromycin (PO) 500mg 24hourly for 3days. 
For Children:  
B: ampicilin+cloxacillin (FDC) (PO) 10mg/kg 24hourly for 3days 
AND 
A: paracetamol (PO) 500mg to 1g 4-8hourly as needed. 
ForChildren ≤ 10kg:  
A: paracetamol (PO) 10mg/kg 4-8hourly as needed 
For Children >10kg: 
A: paracetamol (PO) 15mg/kg 4-8 hourly as needed 
OR 
C: ibuprofen (PO) 200 mg to 400mg 4-8hourly as needed. 
ForChildren ≥ 6 months:  
C: ibuprofen (PO) 5mg to 10mg/kg 4-8hourly as needed 
Surgical management 
•
Incision and evacuation of hematoma
•
Tight wound dressing to prevent re-accumulation of hematoma
15.2.2 Laceration of the Pinna 
Lacerative trauma of the pinna with tear of skin and cartilage through and through. 
Non-pharmacological management 
•
Skin to skin stitching of the wound, avoid through and through stitching this my
compromise blood supply to the cartilage.
Pharmacological management 
B: ampincillin+cloxaccillin (PO) 500mg 8 hourly for 10 -14 days 
ForChildren:  
B: ampicillin+cloxacillin (PO) 15mg/kg 6hourly for 7 -14day 
AND 
A: paracetamol (PO) 500mg to 1g 4-8hourly as needed 
ForChildren ≤ 10kg: 
A: paracetamol (PO) 10mg/kg 4-8hourly as needed 
For Children > 
 A: paracetamol (PO) 10kg: 15mg/kg    4-8hourly as needed 
OR 
A: ibuprofen (PO) 200mg to 400mg 4-8hourly as needed 
For Children ≥ 6 months: 
A: ibuprofen (PO) 5mg to 10mg/kg 4-8hourly as needed. 
OR 
C: diclofenac+ paracetamol (PO) 50mg diclofenac and 500mg paracetamol 4-8hourly as 
needed 
15.2.3 Ear Keloid 
This is abnormal proliferation of scar tissue that forms at the site of cutaneous injury and grows 
beyond the original margins of the scar. Most common causes are ear piercing, trauma or surgical 
incisions.  

320!
Clinical presentation 
•
Swelling of the involved area of the ear, most commonly ear lobe
Non-pharmacological management 
•
Use of pressure therapy e.g. pressure clips
Pharmacological management- Intra-lesional steroid injection 
D: betamethasone (Intra-lesional) 6-12mg depending on the size of the lesion weekly for 4 
weeks before excision and 4weeks after excision 
OR 
D: triamcinolone acetonide (Intra-lesional) 40mg depending on the size of the lesion 
weekly for 4weeks before excision and 4weeks after excision 
Surgical management 
•
Total keloidectomy+/-Steroid injection. (SHOULD BE DONE BY SOMEONE WITH
EXPERTISE)
15.2.4 Cerumen Impaction 
Usually occurs following the use of cotton buds which hinder the natural movement of cerumen 
outwards 
Clinical presentation 
•
Reduced hearing
•
Ear pain
•
Ear fullness
•
Itching
•
Tinnitus
Pharmacological management 
A: hydrogen peroxide 3% ear drops2-4drops each ear 6-8hourly for 7days. 
Non-pharmacological Treatment: 
•
Remove using cerumen hook, syringing or suctioning under direct vision
Note 
Patient should be educated on cleansing mechanism of the ear and not to use cotton bud. 
15.2.5 Foreign Body in the Ear 
Usually happens in children. Common foreign bodies include beads, stones and seeds (bean, 
maize, orange). In adult’s foreign bodies include cotton bud and insect  
Non-pharmacological Treatment: 
•
Restrain the child
•
Remove using a cerumen hook under
direct vision (if the child cannot be
restrained, sedation is advised)
•
An insect should be killed (by soaking
the ear canal with normal saline or spirit)
before removal
Note 
Do not attempt to remove ear foreign body if you don’t have proper instruments and expertise. 
15.2.6 Traumatic Tympanic Membrane/ Ear Drum Perforation. 
Clinical presentation 
•
History of trauma direct or indirect
•
Ear bleeding +/-discharge
•
Ear pain/otalgia
Non-pharmacological Treatment 
•
For indirect trauma avoid ear drops and water in the ear
•
For direct trauma aural toilet can be done then ear drops instilled

321!
Pharmacological management 
A: hydrogen peroxide 3% ear drops 2-4drops each ear 6-8hourly for 7days 
AND 
A: ciprofloxacin ear drops, 2-4drops each ear 6-8hourly for 14days 
AND 
A: ciprofloxacin (PO) 500mg Adults and children above 12years 12hourly for 5-7days 
OR 
C: ciprofloxacin (IV) 400mg 12hourly for 5-7days then for 5-7days 
AND 
A: paracetamol (PO) 500mg to 1g 4-8 hourly as needed. 
For Children ≤ 10kg:  
A: paracetamol (PO) 10mg/kg 4-8 hourly as needed. 
For Children >10kg: 
A: paracetamol (PO) 15mg/kg 4-8 hourly as needed 
OR 
A: ibuprofen (PO) 200 mg to 400mg 4-hourly as needed. 
For Children ≥ 6 months: 
A: ibuprofen (PO) 5mg to 10mg/kg    4-8 hourly as needed 
OR 
C: diclofenac+paracetamol (PO) 50mg diclofenac and 500mg paracetamol 4-8hourly as 
needed 
15.3 Otitis Media (Acute or Chronic) 
It is an inflammation of the middle ear cavity. It is considered acute when the inflammation is of less 
than 2 weeks’ duration, and chronic when the inflammation is of more than 2 weeks’ duration with 
tympanic membrane perforation. 
Clinical presentation 
•
Examine the pinna
•
Using an otoscope carefully examine the external auditory canal and the tympanic membrane
15.3.1 Acute Otitis Media 
Clinical presentation 
•
Previous upper respiratory tract infection
•
Painful ear
•
Restlessness
•
Fever
•
Hearing often reduced
•
Inflamed, bulged tympanic membrane
Non-pharmacological Treatment: 
•
Acute otitis media should be treated with analgesics, antibiotics and/or paracentesis/
(Myringotomy) to reduce pain and to obtain pus for culture and sensitivity)
Pharmacological Treatment: 
B: amoxicillin+clavulanic acid (PO) 375–625mg 12hourly for 10days 
OR 
A: azithromycin (PO) 500mg 24 hourly for 5days (for patients who are allergic to penicillin) For 
Children  
A: azithromycin (PO) 10mg/kg 24hourly for 5days 
OR 
B: ceftriaxone (IV) 1 to 2 g    12hourly for 10days. 
For Children: 
B:  ceftriaxone (IV) 50 to 100mg/kg 24hourly for 10days 
OR 
C: clarithromycin (PO) 500mg 12hourly for 10-14days. 
ForChildren ≥ 6 months:  
C: clarithromycin (PO) 15mg/kg/day in 2divided doses for 10-14days 
OR 
S: cefixime (PO) 400mg 24hourly for 10-4days 

322!
For Children ≥ 6 months to 12 years (weight below 45kg): 
S: cefixime (PO) 8mg/kg 24hourly for 10-14days 
AND 
A: paracetamol (PO) 500mg to 1g 4-8hourly for 3days. 
For Children ≤ 10kg:  
A: paracetamol (PO) 10mg/kg 4-8hourly for 3days 
For Children >10kg: 
A: paracetamol (PO) 15mg/kg 4-8 hourly for 3days. 
OR 
A: ibuprofen (PO) 200mg to 400mg 4-8hourly as needed. 
For Children ≥ 6 months: 
A: ibuprofen (PO) 5mg to 10mg/kg 4-8hourly as needed 
OR 
C: diclofenac+ paracetamol (PO) 50mg diclofenac and 500mg paracetamol 4-8hourly as 
needed 
Note: For antibiotics, treatment periods shorter than 10 days increase the risk of treatment failure 
Referral 
•
Children with high fever, severe ear pain, headache, altered state of consciousness
•
A chronically discharging ear that persists in spite of proper treatment.
•
Foul smelling ear discharge
•
Mastoiditis
•
Otitis in the normal (or better hearing) ear combined with permanent hearing loss in the other
ear
15.3.2 Chronic Suppurative Otitis Media 
This is a perforated tympanic membrane with persistent drainage from the middle ear for more than 
2-6 weeks. Most common causative organisms are Pseudomonas aeruginosa, Staphylococcus
aureus, Proteus species, Klebsiella pneumonia, and diphtheroids.
Clinical presentation 
•
Discharge of pus from the ear
•
Perforated tympanic membrane
•
Reduced hearing
Non-pharmacological Treatment: 
•
Keep ear dry/avoid water into the ear
•
Aural toilet – ear suctioning under direct vision(otomicroscopy/endoscopy), removal of debris
•
Ear wicking regularly, with a dry cotton wick at home
Pharmacological Treatment 
C: ciprofloxacin ear drops, three drops12hourly for 14days  
A: hydrogen peroxide 3% ear drops: 2 to 4 drops each ear 6-8hourly for 14days 
OR 
A: boric acid ear drops: 2-4 drops each ear 6-8hourly for 14days 
OR 
D: ofloxacin ear drops: 2 to 4 drops each ear 6-8hourly for 14days 
AND 
A: ciprofloxacin (PO) 500mg 12hourly for 10days 
ForChildren: 
A: ciprofloxacin (PO) 10–20mg/kg 12hourly for 10days 
Surgical management 
•
Mastoidectomy
•
Endoscopic tympanoplasty
•
Tympano-mastoidectomy
•
Ossiculoplasty

323!
Note 
Treatment of shorter than 10 days will result into treatment failure 
Avoid ototoxic drugs(gentamycin , neomycin and quinine) if there is TM perforation 
15.3.3 Mastoditis with Sub-Periosteal Abscess 
It is due to infection of the mastoid air cells in the middle ear, a complication of chronic suppurative 
otitis media. It presents as a fluctuant painful swelling on the post auricular area. The overlying skin 
is also inflamed. 
Non-pharmacological Treatment 
Aspirate the swelling before incision and drainage, and then refer for mastoidectomy at a 
zonal/national hospital 
Pharmacological Treatment: 
C: ciprofloxacin ear drops, 3drops, 12hourly for 14days 
AND 
A: ciprofloxacin (PO) 500mg 12hourly for 10days; Children 10–20mg/kg 12hourly for 
10days 
Investigations 
•
Culture &sensitivity
•
CT SCAN-Temporal Bone
Surgical management 
•
Incision and drainage
•
Mastoidectomy/Drainage
mastoidectomy
•
Tympano-mastoidectomy
•
Ossiculoplasty
Note 
 Treatment shorter than 10days will result into treatment failure 
15.3.4 Otitis Media with Effusion 
It is a multifactorial, inflammatory condition in the middle ear with serous or mucous accumulation 
without ear discharge. It is a residual condition after acute otitis media and rhino sinusitis with 
Eustachian tube dysfunction.  
Diagnostic Criteria 
 It is often discovered by chance. 
•
Little or no ear pain
•
Gradual loss of hearing
•
No ear discharge
•
Aural fullness
Non-pharmacological Treatment 
•
Close follow-up
•
Valsava maneuver
•
Encourage chewing
Pharmacological Treatment 
D: fluticasone propionate (50mcg/spray) nasal spray. Adults and adolescents more than 
12years: 2sprays in each nostril 24hourly as needed. Children 4-1years: 1spray in each 
nostril 24hourly as needed. 
OR 
S: mometasone (nasal spray) Adults and adolescents from 12years: 1 sprays in each 
nostril 24hourly as needed. Children 6-11years: 1spray in each nostril 24hourly as needed 
AND  
B: ephedrine (0.5% and 1%) nasal drop, Adults and children above 12years: Instill 1 to 2 
drops in each nostril, not more than 4 times a day for 3 to 5 days 

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Note 
Otitis media with effusion with hearing loss that does not improve after 3months should be 
referred to a specialist for myringotomy and grommets insertion 
Surgical management 
Myringotomy+grommet insertion (microscopic/endoscopic) +Adenotonsilectomy (In children) 
15.4 Hearing Loss 
A child with hearing loss should be detected and intervention started immediately after delivery. New 
born hearing screening is done using an otoacustic emission machine. Any child suspected of 
hearing loss (usually presenting with delayed speech development) should be referred to a 
zonal/national hospital immediately since early intervention has a better outcome. 
15.4.1 Sensorineural Hearing Loss (SNHL) 
Loss of hearing that results from defective function of cochlea or auditory pathway. It may be 
congenital or acquired. 
Clinical presentation 
•
Hearing impairment as confirmed by hearing assessment tests.
Investigation 
•
Distraction Test/Free Field Test –
for children
•
Tympamomery
•
Audiometry
•
Otoacoustic emission(OAE)
•
Auditory 
Brainsterm 
Response
(ABR)
•
CT-Scan/MRI for bone cochlea and
auditory nerve assessment for pre
cochlea implantation
Non-pharmacological management (Rehabilitation) 
•
Avoiding exposure to noises
•
Avoiding 
unnecessary 
use 
of
ototoxic drugs
•
Digital programmable hearing aid-
for mild to moderate SNHL
•
Super power digital programmable
hearing 
aid-for 
severe 
and
profound SNHL
•
Bone-anchored hearing Aid(BAHA)
•
Cochlea Implantation (C.I), with
interval
programming/troubleshooting 
–for
severe and profound SNHL.
•
Speech therapy
•
Sign
language/lip 
reading
Pharmacological management 
C: calcium +vitamins 1tablets 24hourly for not less than 3months 
Surgical management 
Posterior tympanotomy for cochlear implantation 
15.4.2 Sudden Sensorineural Hearing Loss 
Clinical presentation 
•
Sudden onset of hearing loss 24-72 hours from onset, unilateral or bilateral.
•
Tinnitus
Investigations 
•
Tympamomery
•
Audiometry
Pharmacological management 
A: prednisolone (PO) 60mg 24hourly for 5days then taper down to 50mg 24hourly for next 
5days. 
For Children: 
A: prednisolone (PO) 1mg/kg 24hourly for 5days then taper down by half for the next 
5days. 
AND 
C: calcium and vitamins 1tablet 24hourly for not less than 3months 

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15.4.3 Otosclerosis 
Otosclerosis is a bony overgrowth that involves the footplate of the stapes. As the overgrowth 
develops, the stapes can no longer function as a piston, it become fixated. Conduction gradually 
becomes worse until a maximal conductive hearing loss of 60 dB is reached. 
Clinical presentation 
•
Hearing loss
•
Dizziness
•
Tinnitus
Investigations 
•
Tympanomety
•
Pure tone Audiometry (PTA)
•
CT- Scan -of temporal bone
Non-pharmacological management 
•
Hearing aids (H/A)-Digital Programmable Hearing Aids
•
Cochlea implantation
Surgical management 
•
Stapedectomy
•
Posterior tympanotomy for Cochlea Implantation
15.4.4 Peripheral Vertigo (Meniere’s disease and Benign Paroxysmal Positional 
Vertigo(BPPV) 
Clinical presentation 
Meniere’s disease 
Benign Paroxysmal Positional Vertigo( PPPV) 
Vertigo 
Vertigo 
Nausea 
Nausea 
Vomiting 
Vomiting 
Tinnitus 
Directional specificity 
Aural Fullness 
Reduced Hearing 
Reduced Hearing 
Investigation 
•
Audiometry
•
Vestibular test
•
Video nystagmogram (vNG)
•
Video head impulse test (vHIT)
•
MRI Brain-to rule out
cerebellopontine angle (CPA)
tumours
Non-pharmacological management (FOR BPPV) 
•
Epley maneuver
•
Berbecure maneuver
•
Vestiulr rehabilitation therapy
•
Stabilometer
Pharmacological management (FOR MENIERES) 
C: betahistidine (PO) 24-48mg 1 hourly for 14days. Maintanance dose 24mg 24hourly for 
14days. 
AND 
B: intratympanic dexamethasone (IV) 4mg  
AND  
C: acetazolamide (PO) 250mg 24hourly for 14days 
15.4.5 Vestibular Neuritis /Vestibular Neuronitis and Labyrinthitis 
Clinical presentation 
•
Rapid onset severe vertigo, nausea, vomiting
•
Spontaneous vestibular nystagmus

326!
•
Gait instability
Pharmacological management 
A: prednisolone (PO) 60mg 24hourly for 5days then taper down to 50mg 24hourly for next 
5days. 
For Children: 
A: prednisolone (PO) 1mg/kg 24hourly for 5days then taper down by half for the next 
5days. 
OR  
D: methylprednisolone (IV) 100mg 24hourly then taper to 10mg over 3weeks. 
15.4.6 Vestibular Migraine 
Clinical presentation 
•
Dizziness/Vertigo
•
Moderate to severe temporal headache
•
Sensory amplification e.g. hyperaccusis
Investigations 
•
Audiometry
•
Vestibular test
•
Video nystagmogram(vNG)
•
Video head impulse test(vHIT)
•
MRI Brain-to rule out
cerebellopontine angle
(CPA)tumours
Pharmacological management 
A: propranolol (PO) 40mg 12hourly for 14days 
OR 
C: amlodipine (PO) 10mg 24hourly for 14days 
15.4.7 Tinnitus 
Clinical presentation 
•
Perception of sound in proximity to the head in the absence of an external source
Non-pharmacological management 
•
Tinnitus masking
Pharmacological management 
C: betahistidine (PO) 16-24mg 8hourly for 14days 
For Children 5-12 years: 
C: acetazolamide (PO) 250mg 24hourly 14days 
15.4.8 Glomus Tumours 
Paragangliomas are rare neuroendocrine tumors that arise from the extra-adrenal autonomic 
paraganglia, small organs consisting mainly of neuroendocrine cells that are derived from the 
embryonic neural crest and have the ability to secrete catecholamines  
Clinical presentation 
•
Neck mass (at angle of
mandible)
•
Pulsatile tinnitus
•
Hearing loss(conductive)
•
Rising sun signs
Investigations 
•
Audiometry
•
CT-Scan-head & neck
•
CT-angiogram
•
MRI-neck

327!
Surgical management 
•
Glomus Tumour excision
15.4.9 Vestibular Schwannomas 
Also known as acoustic neuromas, acoustic schwannomas, acoustic neurinomas, or vestibular 
neurilemomas) are Schwann cell-derived tumors that commonly arise from the vestibular portion of 
the eighth cranial nerve.  
Clinical presentation 
•
Hearing loss
•
Tinnitus
Investigations 
•
Audiometry
•
MRI-brain (with gadolinium as contrast)
Non-pharmacological management 
•
Observation/watchful waiting
•
Radiotherapy
Surgical management 
•
Tumour (schwanoma) excision
15.5 Nose/Paranasal Sinuses Conditions 
15.5.1 Acute Rhinitis 
It is a viral inflammatory condition in the nasal mucous membrane, usually part of a more wide-
spread infection of the upper respiratory tract. 
Non-pharmacological Treatment 
•
Bed rest& warm drinks
Pharmacological Treatment 
A: ephedrine nasal drops (1% for adults and 0.5% for children) 1–2drops into each nostril 
6hourly for not more than 5days 
15.5.2 Acute Non-Allergic Rhinitis 
Clinical presentation 
•
Nasal blockage
•
Post nasal drip
•
Erythematous turbinate
Pharmacological management 
B: ephedrine (0.5% and 1%) nasal drop, Adults and children above 12years: Instill 1-
2drops in each nostril, not more than 4times a day for 3-5days 
OR 
 C: oxymetazoline (0.05%) nasal drops/spray Dosage for adults and children above 6years: 
Instill 2 -3drops or sprays in each nostril 12hourly for 3-5days  
AND 
D: fluticasone propionate (50mcg/spray) nasal spray, Adults and adolescents more than 
12years: 2sprays in each nostril 24 hourly as needed. children 4-11years: 1 spray in each 
nostril 24hourly as needed 
OR 
S: mometasone nasal spray, Adults and adolescents from 12years: 1sprays in each nostril 
24hourly as needed, children 6-11 years: 1spray in each nostril 24hourly as needed 
A: prednisolone (PO), Adults: 60mg 24hourly for 5days then taper down to 50mg 24hourly 
for next 5days. Children: 1mg/kg 24hourly for 5days then taper down by half for the next 
5days. 

328!
Note 
Oral drugs to reduce swelling of the mucous membrane, antihistamines and antibiotics are not 
indicated 
15.5.3 Allergic Rhinitis 
It is an irritation of the nasal mucosa by an allergen in a previously sensitized individual. Common 
allergens include house dust (mite’s feaces), pollens, cockroach antigen, animal dander, molds (in-
door) 
Clinical presentation 
•
Itchy nostrils, throat, eyes
•
Watery nasal discharge
•
Nasal congestion
•
Sneezing
•
Post nasal drip
•
Cough
Investigations: 
•
Anterior rhinos copy – watery nasal discharge, nasal congestion
•
Total or specific IgE
•
Skin prick Allergy test
Non-pharmacological management 
•
The main treatment of allergic rhinitis is the Avoidance of the triggers.
•
Steaming
•
Immunotherapy
Pharmacological Treatment: 
A: ephedrine (0.5% and 1%)nasal drop, Adults and children above 12years: Instill 1 to 
2drops in each nostril, not more than 4 times a day for 3-5days 
OR 
 C: oxymetazoline (0.5%) nasal drops/spray, Adults and children above 6 years: Instill 2- 3 
drops or sprays in each nostril every after 12 hours for 3-5days 
AND 
D: fluticasone propionate (50mcg/spray) nasal spray, Adults and adolescents more than 
12years: 2sprays in each nostril 24 hourly as needed. children 4-11years: 1spray in each 
nostril 24hourly as needed 
OR 
S: mometasone nasal spray, Adults and adolescents from 12years: 1 sprays in each 
nostril 24 hourly as needed. children 6 to 11 years: 1 spray in each nostril 24 hourly as 
needed. 
AND 
A: prednisolone (PO): 60mg 24hourly for 5days then taper down to 50mg 24 hourly for 
next 5days. Children: 1mg/kg 24hourly for 5days then taper down by half for the next 
5days.  
AND 
C: loratadine (PO), Adults: 10mg 24hourly for 30days. Children 2-6years: 5mg 24hourly for 
14days. Children above 6 years: 10mg 24 hourly for 14 days 
OR 
S: desloratadine (PO)Adults: 5mg 24hourly for 30days. Children 2-5 years: 1.25mg 
24hourly for 14days. Children 6 to 12 years: 2.5mg 24hourly for 30days 
AND 
S: montelukast, Adults: 10mg 24hourly for 30days.Children 1-15 years: 5mg 24hourly for 
14days 
15.6 Granulomatous Diseases of the Nose 
15.6.1 Rhinoscleroma 
Clinical presentation 
•
Rhinitis, Fetid rhinorrhea
•
Crusting, Nasal bleeds
•
Intranasal rubbery nodules
•
Dysphonia

329!
•
Fibrosis, Nasal deformity
Non-pharmacological management 
•
nasal douching with saline solution
Pharmacological management 
A: ciprofloxacin (PO), Adults and children above 12years: 500mg 12hourly for 4-12weeks. 
 Continue treatment for at least 2days after signs and symptoms have disappeared. 
OR 
S: cefixime (PO), Adults: 400mg 24hourly for 4-12weeks. Children ≥ 6months to 12years 
(weight below 45kg): 8mg/kg 24hourly for 4-12weeks 
AND 
A: prednisolone (PO) Adults: 60mg 24hourly for 5days then taper down to 50mg 24hourly 
for next 5days. Children: 1mg/kg 24hourly for 5days then taper down by half for the next 
5days. 
Surgical management 
•
Rhinoplasty
15.6.2 Tuberculosis of the Nose 
Clinical presentation 
•
Nasal pain
•
Nasal bleeing
•
Mass in the nose
•
Nasal deformity
Investigations 
•
Nasal mucosal scraping for AFB/gene expert
•
Skin biopsy for Histology and AFB
Pharmacological management 
Refer TB Program 
15.6.3 Syphilis of the Nose 
Clinical presentation 
•
Nasal discharge
•
Nasal crusting
•
Epistaxis
•
Ulceration of nose
•
Saddle nose
Investigations 
VDRL 
Non-pharmacological management 
•
Crusts Removal-Endoscopic
Pharmacological management 
Refer STI chapter 
15.6.4 Rhinosporiodiosis 
Nasal disease caused by rhinosporidium seeberi 
Clinical presentation 
•
Unilateral nasal obstruction
•
Epistaxis
•
Local pruritus
•
Rhinorrhea
•
Pink or deep red polyp, strawberry
like appearance, Bleeds easily on
manipulation

330!
Pharmacological management 
S: dapsone (PO), Adults: 100mg 24hourly for 6months. Children1-2mg/kg 24hourly, not to 
exceed 100mg 24hourly 
Surgical management 
Wide excision with wide area electro-coagulation of the lesion base 
15.6.5. Mucormycosis 
This is fungal infection of nose, caused by mucor, rhizopus species. 
Clinical presentation 
•
Fever, Headache
•
Nasal congestion, Purulent nasal
discharge
•
Eshar of nasal mucosa
•
Proptosis, Blindness
•
Facial
numbness
Pharmacological management 
S: amphotericin B (IV): Adults, Test dose of 1mg IV infused over 20-30 minutes. Loading 
dose of 0.25-0.5mg/kg infused over 2-6hours. Maintenance dose of 0.25-1mg/kg IV 
24hourly for 3-6weeks. Dosage for children: Test dose of 0.1mg/kg not to exceed 1mg: 
infused over 20-60minutes. Loading dose of 0.25mg/kg infused over 2-6hours. 
Maintenance dose of 0.25/kg 24hourly to ensure a total dose of 30-40mg/kg is given over 
3-6weeks
Surgical management 
Endoscopic debridement of the necrotic tissues under general Anastasia(GA) 
Note  
High index of suspicion in patient with DKA and nasal symptoms 
15.7 Other Conditions of the Nose 
15.7.1 Nasal septal Abscess and Hematoma 
Clinical presentation 
•
Nasal pain
•
Fever
•
History of trauma for septal hematoma
•
Nasal swelling
•
Bilateral nasal blockage with boggy
septal mass
•
Aspiration will confirm the diagnosis
Pharmacological management 
B: ampicilin+cloxacilin (FDC) (PO) Adults: 500mg 8hourly for 10-14days. Children: 
15mg/kg 6hourly for 7-14days 
OR 
B: amoxycillin+clavulanate (PO) Adults: 625mg to 1g 12hourly for 7-14days. Children ≤3 
months: 30mg/kg/day in 2 divided doses for 7-14 days. Children >3 months: 25mg/kg/day 
in 2 divided doses for 7-14 days  
AND 
A: paracetamol (PO/IV), adults: 500mg to 1g 4-8hourly as needed. Children ≤10kg: 
10mg/kg 4-8hourly as needed. Children >10kg: 15mg/kg 4 to 8hourly as needed. 
OR 
A: ibuprofen (PO) Adults: 200-400mg 4-8hourly as needed. Children≥6 months: 5-10mg/kg 
4-8hourly as needed
OR 
C: diclofenac+ Paracetamol (PO) Adults: 50mg diclofenac and 500mg paracetamol 4-
8hourly as needed  

331!
Surgical management 
•
Intranasal Incision and drainage
•
Tight bilateral nasal packing or Suturing of mucoperichondrial to prevent re-accumulation
15.7.2. Choanal Atresia 
This is failure of canalization of choanal OR is obliteration or blockage of the posterior nasal 
aperture. 
It can be unilateral or bilateral. If bilateral it is surgical emergency. 
Clinical presentation 
•
New born presenting with cyanosis while at rest which improve on crying
•
Thick nasal discharge on the defective nostril
•
Failure to pass nasogastric tube
•
Thread/cotton test
Investigation 
•
CT-SCAN-Paranasal sinuses(PNS)
Non-pharmacological management 
•
For bilateral choanal atresia put oropharyngeal airway then refer to specialized hospital.
Surgical management 
•
Choanal atresia release (open or endoscopic)
15.7.3 Nasal Turbinate Hypertrophy 
Turbinate hypertrophy is a complication of allergic rhinitis 
Clinical presentation 
•
snoring
•
Nasal obstruction
•
Nasal irritation
•
Enlarged inferior or middle turbinate on rhinoscopy
Pharmacological Management 
As for Allergic Rhinitis 
Surgical management 
Partial submucosal Turbinectomy – (open or endoscopic) 
15.7.4 Nasal Bone Fracture 
Clinical presentation 
•
History of nasal trauma
•
Deviation of nose or septum
•
Nasal bleeding
•
Nasal obstruction
Pharmacological management (antibiotics & analgesics)-As for nasal septal abscess and 
hematoma 
Surgical Management-Closed reduction and alignment of nasal structures under LA or GA this 
should be 1-2weeks if there is edema. Can be done using nasal speculum or endoscopically. 
15.7.5 Nasal Septal Deviation (Non-Traumatic) 
Clinical presentation 
•
nasal obstruction
•
nasal dryness
•
+/_Nasal bleeding

332!
Surgical management 
•
Septoplasty –open or Endoscopic
15.7.6 Adenoid Hypertrophy 
It is hypertrophy of the lymphoid tissues in the nasopharynx; presenting with mouth breathing, 
snoring sleep apnea and otitis media with effusion. It is reported mainly in children. 
Investigations: Nasopharynx lateral view X-ray. 
Pharmacological Treatment: 
A: cetirizine (PO) 10mg nocte for 2weeks. Children: 5mg nocte for 2weeks 
AND 
A: 0.9% sodium chloride nasal spray/drops 4hourly for 2weeks 
AND 
B: azithromycin (PO) 500mg 24hourly for 3days. Children: 10mg/kg 24 hourly for 3days 
OR 
B: amoxicillin+clavulanic acid (PO) (FDC) Adults: 625mg (500mg amoxicillin+125mg 
Clavulanic acid) 8hourly for 7days  
Children: 375mg (250mg amoxicillin+ 125 Clavulanic acid) 12hourly for 7days; 
OR 
S: cefixime (PO) Adults: 400mg 24hourly for 7-14days. Children ≥ 6months to 12years 
(weight below 45kg): 8mg/kg 24hourly for 7-14days 
OR  
C: clarithromycin (PO), Adults: 500mg12 hourly for 7-14days. Children ≥ 6months: 
15mg/kg/day in 2divided doses for 7-14days 
AND 
A: paracetamol (PO) 1gm 8hourly until fever is controlled: Children 10mg/kg body weight 
8hourly until fever is controlled. 
Surgical management 
Adenotonsilectomy/Adenotomy+/-Myringotomy and Gromet insertion 
Note 
An adult with snoaring upper aerodigestive tumours and Obstructive Sleep Apnea (OSA)should be 
considered. 
15.7.7   Acute Rhinosinusitis 
It is the inflammation of the mucosal lining of the nose and paranasal sinuses of not more than 12 
weeks’ duration. In sinusitis of dental origin, anaerobic bacteria are often found. 
Acute Purulent Rhinosinusitis   
Bacterial infection with pus accumulation in one or more of the paranasal sinuses 
Clinical presentation 
•
Nasal discharge (watery or
purulent)
•
Nasal congestion
•
Post nasal dripping
•
Headache worsening on bending
forward and more in the morning
•
Fever
•
Facial pain
•
Ear pain and blockage
•
Anterior rhinoscopy –
watery/purulent nasal discharge
occasionally foul smelling
•
Nasal congestion
•
Plain paranasal sinuses X ray
(Water’s, Caldwell views)
•
Mucosal thickening; air fluid levels
Pharmacological Treatment: 
B: azithromycin (PO) 500mg 24hourly for 3days. Children: 10mg/kg 24hourly for 3days 
OR 
B: amoxicillin+clavulanic acid (PO) 625mg 8hourly for 7days Children: 375mg 12hourly for 
7days; 
OR 

333!
C: clarithromycin (PO), 500mg 12hourly for 7-14days. Children ≥ 6 months: 15mg/kg/day 
in 2divided doses for 7-14days 
OR 
B: ceftriaxone (IV) Adults: 1-2 g12hourly for 7 days. Children: 50 to 100mg/kg once for 
7days 
OR 
S: cefixime (PO) Adults: 400mg 24hourly for 7-14 days. Children ≥ 6 months to 12years 
(weight below 45kg): 8mg/kg 24hourly for 7-14days  
AND (for fungal rhinosinusitis) 
D: itraconazole (PO) Adults: 200mg 24hourly for 30days. Children: 50-100mg/kg once for 
7days 
OR 
S: amphotericin B (IV) Adults: Test dose of 1mg IV infused over 20-30minutes. Loading 
dose of 0.25-0.5mg/kg IV infused over 2 to 6 hourly. Maintenance dose of 0.25-1mg/kg 
24hourly for 3-6weeks for children: Test dose of 0.1mg/kg not to exceed 1mg:  infused 
over 20-60minutes Loading dose of 0.25mg/kg infused over 2-6hours. Maintenance dose 
of 0.25/kg 24hourly to ensure a total dose of 30-40mg/kg is given over 3-6weeks 
AND 
B: ephedrine (0.5% and 1%) nasal drop, Adults and children above 12years: Instill 1 to 
2drops in each nostril, not more than 4 times a day for 3 to 5days      
OR 
S: xylometazoline (0.05% and 0.1%) nasal drops/spray, Adults and children above 6years: 
Instill 2 to 3drops in each nostril 8hourly for 3 to 5days or1 to 2sprays in each nostril 
8hourly for 3 to 5days 
OR 
D: fluticasone propionate (50mcg/spray) nasal spray, Adults and adolescents more than 
12years: 2sprays in each nostril 24hourly as needed. Children 4-11years: 1spray in each 
nostril 24hourly as needed 
OR 
S: mometasone nasal spray, Adults and adolescents from 12years: 1sprays in each nostril 
24hourly as needed. Children 6-11years: 1spray in each nostril 24hourly as needed. 
AND 
A: paracetamol (PO) Adults: 500mg to 1g 4-8hourly as needed. Children ≤ 10kg: 10mg/kg 
4-8hourly as needed. Children >10kg: 15mg/kg 4-8hourly as needed
OR 
A: diclofenac (IM) Adults: 75mg 8hourly as needed 
OR 
C: diclofenac (PO) Adults: 50mg 4-8 hourly as needed 
OR 
C: ibuprofen (PO) Adults: 200-400mg 4-8 hourly as needed. Children ≥ 6 months: 5-
10mg/kg 4-8hourly as needed 
Non-pharmacological management 
•
Saline nasal wash
•
Steaming with or without Vicks
Note: Treatment periods shorter than ten days increase the risk of treatment failure 
Referral: To ENT Specialists 
•
Children with ethmoiditis presenting as an acute periorbital inflammation or orbital cellulitis must
be hospitalized immediately (ophthalmology consultation should be sought)
•
Adults with pronounced symptoms despite treatment
•
If sinusitis of dental origin is suspected
•
Recurrent sinusitis (>3 attacks in a year) or chronic sinusitis (duration of illness of >12 weeks)

334!
Surgical management  
Surgery if associated with complications eg obital/periobital abscess, pottys puffy tumour, Brain 
abscess and nasal polyposis etc. 
•
Frontal Trephination
•
Open ethimoidectomy
•
Functional Endoscopic Sinus Surgery (FESS)
15.7.8 Chronic Rhinosinusitis 
Can be caused byBacterial or Fungal 
Clinical presentation 
•
Anterior and/or posterior nasal mucopurulent drainage
•
Nasal obstruction/nasal blockage/congestion
•
Facial pain, pressure and/or fullness
•
Hyposmia or Anosmia
•
Halitosis
Investigations 
CT Scan of paranasal sinuses (PNS)-gold standard-should be done after adequate medical 
treatment with persistent symptoms. 
Non-pharmacological management 
•
Saline nasal wash
•
Steaming with or without vicks
Pharmacological Treatment: as for acute sinusitis BUT should be for 4-6 weeks 
Surgical Management-Surgery if associated with complications eg obital/periobital abscess, pottys 
puffy tumour, Brain abscess and nasal polyposis etc and Failure of disease resolution after 
adequate medical treatment. 
Frontal Trephination 
OR 
Caldwel Luc operation 
OR 
Open ethimoidectomy 
OR 
Functional Endoscopic Sinus Surgery (FESS) 
15.7.9 Nasal Polyposis 
This is mucosal change due to chronic mucosal inflammation. Ethmoidal polyp- This is a 
complication of allergic rhinitis or chronic rhinosinusitis. Antrochoanal polyp benign tumor of the 
maxillary sinus that prolapse to the nasal cavity. 
Clinical presentation 
•
History of allergy or asthma
•
Nasal congestion/blockage
•
Nasal discharge
•
Snoaring and mouth breathing
•
Post nasal dripping

335!
Investigations 
•
Direct nasal Endoscopy (DNE) or Fiber optic nasopharyngoscopy
•
Serum Total/specific IgE
•
CT-Scan of paranasal sinuses (CT-PNS)
Pharmacological Management-As for allergic rhinitis/acute rhinosinusitis 
Surgical management 
i.
Intranasal polypectomy
ii.
Partial/Medial maxillectomy
iii.
Functional Endoscopic Sinus surgey(FESS)
15.7.10 Nose Bleeding (Epistaxis) 
Nose bleeding is a condition which is common in adults. It may be due to a local cause in the nasal 
cavity (e.g. trauma, tumor, foreign body, septal varices, or septal deviation); or a systemic cause 
(e.g. blood disorders, vascular disorders, renal failure, hepatic failure, or use of anticoagulants 
(warfarin, heparin). Most cases of epistaxis are minor; do not require hospitalization. Patients with 
significant nose bleeding do require hospitalization. 
Non-pharmacological Treatment 
•
Stabilize the patient: put an open intravenous line, do blood grouping and cross matching
•
Put the patient in a sitting position and advise the patient to pinch the soft part of the nose
gently for 5minutes
•
Put on a gown, glasses, head light and sterile gloves and evacuate clots.Do a thorough
head and neck examination
•
Cauterize septal varisces (if any) using a silver nitrate pencil
•
Do an anterior nasal packing by introducing into the nasal cavity as far posterior as
possible sterile Vaseline gauzes (or iodine soaked gauzes if not available) or special
merocele pack,using a dissecting forcep (if bayonet forcep is not available)
•
Put rolled dry gauze on the collumela and plaster it
If the patient is still bleeding 
•
Do a posterior nasal packing using a Foley’s catheter introduced through the nasal cavity
into the oropharynx, balloon it with normal saline up to 10–15cc while pulling it outward to
impinge on the posterior nasal choana, then do anterior nasal packing as above
•
Put dry gauze on the nose to prevent necrosis of the collumela and fix the catheter on the
nose with an umbilical clamp
•
Almost all of the nasal bleedings will be controlled by this way
Note: Remove the packs after 72 hours 
Pharmacological Treatment (to prevent rhinosinusitis) 
B: azithromycin (PO) 500mg 2 hourly for 3days. Children: 10mg/kg 24hourly for 3days 
OR 
B: amoxicillin+ clavulanic acid (PO) Adults: 625mg 8hourly.  Children: 375mg 12hourly for 
7days 
AND 
A: paracetamol (PO) 1gm 8hourly until fever is controlled Children 10 mg/kg body weight 8 
hourly until fever is controlled 
AND 
A: ephedrine (0.5% and 1%)nasal drops, Adults and children above 12 years: Instill 1 to 
2drops in each nostril, not more than 4times a day for 3-5days 
OR 
S: xylometazoline (0.05% and 0.1%) nasal drops/spray. Adults and children above 6 
years: Instill 2 to 3drops in each nostril 8hourly for 3 to 5days or 1 to 2sprays in each 
nostril 8hourly for 3 to 5days. 
AND 
C: tranexamic acid (PO/IM) Adults: 500mg 8hourly for 5 to 8days. Children: 25mg/kg 6 or 
8hourly for 5-8days 

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AND 
C: silver Nitrate Stick-Apply on the lesion once IF the bleeding area is identified. 
Note 
Putting an ice cube on the forehead, extending the neck or placing a cotton bud soaked with 
adrenaline in the vestibule will not help 
Referral: refer the patient to the next facility with adequate expertise and facilities if: 
•
The patient is still bleeding repack and refer immediately
•
Failure to manage the underlying cause, refer the patient
Surgical management 
•
Endoscopic electrical cauterization of the lesion for posterior nasal bleeding
•
Ligation/Clipping/cauterization of bleeding vessel (open or endoscopic)
Note 
 Rule out systemic causes of epistaxis eg. renal, blood dyscrasias and liver failure. 
15.7.11. Foreign Bodies in the Nose 
This situation usually occurs in children.  
Non-pharmacological Treatment: 
•
Restrain the child before removal using a cerumen hook, if the child cannot be restrained
sedation is advised
Note 
 A unilateral foul smelling nasal discharge in a child is due to a foreign body until proven otherwise 
15.8 Throat Conditions 
15.8.1 Pharyngotonsilitis 
Pharyngotonsilitis is an acute inflammation of the pharynx and tonsils, which is characterized by 
fever and a painful throat.  
Pharmacological Treatment 
B: azithromycin (PO) 500mg 24hourly for 3days. Children: 10mg/kg 24hourly for 3days 
OR 
   B: amoxicillin+ clavulanic acid (PO)(FDC) Adults: 625mg 8hourly for 7days Children: 
375mg 12hourly for 7days;  
OR 
C: clarithromycin (PO), Adults: 500mg    12hourly for 7-14days. Children ≥ 6 months: 
15mg/kg/day in 2divided doses for 7-14days 
OR 
S: cefixime (PO) Adults: 400mg 24hourly for 7-14days. Children ≥ 6 months to 12 years 
(weight below 45kg): 8mg/kg 24hourly for 7-14days 
AND 
A: paracetamol (PO) Adult 1gm 10mg/ kg body weight 8 hourly until the fever is controlled 
OR 
A: ibuprofen (PO) Adults: 200-400mg 4-8hourly as needed. Children ≥ 6 months: 5-
10mg/kg 4-8hourly as needed 
OR 
A: diclofenac (IM) Adults 75 mg 8hourly as needed 
OR 
C: diclofenac (PO) Adults: 50 mg 4-8hourly as needed 
OR 
C: diclofenac+ paracetamol (PO) (FDC) Adults: 50mg diclofenac and 500mg paracetamol 
4-8hourly as needed

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Note 
Refer the patient with tonsillitis to the specialist for tonsillectomy if 
•
Chronic tonsillitis
•
Recurrent tonsillitis (>5attacks in a year or 3 or more attacks in 2 consecutive years)
•
Obstructive tonsillitis (causing an upper airway obstruction)
Surgical management 
•
Tonsilectomy
15.8.2 Laryngitis 
This is an infectious or non-infectious, acute or chronic inflammatory condition of the larynx. It 
becomes chronic when the condition lasts for more than 3 weeks. The picture of the disease is 
different in children and adults due to the small size of the larynx in children.  
•
Acute subglottic laryngitis occurs mainly in children under the age of seven, it is a viral
infection
•
Edema of the mucous membrane of the subglottic space causes breathing difficulties,
especially on inspiration
•
Laryngitis in children may require active treatment
15.8.3 Acute Laryngitis 
Acute subglottic laryngitis occurs mainly in children under the age of seven, it is a viral infection. 
Non-pharmacological Treatment 
•
Parents should behave calmly and avoid frightening the child
•
Bed rest
•
Keep the air damp and cool
•
Give extra fluid
Pharmacological Treatment 
A: adrenaline inhalation/nebulization effectively reduces symptoms 
Table15.1: Doses of adrenaline Preparation 
AND 
A: prednisolone (PO) Adults: 60mg 24hourly for 5days then taper down to 50mg 24hourly 
for next 5days. Children: 1mg/kg 24hourly for 5days then taper down by half for the next 
5days.  
OR 
A: hydrocortisone (IV/IM) Adults and children ≥ 12years: 100-500mg/dose IV/IM 4hourly as 
needed. Children <12 years: 1-5mg/kg/day IV/IM divided 12hourly as needed  
AND 
B: amoxycillin + clavulanate (PO) (FDC) Adults: 625mg to 1g 12 hourly for 7-14 days. 
Children ≤ 3 months: 30mg/kg/day in 2divided doses for 7-14days. Children >3 months: 
25mg/kg/day in 2 divided doses for 7-14days  
AND 
A: cough suppressant Syrups-Dosage for adults: as instructed by a physician or 
pharmacist. 
Hospitalization 
If severe symptoms persist or worsen after epinephrine inhalation, hospitalization is indicated. 
Age 
adrenaline(20 mg/ml) 
0.9% Saline 
0-6 months
0.1 ml 
2 ml 
6-12 months
0.15 ml 
2 ml 
>12
0.2 ml 
2 ml 
Note 
The total fluid volume is inhaled in 5 minutes with the use of inhalator 

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15.8.4 Chronic Laryngitis 
Non-pharmacological Treatment: 
•
Voice rest
•
Stop smoking
•
Rehydration
•
Refer to specialist for Rigid
laryngoscopy (Endoscopy) OR
Fiber optic Nasolaryngoscopy
15.8.5 Acute Epiglottitis (AE) 
Epiglottitis is an acute infectious inflammation of the epiglottis, supraglottic and hypopharynx which 
occurs both in children and adults. It is commonly caused by Haemophilus influenzae. Epiglottitis is 
a potentially lethal condition especially in children. Edema of the epiglottis may cause acute airway 
obstruction. 
Clinical presentation 
•
Throat 
pain 
and 
difficulty 
in
swallowing
•
Drooling
•
Husky voice
•
Fever often high and with chills
•
Patient prefers sitting posture with
an extended neck
•
Laborious inspiration
•
Cough in some cases
•
Anxiety
Investigations: Plain X-ray of the neck, lateral view characteristically presents with a positive thumb 
sign (edematous epiglottis). 
Non-pharmacological Treatment: 
•
Immediate hospitalization, preferably in the ICU
•
Transportation: sitting, with oxygen supplementation
•
Be prepared to treat respiratory failure (intubation or tracheotomy)
Pharmacological Treatment 
B: azithromycin (PO) 500mg 24hourly for 3days. Children: 10mg/kg 24hourly for 3days 
OR 
B: amoxicillin+ clavulanic acid (PO)(FDC) Adults: 625mg 8hourly Children: 375mg 12hourly 
for 7days;  
AND 
A: paracetamol (PO) 1gm 8hourly until fever is controlled. Children: 10 mg/kg body weight 
8hourly 
15.8.6 Non-infectious Chronic Laryngitis 
[Laryngopharyngeal reflux disease (LPR) with Vocal cord nodules or Laryngeal polyp] 
Clinical presentation 
•
Dysphonia or hoarseness
•
Dry Cough
•
Globus sensation, Frequent throat
clearing
•
Dysphagia
Investigations - Rigid laryngoscopy (Endoscopy) OR Fiber optic Nasolaryngoscopy 
Non-pharmacological Treatment 
•
Dietary modification, spice foods and feeding times
•
Life style changes; avoid alcohol, tobacco
•
Voice rest
Pharmacological Treatment 
C: pantoprazole (PO) Adults: 40mg 24hourly for 8-12 weeks 
Children ≥ 5 year:  
C: pantoprazole (PO) 20mg 24hourly for 8-12 weeks 
For <40kg 
C: pantoprazole (PO) 20mg 24hourly for 8-12 weeks 
For >40kg  
C: pantoprazole (PO) 40mg 24hourly for 8-12 weeks 

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OR 
C: lansoprazole (PO) Adult 30mg. Paediatric ≥ 1 to 12years: <30kg 15mg;>30kg give 
30mg 24hourly for 8 – 12 weeks. 
OR 
S: esomeprazole (PO) Adult 40mg. Paediatric ≥ 1 to 12 years 10-20mg. Paediatric >12 
years 20-40mg 24 hourly for 8-12weeks.  
C: antiacid liquid/mixture10-15mls 12hourly for 10-14days. 
AND 
A: prednisolone (PO): Adult 60mg 24hourly for 5days then taper down to 50mg 24hourly 
for next 5days.  
For Children:  
A: prednisolone (PO): 1mg/kg 24hourly for 5days then taper down by half for the next 
5days.  
OR 
D: triamcinolone acetonide. Adult (IM) 40-80mg stat. Children 6-12years: 0.2mg/kg stat 
AND 
C: loratadine (PO) Adults: 10mg 24hourly for 14days. Children 2-6years: 5mg 24hourly for 
14days. Children above 6years: 10mg 24 hourly for 14days  
OR 
S: desloratadine (PO) Adults: 5mg 24hourly for 14days. Children 2-5years: 1.25mg 
24hourly for 14days. Children 6-12 years: 2.5mg 24hourly for 14days 
Surgical management 
Direct laryngoscopy+microlaryngeal surgery (D/Scopy+MLS) to remove polyp or cyst-using 
microscope or Endoscope with microdebrider/shaver 
15.8.7 Recurrent Respiratory Papillomatosis (Laryngeal Papillomas) 
It is the commonest benign laryngeal tumor of the larynx caused by Human papilloma virus (HPV), 
occurring in both children and adults. It has a higher recurrence rate in children than in adults, 
among adults it may turn into a malignancy. 
Clinical presentation 
•
Hoarse voice, audible respiration (inspiratory stridor)
•
Progressive difficulty in breathing
•
Progressive inspiratory stridor
•
On and off cough
Investigations 
•
Perform a thorough respiratory system examination
•
Indirect laryngoscopy for papilloma croups on the larynx
•
Rigid laryngoscopy (Endoscopy) OR Fiber optic Nasolaryngoscopy
Non-pharmacological Treatment 
•
If in distress, perform a tracheostomy first then refer
Referral: Refer the patient to the next facility with adequate expertise and facilities 
Surgical management 
•
Tracheostomy if there is upper airway obstruction
•
Direct Laryngoscopy under GA+microlaryngeal surgery(D/Scopy+MLS)
•
D/Scopy+microdebridment
15.8.8. Foreign Bodies in the Throat 
If the foreign body is suspected to be in the hypopharynx, esophagus, trachea or bronchus 
•
Take a thorough history and do a thorough physical examination
•
Do chest X ray to confirm your diagnosis (though some foreign bodies are radiolucent)
•
Refer to a next level hospital with facility for removal

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Surgical management 
•
Oesophagoscopy for oesophageal foreign body(FB)
•
Bronchoscopy for airway FB
15.8.9 Subglottic Hemangioma 
Congenital subglottic hemangiomas are vascular lesions that undergo a phase of rapid growth that 
is initiated during the first few weeks to months of life. They may present as solitary lesions or as 
part of a segmental hemangioma syndrome. 
Clinical presentation 
•
Hoarseness of voice
•
Insipiratory stridor
•
Cough
•
Cyanosis
•
Concomitant
cervical 
facial 
hemangioma
Pharmacological management 
A: prednisolone (PO) Children: 1mg/kg 24hourly for 5days then taper down by half for the 
next 5days. 
AND 
A: propranolol (PO) for children: Starting dose of 0.6mg/kg 12hourly for 1week, then 
increase dose to 1.1mg/kg 12hourly for 2weeks; then Maintenance dose 1.7mg/kg 
12hourly for at least 6months. 
Surgical Management-Tracheostomy- if severe inspiratory stridor is present. 
15.8.9 Laryngomalacia 
This is the most common congenital anomaly of the larynx, characterized by partial or complete 
collapse of supraglottic structures on inspiration. This is the most common cause of noisy breathing 
in infancy. Gastroesophageal reflux disease (GERD) has been implicated. 
Clinical presentation 
•
Insipiratory stridor relieved by lying
prone
•
Difficult breathing/dsypnoea
•
Difficult feeding
•
Chocking on feeding
Investigations 
•
Fiber optic nasolaryngoscopy
•
Microlaryngoscopy and bronchoscopy
Non-pharmacological management 
•
Sleep prone rather than supine
•
Feeding modification
•
Close observation of upper respiratory tract infections
Pharmacological management 
For children 1-12years  
S: esomeprazole (PO) 10-20mg 24hourly 
For children >12years give 
S: esomeprazole (PO) 20 - 40mg 24hourly 
Surgical management 
•
Supraglotoplastly
•
Tracheostomy for severe cases

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15.8.10 Vocal Cords Paralysis 
It is due to total interruption of nerve impulse resulting in no movement of laryngeal muscles. Vocal 
cord paralysis is a sign of disease and not a diagnosis by itself, vocal cord paralysis can be 
unilateral or bilateral. 
Clinical presentation 
•
Change in voice/hoarseness (for
unilateral vocal cord paralysis)
•
Vocal fatigue
•
Dyspnoea/upper airway obstruction
•
Stridor
•
Cough and aspiration
•
History of neck
surgery(thyroidectomy)
•
Neck or mediastinal tumors
Investigation 
•
Fiber optic nasolaryngoscopy
•
Video stroboscopy
Non-pharmacological management 
•
Speech therapy
Surgical management: depends on the severity and desired outcome. 
•
Tracheostomy
•
Arytenoidectomy
•
Vocal cord lateralation through
endoscopy
•
Cordectomy
•
Thyroplasty type i& ii
•
Injection of Teflon paste
•
Muscle or cartilage implant
15.8.11 Infection of Thyroglossal Duct Cyst, Dermoid Cyst, Branchial Cleft 
Cysts 
Clinical presentation 
•
For Thyroglosal cyst- Midline upper neck mass which is cystic just below the hyoid bone. If
infected my present with tenderness. My also present as discharging sinus
•
For branchial cleft cysts mass or discharging sinus along the anterior border of the
sternocleidomastoid muscle.
Investigation 
•
Neck USS
Pharmacological management 
B: ampicillin+cloxaccillin (PO) Adult 500mg. Paediatric 15mg/kg 6-8hourly for 10-14days. 
AND 
B: cephalexin (PO) Adult 500mg 8hourly. Paediatric 75-100mg/kg/day divided in 4doses 
for 7-14days 
OR 
B: amoxycillin + clavulanate (PO): 625mg to 1g 12hourly for 7-14days. 
ForChildren ≤3 months:  
B: amoxycillin + clavulanate (PO) 30mg/kg/day in 2divided doses for 7-14days. 
For Children>3 months:  
B: amoxycillin + clavulanate (PO) 25mg/kg/day in 2divided doses for 7- 14days 
Surgical management 
•
Thyroglosal duct cyst excision (Sistrunk procedure)
•
Branchial cyst/fistula excision

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15.8.12 Deep Neck Spaces Infections 
Clinical presentation 
•
Truisms
•
Induration and swelling below the
angle of mandible
•
Medial bulging of the pharyngeal
wall
•
Difficult 
swallowing
(dysphagia/odynophagi)
•
Difficult breathing
•
Neck stiffness/torticollis
•
Neck swelling, mass, or
lymphadenopathy
•
Systemic toxicity with fever and
rigors 
Pharmacological management 
B: azithromycin (PO) Adult 500mg 24hourly. Paediatric ≥ 6 months10mg/kg/day for 2 to 5 
days 
OR 
A: metronidazole (PO) 400mg 8hourly for 7-14day. Children: 7.5-15mg/kg 8 hourly for 20–
30days 
 OR 
B: metronidazole (IV) 500mg 8hourly. Children: 7.5-15mg/kg 8 hourly for 7-14days 
OR 
B: amoxycillin + clavulanate (PO) 625mg to 1g 12hourly for 7- 14days 
For Children ≤ 3 months:   
B: amoxycillin + clavulanate (PO) 30mg/kg/day in 2divided doses for 7-14days. 
For Children >3 months:  
B: amoxycillin + clavulanate (PO) 25mg/kg/day in 2 divided doses for 7-14days. 
OR 
C: clarithromycin (PO) 500mg 12hourly for 7-14 days. 
ForChildren ≥ 6 months:  
S: clarithromycin (PO) 15mg/kg/day in 2 divided doses for 7-14days 
OR 
C: ceftriaxone (IV) Adult 1-2g 12 hourly. Paediatric 50-100mg/kg 24hourly for 7days 
AND 
A: paracetamol (PO) 500mg to 1g 4-8hourly as needed. 
For Children ≤ 10kg:  
A: paracetamol (PO) 10mg/kg 4-8hourly as needed. 
For Children > 
A: paracetamol (PO) 10kg: 15mg/kg 4-8hourly as needed 
OR 
A: diclofenac (IM) 75mg 8hourly as needed 
C: diclofenac (PO) 50mg 4-8hourly as needed, 
15.8.13 Peritonsillar Abscess (Quincy) 
 Peritonsillar abscess is a collection of pus located between the capsule of the palatine tonsil and 
the pharyngeal muscles. 
Clinical presentation 
•
Severe sore throat (usually unilateral) with Fever
•
"Hot potato" or muffled voice
•
Pooling of saliva or drooling may be present
•
Trismus, neck swelling and pain and may have ipsilateral ear pain
•
Fatigue, irritability
•
Swollen and/or fluctuant tonsil with deviation of the uvula to the opposite side
Pharmacological management 
B: amoxycillin + clavulanate (PO) 625mg to 1g 12hourly for 7-14days. 
ForChildren ≤ 3 months: 
B: amoxycillin + clavulanate (PO) 30mg/kg/day in 2divided doses for 7-14days. 

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For Children >3 months: 
B: amoxycillin + clavulanate (PO) 25mg/kg/day in 2divided doses for 7-14days 
OR 
B: ceftriaxone (IV) 1- 2 g 12 hourly for 7days. 
For Children:  
B: ceftriaxone (IV) 50-100mg/kg 24hourly for 7days 
OR 
C: clarithromycin (PO) 500mg 12hourly for 7-14days. 
For Children ≥ 6 months: 15mg/kg/day in 2divided doses for 7-14days 
OR 
S: cefixime (PO) 400mg 24hourly for 7-14days. 
ForChildren ≥ 6 months to 12years (weight below 45kg):  
S: cefixime (PO) 8mg/kg 24hourly for 7-14days 
Surgical management 
•
Needle Aspiration
•
Incision and drainage (LA/GA)
•
Drainage/quincy tonsillectomy
•
Interval tonsilectomy
15.9 ENT Neoplasms 
15.9.1 Juvenile nasopharyngeal angiofibromas (JNA) 
Are rare vascular tumors exclusively seen in adolescent males. 
Clinical features 
•
Nasal bleeding
•
Nasal blockage
•
May present with eye protrusion
Investigation 
CT-Scan (with contrast) PNS/Skull base-will show widening of sphenopalatine fissure and anterior 
bowing of posterior wall of maxillary sinus. 
Note 
Never take biopsy for suspected case of JNA 
Surgical treatment 
Embolization of internal maxillary artery THEN 
Excision of Angiofibroma (Open or Endoscopic/modified Denkers operation) 
15.9.2 Salivary Gland Tumors 
 Salivary gland tumors include a heterogeneous group of lesions. Most salivary gland tumors are 
composed of more than one cell type. Tumours may arise from major or minor salivary glands. 
(Parotid, Submandibular, Lingual and minor salivary gland tumours) 
Clinical presentation 
•
Painless progressive swelling of a given salivary gland.
Investigation 
•
Fine needle aspiration cytology (FNAC)
•
Do not take incisional biopsy unless lesion is ulcerative.
Surgical management 
-Partial or Total parotidectomy-for parotid tumours
-Submandibular gland tumor excision-for submandibular gland
-Sub lingual gland tumor excision
-Minor salivary gland tumors excision

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15.9.3 Parapharyngeal Tumours 
Both benign and malignant tumors may arise from any of the structures contained in this space. 
Among parapharyngeal space (PPS) tumors; 70-80% are benign, and 20-30% are malignant. Most 
PPS tumors are of salivary or neurogenic origin. 
Clinical presentation 
•
Sore throat
•
Dysphonia
•
Otalgia
•
Snoaring
•
Tonsilar/pharyngeal mass
•
Neck/submandibular mass
Investigation 
•
Fine neddle aspiration cytology (FNAC)
•
CT SCAN-Neck&skull base
•
MRI –Head and neck
Surgical Management 
•
Parapharyngeal tumour excision
15.9.4 Cancer of the Larynx 
It is the commonest ENT malignancy. Risk factors include cigarette smoking, alcohol intake, 
gastroesophageal reflux disease and human papilloma virus. 
 Clinical presentation 
•
Progressive hoarseness of voice
•
Difficulty in breathing (inspiratory stridor)
•
Hemoptysis
Referral: Refer the patient to the next facility with adequate expertise and facilities 
Investigations 
•
Rigid Laryngoscopy (endoscopy) or Fiberoptic nasolaryngoscopy(diagnostic)
Surgical management 
1. Direct Laryngoscopy +Biopsy under General Anaestesia (GA)
2. Tracheostomy
3. Total/Partial laryngectomy +/- neck dissection
Note 
 Any patient with progressive hoarseness of voice for more than two weeks should undergo 
laryngoscopy 
15.9.5 Sino-Nasal Malignancy 
Is a malignancy of the nose and paranasal sinuses? Risk factors include wood dust (both soft and 
hard), wielding dust, lather industry fumes, hydrocarbons fumes, and aflatoxin dust. 
Clinical presentation 
•
Nasal bleeding
•
Nasal discharge
•
Nasal obstruction
•
Teeth loosening
•
Cheek swelling
•
Proptosis
•
Hearing loss
Referral: Refer the patient to the next facility with adequate expertise and facilities 
Investigations 
•
Biopsy-transnasal
biopsy/Endoscopic
•
CT-Scan –paranasal sinus (PNS)
•
Chest x –ray
•
Urinalysis-bence -Jones proteins

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Surgical management 
Total Maxillectomy-Open OR 
Partial Maxillectomy-Open/Endoscopic 
Note 
Refer patient for adjuvant chemo and radiotherapy 
15.9.6 Naso-Pharyngeal Malignancy 
It is a malignancy which arises from the nasopharynx. Risk factors include genetic predisposition, 
Epstein Bar virus, smoked and/or salted foods. 
Clinical presentation 
•
Cervical lymphadenopthy, usually bilateral
•
Nose bleeding
•
Nasal blockage
•
Hearing loss, tinnitus or ear pain
Referral: Refer the patient to the next facility with adequate expertise and facilities 
Note 
A patient presenting with cervical lymphadenopathy has nasopharyngeal carcinoma until proven 
otherwise 

346!
Investigations 
•
Biopsy-Transnasal/Endoscopic
•
Fine needle aspiration cytology for neck mass
•
CT-Scan-head and neck
•
Chest x-ray
•
Serology for Epstein Bar virus(EBV)
Treatment 
•
Radiotherapy
15.9.7 Oropharyngeal Malignancy 
Oropharyngeal squamous cell carcinomas arise in the soft palate, tonsils, base of tongue, 
pharyngeal wall, and vallecula. 
Clinical presentation 
•
Sore throat
•
Throat pain/painful swallowing
•
Voice change (“hot potato” voice)
•
Difficulty in breathing
•
Oropharyngeal mass/ulcer
Investigations 
•
Rigid endoscopy
•
Transoral biopsy
•
Serology for HPV (human papilloma virus)
•
CT-Scan or MRI -Neck
Management 
•
Surgery: open or transoral
•
Definitive Management: Refer Malignancy chapter.
15.9.8 Hypo-Pharyngeal Malignancy 
It is a malignancy which arises from the hypopharynx. Risk factors include cigarette smoking, 
alcohol intake and gastroesophageal reflux disease. 
Clinical presentation 
•
Progressive dysphasia
•
Progressive odynophagia
•
Hematemesis/hemoptysis
•
Ear pain (referred otalgia)
•
Cervical lymphadenopathy
•
Difficulty in breathing (inspiratory
stridor)
•
Excessive salivation/Pooling of
saliva
Referral: Refer the patient to the next facility with adequate expertise and facilities 
Investigations 
•
Rigid Laryngoscopy (endoscopy) or Fiber optic nasolaryngoscopy(diagnostic).
•
CT-Scan-head and neck
•
Chest x-ray
Surgical managemrnt 
1. Direct Hypopharyngoscopy +Biopsy under general anestisia(GA)
Definitive Management 
•
Chemoradiotherapy depending on histological results –Refer to oncology chapter

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15.9.9 Metastatic Lymphadenopathy and Neck Masses 
Cervical lymph nodes are a common site of metastases for malignant tumors that originate at 
primary sites in the head and neck. Primary lymphoma in neck nodes must be considered in any 
differential diagnosis. 
Clinical presentation 
•
Neck mass unilateral or bilateral
•
Neck ulcer
Note 
•
An adult patient with neck mass, should be approached with a presumption of malignancy
until proven otherwise.
•
Once the diagnosis of metastatic squamous cell carcinoma is made, a search for the
primary tumor must be performed. The probable primary site can often be identified by
history and physical examination; panendoscopy and directed imaging may be required.
Investigations 
•
Neck ultrasound
•
Fine needle asypiration cytology(FNAC)
•
Panendoscopy of upper aerodigestive areas (nose and paranasal sinuses, nasopharyngx,
oropharyngx, laryngx, hyponaryngx) and oesophagoscopy.
•
Direct nasal endoscopy (DNE)
•
Fiber optic nasolaryngoscopy
•
Rigid laryngoscopy (endoscopy)
Note: Do not treat patient with cervical lymphadenopathy as a case of TB adenitis until 
malignancy is ruled out and TB adenitis is proved. 
Surgical management 
•
Biopsy for histology from suspected site
•
Neck dissection: Radical or Modified Neck Dissection
15.10. Speech Disorders 
Speech disorder refers to any condition that affects a person’s ability to produce sounds that create 
words. This includes stuttering, apraxia, dysarthria can be caused by brain damage/stroke, muscle 
weakness, hearing loss, dementia etc. 
Investigations 
•
Audiometry
•
Otoacoustic emission (OAEs)
•
Auditory brainstem response
•
Fiber optic nasolaryngoscopy
Non-pharmacological management 
•
Auditory verbal training-for post
cochlea implantation
•
Speech 
therapy 
for 
aphasia,
stuttering, apraxia and dysarthria.
•
Hearing Aids
•
Cochlea implantation
Surgical management 
•
Posterior tympanotomy-for cochlea
implantation.

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CHAPTER SIXTEEN 
ORAL AND DENTAL CONDITIONS 
Oral diseases and conditions are common and range from dental caries, periodontal conditions, 
dental abscess, acute bacterial infections, viral infections, fungal infections, traumatic injuries, 
tumors, and lesions affecting the maxillofacial region (perioral, jaws and face). Before doing oral 
examination or any dental procedures, patients should gurgle with hydrogen peroxide 3% or 
povidone iodine 2% to minimize infectious agent’s contamination between patient and oral health 
care provider. 
16.1 Periodontal Conditions 
16.1.1 Gingivitis 
Inflammatory changes in the gingival develop within a couple of days of undisturbed bacterial growth 
on the gingival margin of the erupted tooth in the oral cavity 
Clinical presentation 
•
Gingival redness
•
Swollen and shiny gingival tissue
•
Increased tendency of the gingival to bleed on gentle probing or spontaneously, during
tooth brushing or even on touch and on biting bread and fruits.
•
Bad breath from the mouth
Prevention and non-pharmacological Treatment 
Proper oral hygiene care counselling. 
Remove accumulated plaque and teach oral hygiene on systematic tooth brushing and other 
adjuvant means of oral hygiene (dental flossing, tongue cleaning on the dorsal part, use of mouth 
washes including saline mouth wash). 
16.1.2 Periodontitis 
This is the progression of the inflammation of gingival into the deep tissue affecting the periodontal 
membrane causing periodontal pockets, introduction of infection and destruction of periodontium. 
Clinical presentation 
•
Reddened, swollen gingiva
•
Easily bleeding gingival on gently
probing
•
Periodontal pocket
•
Loose/mobile teeth
•
Bad breath from the mouth
•
Gingival recession
Investigation
Orthopantomography (OPG) to determine extent of bone loss 
Non-pharmacological Treatment 
Instruct and guide the patients on proper oral hygiene for proper plaque control. 
Plaque control by scaling and root planning. 
Pharmacological Treatment 
Mouth wash: Do not swallow 
A: hydrogen peroxide (PO) 3% 6hourly for at least for 5days 
OR 
B: chlorhexidine gluconate (PO) 0.1% 12hourly at least for 5days 
OR 
Use antibiotics only in severe cases 
A: metronidazole (PO) 400mg 8hourly for 8days 
AND EITHER 
A: amoxicillin (PO) 500mg 8hourly for 8 days 
OR 
A: doxycycline (PO) 100mg 12hourly for 10days 

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16.1.3 Acute Necrotizing Ulcerative Gingivitis (ANUG) 
It is a severe form of gingivitis and is characterized by rapid destruction of gingival tissue, particularly 
in the interdental papilla. Patients usually present with soreness and bleeding of the gums and foul 
smell test (fetor-ex ore/halitosis). It is common in malnourished children and immunocompromised 
individuals especially patients with diabetes and HIV/AIDS. 
Clinical presentation 
•
Painful swollen gingiva which bleeds easily and erythema of the gingival margins
•
Yellowish-white ulceration of the gingival
•
Fever, malaise, and regional lymphadenitis
•
In some patients (especially malnourished children), ANUG may presents with
extensive destruction of the face and jaws in the severe form known as Cancrum Oris
Pharmacological Treatment  
Professional cleaning with hydrogen peroxide 3% (under local anesthesia) 
A: metronidazole (PO) 400 mg 8hourly for 5days 
AND 
A: amoxicillin (PO) 500mg 8hourly for 5days 
16.1.4 Stomatitis 
This is generalized inflammation of the oral mucosal (including the gingiva) due to different 
etiologies such as infections, chemical burn, radiation, and allergy. 
Clinical presentation 
•
Oral sores and ulceration
Pharmacological Treatment 
Mouth wash (do not swallow) 
A: hydrogen peroxide solution 3% (PO) 6hourly for at least 5days 
OR 
B: chlorhexidine 0. % topical oral gel 12hourly 
Note 
Mouth wash should not be used at the same time with the gel. Also, should not be swallowed. 
Oral analgesics can be added 
A: paracetamol (PO) 1gm 8hourly for at least 3days 
OR  
A: ibuprofen (PO) 400 mg 8hourly for at least 3days 
OR 
C: diclofenac (PO) 50 mg 8hourly for at least 3days 
16.2 Dental Caries 
Dental caries is caused by bacteria of the dental plaque which feed on sugary food substrates 
producing acid as by-products which dissolve the minerals of the tooth surface. 
Clinical presentation 
Early stage–asymptomatic 
•
Intermediate stage: black/brown spot which may be visible on any surface of tooth
•
Cavities developing on tooth surface
•
Pain/toothache elicited by hot, cold, or sweet foods/drinks

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Late stage 
•
Pain may be spontaneous, intermittent, sharp, and severe, even interfering with sleep.
•
Tenderness on percussion of the tooth
Investigation
Periapical x-ray of tooth/teeth may need to be done specially to confirm extent of caries for 
treatment decision e.g. the caries contained in the dentine can be distinguished from pulpal caries. 
Prevention 
•
Proper counseling to avoid frequent use of sugary foods and drinks
•
Use fluoridated toothpaste to brush teeth at least twice a day
•
Provide preventive measures to early lesions presenting as a spot on the enamel without
cavitation and softening
Non-pharmacological Treatment 
Lesion with cavitation but confined to dentine–filling/restoration of teeth with suitable filling materials 
(e.g. amalgam, composite, glass ionomer) 
Perform endodontic treatment with combination of antibiotics wherever possible for tooth with lesion 
involving the pulp (with or without periapical abscess otherwise tooth extraction is done 
Pharmacological Treatment 
Analgesics: for toothache 
A: paracetamol (PO) 1gm 8hourly for 3days 
OR 
A: ibuprofen (PO) 400mg 8hourly for at least 3days 
OR 
 C: diclofenac (PO) 50 mg 8hourly for at least 3days 
Antibiotics for endodontic treatment 
B: ampicillin + cloxacillin (FDC) (PO) 500mg 8hourly for 5days 
AND 
A: metronidazole (PO) 400mg 8hourly for 5days 
16.3 Odontogenic and Non-Odontogenic Orofacial Infections 
16.3.1. Periapical abscess 
This clinical condition arises as a complication of inflammation of the dental pulp or periodontal 
pocket. The condition may be acute and diffuse, chronic with fistula or localized and circumscribed. 
It is in the apical aspect of the supporting bone. 
Clinical presentation 
•
The patient complains of tooth ache
•
Pain during intake of hot or cold foods/drinks
•
Pain on bringing the tooth on occlusion
•
Tenderness on percussion (vertical percussion)
•
Swelling of gingiva around the affected tooth
Non-pharmacological Treatment 
•
For posterior teeth: Extraction of the offending tooth under local anesthesia (can perform
root canal treatment for posterior teeth instead of tooth extraction under good clinical
judgement)
•
Perform Incisional and drainage under local anesthesia followed by analgesics.
For anterior teeth (incisors, canine and premolars): extraction is carried out only when root canal 
treatment is not possible  

351!
Pharmacological Treatment 
A: paracetamol (PO) 1gm 6hourly for 3days. 
AND 
A: amoxicillin (PO) 500mg 8hourly for at least 7days 
OR 
A: erythromycin (PO) 500mg 8hourly for 7days (if allergic to penicillin) 
AND 
A: metronidazole (PO) 400mg 8hourly for 7days 
16.3.2 Dental Abscess (Odontogenic Abscess) 
Dental abscess is an acute lesion characterized by localization of pus (caused by polymicrobial 
infection) in the structures that surround the teeth. 
Clinical presentation 
•
Fever and chills
•
Throbbing pain of the offending tooth
•
Swelling of the gingiva and sounding tissues
•
Pus discharge around the gingiva of affected tooth/teeth
•
Trismus (inability to open the mouth)
•
Regional lymph nodes enlargement and tender
•
Aspiration of pus
Investigation 
Pus for Gram stain, culture, and sensitivity if the patient doesn’t respond to initial antibiotic 
treatment. 
Non-pharmacological Treatment 
•
Incision and drainage and irrigation (irrigation and dressing is repeated daily). Irrigation is
done with 3%hydrogen peroxide followed by 0.9% sodium chloride.
•
Supportive therapy carried out depending on the level of debilitation. Most patients need
rehydration and detoxification using 0.9% sodium chloride (IV) or compound sodium
lactate (IV).
Pharmacological Treatment 
A: amoxicillin (PO) 500mg 8hourly for 5days 
AND 
A: metronidazole (PO) 400mg 8hourly for 5days. 
In severe cases, 
B: amoxicillin+ clavulanic acid (FDC) (PO) 625mg 8hourly for 5days 
AND 
A: metronidazole (PO) 400mg 8hourly for 5days. 
If a patient is allergic to penicillin 
A: erythromycin (PO) 500mg 8hourly for 5days 
Where parenteral administration of antibiotics is necessary (especially when the patient cannot 
swallow and has life threatening infection), consider the following 
B: ceftriaxone (IV) 1gm once daily for 5days 
AND 
B: metronidazole (IV) 500 mg 8hourly for 5days 
AND 
A: gentamicin (IV) 80mg 8hourly for 5days 
Note 
Incision and drainage is mandatory in cases of deeper spaces involvement followed by a course of 
antibiotics. The practice of prescribing antibiotics to patients with abscess and denying referral for 
definitive care until pus has established or resolved has been found to lead to more problems for 
orofacial infections therefore early referral for definitive care is important. 

352!
16.3.3 Ludwig’s Angina 
This is a serious life threatening generalized septic cellulitis of the fascia spaces found on the floor of 
the mouth and tongue. It is an extension of infection from mandibular molar teeth into the floor of the 
mouth covering the submandibular, sublingual, and submental spaces bilaterally. 
Clinical presentation 
•
Brawny induration
•
Tissues are swollen, board like, not
pitted and no fluctuance
•
Respiratory distress
•
Dysphagia
•
Tissues may become gangrenous
with a peculiar lifeless appearance
on cutting
•
Three fascia spaces are involved
bilaterally 
(submandibular,
submental, and sublingual)
Non-pharmacological Treatment 
•
Incision and drainage is done (even in absence of pus) to relieve the pressure and allow
irrigation
•
Only when the airway distress is significant and there is evidence that it is not relieved by
incision and drainage then tracheostomy is needed. Supportive care includes high protein
diet and fluids for rehydration and detoxification. During incision and drainage pus should
be taken for culture and sensitivity. Offending tooth should be removed at the same sitting
if the patient can open the mouth.
Pharmacological Treatment 
B: ceftriaxone (IV) 1g 24hourly for 5days 
OR 
B: amoxicillin + clavulanic acid (FDC) (PO) 625mg8hourly for 5days 
AND 
B: metronidazole (IV) 500mg 8hourly for 5days 
If allergic to penicillin use 
A: erythromycin (PO) 500mg 6hourly for 5days 
Once the patient can swallow, replace IV medication with oral treatment. 
Note 
For this condition and other life-threatening oral conditions consultation of available specialists 
(especially oral and maxillofacial surgeons) should go parallel with life saving measures. 
16.3.4 Pericoronitis 
Inflammation of the soft tissues covering the crown of erupting tooth and occurs more commonly in 
association with the mandibular third molar (wisdom) teeth. 
Clinical presentation 
•
High temperature
•
Discomfort 
in 
swallowing 
and
chewing
•
Well localized dull pain, swollen
and tender gum flap
•
Signs of partial tooth eruption
•
Bad smell (Foetor-ox oris)
•
Trismus
Non-pharmacological Treatment 
Excision of the operculum/flap (flapectomy) under local anesthesia. 
Extraction of the third molar associated with the condition. 
Grinding or extraction of the opposing tooth. 
Pharmacological Treatment 
A: hydrogen peroxide solution 3% (PO) 6hourly for 5days (Gurgle /rinse) 
A: amoxicillin (PO) 500mg 6hourly for 5days 

353!
AND 
A: metronidazole (PO) 400mg 8hourly for 5days 
If severe (rare) refer to treatment of dental abscess section 
16.3.5 Osteomyelitis of the Jaw 
Osteomyelitis is an infection involving all layers of bone in which widespread necrosis may occur. It 
is rare in the maxilla due to the rich blood supply, but on occasions may affect the anterior palate 
where the bone is thicker. It is more common in the mandible, usually because of dental infection, 
trauma, or a blood-borne infection. 
Clinical presentation 
•
In the initial stage there is no
swelling
•
Malaise and fever
•
Enlargement of regional lymph
nodes
•
Teeth in the affected area
become painful and loose.
•
Later as the bone undergoes
necrosis the area becomes
very painful and swollen
•
Pus ruptures through the
periosteum and discharged
outside the skin surface
through a sinus
Investigation 
X-ray – OPG (Orthopantomography) or mandibular lateral oblique, water’s view for maxilla/midface.
The x-ray will show sequestra formation in chronic stage. In early stage features seen in x-ray
include widening of periodontal spaces, changes in bone trabeculation and areas of radiolucency.
Perform culture and sensitivity of the pus aspirate to detect the specific bacteria.
Non-pharmacological Treatment  
Incision and adequate drainage to confirmed pus accumulation which is accessible. 
Removal of the sequestrum by surgical intervention (sequestrectomy) is done after the formation of 
sequestrum has been confirmed by X-ray. 
Pharmacological Treatment 
For acute osteomyelitis of the jaw 
B: ampicillin + cloxacillin (FDC) (PO) 500mg 8hourly for 4-6weeks 
AND 
A: metronidazole (PO) 400mg 8hourly for 4-6weeks. If culture is available treat according 
to results. 
For chronic osteomyelitis of the jaw which sequestrectomy has been done 
A: doxycycline (PO) 100mg 12hourly for 5days 
OR 
A: metronidazole (PO) 400mg 8hourly for 5days 
AND 
S: clindamycin (PO) 500mg 8hourly for 5days 
16.4. Fungal Infections 
16.4.1 Oral Candidiasis 
This is a fungal infection of the oral mucosa caused by Candida infection mainly Candida albicans. 
Clinical presentation 
Features of candidiasis are divided according to the types as follows: 
Pseudomembranous 
•
White creamy patches/plaque
•
Cover any portion of mouth but more on tongue, palate, and buccal mucosa

354!
•
Sometimes may present as erythematous type whereby bright erythematous mucosal
lesions with only scattered white patches/plaques
Hyperplastic 
•
White patches leukoplakia-like which are not easily rubbed-off.
Angular cheilitis (angular stomatitis) 
•
Soreness, erythema and fissuring at the angles of the mouth
•
Commonly associated with denture mastitis but may represent a nutritional deficiency or it
may be related to orofacial granulomatosis or HIV infection
Pharmacological Treatment 
A: nystatin suspension (PO) 100,000IU (1 ml) mixture held in the mouth for at least 
3minutes before swallowing, 6hourly  
OR 
C: miconazole gel (PO) 25mg/ml 5–10mls in mouth –hold in the mouth for 60 seconds 
before swallowing. The treatment should be continued for 5days after cure/clearance. Where topical 
application has failed, or candida infection has been considered severe use.  
A: fluconazole (PO) 150mg 24hourly for 7days 
OR  
D: itraconazole (PO) 200mg 24hourly for 7days 
Note 
 Candidiasis has several risk factors; it is recommended that for HIV/AIDS patients with candidiasis, 
refer to the Tanzania HIV/AIDS Guidelines. 
16.5 Viral Infections 
16.5.1 Herpes Simplex Virus 
This is a viral infection commonly affecting the lips and perioral soft tissues presenting as 
papulovesicular lesions which ultimately ulcerate. The primary infection affects mainly the gingiva 
and palate. 
Clinical presentation 
•
A prodromal of tingling, warmth or itching at the site usually precedes the recurrence
•
About 12 hours later, redness appears followed by papules and then vesicles
•
These vesicles then burst, weep, dry, scab and then heal
•
The length of the cycle is variable 5–12days mean time being 7days
Non-pharmacological Treatment 
•
Adequate hydration
•
Avoid salty and acidic drinks
•
Cover lesions on the lips with Petroleum jelly and control any underlying cause
Pharmacological Treatment 
This is an otherwise self-limiting condition but if persistent for 10days or recurrent infection use 
medication: 
For Herpes Labials 
B: acyclovir cream applies 4hourly for 5days 
For Herpes Stomatitis 
B: acyclovir (PO) 200mg 6hourly for 5days 
AND 
B: acyclovir cream 12hourly for 5days 

355!
In immunocompromised patients 
B: acyclovir (PO) 400mg 6hourly for 5days 
For oral facial lesions of herpes zoster treat with 
B: acyclovir (PO) 400–800mg 6hourly for 5days 
Pain control by analgesics 
A: paracetamol (PO) 1g 8hourly for 3days 
OR 
C: diclofenac (PO) 50mg 8hourly for 3days 
OR 
A: ibuprofen (PO) 400mg 8hourly for 3days 
16.6 Aphthous Ulceration 
Aphthous or recurrent aphthous stomatitis (RAS) are painful recurrent mucous membrane 
ulcerations. Usually affect the non-keratinized oral mucous membrane. 
Clinical presentation 
Minor Aphthous Ulcers 
•
Small round or ovoid ulcers 2–4 mm in diameter, surrounded by an erythematous halo and
some edema.
•
Occurs in groups of only a few ulcers (i.e. 1–6) at a time.
•
Found mainly on the non-keratinized mobile mucosa of the lips, cheeks, floor of the mouth,
sulci, or ventrum of the tongue.
Major Aphthous ulcers 
•
Painful ulcers on non-keratinized oral mucous membrane, they are large 1–3 cm edged
ulcers, and several may be present simultaneously.
Herpetiform ulcers 
These occur in a group of multiple ulcers which are small (1–5 mm) and heal within 7–10days. 
Pharmacological Treatment 
B: chlorhexidine gluconate 0.1% mouthwash used 8hourly for 5days 
OR 
D: triamcinolone acetonide cream 0.1% apply 12hourly for 5days 
If systemic therapy is required; 
A: prednisolone (PO) 20mg 8hourly for 3days then dose tapered to 10mg 8hourly for 
2days then 5mg 8hourly for other 2 days. 
A: paracetamol (PO) 1gm 8hourly for 3days when required for pain. 
16.7 Post Extraction Complications 
16.7.1 Bleeding socket 
Commonly due to disturbing the blood clot by the patient through rinsing or inadequate compression 
on the gauze, though at times may be due to bony/tooth remnants. 
Clinical presentation 
Bleeding socket can be primary (occurring within first 24 hours post extraction) or secondary 
occurring beyond 24 hours post extraction. 
Primary Bleeding Socket 
•
Active bleeding from the socket
•
Patient may be dehydrated and pale if has lost significant amount of blood
•
Features of decreased pulse rate and volume, hypotension also if patient has lost
significant amount of blood

356!
Secondary bleeding 
•
The socket may show features of infection or trauma
Non-pharmacological Treatment  
Give local anesthesia (lignocaine 2% with adrenaline 1 in 80,000 IU). 
Clear any clot available and examine the socket to identify source of bleeding. 
Suturing of the wound only when necessary (like significantly traumatized gingiva). 
Give proper instructions to follow (bite on gauze pack for 30 minutes, not to rinse or eat hot foods on 
that day at least for 12 hours and avoid disturbance to the wound). 
Pharmacological Treatment 
Analgesics may be needed: 
A: paracetamol (PO) 1g 8hourly for 3days 
OR 
C: diclofenac (PO) 50mg 8hourly for 3days 
OR 
A: ibuprofen (PO) 400mg 8hourly for 3days 
AND 
C: tranexamic acid (PO) or (IV) 500 mg 8hourly for the first 24hours. 
16.7.2 Infected Socket 
A post extraction complication due to infection of the clot due to contamination (infected socket). The 
condition is painful and if not managed well could lead to osteomyelitis. 
Clinical presentation 
•
Severe painful socket 2–4days after tooth extraction
•
Fever
•
Necrotic blood clot in the socket
•
Swollen gingiva around the socket
•
Sometimes there may be lymphadenopathy and trismus (inability to open the mouth)
Non-pharmacological Treatment 
Socket debridement under local anesthesia with lignocaine 2% and irrigate with hydrogen peroxide 
3% followed with copious amounts of normal saline. The procedure of irrigation is repeated the 2nd 
and 3rd day and where necessary can be extended to the 4th day if pain persists.  
Pharmacological Treatment 
Patient is instructed to rinse with 3% hydrogen peroxide or 2% povidone iodine 3–4 times a day. 
antibiotics should be prescribed to prevent progression to osteomyelitis: 
A: amoxicillin (PO) 500mg 8hourly for 5–7days 
OR 
B: azithromycin (PO) 500mg 24hourly for 3days 
AND 
A: metronidazole (PO) 400mg 8hourly for 5days 
Investigation 
Periapical X-ray of the socket may be necessary when there is limited improvement despite 
treatment. 
16.7.3 Dry Socket 
This is a post extraction complication due to failure to form a clot (dry socket). The condition is very 
painful, and it differs from an infected socket by lack of clotting and levels of severity of pain. 
Clinical presentation 
•
Severe pain 2–4 days’ post-
extraction
•
Pain exacerbated by entry of air on
the site
•
Socket devoid of clot
•
Surrounded by inflamed gingiva

357!
Non-pharmacological Treatment 
Treatment is under local anesthesia with lignocaine 2%, socket debridement and irrigation with 
hydrogen peroxide 3% followed with copious amount of normal saline. The procedure of irrigation is 
repeated on the 2nd and 3rd day and where necessary can be extended to the 4th day if pain 
persists.  
16.7.4 Oro-Antral Communication 
Occasionally, the uncomplicated extraction of a tooth may fracture the thin floor of the sinus and 
cause an oro-antral communication (OAC). More commonly, the communication is produced by 
attempts to remove retained tooth root so that the antrum floor is perforated, or the apex displaced 
into it.  
Clinical presentation 
•
Air passing from the nose into the mouth and the surgeon will be able to see bubbling
through the communication when the patient is asked to breathe out.
•
Blood from the wound, drinks and mouthwashes used to rinse the mouth may pass
through the sinus into the nose.
Non-pharmacological Treatment 
Immediately on diagnosing a communication the tooth should be checked to ensure that it has been 
completely extracted. All pieces of loose bone that might form sequestra are then gently removed. 
The buccal plate of alveolar bone is trimmed if a flap has been raised but is otherwise left alone. 
Buccal advancement flap is the operation of choice to repair the fistula (oro-antral communication) 
Pharmacological Treatment 
A: metronidazole (PO) 400mg 8hourly for 5days 
AND 
B: amoxicillin + clavulanic acid (FDC) (PO) 625mg 12hourly for 7days 
16.8 Tooth Sensitivities 
Teeth become sensitive because of worn enamel, or exposed tooth roots, cavity, gingival collapse, a 
consequence of periodontitis, tartar (calculus) build-up, cracked or chipped tooth and recent filling. 
Non-pharmacological Treatment 
•
Recommend brushing teeth with desensitizing toothpaste for sensitive teeth
•
Desensitizing or bonding –  apply bonding resin material or Glass Ionomer Cement to seal
the area around the tooth
•
Root canal treatment – for severe, prolonged discomfort
•
Prevent tooth-grinding (bruxism) by fabricating to the patient a mouth guard
Pharmacological Treatment 
C: sodium fluoride 1.1 % +potassium nitrate 5% (fluoride gel or varnish), apply 12hourly 
16.9 Tooth Eruption, Shedding and Edentulousness 
16.9.1 Eruption of Teeth 
Eruption of deciduous /primary teeth usually starts at five months of age. Symptoms associated with 
it like fever and diarrhea are normal and self-limiting unless any other causes can be established. 
The following conditions are usually associated with tooth eruption and should be referred to dental 
personnel: eruption cysts, gingival cysts of the newborn and pre/natal teeth. 
Note 
“Nylon teeth” is a myth/belief existing in some traditions. These are conditions associated with the 
eruption of deciduous/primary teeth

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16.9.2 Shedding of Deciduous Teeth 
Phenomenon of losing deciduous/primary teeth occurring between ages of 5–12 years is a normal 
physiological change. Deciduous teeth should be left to fall out themselves unless the teeth are 
carious or there is any other indication. Parents should be counseled accordingly and be instructed 
to assist their children to loosen the already mobile teeth and when there is no success, or the 
permanent teeth are erupting in wrong direction should consult a dentist.  
16.9.3 Edentulousness 
It is the partial or full loss of natural teeth and subsequent resorption of the alveolar bone. 
Diagnosis 
Diagnostic cast, Periapical X-ray, OPG. 
Non-pharmacological Treatment 
•
Design and fabricate dental prosthesis
•
Dental prosthesis may be fixed, partial dentures and complete/full dentures
•
Materials required in fabrication of these prostheses are: alginate impression materials,
silicone impression materials, implant system, gypsum dental stone, Acrylic resins
(monomer and polymer), porcelain, ceramic, metal alloys, wax etc.
16.9.3.1 Dental implant (s) 
A permanent device that is biocompatible and bio-functional placed on or within the bone to provide 
retention for fixed or removable prostheses. 
Indications of Dental Implant(s) 
•
Single tooth replacement.
•
Multiple teeth replacement.
•
Retention of removable prosthesis in partially edentulous patient.
•
Retention of over denture in completely edentulous patient (In mandible two 2 implants are
required for support and in maxilla 4 implants are needed to support the denture.
•
Retention of fixed prostheses completely edentulous patient (In mandible 4 implants
needed and in maxilla - 6-8implants required).
•
Retention of maxillofacial prosthesis.
Investigation 
Radiographic examination
Maxillary and mandibular bone status may be evaluated in combination of periapical X-ray, occlusal 
radiograph, panoramic radiograph, lateral cephalography, MRI and CT-Scan. 
Surgiguids
They are custom made for each patient. They are used as guides for drilling in the optimum 
locations implant placement then removed after placement. 
Study cast
Evaluate occlusal centric relation, including any premature occlusal contacts, the relationship of the 
edentulous area to the adjacent natural teeth and opposing arches. 
Intra-operatively, the following should be observed to have a successful Implant 
•
Assess anatomical variation and abnormalities of vital structures so that implant should
never touch them.
•
Maintain Sterility as interfere with Osseo-integration
Surgical technique 
Adequate blood supply (proper incision design and flap reflection. Using sharp gradual series of drill 
sizes with copious amount of irrigation by normal saline.  

359!
Pharmacological Treatment after implant insertion 
Mouth wash: Do not swallow 
A: hydrogen peroxide 3% 6hourly for at least for 5days 
OR 
B: chlorhexidine gluconate 0.2% 12hourly at least for 5days 
AND 
A: metronidazole (PO) 400mg 8hourly for 8days 
AND 
A: amoxicillin (PO) 500mg 8hourly for 8days 
16.10 Malocclusions 
Malocclusion is any variation in the arrangement of teeth leading to abnormal occlusion to the extent 
that may be functionally harmful or aesthetically objectionable. 
Clinical presentation 
•
Class I malocclusion: Diagnosed when there is any occlusal abnormality or individual tooth
malocclusion in a case with normal arch relationship in anteroposterior plane.
•
Class II malocclusion: Mesiobuccal cusp of upper first permanent molar occludes mesial to
the buccal developmental groove of the lower first permanent molar
•
Class III malocclusion: The upper first permanent molar occludes distal to the buccal
developmental groove of the lower first permanent molar
•
Skeletal malocclusions: These malocclusions are caused by defects in the underlying
skeletal structure itself.
Non-pharmacological Treatment: 
•
Preventive orthodontics
It includes parent counselling, caries control, space maintenance, managing exfoliation of deciduous 
teeth, release of abnormal frenal attachments, treatment of blocked permanent first molars, 
management of abnormal oral musculature and related habits. 
•
Interception orthodontics
o
Correction of anterior or posterior cross bite, relieving crowding of the permanent
dentition, Space closure, treatment of anterior open bite, Deep bite, reverse overjet,
proclination of the upper labial segment and oral habits management by patient
education and monitoring or removable and fixed habit breaker
o
For skeletal malocclusion: Use of extra oral appliances like reverse pull headgear
combined with an RME, high pull head gear and chin cups or functional appliances
are indicated for skeletal malocclusion in growing patients
•
Definitive Orthodontic
Alignment of teeth in patient with dental alveolar malocclusion by using removable, clear aligner or 
fixed appliances. Simple removable appliances are very useful in our local settings especially for 
mild to moderate malocclusion in teenagers and include retainers or space maintainers. 
16.11 Management of Maxillofacial Trauma 
16.11.1 Traumatic Dental Injuries 
It may result in loosening, displacement and or loss of teeth, fracture of teeth and or bone, 
lacerations, and bleeding. The commonest causes are falls (in sports and play) at home or school 
and motor accidents. Most affected are upper incisors. 

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Clinical presentation 
Type 
Presentation 
Tooth 
concussion 
Is an injury to supporting tissues of tooth, without displacement 
Sublaxation 
Is the partial displacement, but is commonly used to describe loosening of a tooth 
without displacement 
Intrusion 
Is the displacement of tooth into its socket often accompanied by fracture of alveolar 
bone 
Luxation 
Is the displacement of tooth laterally, labially or palatally 
Avulsion 
Is the complete loss of tooth from the socket 
Soft tissue Injuries 
Abrasion
Where friction between an object and the surface of the soft tissue causes a wound. This wound is 
usually superficial, denudes the epithelium, and occasionally involves deeper layers. 
Contusion/Bruising 
Indicates that some amount of tissue disruption has occurred within the tissues, which resulted in 
subcutaneous or sub mucosal hemorrhage without a break in the soft tissue surface. 
Laceration
Is a tear in the epithelial and sub epithelial tissues? It is perhaps the most frequent type of soft tissue 
injury, is caused most by a sharp object 
16.11.2 Facial Bones Injuries 
The commonest causes of fractured jaws are fights, road accidents, falls and sport. They occur 
chiefly in males between 15-35years of age and twice as frequently in the mandible as in the 
maxilla. 
Initial assessment 
The initial assessment should not concentrate on the most obvious injury but involve a rapid survey 
of the vital functions to allow management priorities to be established.  
The Mandible 
The commonest sites of fracture in the mandible are the condyle neck, the angle, and the canine 
region.  
Middle third of the face 
Fractures of the middle third of the face involve a complex of bones, which include the paired bones, 
the maxilla, palatine, zygomatic, nasal, lachrymal and inferior conchae, together with the single 
vomer and ethmoid bones. 
Clinical presentation 
Fracture site 
Clinical presentation 
Bilateral condyle 
Pain, tenderness and swelling over both joints 
Gagging on the posterior teeth and an anterior open bite, Restricted lateral 
movements, Absence of movement of condyle heads 
Body of the mandible 
Pain on moving jaw, Trismus 
Movement and crepitus at site of fracture, Step deformity of lower border of 
mandible, Derangement of the occlusion, Mental anaesthesia, Haematoma in 
the floor of mouth and buccal mucosa 
Zygomatic bone 
Depression of the prominence of the cheek, Step deformity in the infraorbital 
ridge, 
Subconjunctival 
haemorrhage 
and 
diplopia, 
Infraorbital 
nerve 
anaesthesia, Haematoma intraorally over the malar buttress, Blood in the 
antrum, Trismus due to the coronoid process impacting against the displaced 

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malar or zygomatic arch, Circumorbital ecchymosis 
Le Fort I 
Floating palate, Blood in the antrum, Bilateral haematoma in buccal sulcus, 
Deranged occlusion with anterior open bite 
Le Fort II 
Gross swelling and, after oedema subside, dish – faced deformity, 
Subconjunctival haemorrhage and diplopia, Bilateral infraorbital nerve 
anaesthesia, 
Bilateral 
haematoma 
intraorally 
over 
malar 
buttresses, 
Retroposed upper dental arch with anterior open bite 
Le Fort III 
Gross swelling and, after oedema subside, dish – faced deformity 
Subconjunctival haemorrhage and sometimes diplopia 
Retroposed upper dental arch with anterior open bite 
Cerebrospinal fluid leak from nose 
Signs of head injury 
Unilateral condyle 
Affected side 
Pain in joint, worse on moving, Tenderness and swelling 
Absence (or abnormality) of movements of 
condyle head, Deviation of mandible towards this side, Gagging on molar 
teeth 
Opposite side 
Open bite 
Limitation of lateral excursion to that side 
Investigation 
Fracture sites 
Type of Investigation 
Mandible 
OPG, Skull x-ray (lateral oblique and PA view) 
Zygoma 
Skull x-ray (Occipitomental and submental vertex view), CT scan 
Maxilla 
Skull x-ray (Occipitomental, submental vertex, lateral face view), CT scan. 
Naso- ethmoidal complex 
CT scan 
Non-pharmacological Treatment 
•
Intra-oral examination: Look for soft-tissue lacerations, dentoalveolar fractures and
damage to teeth.
•
Check for tooth fragments which may be displaced in soft tissues.
•
Examine traumatized teeth for mobility and check mobility.
•
Suture for any soft tissue wounds.
•
Extraction is a treatment of choice for significantly traumatized primary/deciduous teeth
with mobility and or displacement.
Reduction of fractures 
In reducing fractures, the object is to rearrange the bone ends as accurately as possible. Although 
the surgeon should attempt to get perfect reduction, the aim is to treat not a radiograph, but a 
patient, and where displacement is acceptable and function is not impaired the patient should not be 
subjected to unnecessary surgery. 
Open reduction and rigid internal fixation (ORIF) 
It is a standard treatment for most facial fractures. The technique relies on exposing the fractures 
through intra -or extra oral incisions and accurate reduction of the bony fractures, which are then 
held rigidly in place by the application of titanium plates for facial fractures,2 mm used in mandibular 
fractures, 1.7 mm (low profile) and 1 mm used in mid - third fractures. 
Intermaxillary fixation (IMF) 
The mandible is immobilized by fixing it to the maxilla using arch bars and flexible wires of different 
sizes 0.5, 0.6, 0.7 and 0.8mm. This establishes the occlusion and is an accepted part of the 
treatment of maxillary fractures. It may be employed in mandibular fractures, particularly when one 
or both condyles are involved. 

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Note 
Give tetanus toxoid (0.5% IU) if the patient has not received vaccination in the past 10 years.
Pharmacological Treatment 
Pain control by analgesics 
A: paracetamol (PO) 1g 8hourly for 3days 
OR 
C: diclofenac (PO) 50mg 8hourly for 3days 
OR 
A: ibuprofen (PO) 400mg 8hourly for 3days 
Prophylactic antibiotics are indicated in cases of suspected contamination or extensive damage 
B: ampicillin + cloxacillin (FDC) (PO) 500mg 8hourly for 5days 
16.12 Tumours and Tumour-Like Conditions of Oral Cavity and Facial Region 
16.12.1 Benign Odontogenic Tumors 
Each tumour presents with different cardinal features radiologically and on histopathological 
diagnosis. 
16.12.1.1Ameloblastoma 
Clinical Presentation 
•
Recognized between ages of 10 to 80 years
•
80% form in the mandible and 70% develop in the posterior molar region and often involve
the ramus
•
Painless, slow growing tumor that may be solid or cystic
•
Loosening of teeth, with roots resorption
•
Gradual facial asymmetry due to enlargement and destruction of bone
•
Continuous sheet of paper-thin bone covering the tumor
Investigation 
Radiographically, the tumour presents with multilocular radiolucency, honeycomb, or soap bubble 
appearance. 
Note 
Diagnostic confirmation of this tumour is through histopathology. Complete excision e.g. total 
resection of the jaw, segmental resection plus bone grafting is the treatment of choice. Hence refer 
the patient to a centre where there is oral and maxillofacial surgeon and histopathology Unit.
Calcifying odontogenic tumors 
Clinical Presentation 
•
Most often found in the mandibular molar/premolar region, but 33% of cases are found in
the maxilla
•
It is associated with an unerupted or impacted tooth in 50% of cases
Investigation 
Radiographically these lesions can be radiolucent, but more characteristically are mixed lucent and 
opaque masses, exhibiting a snow-driven appearance 
Non-pharmacological Treatment  
Complete excision of the tumour with border of normal lobe should be curative, but recurrence 
follows incomplete excision. 

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16.12.1.2 Amelobastic Fibroma 
Clinical Presentation 
•
Slower growing tumor than the simple ameloblastoma and does not infiltrate between bone
trabeculae
•
75% of ameloblastic fibromas are found in the posterior mandible in the area of a
developing tooth. It is benign and expansile, growing as a pushing front rather than
invading surrounding tissues
Investigation 
Radiographically this lesion appears as a uniocular or bilocular radiolucency, most often in the 
posterior mandible. The radiographic appearance is identical to that of unicystic ameloblastoma, and 
both lesions should be differential diagnoses because they affect similar age groups and have 
similar clinical and radiographic appearances. Histologic examination differentiates the two. 
Non-pharmacological Treatment 
Conservative resection is effective, but if incomplete, recurrence follows 
16.12.1.3. Adenomatoid Tumors (Adenoameloblastoma) 
Clinical Presentation 
•
Two thirds of the cases occur in the anterior maxilla, one third occur in the anterior
mandible, and it is never found posterior to the premolars
•
Two thirds of the cases are associated with an impacted tooth (usually the cuspid)
•
Present with mild swelling or in association with a clinically missing tooth
Investigation 
Radiographically this lesion generally appears as a well-demarcated radiolucency. In 75% of cases, 
it is associated with an unerupted tooth, usually the canine. It may contain radiopaque flecks, which 
represent calcified material.  
Non-pharmacological Treatment 
Enucleation is curative and recurrence is almost unknown. 
16.12.1.4 Odontogenic Myxoma 
Clinical Presentation 
•
Clinically indistinguishable from ameloblastoma
•
The radiographic appearance of this lesion is not distinctive. It appears quite like
ameloblastoma (eg multilocular radiolucency).
Investigation 
Confirmation is through histopathology 
Non-pharmacological treatment 
Wide excision is required.  
16.12.2 Non Odontogenic Benign Tumours 
 (Benign Osteogenic Tumours, Arise from Bone) 
16.12.2.1 Ewing’s tumor 
Clinical presentation 
•
Painful swelling accompanied with fever.
•
It is characterized by extraordinarily fast growth.
Investigation 
Radiographically poorly defined solitary osteolytic lesion, irregular moth–eaten appearance which 
may be undetectable in serial images for a long period. Histological diagnosis is needed. 

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Pharmacological and Non-pharmacological Treatment 
The initial treatment is wide excision, if not possible radiation should be considered. Combination 
chemotherapy should be given. 
16.12.2.2 Pregnancy Tumours 
Clinical presentation 
•
They most commonly appear after first trimester, grow rapidly, and typically regress after
delivery.
•
Found on the gingiva and arise predominantly.
•
They are exophytic, lobulated, or smooth surfaced lesion with a red to purplish color and a
soft, spongy texture.
Non-pharmacological Treatment 
Surgical intervention is often not required. However, pregnancy tumors can be removed during the 
second trimester if they interfere with occlusion, are painful, bleed excessively, or are excessively 
large. Lesions excised during pregnancy often recur. After delivery, pregnancy tumors typically 
recede spontaneously but excision may be necessary for those cases which persist. Other non-
odontogenic tumors are Osteomas, Myxomas, Chondromas, Central giant cell and Fibro-osteoma.  
16.12.3 Benign Soft Tissues Non-Odontogenic Tumours 
Haemangioma 
Clinical presentation 
•
Enlarged, vascular hamartoma appears as a painless, soft, smooth, or lobulated, sessile,
or pedunculated mass but may ulcerate and possibly hemorrhage if traumatized
•
The lesions present with deep red or bluish red in color and moderately firm to palpation.
•
May occur on tongue, lips, buccal mucosa, gingiva, palatal mucosa, salivary glands,
alveolar ridge, and jawbone.
•
They occur early in life and may enlarge rapidly or progressively as the patient grows.
Non-pharmacological Treatment 
Surgery can be beneficial if the lesion is small and has no risk of excessive bleeding. The potential 
for severe hemorrhage caused by the vascular nature of the lesion must be considered. 
Non-pharmacological Treatment of benign tumors 
Enucleation or excision is the treatment of choice depending on the type. Can be hemi 
mandibulectomy, total mandibulectomy, hemi maxillectomy or total maxillectomy. Followed with 
reconstruction when necessary. 
Pharmacological Treatment 
S: bleomycin injection intralesional (sclerotherapy) under ultrasound guidance to cause 
sclerosis of tissues. Surgery may follow if deemed necessary. 
16.12.4 Malignant Soft and Bone 
Tumours 16.12.4.1 Squamous cell carcinoma 
Clinical presentation 
•
A sore in the mouth that does not heal (most common symptom).
•
Pain in the mouth.
•
Persistent lump or thickening of mucosa in the cheek.
•
Persistent white or red patch on the tongue, gums, tonsils, or lining of the mouth.
•
Difficult moving jaw or tongue.
•
Difficult chewing or swallowing.
•
Enlarged cervical lymph nodes may be present.

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Note 
Take tissue biopsy of the lesion and send for histopathology investigation or refer the patient as 
early as possible to a centre where there is oral and maxillofacial surgeon and Histopathology unit. 
Treatment 
Palliative; but this depends on stage of the tumor: stage I and II surgical excision (squamous cell 
carcinoma) with wide margin then curative radiotherapy. Others, surgical excision, radiotherapy 
followed by chemotherapy. 
16.12.4.2 Lymphomas 
These are group of neoplasms of varying degrees of malignancy which are derived from B-cells of 
lymphoid tissues, the lymphocytes and histiocytes in any of their developmental stages. 
Burkitt’s lymphoma (African Jaw Lymphoma) 
Clinical presentation 
•
It shows close association and infection with the Epstein Barr virus. Confined almost
exclusively to children between 2–14years of age.
•
Rapidly growing tumor mass of the jaws, destroying the bone and causing teeth loosening
with extension the maxillary, ethmoid and sphenoid sinuses as well as the orbit.
•
Visceral organ involvement also occurs.
Note 
Diagnostic confirmation is through histopathology; hence, it is emphasized to do early detection 
and referral since Burkitt’s lymphoma responds very quickly on chemotherapy. (For detailed 
management of malignant tumors please refer to the malignancy on chapter twenty-two)
16.12.5. Odontogenic and Non- Odontogenic Cysts 
  Odontogenic cysts
A group of jaw cysts that are formed from tissues involved in odontogenesis (tooth development). 
Odontogenic cysts are closed sacs filled with fluid, and have a distinct membrane derived from rests 
of odontogenic epithelium.  
Non-odontogenic jaw cysts
A group of cysts arising from epithelial remnants of embryonic ducts left behind after embryonal 
facial and jaw development; they are located deep within the tissues in the region of former epithelial 
ridges, epithelial walls, and primary facial fissural and cleft structures. Some few examples of 
frequently encountered cysts I orofacial regions are: 
Dentigerous cyst 
Dentigerous cysts, also called follicular cysts, are slow-growing benign and non-inflammatory 
odontogenic cysts that are thought to be developmental in origin.  
Clinical presentation 
•
Uninfected dentigerous cysts are painless and non - tender on palpation.
•
Larger cysts cause a marked, smooth, rounded expansion of the bone, which may be
reduced to a thin layer of cortical plate.

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Investigation 
Radiographically, they usually present as a well-defined and unilocular radiolucency surrounding the 
crown of an unerupted or impacted tooth within the mandible. 
Radicular (Apical) cyst 
Radicular cyst is an inflammatory jaw cyst originating from epithelial remnants of the periodontal 
ligament because of inflammation that is generally a consequence of pulp necrosis. The resulting 
cyst commonly involves the apex of the affected tooth either by dental caries or trauma.  
Investigation 
Take OPG or Skull X-ray, the cysts appear as rounded, radiolucent areas sharply demarcated from 
normal. Apical periodontal cysts are associated with the roots of dead teeth bone by a thin, 
radiopaque, limiting line of compact or cortical bone. 
Non pharmacological treatment 
Dental cystectomy under local or general anesthesia. 
Globulomaxillary cyst 
The globulomaxillary cyst is a cyst that appears between a maxillary lateral incisor and the adjacent 
canine. The globulomaxillary cyst often causes the roots of adjacent teeth to diverge. 
Investigation 
It exhibits as an "inverted pear-shaped radiolucency" on radiographs, or X-ray films. 
Non-pharmacological Treatment 
Dental cystectomy under local or general anesthesia. 
Dermoid Cyst 
Dermoid cysts are rare masses of the oral cavity derived from ectodermal elements. These are 
benign, slow-growing tumors that are typically asymptomatic but cause complications of inflammation 
or dysphagia, dystonia, and airway encroachment due to mass effects. 
Clinical presentation 
•
Massive swelling of the floor of the mouth, which had displaced the tongue cranially.
•
Painless slowly growing cystic lesion in the sublingual and or submental spaces.
•
A dentigerous cyst may be suspected where a tooth is missing from the arch without any
history of previous extraction.
Non-pharmacological Treatment 
Enucleation through an external approach below the mandible or intraorally though an incision in the 
floor of the mouth. 
Ranular Cyst 
A mucous extravasation cyst involving a sublingual gland and is a type of mucocele found on the 
floor of the mouth.  
Clinical presentation 
•
Translucent, blue, dome-shaped, fluctuant swelling in the tissues of the floor of the mouth.
•
The swelling is not fixed, may not show blanching, and is non-painful unless it becomes
secondarily infected.
•
The usual location is lateral to the midline, which may be used to help distinguish it from a
midline dermoid cyst.
Non-pharmacological Treatment 
Excision of sublingual salivary gland which is affected. 

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16:13 Management of Oral Conditions during Pregnancy 
The oral changes which are seen in pregnancy include gingivitis, gingival hyperplasia, pyogenic 
granuloma, and salivary changes. Gastric acid secretion and the reflux of the acid into the oral cavity 
leads to worsening of enamel erosion, increased caries risk, increased tooth mobility and loss.  
For the first trimester (1-12weeks) 
During the first trimester, it is recommended that the patients be scheduled to assess their current 
dental health, to inform them of the changes that they should expect during their pregnancies, and to 
discuss on how to avoid maternal dental problems that may arise from these changes.  
Recommendations  
Educate the patients about the maternal oral changes which occur during pregnancy. 
Emphasize strict oral hygiene instructions and thereby, plaque control. 
Limit dental treatment to a periodontal prophylaxis, normal filling, and emergency treatments only. 
Avoid routine radiographs. They should be used selectively and only whenever they are needed. 
For the second trimester (13-24weeks) 
During the second trimester, the organogenesis is complete, and the risk to the foetus is low. The 
mother has also had time to adjust to her pregnancy, and the foetus has not grown to a potentially 
uncomfortable size that would make it difficult for the mother to remain still for long periods. 
Recommendations 
Maintenance of oral hygiene and plaque control. 
It’s safe to perform scaling, polishing and curettage if necessary. 
Active oral diseases should be controlled. 
It’s safe to perform elective procedures i.e. Root canal, extraction, restorations. 
Avoid routine radiographs. Use selectively and when they are needed. 
For the third trimester (25-40weeks) 
The fetal growth continues and the focus of the concern now, is the risk to the upcoming birth 
process and the safety and comfort of the pregnant woman. It is safe to perform a routine dental 
treatment in the early part of the 3rd trimester. 
Recommendations 
Maintenance of oral hygiene and plaque control. 
It’s safe to perform scaling, polishing and curettage if necessary. 
Active oral diseases should be controlled. 
It’s safe to perform elective procedures. 
The radiograph use should be minimized. 
Procedures not to be performed after mid time of the third trimester. 
Note 
Pregnancy should not be considered as an absolute reason to deny required dental care. Pregnant 
patients must be educated about the importance of maintaining good oral hygiene, expected 
changes in the oral cavity and routine dental visits.  
16.14 Temporal Mandibular Disorder and Chronic Orofacial Pain 
Temporomandibular disorders (TMD) are disorders of the jaw muscles, temporomandibular joints, 
and the nerves associated with chronic facial pain. 
16.14.1 Chronic Orofacial Pain other than Temporomandibular Disorders 
16.14.1.1 Trigeminal Neuralgia  
A sudden, usually unilateral, severe, brief, stabbing, recurrent pain in the distribution of one or more 
branches of the fifth cranial nerve. 

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Clinical presentation 
•
Episodes of severe, shooting, or stabbing pain that may feel like an electric shock.
•
Spontaneous attacks of pain triggered by things such as touching the face, chewing,
speaking, or brushing teeth.
•
Pain in areas supplied by the trigeminal nerve, including the cheek, jaw, teeth, gums, lips,
or less often the eye and forehead.
•
Pain affecting one side of the face at a time.
Note 
For details of the Investigation and treatment refer a chapter eight (Central Nervous 
System). 
16.14.1.2 Persistent Idiopathic Orofacial Pain (a Typical Facial Pain, a Typical Odontalgia) 
A persistent facial pain that does not have the characteristics of the cranial neuralgias and is not 
attributed to another disorder. 
Clinical presentation 
•
Poorly localized deep pain that does not follow anatomically defined patterns.
•
Patients may have had multiple dental treatments to try and remove the pain.
•
There is a female preponderance in the third to fourth decades.
Investigation 
Thorough clinical history and examination  
Take radiographs of the dentition preferable OPG 
Non-pharmacological Treatment 
Irreversible or invasive procedures should not be undertaken on teeth to try and relieve the pain if the 
clinical picture, vitality testing or radiographic examination would not support the procedure.  
Pharmacological Treatment 
A: amitriptyline (PO) 25mg nocte 24hourly for 1month. 
AND 
A: carbamezepine (PO) 100mg 8hourly for 1month. Dosage can be increased up to 300mg 
at the same frequency and duration. 
16.14.2 Temporomandibular Disorders (TMDs) 
A collective term embracing several clinical problems that involve the masticatory musculature, the 
temporomandibular joint and associated structures, or both. 
Clinical presentation 
•
Facial pain.
•
Limitation of jaw motion.
•
Muscle tenderness and stiffness.
•
Along with any number of associated symptoms in the head, face, and neck region.
Non-pharmacological Treatment 
Reassurance and counseling 
Provide counseling to the patient on the natural history and course of temporomandibular disorders, 
the role of stress and parafunctional habits such as clenching and grinding of the teeth, the 
frequency of the problem in the population, and the self-limited nature of the disorder.  
Heat application 
Application of heat to the sides of the face with a heating pad, hot towel, or hot-water bottle. Vigorous 
treatment may be achieved with ultrasound or short-wave diathermy heat treatments, which are 
widely available in physiotherapy units. 

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Fabrication of Intraoral Occlusal Orthotic Appliances 
These devices are worn on the teeth like a retainer or a removable denture and are usually made of 
processed, hard acrylic.  
Physiotherapy 
Perform manual manipulation, massage, and ultrasonography, which are helpful in reconditioning 
and retraining the masticatory and the other cranio-cervical muscles that are usually involved in 
temporomandibular disorders. 
Pharmacological Treatment 
A: amitriptyline (PO) 25mg nocte for 1month. 
If the treatment is successful, maintenance dose should be given for 2-4months. 
16.14.3 Osteoarthritis and Rheumatoid arthritis of TMJ 
For details management of these two conditions, refer a chapter for disease of musculoskeletal 
system 

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CHAPTER SEVENTEEN 
MUSCULOSKELETAL DISORDERS 
17.1 Infections 
17.1.1   Osteomyelitis 
Osteomyelitis is an infection of the bone or bone marrow caused by pyogenic bacteria or 
mycobacteria or fungi. This condition is most common in children under 12 years. Staphylococci 
aureus are the most frequent responsible organisms. In patients with sickle cell disease Salmonella 
species become more common pathogens than in healthy hosts. Can be classified as acute or 
chronic depending on duration of symptoms. 
 Clinical presentation of acute osteomyelitis 
•
Fever, malaise severe pain at the site of infection, fatigue, irritability, restriction of movement
(pseudo paralysis of limb in neonates) local edema, erythema, and tenderness
•
A history of recent trauma, surgery, or infection of another organ If the infection is close to a
joint there may be a ‘sympathetic’ effusion or concomitant septic arthritis.
Note 
Risk Factor: Poor social economic status, immunosuppression and or malnutrition 
Investigations 
• Total and differential White Blood Cell
count 
• Erythrocyte sedimentation Rate
• C- Reactive protein
• Urinalysis
• Urine for Culture and Sensitivity
• Blood for culture and Sensitivity or
• Aspirated 
pus
for 
culture 
and 
sensitivity 
• Bone Biopsy for Culture and sensitivity
• Polymerase Chain Reaction  (PCR )
for special case like Kingella kingae  
species  
• Bone Scan using Technetium –99  in
acute infection 
• Ultrasound
• Plain X-ray
• CT 
scan 
in 
complex 
anatomical
regions  like shoulder, pelvic, spine 
Pharmacological Treatment 
B: cloxacillin (IV) 1–2g 6hourly then continue with ampicillin + cloxacillin (FDC) (PO) 500mg 
8hourly to complete 3-6weeks course or until CRP and x ray become negative. 
OR 
C: ampicillin+sulbactam (FDC) (IV) 3g 6hourly for two weeks 
THEN 
B: amoxillin+clavulanate (FDC)(PO) 625mg 12hourly for 4weeks. 
Patients with penicillin allergy consider.  
S: clindamycin (IV) 60mg 6hourly for 2weeks then orally to complete 4-6weeks 
AND 
C: ciprofloxacin (IV) 400mg 12hourly for 2weeks then orally to complete 4-6weeks 
For sickle cell patient if salmonella spp is suspected consider 
C: ciprofloxacin (IV) 400mg 12hourly for 4weeks, you may change to oral after 2weeks 
Surgical management  
Surgical drainage and bone window recommended in all cases presenting with history lasting > 24 
hours,  
Clinical presentation of chronic osteomyelitis  
A patient with a history of osteomyelitis who is experiencing a recurrence of pain, erythema, and 
swelling in association with or without pus draining sinus 
Investigations 
•
Total and differential White Blood
Cell count
•
Erythrocyte sedimentation Rate
•
C- Reactive protein

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•
Stop antibiotic for two weeks before
bone biopsy for culture and
sensitivity
•
Polymerase Chain Reaction  (PCR )
for special case like Kingella kingae
species
•
Bone Scan using Technetium –99  in
acute infection
•
Plain X-ray
•
CT scan in complex anatomical
regions like shoulder, pelvic, spine
Pharmacological management 
B: amoxicillin + clavulanate (FDC) (PO) 625mg 12hourly for 6weeks 
Surgical management  
Extensive Surgical debridement of all devitalized tissue and dead bone, dead space filled with 
antibiotic beads,  
Antibiotics cement mixture 
S: vancomycin at a dosage of 2–4g per 40g of cement 
17.1.2   Septic Arthritis 
Inflammation of a synovial membrane with purulent effusion into the joint capsule, often due to 
bacterial infection, but can be caused by fungi and mycobacteria species. If not treated within 24 to 
48hours may cause irreversible joint erosion, septicemia and can be fatal.  
Clinical presentation  
As for acute osteomyelitis however this time sign and symptoms will be localized around the affected 
joint (refers Kocher’s criteria in standard text book for clinical diagnosis ) 
Pharmacological Treatment 
Treat like acute osteomyelitis 
Surgical drainage 
•
Open surgery – incision and drainage followed by meticulous irrigation
•
Laparoscopic drainage
17.1.3: Gonococcal Arthritis 
Pharmacological Treatment  
A: benzyl penicillin (IV) 2.5–5MU 6hourly for 7days 
AND 
B: ceftriaxone (IV) 1g 12hourly for 7days 
OR 
S: cefepime (IV) 2g 12hourly for 7days 
Note 
•
Adjust treatment basing on culture and sensitivity results.
•
Repeat serial CRP, FBP, ESR starting 48hrs after initiation of appropriate treatment until
normalize
Surgical drainage 
•
Open surgery
•
Laparoscopic drainage
17.1.4: Post Open Reduction and Internal Fixation or Arthroplasty Infection 
•
Early < 4/52 post surgery and late >4/52
Clinical presentation of Post arthroplasty infection 
•
Pain
•
Loss of ROM
•
Swelling
•
Local warmth
•
Signs-sinus, effusion, wound
erythema
•
X rays –periosteal reaction,
subchondral bone resorption

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Investigations 
•
Total and differential White Blood
Cell count
•
Erythrocyte sedimentation Rate
•
C - reactive protein
•
Aspirated pus for culture and
sensitivity
•
Synovial or Bone Biopsy for Culture
and sensitivity
•
Bone Scan using Technetium –99
in acute infection
•
Plain X-ray
•
CT scan in complex anatomical
regions like shoulder, pelvic, spine
•
Magnetic Resonance Imaging (MRI)
in Acute Stage
Pharmacological management 
General Principal: Start empirical treatment while awaiting culture and sensitivity results, adjust 
drug according to laboratory results, and continue treatment until CRP become negative. 
S: vancomycin (IV) 1g 12hourly   for 6weeks 
OR 
S: clindamycin (IV) 600mg 8hourly for 6weeks 
AND 
D: ceftazidime (IV) 2g 12hourly for 6weeks 
OR 
S: cefepime (IV) 2g 12hourly for 6 weeks 
OR 
S: meropenem (IV) 500mg to 1g 8hourly for 6weeks 
Surgical management: 
•
Post arthroplasty infection
Stage 1: Removal of prosthesis and replace with cement spacer or postalac and antibiotics for 6/52 
Stage 2:  Use of cement in re implantation and use -stemmed component 
•
Surgical site infection posts open reduction and internal fixation
Stage 1: Extensive surgical debridement, remove metal implant and replace with external fixation, 
traction or orthosis  
Stage 2: Revision surgery once CRP and other inflammatory marker become negative  
Supportive treatment for bone and joint infection 
•
Rest and splintage of affected joint
for 48hrs
•
Nutritional support
•
Addressing the predisposing
condition
•
Physiotherapy to improve range of
motion of nearby joint
•
Walking aid in case of pathological
fracture
•
Hydration
•
Antipyretic for fever
•
Analgesics for pain
17.1.5: Tropical Pyomyositis 
This is a condition whereby there is pyogenic infection of large muscle/muscles with extensive 
necrosis of the involved muscle. This condition occurs more commonly in the tropics, affecting 
immunocompromised individual than normal individual. The cause is uncertain since abscess 
multiple pockets explored early are sterile but later culture of the pus usually yields Staphylococcus 
aureus.   
Clinical presentation  
Fever and painful induration/fluctuation of one or more of the large muscles, mostly in the lower 
extremities. 
Investigations 
•
Complete blood count (CBC)
•
Erythrocyte sedimentation rate (ESR
•
C – Reactive Protein test (CRP)
•
Ultrasound
•
Plain X-ray
•
Muscle biopsy for culture and
sensitivity

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Pharmacological Treatment 
Higher level facilities treatment should be guided by C/S results 
Children 
B: cloxacillin (IV) 1–2g 6hourly for 7-14days 
OR 
A: erythromycin (PO) 500mg 6-8hourly for 7-14days 
OR 
S: vancomycin IV 1g 12hourly for 7days 
OR 
S: clindamycin (IV) 600mg 8hourly for 7days 
Adults 
A: erythromycin (PO) 500mg 6-8hourly for 7-14days; 
OR 
B: amoxillin +clavulanate (FDC) (PO) 625mg 12hourly for 7-14days 
OR 
S: clindamycin (IV) 600mg 8hourly for 7days 
OR 
S: vancomycin (IV) 1g 12hourly for 7days 
Surgical management  
Incision and drainage and irrigation with copious amount of 0.9% sodium chloride 
17.1.6: Necrotizing Fasciitis 
Life threatening progressive rapidly spreading inflammatory infection located in deep fascia, most 
commonly caused by Streptococcus species or polymicrobial   
Clinical presentation of Necrotizing Fasciitis 
•
Early Sign and symptoms mimic
acute osteomyelitis.
•
Foul smelling discharge
•
Late-stage 
multiple 
discoloration
develops a large are of gangrenous
skin,
•
Presence of features of toxic shock
Investigations 
•
Complete blood count (CBC)
•
Erythrocyte sedimentation rate (ESR
•
C – Reactive Protein test (CRP)
•
Ultrasound
•
Plain X-ray
•
Muscle 
biopsy 
for 
culture 
and
sensitivity
Pharmacological Treatment 
A: gentamycin (IV) 80mg 8hourly for 7days 
AND 
B: chloramphenicol (IV) 500mg 6hourly +/_S: clindamycin (IV) 600mg 8hourly for 7days 
Alternatively  
A: benzathine benzylpenicillin (IV) 2-4MU 6hourly for 7days 
AND 
S: clindamycin (IV) 600mg 8hourly +/- ciprofloxacin 400mg (IV) 8hourly for 7days 
Alternatively 
A: benzathine benzylpenicillin (IV) 2-4MU 6hourly for 7days 
AND 
S: clindamycin 600mg (IV) 8hourly for 7days 
OR   
S: vancomycin 1g 12hourly for 7days 
Note 
Adjust treatment basing on culture and sensitivity results Repeat  serial CRP, FBP, ESR starting 
48hours after initiation of appropriate treatment  until normalize. 
Surgical management  
Serial extensive surgical debridement,  
Skin grafting once the wound granulates with no sign of infection 

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Supportive treatment 
•
Hydration
•
Rest
•
Nutritional support
•
Addressing 
the 
predisposing 
condition 
•
Antipyretic for fever
•
Analgesics for pain
•
Physiotherapy to improve range of
motion of nearby joint 
17.2 Inflammatory Conditions 
These are a group of diverse inflammatory conditions due to different causes which affect joints and 
other musculoskeletal tissues.  
General Guidelines 
•
The first-line treatment is a non-steroidal anti-inflammatory drug (NSAID). This group
includes medicines like aspirin, diclofenac and Ibuprofen, (provide dosage and scientific
proof) but does NOT include paracetamol
•
NSAIDs should be used cautiously in pregnancy, the elderly, and patients with asthma and
liver or renal impairment.
•
NSAIDS should be avoided in patients with bleeding disorders
•
NSAIDS increases the risk of heart failure and stroke and should be avoided in patients with
cardiovascular diseases and those who are at high risk
•
NSAIDs should be avoided in patients with current or past peptic ulceration.
•
NSAIDs should be taken with food
•
If dyspeptic symptoms develop in a patient on NSAIDs, try adding magnesium trisilicate
mixture.  If dyspepsia persists and NSAID use considered essential antagonist
•
Physiotherapy is a useful adjunct treatment in many inflammatory joint conditions
Referral: For patients with serious rheumatic disease and peptic ulceration should be referred to 
higher level health facility with adequate expertise and facilities. 
17.2.1 Rheumatoid Arthritis 
Rheumatoid arthritis is an autoimmune condition whereby the immune system attacks the synovial 
membrane of joints, initially of the small joints but progressively involving the big joints. It is a chronic 
multisystem disease of unknown etiology. 
Clinical presentation   
Morning stiffness for >1hr, symmetrical swelling and inflammation of ≥ 3joints (Elbow, Wrist, PIP, 
MCP, Ankle MTP) Rheumatoid nodule, subluxed joints.  
Target population 
Patients who  
•
Have at least1 joint with definite clinical synovitis (swelling)
•
With synovitis not better explained by another disease
Table 17.1: Classification criteria for RA (score- based algorithm): 
 add scores of categories A-D, A score of ≥6/10 is needed for classification of patient as having 
definite RA 
Domain 
Category 
Point score 
A 
Joint involvement (0–5 points)
a 
1 large joint 
0 
2–10 large joints 
1 
1–3 small joints (large joints not counted) 
2 
4–10 small joints (large joints not counted) 
3 
>10 joints including at least one small joint
5 
B 
Serology (at least one test needed for classification: 0–3 points)
b 
Negative RF and negative ACPA 
0 
Low positive RF or low positive ACPA 
2 
High positive RF or high positive ACPA 
3 
C 
Acute-phase reactants (at least one test needed for classification; 
0–1 point)
c  
Normal CRP and normal ESR 
0 

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Abnormal CRP or abnormal ESR 
1 
D 
Duration of symptoms 
<6 weeks 
0 
≥6 weeks 
1 
Investigations 
Note 
No test results are pathognomonic for RA instead they are potential identifier of disease progression 
and monitoring of response to treatment.  
•
Full Blood Picture with differential
(FBP)
•
Erythrocyte Sedimentation Rate
(ESR)
•
Rheumatoid factor (RF)
•
C-Reactive Protein (CRP)
•
Synovial Fluid analysis (WBC
>@2000/ mm³)
•
Antinuclear antibody Test
•
Liver Function test
•
Renal function Test
•
Other test depending on stage of the
disease and expert opinion.
•
Anti-citrullinated protein antibody
(more specific for Rheumatoid
arthritis)
Pharmacological Treatment 
Non-steroidal anti-inflammatory drugs (NSAIDs) should be used in combination, corticosteroids or 
with DMARDs and once DMARDs are effective, NSAIDs and corticosteroids can be reduced in dose 
or discontinued. 
Non selective COX1 and COX2 Inhibitors, until symptoms subside 
A: ibuprofen (PO) 400–800mg 8hourly for 5days 
OR 
D: meloxicam (PO) 7.5mg–15mg 12 hourly for 5-14 days 
OR 
A: Piroxicam 20mg (PO) 24hourly or 10mg 12hourly for 5-14days 
Selective COX 2 inhibitors  
S: ketoprofen (PO) 50-75mg 8hourly for 7-14days 
OR 
S: dexketoprofen trometamol (PO) 12.5mg 6hourly or 25mg (PO) 8hrly for 7-14days 
OR 
Corticosteroid Therapy 
A: prednisolone (PO) 40mg for 3days then taper over a course of 2 to 4 weeks 
OR 
D: triamcinolone (IM) 40mg every 6weeks may be supplemented by additional IM PRN 20-
100mg 
OR 
D: betamethasone dipropionate (Intralesional) 2mg + betamethasone sodium phosphate 
(Intralesional) 10mg once ; not to exceed(4ml) 24hourly repeat every after 2 to 12 weeks, 
maximum of 4 injections per year for a duration of 2years 
Disease-Modifying Ant-rheumatoid Drugs or DMARDs 
S: hydroxychloroquine (PO) 400-600mg 24hourly for 4-12 weeks followed by (PO) 200-400 
mg 24hourly for 12 weeks   
OR 
D: sulfasalazine (PO) 0.5 – 1g 24hourly in two divided doses increase weekly to 
maintenance dose of 2g/day (PO) for 12 weeks 
OR 
S: methotrexate (PO) may be taken with or without food 7.5mg dose weekly; increase PO 
dose to optimum response however should not exceed 20mg/week for 12 weeks. 
Note 
•
Repeat CRP and ESR after every two weeks to determine whether to increase dose or maintain or
taper down.
•
Patient who are using NSAIDs for more than 2 weeks   should be given proton pump inhibitors
•
Combine oral corticosteroid or NSAIDS with one of the DMARDs   to control inflammation
symptoms before DEMARDs become effective.
•
Those on steroid should undergo RBG at least biannual.

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Surgical treatment 
•
Synovectomy
•
Tenosynovectomy
•
Tendon realignment
•
Reconstructive surgery or arthroplasty
•
Arthrodesis
Rehabilitation 
Orthotics and splints: Useful in decreasing pain and inflammation, improve function, reduce 
deformity, and restore joint alignment. Well-padded shoes 
•
Walking aids
•
Braces
Physiotherapy and occupational therapy 
•
30 minutes of daily aerobic exercises at least four times a week
•
Occupational therapy aims at enabling patient to cope with activities of daily life.
17.2.2: Juvenile Idiopathic Arthritis 
Juvenile Idiopathic arthritis (JIA) is the most common chronic rheumatologic disease in children and 
is one of the most common chronic diseases of childhood. JIA should be considered with arthritis 
lasting for at least 6 weeks in children aged < 16 years. All the other causes should be excluded 
including infections, malignancies and hematological conditions like sickle cell anemia. 
Clinical presentation 
History findings in children with JIA may include the following: 
•
Arthritis present for at least 6 weeks before diagnosis (mandatory for diagnosis of JIA)
•
Either insidious or abrupt disease onset, often with morning stiffness or gelling
phenomenon and arthralgia during the day
•
Complaints of joint pain or abnormal joint use
•
History of school absences or limited ability to participate in physical education classes
•
Spiking fevers occurring once or twice each day at about the same time of day
•
Evanescent rash on the trunk and extremities
•
Psoriasis or subtler dermatologic manifestations
Types of JIA include the following: 
•
Systemic-onset juvenile idiopathic arthritis
•
Oligoarticular juvenile idiopathic arthritis
•
Polyarticular juvenile idiopathic arthritis
•
Psoriatic arthritis
•
Enthesitis related arthritis
•
Undifferentiated arthritis
Investigations 
•
ESR and CRP
•
Complete blood count (CBC)
•
LFT
•
Serum creatinine
•
Antinuclear antibody (ANA) testing
•
ASOT and Anti-DNAse B test
•
Urinalysis additional.

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Non-pharmacological Treatment 
•
Psychosocial support
•
Physiotherapy once the pain has subsided
Pharmacological Treatment 
A: ibuprofen (PO) 10mg/kg/dose 6-8hourly (should be given if the duration of arthritis has 
not reached 6 weeks) 
AND 
A: prednisolone (PO) 0.25-0.5mg/kg/day should be given in the initial stage of the 
treatment, and for patients that are responding slowly to treatment, duration should be not 
more than 6 months 
OR 
S: methotrexate (PO) 0.5mg/kg weekly (maximum 20mg) 
Monitor for toxicity with FBP (leucopenia) and ALT (hepatotoxicity) every 1-3months. 
Consider tapering and stopping treatment if the patient is in remission. 
OR 
D: Sulfasalazine (PO) 20-50mg/kg/day in two divided doses (maximum 2000mg/day) 
17.2.3. Gout 
Gout is a recurrent acute arthritis of peripheral joints which results from deposition, in and about the 
joints and tendons, of crystals of monosodium urate from supersaturated hyperuricaemic body fluids. 
The arthritis may become chronic.  
 Clinical presentation 
•
The main clinical features are those of an acute gouty arthritis, often nocturnal, throbbing
crushing or excruciating pain.
•
The signs resemble an acute infection with swelling, hot red and very tender joints.
•
The first metatarsophalangeal joint of the big toe is frequently involved
Investigation 
•
Serum uric acid level.
Non-Pharmacological Treatment 
•
In obese patient, reduce weight
•
Avoid precipitants e.g. alcohol. Red meat
•
Institute anti-hyperuricaemic therapy e adjust the dose depending on response to reduce
uric acid synthesis
•
Prevention or reversal of deposition of uric acid crystals in males
Note: Aim is to maintain serum uric acid level below 8mg/dl (0.48mmol/l) 
Pharmacological Treatment 
Acute state 
A: ibuprofen (PO) 400mg stat then 200mg 8hourly until 24 hours after relief of pain usually 
3-5days.
OR 
A: piroxicam 10–20mg (PO) once a day for 5days 
OR  
A: prenisolone (PO) is 40mg daily for 3days then taper for 2-4 weeks combined with NSAIDs 
and proton pump inhibitor  
OR 
D: methylprednisolone Injection OR triamcinolone OR Betamethasone for monoarticular 
flares (2vials for large joint and 1vial for small joints perday, repeat every after 2-12 weeks, 
maximum of 4 injections per year for a duration of 2years) 
Anti –hyperuricemic therapy for chronic cases 
1st line 
B: allopurinol (PO) 100mg 24hourly. This may be increased every 2-5weeks to until uric acid 
level reaches 6mg/dl or less. Maximum of 600mg daily continue therapy for 6months. 

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2nd line 
S: febuxostat (PO) 10mg 24hourly for 4weeks then 20mg 24hourly for 4weeks then 40mg 
24hourly may increase to reaches 6mg/dl or less. Continue treatment for 6months. 
Nutritional support  
To prevent excessive accumulation of uric acid 
•
Use of low purine diet by restricting consumption red meat, fish, alcohol, stimulants,
and high protein foods to avoid exogenous addition of purines to the existing high
uric acid load is recommended
•
Encourage consumption of alkalizing foods e.g. lemons, tomatoes, green beans,
fruits and milk products 
•
Intake of fluids about 3lts/day to enhance excretion of uric acid based on
assessment is recommended
•
Moderate protein intake (0.8g/kg/day)
•
Maintain adequate CHO intake to prevent ketosis
•
Limit fat intake
•
Avoid large and heavy meals late in the evening
•
Encourage consumption of whole grains
17.2.4 Osteoarthritis 
It is a common form of arthritis, characterized by degenerative loss of articular cartilage, subchondral 
bony sclerosis, and cartilage and bone proliferation subsequent osteophyte formation. Gradual onset 
of one or a few joints involved.   
Clinical presentation 
•
Pain is the commonest symptom
•
Specific clinical features depend on the joint involved e.g. enlargement of distal
interphalangeal joint (Bouchard’s nodes)
Investigation 
•
Plain X-ray of involved joint/ joints.
•
CT scan
•
Diagnostic arthroscopy
•
Synovial fluid analysis
Non-pharmacological Treatment 
•
Rest the joint. Use crutches or walkers to protect weight bearing joints in severe cases.
•
Crepe bandage or braces also can be worn during the active phase of disease.
•
Reduction of weight in obese patients
•
Physiotherapy exercise to the affected joints, TENS
Pharmacological Treatment 
A: ibuprofen (PO) 400mg stat then 200mg 8hourly 7-14days 
OR 
C: diclofenac sodium (PO) 50mg 8hourly for 7-14days 
OR 
D: meloxicam (PO) 7.5-15mg 12hourly-24hourly for 7-14days 
OR 
S: dexketoprofen trometamol (PO) 12.5mg 4-6hourly or 25mg 8hourly for 7-14 
OR 
Topical non-steroidal anti-inflammatory drugs  
A: diclofenac gel 12hourly for 2weeks 
S: ketoprofen gel 12hourly for 2weeks 

379!
Note 
Consider concomitant use of gastro protective treatment in patients with preexistent history of peptic 
ulcers or when giving NSAIDs for a duration of 2 weeks or more 
A: omeprazole 20mg 24hourly 
OR 
C: pantoprazole 40mg 24hourly 
OR 
S: esomeprazole 40mg 24hourly 
OR 
C: lansoprazole 30mg 24hourly for 2-4 weeks 
AND 
B: tramadol (PO) 50mg 8houly for 7-14days 
OR 
B: tramadol+paracetamol (PO) 550mg 8hourly for 14days 
OR 
A: ibuprofen+paracetamol (PO) 900mg 8hourly for 14days 
AND 
A: prednisolone (PO) 5-10mg 24hourly for 
Intra articular injection 
D: methylprednisolone (Intra articular) 80mg/ml for large joint and 40mg/ml for small joints 
per day repeat every after 2-12 weeks, maximum of 4injections per year for a duration of 
2years. 
OR 
S: triamcinolone (Intra articular) 80mg/ml for large joint and 40mg/ml for small joints per day 
repeat every after 2-12 weeks, maximum of 4injections per year for a duration of 2years. 
OR 
D: betamethasone (Intra articular) 12mg/ml for large joint and 6mg/ml for small joints per day 
repeat every after 2-12 weeks, maximum of 4injections per year for a duration of 2years. 
AND 
A: 1% lignocaine 1-2mls. 
AND 
S: hyaluronic acid (Intra articular)16mg once per week for 3 consecutive weeks 
Supplements 
S: glucosamine sulfate1500mg +chondroitin sulfate 1200mg (FDC) (PO) taken with meal 
once a day for 3-6months  
Surgical management for advanced disease 
•
High 
tibia 
osteotomy 
for 
Varus
deformities of knee joint
•
Fibula 
osteotomy 
for 
medial
degeneration of the knee joint
•
Total joint replacement
•
Joint fusion /arthrodesis for limb
salvage
•
Excisional arthroplasty
Note 
For patient who are not fit for surgery consider nerve block option and or radiofrequency ablation.  
Patient should be assessed every after two or four weeks to evaluate response to treatment and 
disease progression 

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!
17.2.5 Heterotopic Ossification 
Heterotopic ossification is defined as bone formation in no osseous tissues. Usually occurs in trauma 
such as fractures and surgical procedures, the exact cause remains unknown. 
Clinical presentation 
• 
Pain and reduced ROM following trauma or post-surgical intervention. 
• 
swelling and tenderness, which can mimic a low-grade infection. 
• 
Bone in soft tissue starts to appear on plain radiographs 4 to 6 weeks after the 
trauma/surgery, 
 
Pharmacological Treatment 
• 
Indomethacin 75- 150mg per day in single daily dose or divided dose 12hrly 
 
Surgical management 
Surgery is delayed for 6 months after the initial trauma/surgery to allow the bone to mature and a 
distinct fibrous capsule to develop. 
 
17.2.6 Tendinopathies 
These are clinical syndrome characterized by chronic, localized tendon pain exacerbated by 
mechanical loading. Caused mostly by tendon overuse and metabolic factors. Classified as Acute or 
Chronic. 
 
Clinical presentation 
• 
Pain with palpation of the affected 
part  
• 
Pain during tendon loading which 
may be also referred pain. 
• 
Kinetic chain changes (muscle 
weakness, abnormal movement 
patterns or joint stiffness) 
• 
Muscle spasm
 
Investigations 
• 
MRI for tendinopathy involving deep tendon like around the shoulder joint 
• 
Greyscale or color Doppler uss. 
 
Non-pharmacological Treatment 
• 
Physiotherapy (active exercise, stretching) 
• 
Activity modification 
• 
Correction of any biomechanical faults 
• 
Reduction of aggravating activities 
• 
Ice heat (chronic tendinopathy) 
• 
Joint mobilization and friction (massage).  
 
Pharmacological Treatment  
Pain management in acute state 
A: ibuprofen (PO) 400mg stat then 200mg 8 hourly 
OR 
C: diclofenac sodium (PO) 50mg 8hourly for 7-14days 
 
OR 
D: meloxicam (PO) 7.5-15mg 12-24hourly for 7-14days 
 
OR 
D: tramadol + paracentamol (PO) 550mg 8hourly for 7- 14days 
 
 
OR 
A: paracentamol + ibuprofen (PO) 900mg 8hourly for 7-14days 
 
Topical analgesics can be added in cases of severe pain, 
A: diclofenac gel applies 12hourly 
 
OR 
S: ketoprofen gel apply 12hourly 
 
Note 
Consider concomitant use of gastro protective treatment in patients with preexistent history of peptic 
ulcers or when giving NSAIDs for a duration of 2 weeks or more. 
 

381!
!
Proton pump inhibitors 
A: omeprazole (PO) 20mg 24hourly 
 
OR 
C: pantoprazole (PO) 40mg 24hourly  
 
OR 
Corticosteroid Therapy 
A: prednisolone (PO) 40mg 24hourly for 3days then taper down over 2-4weeks 
 
OR 
 
 
 
 
D: betamethasone (Intralesional) 12mg 24hourly; repeat every after 2-12 weeks, maximum 
of 4 injections per year for a duration of 2years. 
OR 
S: triamcinolone 40mg per injection site once weekly not to exceed 40mg/day maximum of 
3 injections in one year at interval of 1-3 weeks between injections. 
 
Surgery 
When no improvement after 6month of combined physiotherapy and medical treatment. Open 
surgery or laparoscopic 
 
17.2.7 Plantar Fasciitis 
Planter Fasciitis is a degenerative disease of plantar fascia probably due to overuse trauma that 
leads to micro tears. Depending on duration of symptoms it can be acute 4-6 weeks, subacute 6-12 
weeks and chronic >12weeks with/without refractory. 
Clinical presentation 
• 
Pain in the medial side of the heel, most noticeable with initial steps after a period of 
inactivity 
• 
Paresthesia 
• 
Tightness of Achilles tendon 
 
Investigations 
• 
Plain X-ray 
• 
Ultrasound 
• 
 Nerve conduction and Electromyographic studies 
• 
MRI in chronic with refractory. 
 
Non-pharmacological Treatment 
• 
Weight reduction 
• 
Rest and activity modification  
• 
Stretching/massage  
• 
Ice  
• 
Night splints 
• 
custom orthotic (for client with Pes cavus or planus) 
• 
Extracorporeal shock wave therapy (ESWT) (for subacute and chronic) 
 
Pharmacological Treatment  
Pain management in acute state 
A: ibuprofen (PO) 400mg stat then 200mg 8hourly 
OR 
C: diclofenac sodium (PO) 50mg 8hourly for 7-14days 
OR 
D: meloxicam (PO) 7.5-15mg 12-24hourly for 7-14days 
OR 
D: tramadol and paracetamol (FDC) (PO) 550mg 8hourly for 14days 
OR 
A: ibuprofen and paracetamol (FDC) (PO) 900mg 8hourly for 14days 
  
   Topical analgesics can be added in cases of severe pain, 
A: diclofenac gel apply 12hourly 
OR 
 

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!
 
S: ketoprofen gel apply 12houry 
 
Note 
Consider concomitant use of gastro protective treatment in patients with preexistent history of peptic 
ulcers or when giving NSAIDs for a duration of 2weeks or more. 
 
Proton pump inhibitors 
A: omeprazole 20mg 24hourly for 2weeks or more 
OR 
C: pantoprazole 40mg 24hourly for 2weeks or more 
OR 
Corticosteroid Therapy 
A: prednisolone (PO) 40mg 24hourly for 3days then taper down over 2-4 weeks    
 
 
 
OR 
 
 
S: triamcinolone per injection site 40mg once weekly not to exceed 40mg/day repeat every 
after 2 to 12 weeks, maximum of 4 injections per year for a duration of 2 years  
OR 
D:betamethasone (Intralesional) 12mg 24hourly; repeat every after 2-12 weeks, maximum 
of 4 injections per year for a duration of 2years 
Surgery 
• 
Open partial plantar fascia release with simultaneous release of first branch of lateral 
plantar nerve or 
• 
Endoscopic partial plantar fascia release 
 
17.3: Metabolic Bone Diseases 
17.3.1 Osteoporosis and Brittle Bone Diseases 
Disease which is characterized by low bone mass, microtextural disruption and skeletal fragility and it 
has no clinical manifestation until there is a fracture. Contrary to Brittle bone disease which are 
inheritable with many different phenotypic presentation, however medication for the treatment of 
these two disease are more or less similar. 
Clinical presentation 
• 
Presence of fragility fracture (spine, hip, wrist, humerus, rib and pelvis) 
• 
Family history of osteoporotic fracture 
• 
Bone pain 
 
Investigation 
• 
Complete blood count  
• 
Dual-energy X-ray absorptiometry 
(DEXA) to measure spine and hip 
bone density as reference point 
• 
Serum 25-hydroxyvitamin D,  
• 
Serum Calcium  
• 
Parathyroid stimulating hormone 
• 
Thyroid stimulating hormone 
• 
Serum creatinine  
• 
Urea 
• 
Serum electrolyte 
 
Diagnostic criteria 
T-score chart based on the mineral density measurement by DXA. Osteoporosis is diagnosed when 
a person’s BMD is equal to or more than 2.5 standard deviations below this reference measurement. 
Status 
Hip BMD 
Normal 
T-score of -1 or above 
Osteopenia 
T-score lower than -1 and greater than -2.5 
Osteoporosis 
T-score of -2.5 or lower 
Severe osteoporosis 
T-score of -2.5 or lower, and presence of at least one fragility 
fracture 
 
 

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!
 
Non-pharmacological Treatments 
• 
Fall prevention. 
• 
Diet containing Calcium/vit D. 
• 
Exercise 
• 
Cessation of smoking 
• 
Exposure to sunlight 
 
Pharmacological Treatment 
Pain management 
A: ibuprofen (PO) 400mg start then 200mg 8hourly 
OR 
D: meloxicam 7.5-15mg (PO) once-twice a day for 7-14days 
OR 
Topical analgesics can be added in cases of severe pain, 
A: diclofenac gel applies 12hourly 
OR 
S: ketoprofen gel apply 12hourly 
 
Note 
• 
Consider concomitant use of gastro protective treatment in patients with preexistent history 
of peptic ulcers or when giving NSAIDs for a duration of 2 weeks or more. 
 
Proton pump inhibitors 
A: omeprazole 20mg 24hourly for 2weeks or more 
OR 
C: pantoprazole 40mg 24hourly for 2weeks or more 
OR 
Calcium supplementation 
B: Calcium 600mg + Vitamin D 800IU (PO) 24hourly for 3months then re-evaluate (1mcg of 
Vitamin D=40IU) 
 
Bisphosphonate treatment – should be given for a period of five years. 
S: Ibandronate (IV) 3mg every 3months administered over 15-20minutes (treatment only) 
 
17.3.2: Hypocholecalciferolemia (Vitamin D Deficiency) 
This disease is characterized by hypocalcemia and or hypophosphatemia. The acceptable 
concentration of Vitamin D is between 30-60ng/Ml. 
Clinical presentation 
Adult 
Children 
Mild cases are generally asymptomatic 
Mild cases are generally asymptomatic 
Bone pain and tenderness 
Bone pain and tenderness 
Difficulty rising from a sitting position due to muscle 
weakness 
Muscle weakness 
Bone deformities (osteomalacia) 
Delayed achievement of motor milestones 
Cognitive decline and dementia 
Fatigue and malaise 
Inadequate dietary and supplemental vitamin D 
intake 
Rickets 
 
Investigations 
 
• 
Serum calcium  
• 
Serum alkaline phosphatase  
• 
Parathyroid function test 
• 
Fasting serum phosphate 
 
• 
Renal Function test 
• 
Dual –energy X-ray absorptiometry 
(Bone density scan
• 
Serum 25-hydroxyvitamin D, 
(25(OH)D) levels 

384!
!
Table 17.3: Interpretation of Serum 25-hydroxyvitamin D, (25(OH) D) levels 
Status 
Endocrine Society Guidelines 
Deficient 
Below 20 ng/mL 
Insufficient 
21-29 ng/mL 
Sufficient 
30-60 ng/mL 
Ideal 
40-60 ng/mL 
Considered safe 
<100 ng/Ml 
 
Non-pharmacological Treatment 
• 
Sunlight exposure 
• 
Bracing 
• 
Protective waking 
• 
Isometric exercises  
 
Pharmacological Treatment 
Children1-18years 
D:colecalciferol 2,000 IU 24hourly for 6weeks 
OR 
50,000IU once a week for 6weeks followed by maintenance therapy of 600-1000IU 
24hourly for 3-6months then reevaluate by measuring serum 25(OH)D levels 
 
Adults 
D: colecalciferol 6000IU 24hourly or 50000IU once a week for 8weeks or 6000IU followed 
by maintenance therapy of 1,500-2,000IU/day. 
 
17.4: Condition which may require Amputation.  
Amputation is the surgical removal of part of a limb or extremity such as an arm, leg, foot, hand, toe, 
or finger. This is the treatment of choice for diseased limbs and devastating extremity injuries for 
which attempts at salvage and reconstruction may be lengthy, emotionally, and financially costly and 
have a less than satisfactory results. 
 
Clinical Indication 
• 
Trauma most common reason for 
extremity amputation 
• 
Infection 
• 
Tumor 
• 
Vascular disease 
• 
Metabolic diseases  
• 
Congenital anomalies 
 
Goals of amputation 
• 
Preserve functional length. 
• 
Preservation of useful sensibility 
• 
Prevention of symptomatic 
neuromas 
• 
Prevention of adjacent joint 
contractures 
• 
Early prosthetic fitting 
Early return of patient to work and recreation. 
 
17.4.1: Diabetic Foot Ulcers 
A common surgical complication in diabetic patients. Ulcers can be secondarily infected by 
staphylococci, streptococci, coliforms, and anaerobic bacteria which can lead to cellulitis, abscess 
formation, gangrene, and osteomyelitis. 
 
Clinical presentation  
The three main factors that lead to tissue necrosis in the diabetic foot are: 
• 
Neuropathy 
• 
Infection 
• 
Ischaemia 
 
Non-pharmacological Treatment 
• 
Metabolic control 
• 
Relieve 
pressure: 
non-weight 
bearing  

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•
Smoking cessation is essential.
•
Wound care
•
Frequent (e.g. weekly) removal of
excess keratin and allow efficient
drainage of the lesion.
Pharmacological Treatment 
B: ceftriaxone (IV) 1-2g 24hourly for 7-10days 
AND  
B: metronidazole (IV) 500mg 8hourly for 7-10days 
Depending on culture results 
S: piperacillin-tazobactam (IV) 4.5g 6-8hourly 7-10days (for severe/complicated cases) 
OR  
S: meropenem (IV) 1g 8hourly 7-10days 
Surgical Management 
•
Surgical debridement
•
Amputation depending Wagner’s classification
Table 17:4: Wageners Classification for Diabetic Foot Ulcers 
ULCER GRADING 
DESCRIPTION 
GRADE 0 
No ulcer but high-risk foot 
GRADE 1 
Superficial ulcer 
GRADE 2 
Deep ulcer, no bony involvement or abscess 
GRADE 3 
Abscess with bony involvement (as shown by X-
ray) 
GRADE 4 
Localized gangrene e.g toe, heel etc 
GRADE 5 
Extensive gangrene involving the whole foot 
Note 
Grade 1-3 ulcers are termed non-gangrenous ulcers and Grade 4 and 5 ulcers are termed 
gangrenous ulcers 
17.5 Affection of the Brain and Spine 
17.51 Low Back Pain 
Low back pain is a common presenting complaint especially among the adult population. Severity 
may range from mild, transient symptom to chronic and disabling pain. Causes of low back pain are 
numerous and clues to the underlying cause can usually be found from a good clinical history and 
physical examination. In some patients however, no cause will be found, and these people are 
described as having nonspecific back pain. 
Clinical presentation 
Exclude specific causes of low back pain, for example, suspected or confirmed malignancies, spine 
infection, spine trauma or inflammatory disease such as spondyloarthritis. (flag signs) 
Acute low back pain (pain for <6 weeks’ duration) 
Investigations 
•
Explain to people with acute low back pain with or without sciatica that their pain is likely to
resolve on analgesia and bed rest
•
Do not routinely offer imaging for people with acute low back pain with or without sciatica in
absence of flag signs. Consider imaging only if the result is likely to change management.
Non-pharmacological Treatment 
Self-management: Provide people with advice and information, tailored to their needs and 
capabilities, to help them self-manage their low back pain. 
•
information on the nature of low back pain and sciatica
•
encouragement to continue with normal activities upon pain relief.

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Physical Exercise: Encourage exercise programmes (biomechanical, aerobics, or a combination of 
approaches) based on individual needs, preferences, and capabilities. 
Pharmacological treatment 
The principles of pharmacological treatment include analgesics and muscle relaxants 
 
A: ibuprofen (PO) 400mg stat then 200mg 8hourly 
OR 
C: diclofenac sodium (PO) 50mg 8hourly for 7-14days 
OR 
D: meloxicam (PO) 7.5-15mg 12hourly-24hourly for 7-14days 
OR 
For severe pain 
A: diclofenac (IM) 75 mg 12hourly by deep IM injection for 1-3 days +/- 
B: tramadol (IM) 100mg 12hourly by deep IM injection for 1-3days 
THEN 
C: diclofenac (PO) 50mg 8hourly for 7days +/- 
B: tramadol (PO) 50mg 8hourly for up to 7days. 
 
Topical analgesics can be added in cases of severe pain, 
A: diclofenac gel applies 12hourly 
OR 
S: ketoprofen gel apply 12hourly 
 
Note 
Consider concomitant use of gastro protective treatment in patients with preexistent history of peptic 
ulcers or when giving NSAIDs for a duration of 2weeks or more 
 
Proton pump inhibitors 
A: omeprazole 20mg 24hourly for 2weeks or more 
OR 
C: pantoprazole 40mg 24hourly for 2weeks or more 
OR 
S: esomeprazole 40mg 24hourly for 2weeks or more 
OR 
C: lansoprazole 30mg 24hourly for 2-4weeks 
Muscle relaxant  
S: baclofen (PO) 5mg 8hourly initially, increase by 5mg/dose each after 3days up to 20mg 
8hourly for up to 2weeks  
OR 
S: tizanidine (PO) initially 2mg 8hourly, increase gradually to 4mg per day every after 1-
4days, dose may be extended for 4weeks or more, to discontinue taper gradually; decrease 
by 2-4mg daily.  
 
Chronic Low Back Pain (pain for >6 weeks’ duration) 
Investigations 
• 
Plain Spine x rays 
• 
Dynamic spine x Rays-Flexion/extension views 
• 
Spine CT scan 
• 
Spine MRI 
• 
EMG can be considered for patients in whom the diagnosis is unclear after MRI 
 
Non-pharmacological Treatment 
Non Invasive treatment for chronic low back pain 
Self-management: Provide people with advice and information, tailored to their needs and 
capabilities, to help them self-manage their low back pain. 
 
 

387!
!
• 
information on the nature of low back pain and sciatica 
• 
encouragement to continue with normal activities upon pain relief. 
 
Physical Exercise: Encourage exercise programs (biomechanical, aerobics, or a combination of 
approaches) based on individual needs, preferences, and capabilities. 
Manual therapies: Consider manual therapy (spinal manipulation, mobilization, or soft tissue 
techniques such as massage) for managing low back pain with or without sciatica, but only as part of 
a treatment package including exercises. 
Orthotics: Consider belts or corsets for managing chronic low back pain with or without sciatica in 
selected cases 
Psychological therapy: Consider psychological therapies using a cognitive behavioral approach for 
managing low back pain but only as part of a treatment package including exercise, spinal 
manipulation etc. 
 
Pharmacological Treatment 
The principles of conservative treatment include: 
• 
External spinal immobilization and supportive treatment with analgesics, muscle relaxants, 
bisphosphonates and bed rest  
• 
Monitor for clinical or radiographic evidence of spinal instability and neurological 
deterioration. 
 
A: ibuprofen (PO) 400mg stat then 200mg 8 hourly 
OR 
C: diclofenac sodium (PO) 50mg 8hourly for 7-14days 
OR 
D: meloxicam (PO) 7.5-15mg 12hourly-24hourly for 7-14days 
OR 
For severe pain 
A: diclofenac (IM) 75mg 12hourly by deep IM injection for 1-3 days +/- 
B: tramadol (IM) 100mg 12hourly by deep IM injection for 1-3days 
THEN 
C: diclofenac (PO) 50mg 8hourly for 14 days +/- 
B: tramadol (PO) 50mg 8hourly for up to 14 days. 
 
Topical analgesics can be added in cases of severe pain, 
A: diclofenac gel applies 12hourly 
OR 
S: ketoprofen gel apply 12hourly 
 
Note 
Consider concomitant use of gastro protective treatment in patients with preexistent history of 
peptic ulcers or when giving NSAIDs for a duration of 2 weeks or more 
 
Proton pump inhibitors 
A: omeprazole (PO) 20mg 24hourly for 2-4 weeks 
OR 
C: pantoprazole (PO) 40mg 24hourly for 2-4 weeks 
OR 
S: esomeprazole (PO) 40mg 24hourly for 2-4 weeks 
OR 
C: lansoprazole (PO) 30mg 24hourly for 2-4 weeks 
 
For radicular symptoms add neuromodulators, neurovitamins and muscle relaxants: 
 
Neuromodulator  
D: pregabalin (PO) 75-150mg 24hourly for 4weeks (dose can be escalated based on 
individual response)  
AND 
Neurovitamins  
C: Vit B1+B6+B12 (PO) 24hourly for 4weeks 
AND 

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!
Muscle relaxant 
S: baclofen (PO) 5mg 8hourly initially, increase by 5mg/dose each after 3days up to-20mg 
8hourly for up to 2 weeks 
OR 
S: tizanidine (PO) initially 2mg   8hourly, increase gradually (PO) to 4mg 24hourly every 
after 1-4days, dose may be extended for 4weeks or more, to discontinue taper gradually; 
decrease by 2-4mg daily 
 
Invasive treatments for Chronic Low Back Pain 
Non-surgical interventions 
• 
Consider epidural injections of local anesthetic and steroid in people with severe refractory 
pain. 
• 
Consider referral for assessment for radiofrequency (RF) denervation for people with 
chronic low back pain when non-surgical treatment has not worked for them and the main 
source of pain is thought to come from structures supplied by the medial branch nerve and 
they have moderate or severe levels of localized back pain, or surgical treatment is not 
possible due to other comorbid conditions. 
Surgical interventions 
• 
Spinal decompression: Consider spinal decompression for people with sciatica when non-
surgical treatment has not improved pain or function and their radiological findings are 
consistent with their symptoms. The surgical approach might entail an open or minimal 
invasive technique based on patient factors, availability of resources and expertise. 
• 
Spinal fusion: Consider spinal decompression and fusion with transpedicular screws and 
rods, or interbody devices in unstable spine patients when non-surgical treatment has not 
improved pain or function and their radiological findings are consistent with their symptoms. 
The surgical approach might entail an open or minimal invasive technique based on patient 
factors, availability of resources and expertise. 
17.5.2: Cervical Degenerative Disorders 
Cervical degenerative spine disorders (DSD)are common among the adult population. Clinical 
characteristics include neck pain radiating to upper extremities related to compression and/or 
irritation of one or more cervical nerve roots, resulting into varying degrees of sensory, motor and 
reflex changes. Severity may range from mild, transient symptom to chronic and disabling pain. 
 
Clinical presentation 
• 
neck pain, dermatomal arm pain, scapular/periscapular pain 
• 
upper limb paresthesias, numbness and sensory changes, 
• 
muscle cramps, weakness, or abnormal deep tendon reflexes 
 
Investigations 
• 
Plain Spine x rays 
• 
Dynamic spine x-Rays-Flexion/extension views 
• 
Cervical Spine MRI 
• 
EMG can be considered for patients in whom the diagnosis is unclear after MRI 
 
Non-pharmacological Treatment 
Non Invasive treatment for neck pain and radiculopathies 
Physical Exercise: Encourage exercise programs based on individual needs, preferences, and 
capabilities. 
Manual therapies: Consider manual therapy (spinal manipulation, mobilization, or soft tissue 
techniques such as massage) for managing pain as part of a treatment package including exercises. 
Orthotics: Consider neck collars for managing neck pain with or without radicular symptoms 
Psychological therapy: Emotional and cognitive factors (eg, job dissatisfaction) should be 
considered when addressing surgical or medical/interventional treatment for patients with cervical 
radiculopathy from degenerative disorders 
Pharmacological Treatment 
For mild to moderate pain 
A: ibuprofen (PO) 400mg stat then 200mg 8hourly 
OR 

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!
C: diclofenac sodium (PO) 50mg 8hourly for 7-14days 
OR 
D: meloxicam (PO)7.5-15mg 12-24hourly for 7-14days 
OR 
For severe pain 
A: diclofenac (IM) 75 mg 12 hourly by deep IM injection for 1-3 days +/- 
B: tramadol (IM) 100mg 12hourly by deep IM injection for 1-3days 
THEN 
C: diclofenac (PO) 50mg 8hourly for 14days +/- 
B: tramadol (PO) 50mg 8hourly for up to 14days. 
 
 
Topical analgesics can be added in cases of severe pain, 
A: diclofenac gel applies 12hourly 
OR 
S: ketoprofen gel apply 12hourly 
 
Note 
Consider concomitant use of gastro protective treatment in patients with preexistent history of peptic 
ulcers or when giving NSAIDs for a duration of 2 weeks or more 
 
Proton pump inhibitors 
A: omeprazole (PO) 20mg 24hourly for 2-4 weeks 
OR 
C: pantoprazole (PO) 40mg 24hourly for 2-4 weeks 
OR 
S: esomeprazole (PO) 40m24hourly for 2-4 weeks 
OR 
C: lansoprazole (PO) 30mg 24hourly for 2-4 weeks 
 
For radicular symptoms add neuromodulators, neurovitamins and muscle relaxants: 
Neuromodulator 
D: Pregabalin (PO) 75-150mg24hourly for 4 weeks (dose can be escalated based on 
individual response) 
AND 
Neurovitamins 
C: Vit B1+B6+B12 (PO) once daily for 4 weeks 
AND 
Muscle relaxant 
S: baclofen (PO) 5mg three times a day initially, increase by 5mg/dose each after 3days up 
to-20 mg 8hourly for up to 2 weeks 
• 
OR 
 
S: tizanidine (PO) initially 2mg 8hourly, increase gradually to 4mg 24hourly every after 1-
4days, dose may be extended for 4weeks or more, to discontinue taper gradually; decrease 
by 2-4mg daily 
 
Invasive treatments for Dervical Degenerative Disease 
Non-surgical interventions 
Consider transforaminal epidural steroid injections for severe symptoms while developing 
interventional or surgical plan of management. 
 
Surgical interventions 
• 
Spinal decompression: Surgical intervention is recommended for cervical myelopathy and 
suggested for relief of symptoms of cervical radiculopathy from degenerative disorders. 
• 
The surgical technique (minimal invasive v/s open) approach via anterior/posterior or 
combined, and the appropriate implants required will be guided by patient factors, 
availability of resources and expertise. 
 
 
 

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17.5.3 Pyogenic Spondylodiscitis 
 
Spinal infections constitute an important clinical problem that often requires aggressive medical and 
surgical management to avoid serious complications and long-term sequelae. Common causative 
agents are S. aureaus, E. coli and Proteus spp. 
 
Clinical presentation 
• 
Back pain,  
• 
Fever,  
• 
Muscle spasms 
• 
Extremities weakness,  
• 
Numbness,  
• 
Paresthesias 
 
Investigations 
• 
CBC, ESR, CRP 
• 
Blood and urine cultures 
• 
Spine Xrays 
• 
CT-guided biopsy or a surgical 
biopsy is advisable if diagnosis is 
uncertain Spine MRI with contrast 
• 
Radionuclide bone scan 
Pharmacological treatment 
The principles of conservative treatment include: 
• 
accurate microbiological diagnosis and treatment with appropriate antibiotics 
• 
Treatment should include analgesics, antibiotics, muscle relaxants, bed rest and external 
spinal immobilization with spinal orthotics 
• 
Monitor for clinical/radiographic evidence of spinal instability and neurological deterioration 
 
Pain management 
 
A: ibuprofen (PO) 400mg stat then 200mg 8hourly 
OR 
C: diclofenac sodium (PO) 50mg 8hourly 
OR 
D: Meloxicam (PO) 7.5-15mg 12-24hourly for 7-14days 
OR 
For severe pain 
A: diclofenac (IM) 75mg 12hourly by deep IM injection for 1-3 days +/- 
B: tramadol (IM) 100mg 12hourly by deep IM injection for 1-3days 
 
THEN 
A: diclofenac (PO) 50mg 8hourly for 14 days +/- 
B: tramadol (PO) 50mg 8hourly for up to 14 days. 
 
Topical analgesics can be added in cases of severe pain, 
A: diclofenac gel apply 12hourly 
OR 
S: ketoprofen gel apply 12hourly 
 
Note 
Consider concomitant use of gastro protective treatment in patients with preexistent history of peptic 
ulcers or when giving NSAIDs for a duration of 2 weeks or more 
 
Proton pump inhibitors 
A: omeprazole (PO) 20mg 24hourly for 2-4weeks 
OR 
C: pantoprazole (PO) 40mg 24hourly for 2-4weeks 
OR 
S: esomeprazole (PO) 40mg 24hourly for 2-4weeks 
OR 
C: lansoprazole (PO) 30mg 24hourly for 2-4weeks 

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!
For radicular symptoms add neuromodulators, neurovitamins and muscle relaxants: 
Neuromodulators 
D: pregabalin (PO) 75-150mg 24hourly for 4 weeks (dose can be escalated based on 
individual response) 
AND 
Neurovitamins 
C: vit B1+B6+B12 (PO) 24hourly for 4 weeks 
 
 
 
AND 
Muscle relaxant 
S: baclofen (PO) 5mg 8hourly initially, increase by 5mg/dose each after 3days up to 20 mg 
8hourly for up to 2 weeks 
OR 
S: tizanidine (PO) initially 2 mg   8hourly, increase gradually to 4mg 24hourly after 1-4days, 
dose may be extended for 4weeks or more, to discontinue taper gradually; decrease by 2-
4mg daily 
 
Antibiotic treatment 
B: ceftriaxone (IV) 2g 12hourly for 4-6 weeks 
OR 
C: amoxicillin+clavulanate (IV) 1.2g 12hourly 
 
 
AND 
B: metronidazole (IV) 500mg 8hourly for 4-6 weeks 
(shift to organism specific drugs after C/S results) 
 
Surgical management for extensive debridement of the disc and vertebral bodies, and subsequent 
autologous bone grafting via a least disrupting approach to the stabilizing element is preferred in the 
following situations 
• 
Failure to respond to conservative therapy. 
• 
Significant or progressive neurologic deficits 
• 
Large paraspinal abscess with local mass effect or septic embolization 
• 
Progressive spine deformity with or without incapacitating spinal pain 
 
17.5.4: Tuberculous Spondylodiscitis 
Tuberculous spondylodiscitis, also called Pott’s disease is a common form of spinal infection that left 
untreated can result in serious complications and long-term sequelae. 
 
Clinical presentation 
• 
Back pain,  
• 
Fever,  
• 
Muscle spasms 
• 
Extremities weakness,  
• 
Numbness, paresthesia 
• 
Spine deformity 
Investigations 
• 
CBC, ESR, CRP 
• 
serology for HIV 
• 
Chest x-rays 
• 
Spine Xrays 
• 
Spine CT scan 
CT-guided biopsy or a surgical biopsy is advisable if diagnosis is uncertainSpine MRI with contrast 
 
Pharmacolological treatment 
The principles of conservative treatment include: 
• 
antituberculous treatment in accordance with current national TB treatment guidelines 
• 
supportive treatment with analgesics, muscle relaxants, bed rest and external spinal 
immobilization with spinal orthotics 
 
Monitoring for clinical and radiographic evidence of spinal instability and neurological 
deterioration. 
A: ibuprofen (PO) 400mg stat then 200mg 8 hourly 
OR 
C: diclofenac sodium (PO) 50 mg 8hourly 
OR 
D: meloxicam (PO) 7.5-15mg 12-24hourly  
OR 

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!
For severe pain  
A: diclofenac (IM) 75 mg 12hourly by deep IM injection  
OR 
B: tramadol (IM) 100mg 12hourly by deep IM injection for 1-3days 
THEN 
B: tramadol (PO) 50mg 8hourly for up to 14days. 
 
For radicular symptoms add neuromodulators, neurovitamins and muscle relaxants: 
Neuromodulator  
D: pregabalin (PO) 75-150mg 24hourly for 4 weeks (dose can be escalated based on 
individual response) 
AND 
Neurovitamins 
C: vit B1+B6+B12 (PO) once daily for 4 weeks 
 
 
 
AND 
Muscle relaxant 
S: baclofen (PO) 10-20mg 8hourly for up to 2weeks 
OR 
S: tizanidine (PO) 2mg to 4mg 8hourly for up to 2weeks 
 
Surgical management 
Surgical management for extensive debridement of the disc and vertebral bodies, and subsequent 
autologous bone grafting with or without instrumented spine stabilization via a least disrupting 
approach to the stabilizing element is preferred in the following situations; 
• 
Failure to respond to pharmacological therapy. 
• 
Progressive neurologic deficits from compromised neural structures. 
• 
Large paraspinal abscess with local mass effect or septic embolization Progressive spine 
deformity 
 
17.5.5: Osteoporotic Vertebral Compression Fractures (VCFs) 
Osteoporotic fractures are common in the elderly and in particular post-menopausal women. 
Vertebral compression fractures (VCFs) are among the most common types of osteoporotic 
fractures. Other causes of VCFs include primary or metastatic vertebrae tumors and chronic steroid 
usage. 
 
Clinical presentation 
• 
Severe back pain 
• 
Extremities weakness,  
• 
Numbness,  
• 
Paresthesia 
• 
Muscle spasms, Spine deformity 
 
Investigations 
• 
CBC, ESR, CRP 
• 
Serum calcium levels 
• 
Spine X-rays 
• 
Spine CT scan  
• 
Spine MRI with contrast 
• 
Radionuclide bone scan 
 
Non-pharmacological Treatment 
Consider referral for image guided vertebral cement augmentation procedures in patients with poor 
response to medical treatment and spinal support. 
• 
Vertebroplasty 
• 
kyphoplasty 
Surgical management—spinal decompression and instrumented stabilization in 
• 
Progressive neurologic deficits from compromised neural structures. 
• 
Progressive spine deformity with disabling pain. 
 
 

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Physical and occupational therapy 
• 
strengthening back muscle, balance training 
• 
consider 3-5sessions of weight bearing exercises such’s walking or jogging with each 
session lasting 45-60minutes 
• 
also encourage aerobic low impact exercises such as walking and bicycling 
 
General measures 
Behavioral modification 
Counsel on smoking cessations, and moderation of intake of alcohol, caffeine and encouraged to 
engage in physical activities 
 
Fall prevention 
• 
installing handrails in bathroom, halls, stairways 
• 
ensures hallways,stairwells and entrance are well lighted 
• 
encourage patient to wear sturdy, low heeled shoes. 
• 
Use of walking aid 
 
Pharmacological Treatment 
The principles of conservative treatment include: 
• 
External spinal immobilization and supportive treatment with analgesics, muscle relaxants, 
bisphosphonates and bed rest  
• 
Monitor for clinical or radiographic evidence of spinal instability and neurological 
deterioration. 
 
For mild pain provide one of the following NSAIDS as 1st line treatment 
A: ibuprofen (PO) 400mg stat then 200mg 8hourly 
OR 
C: diclofenac sodium (PO) 50mg 8hourly for 7-14days 
OR 
D: meloxicam (PO) 7.5-15mg 12-24hourly for 7-14days 
OR 
For severe pain 
A: diclofenac (IM) 75 mg 12 hourly by deep IM injection for 1-3 days +/- 
B: tramadol (IM) 100mg 12hourly by deep IM injection for 1-3days 
 
 
THEN 
A: diclofenac (PO) 50mg 8hourly for 14 days +/- 
B: tramadol (PO) 50 mg 8 hourly for up to 14 days. 
 
Topical analgesics can be added in cases of severe pain, 
A: diclofenac gel applies 12hourly 
OR 
S: ketoprofen gel apply 12hourly 
 
Note 
Consider concomitant use of gastro protective treatment in patients with preexistent history of peptic 
ulcers or when giving NSAIDs for a duration of 2 weeks or more 
 
Proton pump inhibitors 
A: omeprazole (PO) 20mg 24hourly for 2-4weeks 
OR 
C: pantoprazole (PO) 40mg 24hourly for 2-4weeks 
 
 
OR 
C: lansoprazole (PO) 30mg 24hourly for 2-4weeks 
OR 
S: esomeprazole (PO) 40mg 24hourly for 2-4weeks 
 
 
 

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!
For radicular symptoms add neuromodulators, neurovitamins and muscle relaxants: 
Neuromodulators 
D: pregabalin 75-150mg 24hourly for 4weeks (dose can be escalated based on individual 
response) 
AND 
Neurovitamins 
C: vit B1+B6+B12 (PO) 24hourly for 4weeks 
AND 
Muscle relaxant 
S: baclofen 5mg 8hourly initially, increase by 5mg/dose each after 3days up to 20 mg 
8hourly for up to 2 weeks 
OR 
S: tizanidine initially 2mg 8hourly, increase gradually to 4mg per day every 1-4days, dose 
may be extended for 4weeks or more, to discontinue taper gradually; decrease by 2-4mg 
daily 
 
Calcium supplementation 
B: Calcium 600mg + Vitamin D800IU (PO) 24hourly for 3 months then re evaluate 
(1mcg of Vitamin D=40 international unit) 
 
Bisphosphonate treatment – should be given for a period of five years. 
S: ibandronate (IV) 3mg every 3months administered over 15-20minutes (treatment only) 
for 5years 
 
17.6: Common Congenital Anomalies of Musculoskeletal System 
17:6:1 Talipes equinovarus (congenital clubfoot) 
Talipes equinovarus is one of the most common musculoskeletal birth defect affecting approx. 
1/1,000 live births. If untreated it causes long-term functional disability. The condition can vary in its 
degree of severity ranging from quite mild to very severe.  It may present with other defects such as 
spina bifida, arthrogryposis, multiplex congenita, congenital myotonic dystrophy, or diastrophic 
dysplasia. 
 
Clinical presentation 
Birth deformities of the foot with  
• 
Small foot and calf  
• 
Cavus (tight intrinsics muscles) 
• 
Adductus of forefoot (tight tibialis 
posterior) 
• 
Varus (tight tendoachilles, tibialis 
posterior, tibialis anterior) 
• 
Equinus (tight tendoachilles) 
Diagnosis  
• 
Most clinical diagnosis 
• 
Plain X-ray  
 
Management   
Non operative management - Ponseti method of serial manipulation and casting,  
The goal is to rotate foot laterally around a fixed talus, order of correction follows acronym (CAVE) 1. 
Cavus 2. Adductus3.Varus4. Equinus. Heel cord tenotomy needed in at least 80-90% of children. 
Followed by Foot abduction orthosis (FAO). Non noncompliance to FAO is the biggest risk factor for 
deformity recurrence  
 
 
Table 17:5: Ponseti Method 
Month 
1-4 
Weekly serial casting (with knee 
in 90° of flexion ) with forefoot 
supination, 
then 
forefoot 
abduction 
• First correct cavus with forefoot SUPINATED (NOT 
pronated) by aligning the less varus forefoot with the 
more varus hindfoot (pronation would increase cavus 
deformity)   
• 
Secondly correct 
adduction and heel 
varus by 
rotating calcaneus and forefoot around talus (head of 
talus acts as a fulcrum) into forefoot ABDUCTION 

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Tendon 
Achilles 
lengthening 
(Tenotomy) (TAL) at week 8 
required in > 80-90% 
• 
Equinus 
correction 
last with 
tendon 
Achilles 
tenotomy  
• Perform when foot is at least 60° abducted, heel is 
in 
valgus 
and 
equinus 
persists   
• Cast in maximal dorsiflexion for 3 weeks after 
tenotomy 
Month 
4-8 
Foot abduction orthosis (FAO)  
• 23 hours a day for 3 months 
after 
correction  
• night time/nap time only until 
age 4 years 
• With FAO holding affected feet at least 60°external 
rotation and 30° in normal foot for unilateral cases 
 
• Feet are measured prior to tenotomy so FAO is 
available on the day of post-tenotomy cast removal 
2-4 
years 
Tibialis anterior tendon transfer 
(TA transfer)  at 2-5 yrs of age 
(30-50% will require) 
• 30-50% will need TA transfer with or without repeat 
TAL or gastrocnemius recession for recurrent 
deformity 
• Indicated if the patient demonstrates supination 
during gait 
Operative management  
I. 
posteromedial soft tissue release and tendon lengthening for children of <2years  
II. 
medial column lengthening or lateral column-shortening osteotomy, or cuboid 
decancellation indicated for children older than 2years 
III. 
talectomy-n severe, rigid recurrent clubfoot in children between 6-10yeras or those 
with arthrogryposis 
 
Note 
Surgical management are complemented by serial casting and   foot adduction orthosis 
 
17.7: Musculoskeletal Tumour  
Musculoskeletal tumors are tumors that develop in muscles, bones and nerves Bone tumors are 
divided into primary and secondary (metastatic) tumours. Primary tumours arise from cells which 
constitute the bone and are divided into benign and malignant types. Metastatic type is most 
common cause of bone cancer, the most common primary sites being renal, thyroid, lung, prostate, 
and breast. 
 
Clinical presentation 
• 
Dull and aching pain which worsen at night is deemed a ‘red flag’ symptom 
• 
Swelling where the tumor is located  
• 
Pathological fracture  
• 
Fever, weight loss, anemia and general body malaise are late symptoms  
 
Note 
For detailed clinical presentations, investigations and management of specific bone tumor refer to 
malignancy chapter  
 
17:8 Angular Deformity of Limbs 
17.8.1 Rickets 
Refers to softening and weakening of bones in children, usually due to inadequate vitamin D. Vitamin 
D promotes the body’s absorption of calcium and phosphorus. Extreme or prolonged lack of vitamin 
D makes it difficult to maintain proper calcium and phosphorus levels in bones, which can cause 
rickets. 
Clinical presentation  
• 
delayed growth,  
• 
bow legs,  
• 
weakness and pain in the spine,  
• 
pelvis and leg 

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!
Pharmacological Treatment  
Treatment may involve adding vitamin D or calcium to the diet,   
 
17.8.2 Physiological Bowing/Knocked Knees 
Is considered bending of knees at an early age due to early walking and overweight below the age of 
2years 
 
Diagnosis process 
I. 
Diagnosis is mainly by physical examination – obvious varus/valgus deformity and 
metaphysical widening. 
II. 
Blood tests to measure the levels of calcium and phosphate in the blood (Refer to table 
17:3.) 
III. 
Bone X-rays to check for bone deformities. 
 
Treatment 
• 
First consultation: rule out if it’s physiological – bow legs at young age before the age of 3 
years without signs of rickets 
• 
If it’s physiological then consider follow up every 6 months +/- vitamin d supplements 
• 
At the age of 3 years if deformity more than 8degrees consider–hemiepiphysiodesis at 
around the age of 3years if the deformity is due to Blount’s disease consider 
hemiepiphysiodesis/corrective osteotomy. 
 
Note 
For details on specific surgical option kindly refer to standard orthopedic text books. 

!
397!
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CHAPTER NINETEEN 
METABOLIC AND ENDOCRINE DISEASE CONDITIONS 
 
19.1 Diabetes Mellitus 
Diabetes mellitus is a clinical syndrome characterized by persistently high blood glucose values due 
to deficiency or diminished effectiveness of insulin.  
 
Classification 
Diabetes mellitus can be classified as follows:  
• Type 1 Diabetes Mellitus (T1DM) – due to autoimmune β-cell destruction  
• Type 2 Diabetes Mellitus (T2DM) – due to a progressive loss of β-cell insulin secretion 
frequently with underlying insulin resistance  
• Gestational Diabetes Mellitus (GDM) – diabetes diagnosed in the second or third trimester of 
pregnancy that was not clearly overt diabetes prior to gestation  
• Specific types of diabetes – due to other causes e.g., monogenic, diseases of the exocrine 
pancreas and drugs or chemicals. 
 
Diagnostic Criteria  
• Main clinical features of diabetes are thirst, polydipsia, polyuria, tiredness, loss of weight, 
blurring of vision.  
• Many people have no classical symptoms and may only present late with the symptoms 
related to complications e.g., pruritus vulvae and balanitis due to infections, paraesthesia or 
pain in the limbs, non-healing ulcers, and recurrent bacterial infections.  
 
WHO diagnostic Criteria 2006  
• Fasting plasma glucose level ≥ 7.0 mmol/L (126 mg/dL)  
• Plasma glucose≥ 11.1 mmol/L (200 mg/dL) two hours after a 75 g oral glucose load in a 
glucose tolerance test  
• Symptoms of hypogycaemia and casual plasma glucose ≥11.1 mmol/L (200 mg/dL)  
• Glycatedhemoglobin (HbA1c) ≥ 6.5%.  
 
Diagnosis of gestational diabetes (WHO criteria 2013)  
• Fasting plasma glucose 5.1–6.9 mmol/l  
• 2–hour plasma glucose 8.5–11.0 mmol/l following a 75g oral glucose load.  
 
Note 
Fasting plasma glucose higher than 6.9 mmol/l or 2–hour plasma glucose higher than 
11.0 
mmol/l are considered overt diabetes rather than GDM 
 
At risk screening  
Early diagnosis and good control reduce the risk of costly complications and reduces the 
deterioration of islet function in T2DM. The following people should therefore be screened with 
fasting blood glucose or HbA1c at least yearly when they visit health facilities:    
• Those aged ≥40 years 
• Children and adults <40 years who are overweight or obese and who have two or more 
additional risk factors for diabetes 
• Individuals with impaired glucose tolerance or impaired fasting glucose or a history of a 
cardiovascular event  
• People on long-term steroids or immunosuppressants 
• Women with a history of gestational diabetes mellitus or polycystic ovary syndrome  
• All pregnant women at the first antenatal visit if overweight, have had gestational diabetes, 
babies with birth weight >4 kg, previous stillbirths or neonatal deaths. Screening should be 
repeated in the second trimester if negative. 
• All women during the 2nd or 3rd trimester (for gestational diabetes). 
 
Impaired glucose tolerance 
For people with glucose intolerance the risk of T2DM and its associated mortality may be reduced 
by: 

!
398!
!
• dietary modification (see chapter on Nutrition) 
• physical activity (see chapter on Nutrition)   
• weight reduction 
• medication with metformin. 
 
Goals of diabetes management 
Table 19.1: Goals for Optimum Management Of Diabetes 
Diet 
Advise same as for people without diabetes 
Body mass index  
Therapeutic goal is 5–10% weight loss for people who are overweight or 
obese, but aim for BMI<25 kg/m2 
Waist circumference  
<102 cm for men, <88 cm for women  
Physical activity  
At least 30 minutes of moderate physical activity on most days of the 
week (total ≥150 minutes/week) 
Cigarette consumption  0 per day 
Alcohol consumption   
Not more than 2 standard unit  drinks (20 g) per day for men and 1 unit 
for women 
Blood glucose level  
Non-pregnant: 4–6 mmol/L fasting; 6–8 mmol/L postprandial     
Pregnant: ≤5.0 mmol/L fasting, ≤6.7 mmol/L postprandial 
Self-monitoring of blood glucose is essential to improve outcomes   
HbA1c  
Target ≤7% (6.5–7.5%). Should be measured every three months until 
stable, thereafter at least twice a year 
Lipids  
Total cholesterol: <5.2 mmol/L 
HDL-C: ≥1.0 mmol/L 
LDL-C: <2.6 mmol/L 
Triglycerides: <1.7 mmol/L 
Blood pressure   
Target ≤140/90 mmHg 
For those with albuminuria/proteinuria <130/80 mmHg   
Urine albumin  
Spot collection: <20 mg/L  
 
Urine albumin-to-creatinine ratio (UACR): women: <3.5 mg/mmol; men: 
<2.5 mg/mmol 

399!
Algorithm for the Glycemic Management of T2DM 
Non-pharmacological Management 
Healthy lifestyles 
Dietary control 
•
Objectives:
o To meet requirements for growth and development, physical activity, and
maintenance of desirable body weight. Majority of people with T2DM are overweight
or obese and need to lose weight.
o Attain and maintain near normal blood glucose levels to prevent hypo- and
hyperglycaemia and so minimize the onset of chronic complications.
o Attain optimum blood lipids and blood pressure control and so reduce the risk of
macrovascular disease.
•
Appropriate measures
STEP 1:
Lifestyle changes: 
Diet,
Physical activity,
Stop smoking, & 
Stop/reduce alcohol
STEP 2:
Oral monotherapy
Sufonylurea or
Metformin
Sick-looking
Severe symptoms
Infections
STEP 3:
Oral combination
therapy
SU+Biguanides
STEP 4:
Oral therapy
PLUS Insulin
STEP 5:
Insulin therapy in 
a secondary or 
tertiary service
Recommend Llifestyle change
Wait Three Months
Glycaemic goal met?
Is Metformin contraindicated?
Start with low dose;
increase monthly as needed to 
glucose target or maximum dose
Glycaemic control met?
Add another class of oral agents
Start with low dose and increase 
monthly as needed to glucose target 
or until maximum dose
Glycaemic control met?
Continue above
Add bedtime Intermediate-acting Insulin
Wait three months
Glycaemic control met?
Continue to 
monitor
Refer to secondary or tertiary care for 
more than once daily Insulin therapy:
Admit patient.
Consider insulin
Continue to 
monitor
Metformin
Continue to 
monitor
Continue to 
monitor
Sulfonylurea
  Yes
No
Yes
Yes
No
Yes
No
Yes
No
No
No
Yes

400!
o Each meal should consist of a variety of foods from the core food groups
(vegetables, fruits, whole grains, meat and proteins, dairy products)
o Distribute foods evenly throughout the day with small/light meals in between the
three main meals.
•
Food composition
o Protein: 15-20% of total energy (1g/kg/day)
o Energy from carbohydrates: 45-60% of total calories
ü
Less than 100gms carbohydrates per day is not advisable as it
leads to ketosis
ü
The distribution and amount of carbohydrates between meals
should be synchronized with the action of insulin and drugs.
ü
Distribute the food over three meals with snacks in between rather
than 1 or 2 large meals
ü
Give more of carbohydrate as complex starches e.g. whole grain
cereals, whole grain bread, roots and stem tubers, because they
breakdown more slowly to releaseglucose.
ü
Avoid simple sugars, sugar-sweetened beverages and honey.
o Fats should provide < 30% ofenergy
ü
A lower fat intake of up to 20% or less of the daily energy in case
of obese adult with diabetes.
o Limit salt to less than 1 teaspoonful/day
o Limit fat intake
•
Physical activity
o Aerobic (e.g. brisk walking) and muscle strengthening activities improve glucose
tolerance, energy expenditure, feeling of wellbeing and mood, work capacity, improved
blood pressure, lipid profiles and increased functional mobility in older people.
o Adjust medicine dosages and or food intake to avoid hypoglycaemia.
•
No smoking
•
Avoid or limit alcohol intake to one drink/day for women, two drinks/day for men.
Pharmacological Treatment  
Treatment with oral hypoglycemics 
•
Review the blood glucose at follow-up clinic and adjust medicines as needed until blood
glucose is controlled.
•
If lifestyle measures on their own failure achieve blood glucose control or blood glucose
levels are persistently high (fasting >11 mmol/l or random >15 mmol/l) initiate:
67267 
A: metformin (PO) 500mg 12hourly with or after meals. Increase, as required, until a 
maximum of 2000mg in 2–3 divided doses. 
If Metformin is contraindicated, then use 
A: glibenclamide (PO) 2.5–10mg 12hourly 
OR   
C: glimepiride (PO) 1–4mg 12hourly 
OR 
A: gliclazide (PO) 40–160mg 12hourly 
•
If the maximum dose of metformin does not result in adequate glycaemic control, either one
of the above sulphonylureas may be added, starting with the lower dose and increasing until
control is achieved or the maximum dose is reached.
•
If a combination of both medicines is still inadequate, then insulin should be added as
detailed below in the section on insulin.
•
Activity of sulphonylureas is prolonged in both hepatic and renal failure
•
Metformin is contraindicated in those with severe renal, liver and cardiac failure.
•
The lower dosage is appropriate when initiating treatment in elderly patients with
uncertain meal schedules, or in patients with mild hyperglycemia
•
Sulphonylureas are best taken 15 to 30 minutes before meals
Treatment with Insulin Injection in Type 2 Diabetes 
Insulin injections are indicated in T2DM in the following conditions:  
Note 

401!
•
Initial presentation with fasting blood glucose more than 15 mmol/l
•
Presentation in hyperglycaemic emergency
•
Peri-operative period especially major or emergency surgery
•
Other medical conditions requiring tight glycaemic control
•
Organ failure: Renal, liver, heart etc,
•
Diabetes not well controlled with diet or oral drugs
•
Latent autoimmune diabetes of adults (LADA)
•
Contraindications to oral drugs
Note 
The maximum glucose lowering efficacy of oral drugs is usually evident by six months. 
Therefore, the efficacy of any added therapy must be assessed within six months and 
an alternative drug instituted in case of failure 
Insulin injections should be initiated by a doctor able to fully instruct the patient in its use but insulin 
will be available at lower health facilities for management of stable patients who require 
prescription refills. 
  Table 19.2: Types of Insulin as per WHO Essential Medicine List 
Type of Insulin 
Name 
Basal or short acting 
Short acting 
A: Insulin–short acting (human) 
soluble  
Short acting 
Intermediate acting  A: Insulin–intermediate acting (human)  Basal 
Pre-mixed insulin 
A: Intermediate and short acting 
insulin (70/30)  
Basal + Short acting 
Insulin as substitution therapy 
Oral medicines are discontinued (except metformin if patient is obese) 
S: Pre-mixed insulin is introduced at a dosage of 0.2 IU/kg body weight and this is split    into: 
⅔ in the morning and ⅓ in the evening  
•
Inject 30 minutes before the morning and the evening meals for human insulins
•
Inject 0 to 15minutes before meal for analog insulins.
Insulin as supplemental therapy 
Oral medicines are continued 
A: neutral protamine hagedorn (isophane) insulin administered at night before 22:00h at a total 
daily dose of 0.1–0.2 IU/kg body weight.  
•
The oral medicines are continued (half maximum dose of sulphonylureas and
metformin dose of 2 g/day)
•
Blood glucose levels are monitored.
Self-monitoring in patients with T2DM   
Self-Monitoring Blood Glucose (SMBG) is usually recommended in the following patients: 
•
patients on insulin and glucose lowering agents that can cause hypoglycaemia
(sulphonylureas)
•
when monitoring hyperglycaemia arising from illness
•
with pregnancy and pre-pregnancy planning
•
when changes in treatment, lifestyle or other conditions requires data on glycaemic
patterns
•
when HbA1c estimations are unreliable (eg haemoglobinopathies)
 TYPE 1 Diabetes Mellitus (Childhood 
diabetes) Non-pharmacological Treatment 
•
Nutrition (refer to nutrition chapter)
•
Exercise requirements are as for children without diabetes
•
Psychological support is important to cope with this chronic illness.
Pharmacological Treatment 
Total dose of insulin contains soluble and intermediate/long-acting insulin. 

402!
•
Give total dose of insulin
o pre puberty 0.5 IU/kg/day subcutaneously for life
o puberty 1-2 IU/kg/day subcutaneously for life
o after puberty < 2 IU/kg/day subcutaneously for life
•
Divide total insulin dose as per recommended percentage below
Table 19.3: Recommended Insulin Dosage 
Time 
Type of insulin 
Proportion 
Break-fast 
Short acting 
30% of total daily dose 
Lunch 
Short acting 
20% of total daily dose 
Supper 
Short acting 
10% of total daily dose 
Bedtime 
Long/intermediate acting 
40% of total daily dose 
Note 
•
Diabetes in children is often misdiagnosed as some other condition – e.g. as pneumonia or
asthma (laboured breathing),
•
Insulin should be given for life and the dose adjusted according to weight and glucose response
•
Self-glucose monitoring by glucometer at home 3-4times/day
•
Pre-mixed insulins not advised in children
Clinical monitoring of people with diabetes 
Table 19.4: Clinical Monitoring of People with Diabetes 
Initial visit 
3 Month visit 
Annual visit 
History and diagnosis 
Physical examination 
•
Height and weight
•
Waist/Hip circumference
•
Blood pressure
•
Detailed foot examination
•
Tooth inspection
•
Eye examination
•
Visual acuity+ Fundoscopy
•
ECG
•
Biochemistry
o
Blood sugar
o
Glycosylated Haemoglobin
(HbA1c)
o
Lipid profile (TC, HDC, LDLC,
TG)
o
Serum creatinine
o
Urine: glucose, ketones, protein
•
Education
•
Nutritional advice
•
Medication if needed
•
Relevant history
•
Weight
•
Blood pressure
•
Foot inspection
•
Blood Glucose
•
Urine protein
•
Education advice
•
Nutrition advice
•
Review therapy
•
HbA1c every six
months
History and examination 
– as at initial visit
Biochemistry as at initial visit 
TC=Total cholesterol, HDLC=high density lipoprotein, LDLC= low density lipoprotein, G=Triglycerides 
Surgery in diabetes  
General measures  
Correct pre-operative management depends on type of surgery (major or minor), type of diabetes 
and recent diabetes control.  
•
Surgery should be delayed if possible if HBA1C >9% or blood glucose fasting >10 mmol/l or
random glucose > 13 mmol/l.
•
Screen for nephropathy, cardiac disease, retinopathy and neuropathy and inform surgical
team.
If diabetes is well controlled and surgery is minor: 
•
If on diet or oral agent therapy, omit therapy on morning of surgery and resume therapy
when eating normally
•
For T1DM, continue with normal dose of insulin

403!
If on insulin therapy or poor glycaemic control or major surgery: 
•
Use continuous IV insulin infusion
•
Start at 8 am and stop when eating normally.
•
Monitor blood glucose before, during and after surgery: aim for blood glucose levels of 6–10
mmol/l.
For major surgery (glucose-insulin potassium regimen) 
•
Once snack is missed, start an IV regimen irrespective of the size of the procedure
•
Maintain insulin administration (hourly) to avoid lipolysis and ketoacidosis in patients with
restricted oral intake and thus prevent DKA
•
Administer 5% dextrose in maintenance IV fluids AND
•
Short-acting insulin (16 Units) + KCl 10mmol/L added to 500mls of 10% dextrose.
o
Infuse at 80ml/hr IV.
o
If obese or initial blood glucose is high (>14mmo/l) consider higher dose of insulin (20
Units)
o
If very thin or usual insulin dose is very low, consider lower dose (12 Units)
•
Monitor blood glucose levels hourly (aim for 6–10 mmo/l)
o
If blood glucose is low or falling reduce dose by 4 Units
o
If blood glucose is high or raising increase dose by 4 Units
•
Patients receiving Multiple Daily Insulin Therapy (MDIT) should receive preoperative basal
insulin dose without interruption in the perioperative period. When oral intake is restricted,
regular insulin may be given every 4–6 hrs to control hyperglycemia. When a diet is
tolerated, the MDIT regimen should be resumed
•
Post operatively: give 5–10% dextrose IV 1 litre + KCl 20ml + 2/3 of total daily dose of
insulin over 8hrs and repeat until able to take orally. Continue the infusion until 60 minutes
after the first meal.
•
Resume usual therapy after first meal
•
Check electrolytes daily.
19.2 Management of Diabetes During Religious Fasting 
There are several types of fasting:  
•
Normal fast (the common fast): the person abstains from all foods but can take water for a
limited time.
•
Total fast = total abstinence from both food and water. This should not go beyond a
maximum of three days and is not recommended for those people taking insulin
secretagogues or insulin.
•
Partial fast = abstain from selected foods and drinks, or omit a certain meal each of the
fasting days.
Those with very poor glucose control should be discouraged from fasting 
•
A total fast is not recommended for anyone with diabetes. Adequate hydration is important
even during the period of fasting.
•
For those on insulin, a partial fast is preferred to total or normal forms of fasting.
•
Self-blood glucose monitoring is mandatory for people with diabetes who elect to fast.
o Once-a-day is adequate for patients on diet only or diet with metformin.
o At least 3 times a day in patients on insulin secretagogues
o More frequently if hyperglycaemia is marked and the urine tested for ketones.
•
Consider terminating the fast if frequent hypoglycaemia or intercurrent infections.
•
Vigorous activity should be avoided during period of fast.
•
Ensure ready access to a healthcare provider during the period of fast.
Management of normal fasting for people treated with oral hypoglycaemic agents 
•
Fasting is possible in this situation.
•
Usual dietary advice should be followed at this time.
•
Patients on metformin, alpha-glucosidase inhibitors and thiazolidinediones (glitazones) can
continue taking the usual doses at the usual times.
•
If on a second or third generation sulphonylurea (glibenclamide, gliclazide, glipizide,
glimepiride), this should be taken at the time of breaking the fast and not before dawn.

404!
Management of normal fasting for T2DM patients on insulin 
•
If on once daily insulin before bed, this can be given as usual
•
If on twice daily short- and intermediate-acting insulin:
o
Before the dawn meal, give the usual evening dose of short-acting insulin without any
intermediate-acting insulin.
o
Before the evening meal give the usual morning dose of short-acting and
intermediate-acting insulin.
•
If on basal bolus regimen:
o Usual doses of the short-acting insulin can be given before the dawn and evening
meals, and usual doses of the intermediate-acting insulin can still be given at 10pm.
o Regular SBGM is essential to ensure prevention of hypoglycaemia
o Titration of doses should occur according to SBGM results.
•
Neither the insulin injection nor the breaking of the skin for SBGM will break the fast.
Management of other fasting types  
Table 19.4: Types of Fasting and Recommended Diabetic Treatment 
Treatment regimen 
Fasting regimen 
When to take antidiabetic 
agents 
Diet only 
Total, normal of partial fast 
Not applicable 
Metformin, Thiazolidinediones 
Normal or partial fast 
With meals 
Insulin secretagogues 
Sulphonylureas  
Partial fast 
Before meals 
Daily intermediate or long-acting 
insulin 
Partial fast 
Before first meal 
Multiple insulin doses using 
intermediate and short acting insulin 
Avoid fasting 
Not applicable 
Long-acting plus bolus fast acting 
insulin 
Avoid fasting or partial fast 
Lantus am and analogue 
with meals  
19.3 Hyperglycaemia in Pregnancy 
Gestational Diabetes Mellitus (GDM) is any degree of glucose intolerance first recognized in 
pregnancy. Diabetes in pregnancy refers to those with pre-existing diabetes, whether diagnosed or 
not. 
Screening at first antenatal visit 
•
Perform screening in all women at the first antenatal clinic attendance if they have:
o BMI > 25 kg/m2
o previous history of GDM
o previous big baby
o poor obstetric history
o family history of DM
o known impaired glucose
tolerance/impaired fasting
glucose.
o grand multipara
o glycosuria.
•
Women in early pregnancy with levels of HbA1c≥6.5% or blood glucose levels fasting ≥7.0
mmol/l or two hours ≥11.1 mmol/l which are diagnostic of diabetes should be treated as
having pre-existing diabetes.
•
Women with HbA1c 6.0–6.4%, fasting glucose 5.1– 6.9 mmol/l or two-hour glucose 8.6–11.0
mmol/l should be assessed to determine the need for immediate home glucose monitoring
and, if the diagnosis remains unclear, assessed for gestational diabetes by 75 g oral glucose
tolerance test (OGTT) at 24–28 weeks.
Screening later in Pregnancy 
•
All women with risk factors (see above) should have a 75 g OGTT at 24–28 weeks
•
A fasting plasma glucose at 24–28 weeks is recommended in low-risk women
Non-pharmacological Treatments 
•
All women intending to become pregnant should:

405!
o Be encouraged to achieve excellent glycaemic control using glucose monitoring of both
fasting and postprandial values
o Be prescribed high-dose (5mg) pre-pregnancy folate supplementation, continuing up to
12 weeks’ gestation
o Have an eye exam and be informed of the risk of developing and/or progression of
diabetic retinopathy
o Have a kidney assessment (random urine albumin/creatinine ratio and serum
creatinine) and referred if urine protein ≥ 1g.
•
A combined health-care team (obstetrician, diabetologist or internist, diabetes educator,
pediatrician/neonatologist) is required.
•
Review SMBG, blood pressure and urine protein and ketones by dipstick at each visit and
eye examination in each trimester.
•
Target glycaemia:
o Preprandial blood glucose 3.5–5.5mmol/L
o Postprandial blood glucose 5–7.5mmol/L
•
Lifestyle management is the preferred means of managing gestational diabetes.
o Diet is based on the principles of optimal nutrition and controlled weight gain.
o Exercise can be helpful in lowering BG levels: the most acceptable form of exercise for
most women is walking in their normal daily routine.
•
Glucose-lowering therapy should be considered in addition to diet where fasting or two
hours glucose levels are above target, for example, where two or more values per fortnight
are:
o fasting or preprandial ≥5.5 mmol/L, or two hours postprandial ≥7 mmol/L at ≤35 weeks
o fasting or preprandial ≥5.5 mmol/L, or two hours postrandial ≥8 mmol/L at >35 weeks
o any postprandial values are >9 mmol/L.
•
When pharmacologic treatment of gestational diabetes is indicated, insulin and oral
medications are equivalent in efficacy, and either can be an appropriate first-line therapy.
Pharmacological Treatment 
A: metformin 500 mg 12hourly, maximum 2000mg in 2–3 doses 
OR 
A: glibenclamide 2.5mg 24hourly to a maximum of 10mg daily 
Note 
Oral hypoglycaemics (except for metformin and glibenclamide) are contraindicated in pregnancy 
Insulin  
The rapid-acting insulin analogs (lispro and aspart) lower postprandial blood glucose and decrease 
the risk of nocturnal hypoglycemia. Patients on lispro and aspart prior to conception may continue 
them during pregnancy. Patients on regular insulin may be switched to lispro or aspart if 1–hour 
postprandial blood glucose levels are above target and/or the patient is also experiencing pre-meal 
or nocturnal hypoglycemia.  
Postnatal Follow Up 
•
Women with gestational diabetes should be screened at 6–12 weeks postnatal to ensure
return to normal glucose tolerance. Thereafter, a 1–2 yearly follow up is recommended.
•
Metformin and glibenclamide may be used even if a woman is breastfeeding.  Encourage
women to breastfeed.
•
If retinopathy, check eyes 1 year postpartum
19.4 Diabetes and HIV 
The management of people with both diabetes and HIV need to consider the following: 
•
ARVs are associated with increased metabolic dysfunction, including insulin resistance,
dyslipidemia and lipodystrophy
•
Protease inhibitors (PIs) increase insulin resistance and reduce insulin secretion by
interfering with GLUT–4 mediated glucose transport
•
Standards of treatment and management of diabetes for patients with HIV are generally the
same as those for diabetic patients without HIV and patients who acquire HIV may continue
to be managed with the same drug therapy as before

406!
•
Sulfonylureas may not be effective in the face of severe insulin resistance. In case glycemic
control deteriorates, insulin should be initiated, rather than increasing dosage or number of
oral medications
•
People who are on ARTs need to be screened for diabetes at least once a year and
especially if they have other CVD risk factors
19.5 Diabetes and Tuberculosis 
Diabetes and tuberculosis are interlinked as follows: 
•
People attending TB clinics should be screened for diabetes and those attending diabetes
clinics should be screened for TB if presenting with symptoms.
•
Diabetes may be associated with delayed sputum conversion (>60 days), higher probability
of tuberculosis treatment failure, higher recurrence and relapse rates, higher overall
mortality, higher rates of multi-drug resistance TB and more atypical presentation in
hyperosmolar hyperglycemic nonketotic coma or ketoacidosis
•
For both conditions, controlling blood sugar, being more physically active, avoiding chronic
stress, getting enough sleep and maintaining ideal weight are recommended.
Review Drug Requirements 
•
Rifampicin is a potent hepatic enzyme-inducing agent, accelerates the metabolism of oral
hypoglycemic agents and shortens the plasma half-life of sulphonylureas
•
Isoniazid antagonizes sulphonylureas, impairs insulin release and action and leads to
increased requirement of insulin and oral antidiabetic medication
•
Therefore, people with diabetes may require an increase in dosage of antidiabetic
medication if they develop tuberculosis.
Use Oral Antidiabetic Medicines Carefully in Tuberculosis 
•
People with diabetes mellitus and tuberculosis should be treated with insulin injection, or in
case a diabetic with tuberculosis is on oral hypoglycemic agents, it may be necessary to
switch to insulin.
•
Tuberculosis affects both the liver and pancreas: oral antidiabetic drugs are contraindicated
in hepatic disease, which is a common adverse effect of antituberculous therapy.
•
Metformin produces weight loss, particularly in high doses, and it is also an anorectic.
•
Marked weight loss and higher insulin and caloric needs in tuberculosis are other important
indications for reviewing oral antidiabetic therapy in diabetes mellitus.
19.6 Hypoglycaemia 
Hypoglycaemia is defined as blood glucose <3.9mmol/L. 
Diagnostic Criteria 
•
Hunger
•
Sweating
•
Trembling or shaking
•
Anxiety
•
Dizziness
•
Lightheadedness
•
Palpitation
•
Numbness around the lips and fingers
•
Headache
•
Confusion
•
Lack of concentration
•
Weakness
•
Changes in behaviour (e.g. irritability,
tearfulness, crying), paraesthesiae.
Patients may also present with convulsions, seizures or coma due to delayed corrective action or 
impaired hypoglycaemia awareness where the patient loses the ability to detect the early 
symptoms of hypoglycaemia due to repeated episodes of mild hypoglycaemia or long duration of 
diabetes leading to loss of adrenergic and glucagon response, with eventual loss of adrenergic and 
neuroglycopaenic symptoms.  
Non-pharmacological 
Treatment for conscious Patients: 
Quickly take a glass of a sugar-rich drink 
OR  
Eat one table spoon of sugar or honey 
AND 
Have a meal. 

407!
If symptoms persist after 5 minutes repeat the above. 
Treatment for unconscious Patients: 
C: 50% dextrose (IV) (40–50ml) 
OR 
C: 10% dextrose (IV) (200–300ml). 
•
Repeat if patient is not responsive or if after 15 minutes, the blood glucose is
still below 4mmol/l.
•
Follow by 8–10 % glucose infusion. Use 5% dextrose if the higher
concentrations are not available.
OR  
S: glucagon (IM or SC) 1mg stat 
Note 
 If IV access is impossible, consider nasogastric tube or rectal glucose 
On Recovery 
•
Give long-acting carbohydrate snack e.g. a piece of bread
•
Identify the cause of hypoglycaemia and correct it
•
If hypoglyceamia is a result of long acting suphonylureas, long- or intermediate acting insulin or
alcohol, frequently monitor blood glucose (2hourly) and give IV dextrose infusion (5–10%) for 12–
24 hours
•
If patient is not responding look for another cause or refer.
19.7 Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic States 
These are acute metabolic complications of diabetes mellitus that may lead to severe dehydration, 
altered level of consciousness and electrolyte imbalance. The presence of acidosis, ketonemia and 
ketonuria in diabetic ketoacidosis (DKA) differentiates it from hyperglycemic hyperosmolar state 
(HHS). 
Symptoms 
•
Nausea/vomiting
•
Shortness of breath
•
Obtundation/drowsiness
•
Thirst/polyuria
•
Fruity smellingbreath
•
Confusion
•
Abdominal pain
•
Fever
•
Altered mental function
•
Dehydration
•
Lethargy
•
Coma
Note 
•
When you suspect DKA, confirm diagnosis immediately
•
All patients minimum should be admitted in hospital for intensive management
Table: 19.5: Diagnostic Criteria for DKA and HHS 
Parameter 
Mild DKA 
Moderate DKA 
Severe DKA 
HHS 
Blood Glucose 
>13.9
>13.9
>13.9
>30
Arterial PH 
7.25-7.3 
7.00-7.24 
<7.00 
>7.30
Serum bicarbonate 
15-18
10-15
<10 
>18
Urine ketones 
Positive 
Positive 
Positive 
Small 
Serum ketones 
Positive 
Positive 
Positive 
Small 
Serum osmolality 
Variable 
Variable 
Variable 
>320
Alteration in sensorium 
Alert 
Alert/drowsy 
Stupor/coma 
Stupor/coma 
Investigations 
Apart from the ones in the table above, check serum electrolytes, urea and creatinine. 
DKA and HHS Treatment 
Treatment of DKA and HHS is similar. 
•
Frequent monitoring of patients
•
Improvement of circulatory volume and tissue perfusion

408!
•
Replacement of electrolyte losses (potassium)
•
Administration of insulin
•
Careful search and management of the precipitating causes
With proper treatment, the average time to resolution is between 10–18 hours for DKA and ~9–11 
hours for HHS. 
I.
Fluid management protocol
•
The first step - infusion of isotonic saline to expand extracellular volume and stabilize
cardiovascular status. Fluid replacement alone results in:
o Improvement of hyperglycemia, reduce insulin resistance
o lowering the plasma osmolality,
o reducing vasoconstriction and improving perfusion,
o restores renal perfusion
o Reduce insulin resistance by ↓ stress/counterregulatory hormone levels
•
Both DKA and HHS patients have severe volume depletion -- estimated water deficit of
100mls/kg body weight
•
Usual initial fluid → isotonic saline (0.9% NaCl)
•
Optimal rate of fluid infusion depends on the clinical state of the patient. On average
15 to 20 ml/kg/hour (about 1000 ml/hour) max. <50ml/kg in the first four hours.
For children 
o Detailed management of DKA is presented in the alogarithm for management of
paediatric diabetic ketoacidosis in low resource centre below.
o Give NS or RL for 48 hours
o Fluid Requirements = DEFICIT + 48 hours’ maintenance
Table: 19.6: Maintenance Fluid 
Age 
(years) 
Weight 
(kg) 
Maintenance fluid 
(ml/kg/hr) 
<1 
3-9
80 
1-5
10-19
70 
6-9
20-29
60 
10-14
30-50
50 
>15
>50
30 

409!
II.
Electrolyte management protocol
Almost all patients with DKA or HHS have a substantial potassium deficit.
•
Acidosis –shift to extracellular
•
Urinary losses related to the glucose osmotic diuresis
•
Secondary hyperaldosteronism.
•
Loss is high 3-10mEq/kg
Despite total body potassium deficit, concentration is usually normal or elevated due to 
•
insulin deficiency and hyperosmolality
•
both result in potassium movement out of the cells
•
Insulin treatment reverse distribution
Good approach checks ECG for signs of hyperkalemia (peaked T wave, QRS widening) 
•
Give KCL if signs absent and if K <5.3
•
If Patient oliguric give KCL when K <4 or ECG signs of hypokalemia (U wave)
Table 19.7: Potassium Repletion in DKA and HHS 
K+>5.2 mEq/L 
Do not give K+ initially, but check serum K+ with basic metabolic profile every 
2 h 
K+<3.3 mEq/L 
Hold insulin and give K+ 20-30 mEq/hr until K+>3.3 mEq/L 
K+ = 3.3-5.2 mEq/L 
Give 20-30 mEq K+ in each L of IV fluid to maintain serum K+ 4-5 mEq/L 
Delay insulin treatment until the serum potassium is above 3.3 mEq/L 
•
insulin Rx worsen hypokalemia by driving potassium into the cells.
•
To avoid possible arrhythmias, cardiac arrest, and respiratory muscle weakness
Shock
Reduced conscious level
Coma
Dehydration 5-10%
Clinically acidotic
Vomiting
Dehydration <5%
Clinically well
Tolerating fluids
Follow ABC concept
Give IV Fluids
IV THERAPY
Correct over 48hrs by 0.9% NS
Add 20mmol KL in every 500mls
Give 0.1IU/kg/hr as an infisuion
THERAPY
Start with SC Insulin
Oral fluids e.g. ORS
No Improvement
OBSERVATION
Blood glucose 1-2 hourly
Neurological status 1hourly
Fluid input/output
Serum electrolytes 2hrs after starting IV 
therapy then 4-6 hourly
No Improvement
Reevaluate
Fluid balance + IV therapy
If acidosis manage
Check insulin dose and correct
Consider sepsis
Blood glucose <14
Neurological deterioration
Reduced conscious level
Irritability
Signs of raised ICP
Headache
Slowing heart rate
INSULIN
Maintenance dose of insulin
Child who was on insulin can 
resume normal dose before DKA
Newly diagnosed start insulin as 
shown in table
Change NS to 5% dextrose
Monitoring
Exclude hypoglycaemia
Possible cerebral oedema
IMPROVEMENT
Clinically well
Drinking and tolerating food
Urine ketones may still be positive
Management of Diabetic Ketoacidosis in Low Resource Centre
MANAGEMENT
Give manitol 0.1g/kg
Transfer to ICU
CT Scan when stable

410!
III.
Insulin therapy management protocol
Continuous IV infusion of regular insulin is the treatment of choice
•
Correct hypovolemic shock and hypokalemia if present, before starting insulin
•
Low dose IV insulin for both DKA and HHS
•
Serum potassium <3.3 mEq/L only contraindication for insulin
IV regular/Soluble insulin and rapid-acting insulin analogs are equally effective 
Insulin therapy   
•
Lowers serum glucose concentration (↓ hepatic glucose production>> ↑ peripheral utilization)
•
Diminishes ketone production (reducing both lipolysis and glucagon secretion)
•
Augment ketone utilization.
Conventional Insulin Guidelines  
Both HHS and moderate to severe DKA 
•
IV bolus of regular insulin (0.1 U/kg body weight) followed within 5 minutes by a continuous
infusion of regular insulin of 0.1 U/Kg/hour = 7 U/hour in a 70 kg patient
•
Alternatively, omit bolus dose →continuous IV infusion of regular insulin at a rate of 0.14 U/kg
per hour (equivalent to 10 U/hour in a 70 kg patient)
o But bolus insulin is a priming dose, saturates insulin receptors full before continuous
insulin
o Avoid lag time in achieving steady state insulin levels
ü
In practice -100iu in 100mls of NS titrate in 5-7cc/h in the first 24hours
ü
Or 60iu in 60mls of NS titrate 6-7cc/hour in 24hours
•
Insulin dosing same in DKA and HHS
•
If plasma glucose does not decrease by 2.8-4.2mmol/l in the first hour, increase the infusion
rate of insulin by 50% to 100%
•
Optimal rate of glucose declines 5.5mmol/l/hour
•
Glucose drop not allowed to less than 14mmol/l during first 4-5hrs of treatment.
•
It takes 12-24 hours to clear ketones from circulation after hyperglycemia is controlled
19.8 Diabetes and Cardiovascular Diseases 
Diabetic patients are 2–4 times likely to develop cardiovascular diseases mainly due to 
atherosclerosis and hypertension. 
The clinical spectrum of cardiovascular diseases includes:  
•
Coronary heart disease
•
Angina (which may be silent)
•
Acute coronary artery syndrome
•
Congestive cardiac failure
•
Sudden death
•
Cerebral vascular accident (stroke, transient ischaemic attacks and dementia)
•
Peripheral vascular disease (intermittent claudication, foot ulcer and gangrene).
Assessment (annual) 
•
ECG, Chest X-Ray, if with symptoms/signs of heart failure.
•
Peripheral vascular disease evaluation includes doppler and angiography of lower limbs.
Pharmacological Treatment 
Acute coronary syndrome  
All adults with T2DM and recent acute coronary syndrome and/or coronary stent should receive dual 
anti-platelet therapy for 12 months after the event or procedure:  
A: acetyl salicylic acid (PO) 75–100mg 24hourly 
AND  
D: clopidogrel (PO) 75mg 24hourly 
Note 
•
acetyl salicylic acid is also indicated for primary prevention for people with T2DM >40years with
family history of ischaemic heart disease (IHD), cigarette smoking, obesity, proteinuria, or
dyslipidemia.
•
It is contraindicated in peptic/duodenal ulcer, dyspepsia, heartburn, malignant hypertension,
haemorrhagic stroke.

411!
Hyperlipidaemia 
Statin therapy results in a significant decrease in CVD morbidity and mortality in T2DM and are 
indicated in Type 2 diabetics > 40 years of age, or diabetes for > 10years 
B: atorvastatin (PO) 10mg 24hourly. Dose may be increased to 80mg daily if required. 
OR 
S: rosuvastatin (PO) 10mg 24hourly. Dose may be increased to 40mg daily if required 
Fenofibrate reduces incidence of retinopathy and need for laser surgery, peripheral neuropathy, and 
improvement in proteinuria, suggesting a more generalized effect on microvascular disease 
independent of dyslipidaemia. 
•
Fibrates:
o Should be used in mixed hyperlipidemias which have not responded adequately to diet
or other therapy.
o Are more effective in lowering triglycerides and increasing HDL, but less effective in
lowering cholesterol.
o Should be used with caution in combination with statins.
o Can enhance the effects of warfarin and antidiabetic agents
o Are contraindicated in patients taking Orlistat.
D: fenofibrate (PO) 67–267mg 24hourly
Hypertension  
In people with T2DM, antihypertensive therapy with an angiotensin receptor blockers (ARB) or 
angiotensin-converting enzyme inhibitors (ACEI) decreases the rate of progression of albuminuria, 
promotes regression to normal albuminuria and may reduce the risk of decline in renal function. 
Therefore: 
•
BP-lowering therapy in people with diabetes should preferentially include an angiotensin
converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) e.g.
C: enalapril (PO) 10 – 40mg 24hourly, taken either as a single dose or two divided doses
(enalapril (PO) 5 mg–10mg 12hourly)
OR
C: losartan (PO) initial dose 50mg stat. Maintenance dose; losartan (PO) 25–100mg
24 hourly in single or 2 divided doses.
•
The target level for optimum BP is controversial. It is reasonable to target BP levels of
<140/90 mmHg for people with diabetes, with lower targets for younger people and those at
high risk of stroke. The target BP for people with diabetes and microalbuminuria or
proteinuria remains <130/80 mmHg.
•
Combining an ARB and an ACEI is not recommended.
•
If monotherapy does not sufficiently reduce blood pressure add one of the following:
C: amlodipine (PO) 5–10mg 24hourly
OR 
A: bendrofluazide (PO) 5mg 24hourly 
•
ACE-inhibitors and ARBs should be stopped pre-conception. Diltiazem (PO) 60mg 24hourly
may be a useful substitute.
19.9 Diabetic Peripheral Neuropathy 
All patients should be screened for distal symmetric polyneuropathy starting at diagnosis of T2DM 
and at least annually thereafter.    
Diagnostic Criteria 
•
Unsteady gait
•
Burning, aching pain or tenderness in legs or feet (occurring at rest or at night, not related to
exercise)
•
Prickling sensations in legs and feet (occurring at rest or at night, distal>proximal, stocking
glove distribution)
•
Numbness in legs or feet (distal>proximal, stocking glove distribution)
•
History of previous foot ulceration and/or amputation.

412!
Investigations Test for: 
•
Sensation (10g monofilament or cotton wool)
•
Vibration (128Hz tuning fork)
•
Postural hypotension and pulse (tibial and dorsalis)
•
Inspect foot for structural abnormalities and ulceration.
Pharmacological Treatment  
It is difficult to treat. Some of the drugs used include: 
D: pregabalin (PO) 75-150mg (24hourly–12hourly) for 4weeks 
Tricyclic antidepressants may help 
A: amitriptyline (PO) 25-75mg 24hourly 
OR 
C: imipramine (PO) 100mg 24hourly 
Gastroparesis 
Due to autonomic neuropathy 
C: metoclopramide (PO) 10mg 8hourly 
OR 
D: domperidone (PO) 10mg 8hourly 
Diabetic Foot: 
Give foot care education and advice on appropriate footwear. 
19.10 Diabetic Nephropathy 
It is one of the most important causes of chronic renal failure. Persistent microalbuminuria is both a 
marker for the development of overt nephropathy and cardiovascular risk. Patients with 
microalbuminuria who progress to macroalbuminuria (>300 mg/24 h.) are likely to progress to end–
stage renal disease over a period of years. Patients with diabetes and chronic kidney disease (CKD) 
should be treated with a comprehensive strategy to reduce risks of kidney disease progression and 
cardiovascular disease.  
Non-pharmacological Treatment 
Patients with diabetes and CKD should be advised to: 
Intensify management of modifiable risk factors: 
•
Stop smoking.
•
Treat urinary infection aggressively.
•
Avoid drugs toxic to the kidney.
•
Consume an individualized diet high in vegetables, fruits, whole grains, fiber, legumes, plant-
based proteins, unsaturated fats, and nuts; and lower in processed meats, refined
carbohydrates, and sweetened beverages
•
Undertake moderate-intensity physical activity for a cumulative duration of at least 150
minutes per week, or to a level compatible with their cardiovascular and physical tolerance
Pharmacological Treatment 
•
Renin–angiotensin system (RAS) inhibition is recommended for patients with albuminuria and
hypertension
•
Most patients with T2D, CKD, and eGFR => 30 ml/min per 1.73 m2 would benefit from
treatment with both metformin and an SGLT2i.
•
Patient preferences, comorbidities, eGFR, and cost should guide selection of additional drugs
to manage glycemia, when needed, with glucagon-like peptide-1 receptor agonist (GLP-1 RA)
generally preferred.
A: metformin (PO) 500mg or 850mg (12hourly – 24 hourly); usual maintenance dose: 1g
twice daily
SGLT-2 Inhibitors 
S: empagliflozin (PO) 10–25mg 24hourly 
•
Advise contraception in women who are receiving ACEI or ARB therapy and discontinue
these agents in women who are considering pregnancy or who become pregnant.

413!
•
Monitor serum creatinine and potassium annually and more frequently if there is evidence of
renal impairment.
•
Hyperkalaemia associated with the use of an ACEI or ARB can often be managed by
measures to reduce serum potassium levels rather than decreasing the dose or stopping the
ACEI or ARB immediately
o Avoid potassium-containing salt substitute or food products containing the salt substitute.
o Avoid drugs that can impair kidney excretion of potassium: over-the-counter nonsteroidal
anti-inflammatory drugs, supplements, and herbal treatments
o Avoid constipation by ensuring enough fluid intake and exercise.
o Consider diuretics treatment to enhance the excretion of potassium in the kidneys
especially when there is concomitant volume overload or hypertension.
o Consider oral sodium bicarbonate especially in patients with CKD and metabolic
acidosis.
•
Metformin should not be used once the serum creatinine is > 200µmol/l.
•
Treat blood pressure aggressively with target of <130/80 mmHg.
•
Add diuretics if necessary (but in large doses inhibit insulin release).
19.11 Diabetic Retinopathy 
It is one of the major causes of blindness. Poor glycaemic control, nephropathy, hypertension and 
pregnancy, long duration of diabetes are among the risk factors. It is preventable and its progression 
retarded by improved glycaemic control and blood pressure. Screening for early detection and laser 
therapy can prevent blindness. 
Screening for Diabetic Retinopathy 
For all people with diabetes, yearly screening is necessary for early detection of ocular complications. 
The screening should begin: 
•
Comprehensive eye examination in woman planning pregnancy, and during the first trimester,
preferably at booking of antenatal clinic (ANC). Further screening should be determined by
the degree of retinopathy detected at the initial appointment.
•
Five years after the diagnosis of diabetes for individuals with Type 1 diabetes diagnosed after
puberty (around 14years).
•
At puberty for individuals diagnosed with type 1 diabetes before puberty
•
At the time of diagnosis of diabetes for individuals with type 2 diabetes
For each of the scheduled screening visits, detailed patient’s assessment should include a complete 
ophthalmic examination in the following steps: 
a. Take visual acuity (VA) without and with spectacles
b. If VA less than 6/9 take VA with pin hole
c. Dilate the pupil by using the mydriatic agents (Tropicamide)
d. Identify presence of cataract or other causes of media opacification.
e. Perform retinal evaluation by direct or indirect Ophthalmoscope or Fundus Photography
f. Identify retinal changes, document and if applicable grade the diabetic retinopathy and
maculopathy as shown in Table XX.
g. Explain the results of screening to the patient and schedule rescreening (Table XX).
Table 19.8:Grading of Diabetic Retinopathy for Screening at Community/ Diabetic Clinic: 
Features and Outcome  
Grade 
Features 
Outcome/action 
R0 
No disease 
Rescreen in12 months 
R1 
Mild background DR Including: micro-aneurysms, flame exudates, 
>4 blot haemorrhages in one or both hemifields and/or cotton wool
spots
Rescreen in12months 
R2 
Moderate background DR: >4blot haemorrhages in one 
hemifield 
Rescreen in 6months 
R3 
Severe non-proliferative or pre proliferative DR: >4 blot 
haemorrhages in both hemi fields, intra-retinal microvascular 
anomalies (IRMA),venous bleeding 
Refer to Eye Clinic 
R4 
Proliferative retinopathy, Neovascularization of the Disc (NVD), 
Neovascularization Elsewhere (NVE), vitreous haemorrhage, retinal 
detachment 
Refer to Eye Clinic 
M0 
No macular findings 
Rescreen in 12months 
M1 
Hard exudates within 1–2 disc diameters of fovea 
Rescreen in 6 months 

414!
M2 
Blot haemorrhage or hard exudates within 1disc diameter of fovea 
Refer to Eye Clinic 
P0 
Photocoagulation Laser: Absent 
Refer to Eye Clinic 
P1 
Photocoagulation Absent/Present (Any PRP or evidence of Grid 
Laser 
Refer to Eye Clinic 
U 
Unclassifiable (When there is Cataract, small Pupil, Vitreous 
Haemorrage, Tractional Retinal Detachment or Corneal Opacity 
Refer to Eye Clinic 
KEY: R=Retinopathy; M=Maculopathy; P=Photocoagulation, U=Unclassified 
At all times, remind patients to stop smoking and intensify blood pressure, lipids and glycaemic 
control. 
19.12 Thyroid Disorders 
Thyroid disorders are conditions that affect the thyroid gland. There are specific kinds of thyroid 
disorders that includes hypothyroidism, hyperthyroidism, goiter, thyroid nodules and thyroid 
cancer.  
19.12.1 Hypothyroidism 
Hypothyroidism is a condition in which a person's thyroid hormone production is below normal. 
Common causes of the disease are chronic autoimmune thyroiditis, post-surgery and post 
radioactive iodine.   
Diagnostic criteria  
The symptoms depend on the deficiency of thyroid hormone, but can include: 
•
Increased cholesterol levels,
•
Depression
•
Fatigue
•
Hair loss
•
Memory loss
•
Dry, rough skin
•
Constipation
•
Hoarse voice
Investigation 
A blood test is used to confirm hypothyroidism 
Indications for Treatment 
•
TSH level persistently >10mU/L; treat all patients due to, increased likelihood of progression
to overt disease and a higher risk of congestive heart failure, cardiovascular disease and
mortality.
•
TSH levels (4.5–10mU/L); consider, treatment in patients younger than 65 with increased
cardiovascular risk (e.g., previous cardiovascular disease, hypertension, documented
diastolic dysfunction, atherosclerotic risk factors (dyslipidaemia, diabetes mellitus, smoker),
goitre, positive antithyroid peroxidase antibodies, evidence of autoimmune thyroiditis by
ultrasound, pregnancy, or infertility), particularly when TSH level is persistently >7mU/L.
•
Levothyroxine therapy could be considered also for symptomatic middle-aged patients for a
short period of time. If a clear beneficial effect is observed, levothyroxine therapy could be
maintained.
•
Persistently mildly increased TSH levels (>4.5–10mU/L) with positive Thyroid Antibody and
thyroid sonographic findings typical of autoimmune thyroiditis.
Pharmacological Treatment 
Initial dose:  
Clinical hypothyroidism– 
D: levothyroxine 1.6–1.8µg/kg ideal body weight 
Subclinical hypothyroidism– 
D: levothyroxine 1.1–1.2µg/kg is recommended 
•
Take at least after 2hours fast, 30minutes before food intake. Alternatively, at bedtime (3 or
more hours after the evening meal).
•
When initiating therapy in young healthy adults with overt hypothyroidism, consider beginning
treatment with full replacement doses
•
Routine use of combined therapy with levothyroxine and triiodothyronine for hypothyroid
patients is not recommended

415!
•
Assess TSH and adjust dosage when there are large changes in body weight, with aging, and
with pregnancy.
•
There is no convincing evidence to support routine use of thyroid extracts, L-T3 monotherapy,
compounded thyroid hormones, iodine containing preparations, dietary supplementation, and
over the counter preparations in the management of hypothyroidism.
Monitoring 
•
TSH monitoring 6–8weeks after any levothyroxine dose change, and yearly life–long
monitoring once euthyroidism is achieved (target TSH 0.2–4.0um/l). FT4 can be measured in
early stages of treatment.
•
In patients with central hypothyroidism, assessments of serum free T4 should guide therapy
and targeted to exceed the mid normal range value for the assay being used.
•
Wait for TSH equilibration–TSH equilibration requires eight to 12 weeks after any thyroxine
dosage change. Once a stable dose is achieved–yearly TSH is sufficient.
In Pregnancy  
When the elevation of the TSH level is confirmed, free T4 should be measured in order to classify 
the hypothyroidism as clinical or overt (OH) and subclinical (SH).  
•
TSH > 2.5–10.0mU/L with normal free T4: SH.
•
TSH > 2.5 –10.0mU/L with low levels of free T4: OH.
•
TSH =10.0mU/L, despite the level of free T4: OH
Women in reproductive period should be euthyroid before conceiving, as the hypothyroidism is 
associated with neural development. Dose may be doubled during pregnancy and returned to 
normal dose after delivery  
19.12.2 Hyperthyroidism 
Hyperthyroidism is a condition in which an overactive thyroid gland is producing an excessive 
amount of thyroid hormones that circulate in the blood. Graves' disease, multinodular goiter 
(TMNG), inflammation of the thyroid gland (thyroiditis) and excessive iodine intake are the most 
common cause of hyperthyroidism.  
Diagnostic criteria  
Hyperthyroidism can be suspected in patients with 
•
Tremors
•
Excessive sweating
•
Smooth velvety skin
•
Fine hair
•
A rapid heart rate
•
An enlarged thyroid gland
•
Frequent bowel movements
Investigations 
•
Baseline complete blood count, including white count with differential, and a liver profile
(bilirubin and transaminases)
•
Differential white blood cell count should be obtained during febrile illness and at the onset
of pharyngitis in all patients taking antithyroid medication. Routine monitoring of white blood
counts is not recommended
•
Test for THS and T4
•
When thyrotoxicosis is confirmed, if cause is not known request thyroid uptake scan
Note 
Management of hyperthyroidism depends on the cause 
19.12.3 Toxic Multinodular Goitre or Thyroid Antibody Positive 
Patients with overtly Toxic multinodular goitre or Thyroid antibody are treated with either: 
Non-pharmacological Treatment 
S: Radio iodine (131-I) therapy 
OR  
S: Thyroidectomy 
Note 
Long term, low-dose carbimazole should not be used for either conditions except in some elderly 

416!
Surgery 
•
Patients with overt hyperthyroidism should be rendered euthyroid prior to the procedure with
carbimazole pre-treatment (15–40mg daily, divided into 2–3doses a day for 4–8 weeks then a
maintenance dose of 5–15mg, taken once daily) with or without beta–adrenergic blockade
(e.g. propranolol 1—40mg 6hourly). Preoperative iodine should not be used in this setting.
•
Following thyroidectomy for Toxic multinodular goitre, it is suggested that serum calcium or
intact parathyroid hormone levels be measured, and that calcitriol and oral calcium
supplementation (maximum 1,200mg of calcium per day in two divided doses) be
administered based on these results.
•
Following surgery for Toxic multinodular goitre, thyroid hormone replacement should be
started at a dose appropriate for the patient’s weight (0.8µg/lb or 1.7µg/kg) and age, with
elderly patients needing somewhat less. TSH should be measured every 1–2months until
stable, and then annually.
Radioiodine 
•
Radioactive iodine therapy should be used for retreatment of persistent or recurrent
hyperthyroidism following inadequate surgery for Toxic multinodular goitre or Thyroid
antibody.
19.12.4 Grave’s Hyperthyroidism 
Patients with overt Graves’ hyperthyroidism should be treated with: 
Medicine 
Initial therapy  for 4–6 
weeks 
Maintenance therapy   
(gradual reduction over 3–6 months from initial dose) 
C: carbimazole 10–60mg/day in 2-3 
divided dose  
5–10mg/day  
Continue for approximately 12–18months, then taper or 
discontinue if TSH is normal.  
Beta Blockers are used for excessive sympathetic symptoms. 
A: propranolol (PO) 40 to 120mg (24hourly or 12hourly) 
OR  
B: atenolol (PO) 50–100mg 12hourly 
Factors which favour use of antithyroid medicines 
•
High likelihood of remission (patients, especially females, with mild disease, small goitres,
and negative or low-titre TSH-receptor antibody)
•
Elderly or others with comorbidities increasing surgical risk or with limited life expectancy or
unable to follow radiation safety regulations
•
Previously operated or irradiated necks
•
Moderate to severe active Graves’ ophthalmopathy
Radioactive Iodine  
Potassium iodide (B) should be given in the immediate preoperative period as 5–7drops (0.25–
0.35 mL) Lugol’s solution (8 mg iodide/drop) or 1–2 drops (0.05–0.1 mL) saturated solution of 
potassium iodide (50 mg iodide/drop) three times daily mixed in water or juice for 10 days before 
surgery 
Factors which favour use of radioiodine 
• Individuals 
with 
comorbidities 
increasing surgical risk 
•
Patients with previously operated or
externally irradiated necks
•
Lack of access to a high-volume
thyroid surgeon
•
Contraindications
to 
antithyroid 
medicines use
•
Females who are not pregnant and
are not planning a pregnancy in the
future 
(4–6months) 
following
radioiodine therapy
Surgery  
Consider the following factors 
•
Symptomatic compression or large goitres
•
Low uptake of radioactive iodine
•
Thyroid malignancy is documented or suspected or large non-functioning nodule
•
Coexisting hyperparathyroidism requiring surgery

417!
•
Females planning a pregnancy in <4–6months
•
Patients with moderate to severe active Graves’ ophthalmopathy
•
If a patient with Grave’s disease becomes hyperthyroid after completing a course of
carbimazole, consideration should be given to treatment with radioactive iodine or
thyroidectomy. Low-dose carbimazole treatment for longer than 12–18months may be
considered in patients not in remission who prefer this approach but evidence is that
remission rate in adults is not improved by a course of medicines longer than 18 months
•
Whenever possible, patients with Grave’s disease undergoing thyroidectomy should be
rendered euthyroid with carbimazole.
19.12.5 Thyroid Storm (Crisis) 
Thyroid storm is one of the most life-threatening endocrine emergencies, resulting from 
exacerbation of manifestations of thyrotoxicosis.  
Triggers of thyroid storm include: 
•
Antithyroid withdraw
•
Acute infections
•
Thyroidal or nonthyroidal surgeries
•
Iodinated contrast dyes
•
External beam radiation therapy.
•
It should be considered in very sick patients if they present with recent history of
thyrotoxicosis and a recent history of precipitating factor.
Patients with thyroid storm (tachycardia, arrhythmias, congestive heart failure, hypotension, 
hyperpyrexia, agitation, delirium, psychosis, stupor and coma, as well as nausea, vomiting, 
diarrhoea, and hepatic failure) should receive a multimodal treatment including:  
•
Beta-adrenergic blockade
•
Antithyroid medicine therapy
•
Inorganic iodide
•
Corticosteroid therapy
•
Aggressive cooling with
acetaminophen and cooling blankets
•
Volume resuscitation
•
Respiratory support
•
Monitoring in an intensive care unit.
Thyroid storm is not a matter of thyroid levels increased beyond those of uncomplicated 
thyrotoxicosis, but the systemic decompensation that occurs. 
Table 19.7: Pharmacological Treatment 
Medicine 
Dosing 
Comment 
D: propylthiouracil* 
500–1000mg load, then 
250mg 4hourly 
Blocks new hormone synthesis Blocks 
T4–to–T3 conversion  
C: carbimazole 
40–60 mg/day 
Blocks new hormone synthesis 
A: propranolol 
60–80mg every 4hourly 
Consider invasive monitoring in congestive heart 
failure patients  
Blocks T4–to–T3 conversion in high doses.  
Alternate medicine: esmolol infusion  
B: iodine (saturated 
solution of potassium 
iodide)  
5drops (0.25mL or 250mg) 
(PO) 6hourly 
Do not start until 1hour after antithyroid medicines  
Blocks new hormone synthesis  
Blocks thyroid hormone release  
A: hydrocortisone 
300 mg intravenous load, 
then 100mg  
8hourly 
May block T4–to–T3 conversion  
Prophylaxis against relative adrenal insufficiency 
Alternative medicine: dexamethasone  
Note 
In thyroid storm, propylthiouracil is preferred to carbimazole 

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19.13 Cushing's Syndrome 
Cushing syndrome is a clinical condition resulting from prolonged exposure to excessive 
glucoccorticoids from either endogenous or exogenous sources. The most common cause of 
Cushing’s syndrome is from the administration of exogenous sources. 
Classification 
Cushing syndrome can be divided into two categories based on pathophysiology, ACTH dependent 
or ACTH – Independent 
•
ACTH-dependent States
o
Pituitary Adenoma (Cushing’s Disease) 90-95%
o
Ectopic ACTH Syndrome
•
ACTH-independent States
o
Adrenal adenoma
o
Adrenal carcinoma
•
Exogenous Sources
o
Glucocorticoid intake
•
Psychiatric Conditions (Pseudo-Cushing Disorders)
o
Depression
o
Alcoholism
•
High Cortisol Secretion Rate without Convincing Clinical Features of Cushing Syndrome
•
Pregnancy
Symptoms and signs of Cushing’s syndrome 
•
The symptoms and signs of Cushing's syndrome result directly from chronic exposure to
excess glucocorticoid
•
Establishing the diagnosis is often difficult because none of the symptoms or signs are
pathognomonic of the syndrome.
•
An important clinical clue to the presence of glucocorticoid excess is the simultaneous
development and increasing severity of several of these symptoms
•
Common presenting symptoms include
o Central obesity
o Facial plethora
o Weakness of the proximal muscles
o Easily bruises and striae
o Hirsutism
o Glucose intolerance
Diagnosis of Cushing’s syndrome  
At least two first-line tests should be abnormal to establish the diagnosis of Cushing's syndrome 
•
The low-dose dexamethasone suppression tests
•
24hrs urinary cortisol,
•
Late night salivary cortisol
•
Differential Diagnostic Testing to established, the cause of Cushing’s syndrome
o Morning serum ACTH
o High dose dexamethasone suppression test
Imaging diagnosis 
•
Pituitary CT - sensitivity of about 50% for identifying microadenomas
•
MRI pituitary   sensitivity up to 100%
•
Adrenal ultrasonography/CT for suspected Adrenal source
Treatment of Cushing’s syndrome 
Without therapy, Cushing’s syndrome is often fatal. 
•
Typically, due to CV, HTN or infectious complications.
•
With therapy Symptoms improve over 2-12 months.
Definitive Therapy 
Surgery by source when possible 
•
Adrenal source - Adrenalectomy
•
Pituitary source - Transphenoidal resection
•
Ectopic source - Tumor Resection

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Medical therapy 
S: metyrapone (PO) 30mg/kg, maximum dose 3,000mg, administered at midnight usually 
with a snack 
19.14 Prolactinoma 
Are prolactin – secreting pituitary tumors 
Classification 
May present as Microprolactinomas (<10mm) or Macroprolactinomas (>10mm) 
Clinical Presentation 
Symptoms are due to hyperprolactinemia which include galactorhea, oligo/amenorrhea, infertility, 
reduced libido, impotence and gynacomastia in male, headache and visual abnormality in large 
adenomas. 
Diagnosis 
Serum prolactin levels 
<100ng/ml possible prolactinoma 
100-200ng/ml likely prolactinoma
>200 ng/ml –diagnostic of prolactinoma
Treatment 
Proactinomas are unique among pituitary tumors in that first line treatment is medical not surgical. 
The mainstays of management for prolactinomas are the dopamine agonist which are: 
C: bromocriptine (PO) 2.5-20mg (24hourly or 12hourly) 
OR 
S: cabergoline (PO) 0.25-1mg (twice a week) 
19.15 Diabetic Insipidus (DI) 
DI is a disorder of water balance caused by non-osmotic renal loss of water leading to excretion of 
large volume of dilute urine  
Classification 
Central DI: Is caused by either complete or partial deficiency of antidiurectic hormone (ADH) 
secretion from the posterior pituitary gland 
Nephrogenic DI: Is caused by end organ unresponsiveness of the kidney to ADH 
Dipsogenic DI: Is caused by excessive and inappropriate fluid intake due to a defective in thirsty 
mechanism 
Clinical Presentations 
Polyuria especially nocturnal 
Diagnostic criteria 
•
Polyuria and urine osmolality of <300 for a given plasma osmolality
•
Volume depletion and orthostatic hypotension may be found
•
Plasma Sodium may be normal or elevated
Pharmacological Treatment 
In case of water deficit - water replacement. Treating of the underlying defect 
Central DI: 
S: desmopressin (IV) 2-4 µg/day divided 12hourly 
OR 
S: desmopressin (PO) Initial dose 0.05mg 12hourly; effective range: 0.1-1.2mg divided 8-
12hourly  
OR 
D: desmopressin (Intranasal) 10-40µg (0.1-0.4mL) 24hourly, either as a single dose or 
divided into 2 or 3doses; usual dose is 20µg (0.2mL) 24hourly in 2divided doses 
Nephrogenic DI: 
A: thiazide diuretic (e.g bendrofluazide (PO) 5mg 24hourly OR hydroclorothiazide 12.5-
25mg 24hourly)  

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19.16 Pheochromocytoma 
Pheochromocytoma are neuroendocrine tumors arising from catecholamine producing chromaffin 
cells of the adrenal medullar but about 15–20% are extra-adrenal in origin 
Clinical presentation 
•
The classic symptoms of pheochromocytoma are due to episodic release of excess
catecholamines into circulation (Norepinephrine and Epinephrine)
•
Typical symptoms
o headaches
o palpitations
o anxiety and diaphoresis
o hypertension which can be paroxysmal (∼48%) or persistent (∼29%).
       Table: Biochemical Tests Comparisons 
Test 
Sensitivity 
Specificity 
Urine Catecholamine 
83 
88 
Urine Total Metanephrines 
76 
94 
Urine Catecholamines + Metanephrines 
90 
98 
Urine VMA 
63 
94 
Plasma Catecholamines 
85 
80 
Plasma Metanephrines 
99 
89 
Tumor Localization 
•
Anatomic localization of a catecholamine-secreting tumor should be performed only after
biochemical diagnosis has been confirmed
•
Approximately 85% of catecholamine-secreting tumors are found in the adrenal glands, and
95% are found in the abdomen and pelvis
•
Either CT or MRI are effective for localization of catecholamine-secreting tumors -sensitivity
89 vs 98% resp.
Management of Pheochromocytoma 
•
After definitive diagnosis, the mainstay of definitive therapy is complete surgical resection of
the tumor
•
Prior to planned surgical intervention, the effects of excess catecholamines must be
ameliorated in order to avoid perioperative complications and improve outcome, by using α -
adrenergic antagonists
None selective α-antagonist 
S: phenoxybenzamine (PO) 10mg 12hourly initially; increase to 20-40 mg 8-12hourly 
OR 
Selective α-antagonist 
S: doxazocin (PO) 1-2mg 24hourly 
Combined α + β blockade 
19.17 Disorder of Sexual Development (DSD) 
DSD formerly known as intersex conditions are classified on the basis of genetics and the state of 
gonads. They may be caused by virilization 64XX or under virilization 46XY. As well as mosaism 
(streak Ovary, Ovotestis, dysgentic testis). The most common DSD is Congenital Adrenal 
Hyperplasia (CAH). 
Diagnostic criteria 
•
Infant born with ambiguous or abnormal genitalia
•
Infant with undescended testis, unilateral or bilateral
•
Infant with hypospadias

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Investigations 
•
Serum electrolytes
•
Chromosomal analysis
•
Karyotyping in a male looking male with undescended testis and/or hypospadias whether the
genitalia appears normal or not
•
Endocrine screening
•
Antimurellian Hormone (AMH)
Non-pharmacological Treatment 
Counseling of the parents on  
•
The condition
•
Naming of a child and
•
Gender assignment
Pharmacological Treatment 
Depends on type of the DSD it is either CAH or other forms of DSD (Non CAH DSD) 
CAH DSD 
Salt losing in crisis- 
•
Bolus normal saline (0.9% NaCl) and maintenance,
•
Hypoglycemic 2-4 ml of 10% dextrose
Long-term treatment 
S: fludrocortisone (PO) 0.05-0.3mg 24hourly 
Non CAH DSD 
D: testosterone 50-400mg monthly for 3cycles, then asses +/- 
D: testosterone cream 
19.8 Obesity in Adults 
Diagnosis 
•
Body mass index (BMI) = weight divided by height squared (weight in kg, height in meters)
•
Ideal BMI is from 18.5-24.9: less than 18.5 is underweight, 25-29.9 is overweight and 30+ is
obese.
•
Overweight/obesity increases risk of CVD, type 2 diabetes, pulmonary embolism, gallbladder
disease, colorectal cancer, osteoarthritis, chronic back pain and all-cause mortality, especially
for those with high blood pressure,hyperlipidemia, and hyperglycemia.
•
Individuals living with obesity are subject to considerable stigma, which they may internalize
and experience as shame, depression and anxiety.
•
As part of prevention of non-communicable diseases, for all adults attending health facilities,
height, weight and waist circumference should be measured at least yearly and appropriate
action taken:
o Everyone should be educated on the risks of overweight/obesity and the need to avoid
weight gain by adjusting food intake and engaging in regular physical activity
o Weight loss treatment is indicated for the obese or those overweight with increased
cardiovascular risk (e.g. diabetes, prediabetes, hypertension, dyslipidemia, elevated
waist circumference) or other obesity-related comorbidities.
o Evaluate diet, previous and current physical activity, and disorders of sleep, eating and
mood
o Assess the patient's medication regimen for drugs that may contribute to weight gain and
consider adjustments
o Determine diabetes and CVD risk
▪
High Blood Pressure
▪
Hyperlipidemia
▪
Hyperglycemia
▪
Elevated liver enzymes (Non-alcoholic liver disease)
Non-pharmacological Management 
•
Even modest, sustained weight loss of 3%–5% produce clinically meaningful reductions
in triglycerides, blood glucose, hemoglobin A1c, and the risk of developing type 2 diabetes.

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•
Greater amounts of weight loss will reduce blood 
pressure, improve LDL-Cholesterol
and HDL-Cholesterol, and reduce the need for medications to control BP, blood glucose,
and lipids as well as further reduce triglycerides and blood glucose.
•
Weight loss requires creating an energy deficit through caloric restriction, physical activity, or
both
o Aim for a loss of 5%-10% of baseline weight within 6 months (0·5 kg per week for 6
months: total about 8kg)
o Prescribe a diet to achieve energy deficit of ≥500 kcal/d: may be achieved with dietary
intake of 1200-1500 kcal/d for women and 1500-1800 kcal/d for men (25-30kcal/kg/day)
o The choice of diet should address a patient’s preference and ease of adherence and be
directed towards long-term lifestyle changes that include eating patterns that are
practical, achievable, and sustainable
o Use of very-low-calorie diets (<800 kcal/d) should be advised only under medical
supervision
o Proteins
▪
Aim for approximately 20% of total energy from good quality proteins, lean meats
and whole pulses
▪
Proteins induce a feeling of satiety and any excess is deaminated.
o Fats
▪
Aim for 20% or less of total energy from fats
▪
Avoid saturated fats to reduce the risk of heart problems
▪
Restrict or avoid fried foods
▪
Choose low fat milk.
o Carbohydrates
▪
Aim for 60% of energy from complex carbohydrates
▪
Whole grains, roots & tubers, e.g. sweet potatoes, yams
▪
Limit sugars and honey.
▪
Vegetables e.g. broccoli, mushroom, zucchini, cabbage, lettuce, cucumber, celery
▪
Fruits such as pineapple, apples, cherimoya, peach, grapefruit, watermelon
o Avoid
▪
Alcohol as it provides calories without nutrients, and excessive use is harmful in
many ways
▪
Omit fad diets and other unhealthy practices
•
Tailored physical activity program
o Initially 30 min of moderate intensity 3-5 times per week
o eventually ≥60 min on most days; add muscle strengthening on at least two days/week
o Weight regain following weight loss is reduced by physical activity equivalent to 60 min
of brisk walking daily and lifestyle activity that increases energy expenditure throughout
the day without concern for the intensity or duration can be as effective for weight control
as jogging, swimming, or cycling.
•
Offer behavioural support
o identify cues that prompt overeating or inactivity, and restructure thoughts and
behaviours to prompt healthy responses
o Advise patient to
▪
set goals that specify what, when, where, how, and for how long they will engage in
a selected activity
▪
keep detailed records of food intake, physical activity, and bodyweight
▪
eat breakfast regularly and maintain a consistent eating pattern across weekdays
and weekends
▪
engage family members for ongoing support
▪
participate for ≥6 months in a lifestyle program that assists participants in adhering
to a lower-calorie diet and in increasing physical activity
o For those who have lost weight, prescribe face-to-face or telephone-delivered weight
loss maintenance programs that provide regular contact (monthly or more frequently)
and helps participants to engage in high levels of physical activity (ie, 200–300
min/wk), monitor body weight regularly (ie, weekly or more frequently), and consume
a reduced-calorie diet (needed to maintain lower body weight).
•
Facilitate referral to a specialist team (metabolic obesity clinic and/or metabolic surgery) if
patient:

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o is unable to achieve >= 5% weight loss at 3 months on a lifestyle intervention consisting
of reduced energy/low-energy diet, increased physical activity, and/or pharmacotherapy
o has a BMI ≥40 kg/m2 or BMI ≥35 kg/m2 with obesity-related comorbid conditions and
has not responded to behavioral treatment with or without pharmacotherapy to consider
bariatric surgery
o Monitor the patient's requirements for medication as weight loss progresses, particularly
for antihypertensive and diabetes medications that can cause hypotension and
hypoglycemia.
Pharmacological Treatment  
Drug therapy may be considered for those with a BMI ≥30kg/m2, BMI ≥27kg/m2 with obesity-related 
comorbid conditions, or if patient has not lost 0·5kg per week by 3–6months after lifestyle changes 
S: orlistat (PO) 120mg 8hourly with each main meal containing fat (during or up    to one 
hour after the meal). It inhibits pancreatic and gastric lipase, reducing fat absorption by 
approximately 30% 
•
Anti-obesity pharmacotherapy should be continued beyond 12weeks only if at least 5% of
initial body weight has been lost since starting medication and should be prescribed as an
adjunct to lifestyle interventions.
Innovative strategies for delivery and management of obesity care 
Primary care should be enhanced with: 
•
patient registries and methods for systematic tracking to assess clinical interventions
(electronic health records)
•
care teams to manage patients with chronic illnesses
•
health information systems that support the use of evidence-based practices at the point-of-
care to provide longitudinal care for chronic illnesses.
•
Electronic support
o text messaging to provide outreach, support for behaviour change to patients and
educational messages
o Blood pressure, blood glucose and wi-fi scales, which automatically transmit results from
machine to a server
o smartphones and tablets with weight loss applications to simplify monitoring of food
intake, physical activity, and weight
o interventions by telephone, study-specific website, and email
o Remote support offers flexibility to patients and practitioners and can be scaled up or
down according to patients’ needs.
Hospitals and health professionals as role models 
•
An overweight/obese health worker is less likely to counsel patients with obesity
•
Provide healthy food choices for patients, employers, visitors, and communities, with pricing
incentives
•
Label drinks sold in hospital cafeterias as red, yellow, or green to shift consumption towards
healthier beverages
•
Prohibit fast food outlets in hospital premises
19.19 Physical Activity 
•
Physical fitness is the ability to perform physical activities without undue fatigue and is
achieved through proper nutrition, moderate to vigorous physical activity, and sufficient rest.
•
Physical activity
o Improves insulin resistance, reduces HbA1c by 0.7% in Type II diabetes and protects
against the development of Type II diabetes
o Improves lipid profile, lowers blood pressure and helps maintain appropriate body
weight.
•
Physical activities
o Include:
▪
Those associated with the performance of a job e.g. walking, hauling, lifting,
pushing, carpentry, farming, shoveling, packing boxes, etc.
▪
Those done during free time e.g. structured exercise as well as walking, hiking,
gardening, sport, dance, etc.

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o Require contraction of skeletal muscle and increased energy expenditure above the
resting level.
•
The types of physical activity for optimal fitness include aerobic, muscle-strengthening,
stretching and coordination.
Aerobic Activities 
•
These improve the body composition (fat, muscle and bone) and cardiorespiratory fitness
•
Examples:
o brisk walking, climbing stairs, cycling, swimming, dancing, jogging, running, washing
windows or car, sweeping floors or carpet, vacuuming, mopping, shoveling, digging
ditches, carrying heavy loads such as bricks
o Sports: badminton, golf, tennis, volleyball, swimming, basketball, football, jumping jacks,
jumping rope.
•
For optimal effect, the activity has to be:
o Moderate intensity (a person doing moderate-intensity aerobic activity can talk, but not
sing, during the activity) or vigorous (cannot say more than a few words without pausing
for a breath).
o For at least 30 minutes per day at least five days per week.
Muscle-strengthening Activities 
•
These enable the major muscle groups of the body (the legs, hips, back, chest, abdomen,
shoulders, and arms) to do more work than they are accustomed and thus increase muscle
mass, strength and endurance.
•
Examples: pull-down, pull-ups, push-ups, dips, abdominal crunch/curl-up, calf raises,
jumping, carrying heavy loads, and heavy gardening (digging or hoeing).
•
For optimal effect:
o Each activity should consist of at least 8 repetitions of the movement (e.g. 8 push-ups)
o Each muscle group should be active on at least two days per week.
Stretching Activities 
•
Improve flexibility such as range of motion, e.g. ability to bend down to tie your shoe.
•
Examples: neck flexions, arm rotations, trunk rotations, and stretching of muscles.
Coordination Activities 
•
Improve neuromuscular fitness such as balance, agility and proprioception necessary for
example to prevent falls in the elderly
•
Examples: Standing on the toes of one leg.
Improving Exercise Adoption and Maintenance 
As part of risk factor assessment in disease prevention, the physical activity level of all patients 
attending health facilities should be assessed, followed by brief advice, if required, about 
recommended levels. 

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CHAPTER TWENTY 
CARDIOVASCULAR DISEASE CONDITIONS 
20.1 Prevention of Atherosclerotic Ischaemic Heart Disease and Stroke 
Cardiovascular disease (CVD) prevention is a coordinated set of actions, at the population level or 
targeted at an individual at risk of developing cardiovascular disease, that are aimed at eliminating or 
minimizing the impact of CVDs and their related disabilities. 
Diagnostic/screening Criteria  
Major risk factors for ischaemic cardiovascular and cerebrovascular disease are: 
•
Diabetes mellitus
•
Hypertension
•
Central obesity: waist circumference ≥ 94cm (men) and ≥ 80cm (women)
•
Dyslipidaemia (fasting levels): Total cholesterol > 5 mmol/L, or LDL> 3mmol/L, or HDL< 1
mmol/L in men and < 1.2mmol/L in women
•
Smoking
•
Age: Men >50 years, Women >60 years
•
Family history of early onset cardiovascular disease; Male relatives <55 years and Female
relatives <65 year
Estimation of total cardiovascular risk is important for prevention of CVD in an individual, should be 
adapted to his or her total CV risk: the higher the risk, the more intense the management should be 
(See Table 20.1). 
Table 20.1: Cardiovascular Disease Risk Classification and WHO Risk estimation 
Very 
High 
Risk 
Subjects with any of the following: 
• Documented CVD, clinical or unequivocal on imaging: previous AMI, ACS, coronary
revascularization and other arterial revascularization procedures, stroke and TIA, aortic
aneurysm and PAD. Unequivocally documented CVD on imaging includes plaque on coronary
angiography or carotid ultrasound. It does NOT include some increase in continuous imaging
parameters such as intima–media thickness of the carotid artery.
• DM with target organ damage such as proteinuria or with a major risk factor such as smoking
or marked hypercholesterolaemia or marked hypertension.
• Severe CKD (GFR <30mL/min/1.73m²).
• A calculated CVD Risk Score ≥10%.
High Risk 
Subjects with: 
• Markedly elevated single risk factors, in cholesterol >8mmol/L (>310mg/dL) (e.g. in familial
hypercholesterolaemia) or BP ≥180/110mmHg.
• Most other people with DM (except for young people with type 1 DM and without major risk
factors that may be at low or moderate risk).
• Moderate CKD (GFR 30–59mL/min/1.73m²).
• A calculated CVD Risk Score ≥5% and <10%.
Moderate 
Risk 
CVD Risk Score is ≥1% and <5% at 10years. Many middle–aged 
subjects belong to this category 
Low Risk 
CVD Risk Score <1% 
Non-pharmacological Treatment 
General measures:  
•
Lifestyle modification (refer to table 20.2)
Table 20.2: The Summarized Preventive Measures to be Individualized on Targeted Goals 
Risk factor goals and target levels for important cardiovascular disease risk factor reduction 
1 
Smoking 
No exposure to tobacco in any form. 
2 
Diet 
Reduce dietary sodium intake no more than 1000mmol/L (2.4gm sodium or 6gm 
sodium chloride per day) 
Low in saturated fat with a focus on wholegrain products, vegetables, fruit, and 
fish. 
Reduce alcohol intake to ≤ 2 units/day for men and ≤1 unit for women, not more 
than 5 out of 7days per week (1 unit is equivalent to 25mL of spirits, 125mL of 
wine, 340mL of beer or sorghum beer, or 60mL of sherry). 
3 
Physical activity 
At least 150minutes a week of moderate aerobic exercise (30minutes for 

442!
5days/week) or 75minutes a week of vigorous aerobic exercise (15minutes for 
5days/week) or a combination thereof 
4 
Body weight 
Body weight BMI 18.5–24.9kg/m² 
Waist circumference <94 cm (men) or <80 cm (women) 
5 
Blood Pressure 
<140/90mmHg 
6 
Lipids 
LDL–C is the 
primary target 
Very high risk: <1.8 mmol/L (<70mg/dL), or a reduction of at least 50% if the 
baseline is between 1.8 and 3.5mmol/L (70 and 135mg/dL)  
High risk:<2.6mmol/L (<100mg/dL), o r a reduction of at least 50% if the baseline 
is between 2.6 and 5.1mmol/L (100 and 200mg/dL) 
Low to moderate risk:<3.0mmol/L (<115mg/dL) 
HDL–C 
No target but >1.0mmol/L (>40mg/dL) in men and >1.2mmol/L (>45mg/dL) in 
women indicate lower risk 
Triglycerides 
No target but <1.7mmol/L (<150mg/dL) indicates lower risk and higher levels 
indicate a need to look for other risk factors. 
7 
Diabetes 
HbA1c <7%. (<5.3mmol/l) 
Recommended to repeat CV risk assessment every 5years, and more often for individuals with risks 
close to thresholds mandating treatment. 
Pharmacological Treatment: Forspecific pharmacological treatment for hypertension, diabetes, 
dyslipidemia refer specific sections, respectively. 
20.2 Management of Dyslipidemias 
Lowering blood cholesterol levels using statins is recommended to reduce the impact of 
cardiovascular morbidity and mortality 
Clinical indication for lipid lowering medicine therapy 
•
Established atherosclerotic disease
•
Ischaemic heart disease
•
Peripheral vascular disease
•
Atherothrombotic stroke
Note 
Lipid lowering medicines should be administered in this setting even if the level of cholesterol is 
normal 
•
Type 2 diabetics >40 years of age, or diabetes for >10 years,
•
Existing cardiovascular disease,
•
Chronic kidney disease (eGFR < 60mL/min).
•
CV risks of more than >20% in 10years Such high-risk patients will benefit from lipid lowering
(statin) therapy irrespective of their baseline LDL levels.
Pharmacological Treatment 
B: atorvastatin (PO) 20mg to 80mg 24hourly 
OR 
S: rosuvastatin (PO) 10mg-40mg 24hourly 
AND 
D: fenofibrate (PO) 120mg /160mg /200mg 24hourly 
Note 
•
Criteria for initiating lipid lowering therapy are the same as for HIV uninfected patients. Fasting
lipid levels should be done 3months after starting lopinavir/ritonavir and atazanavir/ritonavir.
•
Patients at high risk (>20% risk of developing a CVS event in 10years) should switch to
atazanavir/ritonavir and repeat the fasting lipid profile in 3 months.
•
Concomitant use of Ezetimibe andAtorvastatin can lead to liver damage and rhabdomyolysis.
•
Fenofibrate indicated Hypertriglyceridemia, in which statin alone is not enough to treat & lower
the hypertriglyceridemia.

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20.3   Chronic Stable Coronary Artery Disease (CSCAD) / ISCHAEMIC Heart 
Disease (IHD) 
Clinical history characterized by chest pain due to myocardial ischaemia usually inducible by 
exercise, emotion, or other stress and reproducible, relieved by rest but may occur spontaneously 
and stable in nature, occurs in high-risk patient.   
Non-pharmacological Treatment 
General Measures 
•
Lifestyle modification (refer to table 20.2).
•
Annual control of lipids, glucose metabolism and creatinine are recommended in all patients with
known IHD.
•
A resting ECG is recommended in all patients at presentation and during or immediately after an
episode of chest pain suspected to indicate clinical instability of CAD, Consider immediate
referral.
•
A resting transthoracic echocardiogram is recommended in some patients for:
a) exclusion of alternative causes of angina
b) regional wall motion abnormalities suggestive of CAD
c) measurement of LVEF for risk stratification purpose
d) evaluation of diastolic function.
Consider referral if no echocardiogram available or unavailability of skilled personnel to perform
transthoracic.
•
Stress ECG
•
Stress Echocardiography; a) Physical (Exercise) Stress Echo; b) Dobutamine (Pharmacological)
Stress Echo performed to Orthopaedic related disorders pt who cannot walk on the Treadmill
machine).
Pharmacological Treatment 
A: acetylsalicylic acid soluble (PO) 75–150mg 24hourly 
AND 
C: isosorbide dinitrate (PO) 20mg-40mg 12hourly 
If nitrates cannot be tolerated, consider stepwise approach below. 
S: ivabradine (PO) 2.5mg /5mg 24hourly 
Step 1: add ß-blocker if not contraindicated: 
B: atenolol (PO) 12.5/25mg 24hourly 
OR 
S: metoprolol tartrate (IV) 5mg 2min for max 3doses, then (PO) 50-100mg 12hourly 
OR 
C: metoprolol succinate (SR) (PO) 25–200mg 24hourly 
OR 
S: bisoprolol (PO) 2.5mg /10mg 24hourly 
Consider long-acting calcium channel blocker, if a ß-blocker cannot be tolerated or contraindicated. 
Step 2: add long-acting calcium channel blocker. 
S: verapamil (PO) 60mg -120mg 8hourly 24hourly 
OR  
D: diltiazem (PO) 60mg 6 to 8hourlydaily; if suspects Prinzmetal Angina. 
Key Points 
•
All patients with chronic stable angina are high-risk for cardiovascular events, lipid lowering
medicines should be initiated (See Section 20.2).
•
Consider immediate referral to high level of care where there are adequate resources for the
case management.
Indications for Referral 
•
Angina or chest pain suspected to indicate clinical instability of CAD
•
When diagnosis is in doubt/ failed medical therapy; no echocardiogram available or
unavailability of skilled personnel to perform transthoracic echocardiogram.

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Before referral when high likelihood of clinical instability of stable CAD consider giving: 
A: acetylsalicylic acid(PO) 300mg stat. 
AND 
B: atorvastatin (PO) 80mgstat 
AND  
D: clopidogrel (PO) 300mg stat 
20.4    Acute Coronary Syndrome 
20.4.1 Unstable Angina (UA) 
Unstable angina is a medical emergency and if untreated can progress to Non-ST Elevation 
Myocardial Infarction (NSTEMI)  
Diagnostic Criteria 
Presents as chest pain or discomfort like stable angina but with the following additional 
characteristics: 
•
Angina at rest or minimal effort, occurring for the first time, particularly at rest and prolonged
>10minutes, not relieved by sublingual nitrates.
•
The pattern of angina accelerates and gets worse.
•
The chest pain may be associated with ST segment depression or T wave inversion or
normal ECG without rise in cardiac enzymes (biomarkers ie. Total Createnine, Creatine -
MB and Troponin).
20.4.2 Non-ST Elevation Myocardial Infarction (NSTEMI) 
Non-ST Elevation Myocardial Infarction is a medical emergency characterized with chest pain that is 
increasing in frequency and/or severity or occurring at rest, associated with elevated cardiac 
enzymes and ST segment depression or T wave inversion or normal ECG.  
Diagnostic Criteria  
Presents with typical chest pain with the following additional characteristics. 
•
Electrocardiogram (ECG) may show ST segment depression or transient ST segment
elevation, or normal ECG does not exclude the diagnosis (serial ECG is important).
•
Raised Cardiac Biomakers – Total Creatine Kinase (Total-CK), Creatine Kinase - MB (CK-
MB) and standard/high sensitive Troponin I or T.
Non-pharmacological Treatment  
Both UA and NSTEMI are medical emergencies with the same pathophysiological progressive 
instability of CAD, which share similar management approach. 
Supportive Therapy 
•
Admit patient into high dependent ward/ICU/CCU for haemodynamic monitoring, bed rest
in Fowler’s position and reassurance.
•
Oxygen via nasal blog cannula or face mask if saturation < 92%.
•
Establish Peripheral Intravenous line for intravenous fluid or drug administration.
•
Haemodynamics blood pressure, heart rate and electrocardiogram rhythm monitor.
Pharmacological Treatment 
Adjunctive therapy 
Control cardiac pain 
C: glyceryl trinitrate (Nitroglycerin) sub–lingual/ spray 0.5mg (make sure patient has not 
taken phosphodiesterase–5 inhibitor). 
For persistent pain and if oral therapy is insufficient. 
S: glyceryl Trinitrate (Nitroglycerin) (IV), 1–2µg/kg/min titrated with chest pain over 8–
24hours. 
OR 
C: morphine (IV)1–2mg/minute dilute 10mg up to 10mL with sodium chloride solution 0.9%. 
Total maximum dose10 mg, repeat after 4hours if necessary 

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Note 
•
If pain is not responsive to this dose, it is suggestive for ongoing unresolved ischaemia. This
requires immediate referral to high level of care where resources available to manage Acute
Coronary Syndrome or to exclude differential diagnosis.
Antiplatelet Therapy 
A: acetylsalicylic acid (PO) 300mg stat then followed by 75mg/100mg 24hourly 
AND 
D: clopidogrel (PO) 300mg /600mg start then followed by 75mg 24hourly 
OR 
S: ticagrelor (PO) 180mg stat. 
For first year following ACS event: 90 mg 12hourly. 
After 1year of maintenance: 60mg 12hourly. 
Statin high dose 
B: atorvastatin (PO) 80mg stat then 40mg 24hourly 
OR 
S: rosuvastatin (PO) 10mg-40mg 24hourly 
Anticoagulant 
B: heparin UFH (IV) 70–100U/Kg body weight a 24hourly 
OR 
S: low molecular weight heparin (SC) 1mg/kg body weight 12hourly 
Beta blocker (ß –blockers) 
In case of LV dysfunction 
C: carvedilol initial dose (PO) 6.25mg 12hourly preferred, titrate the dose upward. Max. 
Dose 25mg 12hourly 
OR  
In the settings of normal LV systolic function 
B: atenolol 25–50mg (PO) 24hourly, 
OR 
S: metoprolol tartrate 5mg (IV) 2min for maximum of 3 doses, then (PO) 50-100mg 
12hourly  
OR 
C: metoprolol succinate (SR) (PO) 25 – 200mg 24hourly. 
OR 
S: bisoprolol (PO) 2.5mg – 10mg 24hourly 
Angiotensin Converting Enzyme Inhibitors (ACEIs) 
B: captopril (PO) 6.25mg–25mg 8hourly 
OR 
C: enalapril (PO) 10mg 12 hourly 
OR  
C: lisinopril (PO) 5mg /10mg 24hourly  
Referral 
High suspicion index of acute coronary syndrome immediate consider referral to high level of care 
where resources are available to manage. In acute settings before referral from low to high level of 
care if available consider giving the following urgently:  
•
glyceryl trinitrate (Nitroglycerin) sub-lingual 0.5mg spray prn for intolerable chest pain
•
acetylsalicylic acid (PO)300mg stat (chew)
•
clopidogrel (PO) 300mg/600mg stat
•
High dose statin simvastatin (PO) 80mg stat OR atorvastatin (PO) 80mg stat
20.4.3 ST Elevation Myocardial Infarction (STEMI) 
STEMI is a medical emergency caused by the complete or partial occlusion of a coronary artery and 
requires prompt hospitalization and intensive care intervention management. 

446!
Clinical Presentation 
Severe chest pain with the following characteristics 
•
Site: retrosternal or epigastric, quality: crushing, constricting, or burning pain or discomfort.
•
Radiation to the neck and/or down the inner part of the left arm.
•
Duration: at least 20 minutes and often not responding to sublingual nitrates.
•
Occurrence: at rest. May be associated with pulmonary oedema sweating, hypotension or
hypertension, arrhythmias.
Diagnostic Criteria  
Simple recognition triage: Two out of three points most likely point to STEMI diagnosis 
•
Symptoms - typical/atypical chest pain
•
ECG – ST elevation in in two contiguous leads ≥0.1mV
•
Raised cardiac biomakers– Total Creatine Kinase (Total-CK), Creatine Kinase -MB (CK-MB)
and Standard/Highly Sensitive Troponin I or T
Non-pharmacological Treatment: 
Supportive therapy  
•
Consider cardio-pulmonary resuscitation if necessary, before transfer (cardiac arrest–
cardiopulmonary resuscitation).
•
Oxygen 40% via facemask, if saturation < 92% or if in distress
•
See section 20.4.2 above on supportive therapy for NSTEMI
Adjunctive therapy 
Control cardiac pain 
C: glyceryl trinitrate sub-lingual/ spray 0.5mg (make sure patient hasn’t taken 
phosphodiesterase-5 inhibitor). 
For persistent pain and if oral therapy is insufficient 
S: glyceryl Trinitrate (IV) 1–2 µg/kg/min titrated with chest pain over 8–24 hours. 
OR 
C: morphine (IV) 1–2 mg/minute dilute 10 mg up to 10 mL with sodium chloride solution 
0.9%. Total maximum dose: 10 mg, repeat after 4 hours if necessary. 
Anti-platelets therapy 
A: acetylsalicylic (PO) 300mg stat then followed by 75mg/100mg (PO) 24hourly 
AND  
D: clopidogrel (PO) 300mg/600mg stat then followed by 75mg 24hourly 
OR 
S: prasugrel (PO) 60mg stat, given after defining coronary anatomy prior to onset of PCI, 
then 10mg as maintenance dosage. 
Statin high dose 
B: atorvastatin (PO) 80mg start then 40mg 24hourly 
OR 
S: rosuvastatin (PO) 10mg-40mg 24hourly 
Anticoagulant 
B: heparin UFH (IV) 70–100U/Kg 24hourly 
OR 
S: low molecular weight heparin (SC) 1mg/kg 12hourly, Reduce dose in renal failure patient 
to 0.5mg/kg 
Beta blocker (ß –blockers) 
In case of LV dysfunction 
C: carvedilol (PO) initial dose 6.25mg 12hourly daily preferred, titrate dose upward to 
maximum dose 25mg hourly daily 
In the settings of normal systolic function 
B: atenolol (PO) 12.5mg or 25mg or 50mg 24hourly 
OR  
S: metoprolol tartrate (IV) 5mg 2min for max 3doses, then (PO) 50-100 mg 12hourly 
OR 

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C: metoprolol succinate (SR) (PO) 25 – 200mg 24hourly 
OR 
S: bisoprolol (PO) 2.5mg – 10mg 24hourly 
OR 
S: verapamil SR (PO) 240 mg – 480 mg daily in 1-2 divided doses 
Note 
Verapamil SR should be initiated from 7 days’ post myocardial infarction; any single dose should 
not exceed 240mg as secondary prevention of myocardial infarction. 
Angiotensin-Converting Enzyme Inhibitors (ACEIs) 
B: captopril (PO) 6.25mg or 12.5mg 8hourly 
OR  
C: enalapril (PO) 10mg 12hourly 
OR 
C: lisinopril (PO) 5mg-10mg 24hourly 
Definitive management of STEMI – Reperfusion therapy (Myocardial reperfusion) 
Myocardial reperfusion with rapid recanalization of infarct related artery is the key to success in the 
management of ST Elevation Myocardial Infarction (STEMI). Timely reperfusion is crucial for 
minimization of infarct size and thereby for preservation of left ventricular function and reduction in 
mortality in STEMI patients. The two main reperfusion strategies for STEMI patients are;  
•
Thrombolytic/Fibrinolytic therapy (preferably chest pain duration less 12 hrs)
•
Primary percutaneous coronary intervention (PPCI) (preferably less than 90 mins of Door to
Needle Time)
Thrombolytic agents 
S: streptokinase (IV) 1.5 million units diluted in 100 mL sodium chloride 0.9%, infused over 
30–60minutes 
OR 
S: alteplase (TPA) (IV) 15mg as bolus, 0.75mg/kg over 30min, then 0.5mg/kg over 60min
Absolute contraindication for Thrombolytics 
•
Previous allergy to streptokinase or used within the last year for streptokinase only.
•
Stroke CVA within the last 3 months
•
History of recent major trauma
•
Bleeding within the last month
•
Aneurysms
•
Brain or spinal surgery or head injury within the preceding month
•
Active bleeding or known bleeding disorder.
Relative contraindication for Thrombolytics 
•
Refractory hypertension
•
TIA in the preceding 6 months,
•
Subclavian central venous catheter
•
Warfarin therapy
•
Pregnancy
•
Traumatic resuscitation
•
Recent retinal laser treatment
Referral is urgent for all suspected or diagnosed cases to high level care equipped with cardiac 
catheterization laboratory for Coronary angiogram (CAG) followed by Percutenous Coronary 
Intervention (PCI). 
20.5 Hypertension 
Hypertension is elevation of Blood Pressure SBP ≥ 140 mmHg and DBP ≥90 mmHg measured 
atleast three separate occasions. Hypertension is a major independent risk factor for the 
development of CAD, stroke, and renal failure. 
Diagnostic Criteria  
Blood Pressure should be measured on three separate occasions, a minimum of 2 days apart and/or 
taken over period of two months. Minimum of 3 blood pressure readings must be taken at the first 
visit to confirm hypertension. 
Ambulatory Blood Pressure monitoring should be done to exclude Masked or white coat hypertension 
and monitoring of Blood Presure response to anti-hypetensives. 

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Table 20.3: Classification of Hypertension 
Class 
of 
hypertension 
SBP 
mmHG 
DBP 
mmHg 
Confirm diagnosis 
Grade 1 
140-159
90-99
After 3 months of life style modification 
Grade 2 
160-179
100-109
Same visit 
Grade 3 
>180
>110
Same visit 
Consider secondary hypertension with identifiable cause in young patients < 40 years or elderly 
patient > 60 years presenting for first time with hypertension. 
Note 
•
Recommend an alternative contraceptive method for women using oestrogen containing oral
contraceptive.
•
Evidence of end organ damage, i.e. cardiomegaly, proteinuria or uraemia, retinopathy or
evidence of stroke, dictates immediate treatment.
Treatment goal of Hypertension 
•
In patients aged 18 - 59 years without major comorbidities, and in patients 60 years or older
who have diabetes, chronic kidney disease (CKD), or both conditions, the blood pressure goal
level should be <140/90 mm Hg.
•
In patients aged 60 years or older who do not have diabetes or chronic kidney disease, the
blood pressure goal level should be <150/90 mm Hg.
Non-pharmacological Treatment 
Lifestyle modification: 
•
Lifestyle modification (refer to table 20.2)
Assess or stratify according to risk factors and target organ damage see figure 20.1 below. 
Figure 20.1:Non-Pharmacological Management flow diagram of hypertension 
Pharmacological Therapy 
First-line treatment without compelling indications, Thiazide diuretics should be initiated.  
Combination therapy may be considered if SBP >20mmHg or DBP> 10mmHg above target. 
Refer Figure 20.2, Algorithm II and Table 20.4 below show choice of anti-hypertensives. 

450!
Figure 20.2: Approach of Pharmacological Treatment of hypertension in Primary Healthcare 
Facility. 

451!
Figure 20.3: Approach of Pharmacological Treatment in Hypertensive Emergency and 
Hypertensive Urgency. 

452!
Table 20.4: Compelling Indications and Anti-Hypertensive Drug Combination 
Compelling indications 
Drug class 
Angina 
Prior or Post–myocardial 
infarct 
• ß–blocker or Long-acting calcium channel blocker
• ß–blocker and ACEI or ARB if patient sensitive to ACEIs
•If ß–blocker contraindicated: Long-acting calcium channel blocker
eg Verapamil Sustained Release / Diltiazem Extended Release.
Heart failure 
Volume overload 
• ACE inhibitor and ß–blocker eg carvedilol
• Diuretics–Loop diuretics eg furosemide and/or spironolactone
*(exclude Renal Failure before adding spironolactone)
Left ventricular hypertrophy 
(confirmed by ECG or 
Echocardiography) 
ACE inhibitor or ARB if patient sensitive to ACEIs 
Stroke: secondary 
prevention 
Hydrochlorothiazide or Indapimide and ACE inhibitor 
Diabetic mellitus 
ACE inhibitor or ARB, usually in combination with diuretic 
Chronic kidney disease 
ACE inhibitor, usually in combination with diuretic 
Isolated systolic 
hypertension 
Hydrochlorothiazide or Long-acting calcium channel 
Blocker 
Pregnancy 
Labetalol, Nifedipine, Methyldopa or Hydralazine (Avoid ACEI/ARB 
due to teratogenic effect) 
Prostatism 
alpha–blockers 
Elderly 
Calcium channel blocker CCB 
Anti-hypertension therapy:  
Thiazide diuretics: Refer Figure 20.2, Step2 above 
Loop diuretics 
B: furosemide initial dose (PO) 40mg 12hourly 
OR 
S: torsemide (PO) 2.5mg /5mg/10mg 24hourly 
Dose can be up scaled depending on congestive status to maximum dose 
Mineralocorticoid (Aldosterone) Receptor antagonist 
C: spironolactone (PO) 25mg 24hourly 
OR  
S: eplerenone (PO) 25mg 24hourly 
Angiotensin Converting Enzyme Inhibitor (ACEI) 
B: captopril (PO) 6.125mg, 12.5mg or 25mg 8hourly 
OR  
C: enalapril (PO) 10mg 12hourly 
Angiotensin Receptor Blocker–ARB (*Do not combine with ACEI, indicated in patient sensitive to 
ACEIs) 
C: losartan (PO) 25mg/50mg 24hourly 
OR 
S: candesartan (PO) 8mg/16mg 24hourly 
OR 
S: telmisartan (PO) 40mg / 80mg 24hourly 
OR 
S: irbesartan (PO) 150mg / 300mg 24hourly 
Note 
The prescription of ARBs should depend on patient’s presenting conditions 
Beta blocker (Beta 1 selective Beta Blocker) 
B: atenolol (PO) 25mg /50mg/ 100mg 24hourly 
OR 
C: metoprolol succinate (SR) (PO) 50- 200mg 24hourly 
OR 
S: metoprolol injection (IV) 1mg/ml in 5ml stat 
OR 
S: bisoprolol (PO) 2.5mg – 10mg 24hourly 

453!
Beta  blocker (Non-selective Beta) 
A: propranolol (PO) 40mg 24hourly 
OR 
C: carvedilol (PO) 6.25mg/12.5mg 24hourly 
OR 
C: labetalol (PO) 100mg 24hourly 
OR 
C: labetalol injection (IV) 5mg/ml in 2ml or 10mg/ml 
Calcium Channel Blocker 
Dihydropyridines:  
B: nifedipine (PO) 10mg/20mg 24hourly 
OR 
B: nifedipine (Slow Release/Long Acting) (PO) 20mg/30mg/ 60mg/90mg/daily 
OR  
C: amlodipine (PO) 5mg or 10mg 24hourly 
OR 
S: nimodipine (PO) 30mg 24 hourly (indicated in subarachnoid hemorrage, less 
anti-hypertensive effect) 
Non–dihydropyridine  
S: verapamil (PO) 30mg 8-12hourly for 24hours 
OR 
S: verapamil (Sustained Release) (PO) 120mg 24hourly (Initial daily dose), 
Maximum dose: 120mg 12hourly (single dose should not exceed 240mg) 
OR 
D: diltiazem (Extended Release) (PO) 60mg / 120mg 24hourly 
OR 
D: diltiazem (PO) 30mg 8-12hourly for 24hours 
Alpha-2 adrenergic agonists 
A: methyldopa (PO) 250mg 24hourly 
OR 
S: clonidine (PO) 50mcg/100mcg 24hourly 
Alpha-1 adrenergic blockers 
S: doxazocin (PO) 1mg / 2mg 24hourly 
OR 
D: tamsulosin (PO) 0.4mg24hourly 
Vasodilators 
B: hydralazine (PO) 25mg 8hourly 
OR 
C: hydralazine (IV) 20mg/ml in 1ml injection 
OR 
S: nitroglyceride/glyceryl trinitrate Injection (IV) 50mg/ml in 10ml 
Fixed Dose Combination (Poly Pills) - FDCs 
C: losartan + hydrochlorothiazide (FDC) (PO) 50mg/12.5mg 
OR 
S: candersatan+hydrochlorothiazide (FDC) (PO) 16/12.5 mg 
OR 
S: telmisartan + hydrochlorothiazide (FDC) (PO) 40/12.5mg, 80/12.5mg 
OR 
S: irbersatan + hydrochlorthiazide (FDC) (PO) 150/12.5mg 
Referral indicated when: 
•
Resistant (Refractory) hypertension suspected,
•
Secondary hypertension is suspected
•
Complicated hypertensive urgency/emergencies,
•
Hypertension with Heart failure.
•
When patients are young (<30 years).
•
Blood pressure is severe or refractory to treatment.

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20.6   Resistant (Refractory) Hypertension 
Hypertension that remains >140/90mmHg despite the use of 3 antihypertensive drugs in a rational 
combination at full doses and including a diuretic i.e. thiazide. Consider all correctable causes of 
refractory hypertension before you refer. 
20.7 Hypertensive Urgency 
Symptomatic severe hypertension SBP 180mmHg and/or DBP >110 mmHgwithout evidence of 
target organ damage, such as pulmonary edema, cardiac ischemia, neurologic deficits, or acute renal 
failure.   
Note 
All patients with hypertensive urgency should be treated in hospital 
Pharmacological Treatment  
The goal is to lower DBP to 100mmHg slowly over 48–72hours. This can be achieved with two or 
more oral agents preferably, Refer to Figure 20.3. 
20.8 Hypertensive Emergency 
A marked elevated systolic blood pressure SBP≥180mmHg and/or a diastolic DBP≥130mmHg 
associated with life threatening situations (target end organ damage) one or more of the following: 
•
Unstable angina/myocardial infarction
•
Hypertensive encephalopathy e.g. severe headache, visual disturbances, confusion, coma,
or seizures which may result in cerebral haemorrhage
•
Acute left ventricular failure with severe pulmonary oedema (extreme breathlessness at
rest)
•
Excessive circulating catecholamine: e.g. pheochromocytoma – rare cause of emergency;
food or drug interaction with monoamine oxidase inhibitors
•
Rapidly progressive renal failure
•
Acute aortic dissection
•
Eclampsia and severe pre-eclampsia
Pharmacological Treatment 
C: labetolol (IV) 20–80mg bolus every 10 minutes or 0.5–2mg/min infusion stat 20 mg, then 
20–80 mg every10 min as needed, or stat with 0.5 mg/min infusion, then 1–2 mg/min (may be 
up to 4 mg/min) IV infusion up to 300 mg/d max.  
Onset: 5–10 min; duration: 3–6 hours 
AND / OR 
S: nitroglycerin (glyceryl trinitrate; highly effective in setting of coronary ischemia, acute 
coronary syndromes. Dose is (IV) 5–100µg/min as infusion  
S: nitroglycerin (IV) initially 5–10 ug/min then may be up to >200 ug/min as needed 
Onset: immediate; Duration: 1–5 minutes 
AND / OR 
C: hydralazine (IV) 5mg slow push over 1–2 minutes, repeat 5–10mg as needed 
20.9 Heart Failure 
Heart Failure is a clinical syndrome characterized by typical symptoms (e.g. breathlessness, ankle 
swelling and fatigue) that may be accompanied by signs (e.g. elevated jugular venous pressure, 
pulmonary crackles and peripheral oedema) caused by a structural and/or functional cardiac 
abnormality, resulting in a reduced cardiac output and/or elevated intracardiac pressures at rest or 
during stress. 
Heart Failure in Pregnancy 
Symptoms and signs of heart failure in a pregnant woman are an indication for urgent assessment to 
establish a diagnosis and appropriate management. This is best accomplished through a 
multidisciplinary approach in which both cardiologists and obstetricians need to participate in order to 
provide expert counselling and care in pursuit of safe motherhood, as well as to exclude underlying 
cause of heart failure.  

455!
Acute Heart Failure (AHF) or Decompensated Acute Heart Failure (ADHF) 
AHF is defined as rapid or gradual onset of signs and symptoms of heart failure that results in urgent 
unplanned hospitalization or Emergency Medicine Department visits. The clinical signs and 
symptoms are significantly life threatening if the above features occur in patients with established 
diagnosis with structurally heart disease categorized as Acute Decompensated Heart Failure 
(ADHF). The cause and immediate precipitating factor(s) of the AHF must be identified and treated to 
prevent further damage to the heart. 
Non-pharmacological Treatment: 
Oxygen therapy and/or ventilatory support. 
•
Non-invasive positive pressure ventilation includes both CPAP and bi–level positive
pressure ventilation (PPV)
•
Mechanical ventilation
Note 
In AHF, oxygen should not be used routinely in non–hypoxaemic patients, as it causes 
vasoconstriction and a reduction in cardiac output 
Pharmacological treatment 
Recommendations for the management of patients with acute heart failure: 
Diuretics: Diuretics are a cornerstone in the treatment of patients with AHF. In patients with new-
onset AHF or those with chronic, decompensated HF not receiving oral diuretics the initial 
recommended dose should be 20–40 mg intravenous furosemide (or equivalent); for those on 
chronic diuretic therapy, initial intravenous dose should be at least equivalent to oral dose.  
Diuretics should either be given as intermittent boluses or as a continuous infusion, and the dose and 
duration should be adjusted according to patients’ symptoms and clinical status. Combination of loop 
diuretic with either thiazide-type diuretic or spironolactone may be considered  
Loop diuretic  
B: furosemide (IV) 20–120mg 24hourly 
OR 
S: torsemide (PO) 5–20mg 24hourly 
AND  
Mineralocorticoid (Aldosterone) Receptor Antagonists: 
C: spironolactone (PO) 25–50mg 24hourly 
OR 
S: eplerenone (PO) 25–50mg 24hourly 
Vasodilators: theseare the cornerstone of treatment of AHF and have dual benefit by decreasing 
venous tone (to optimize preload) and arterial tone (decrease afterload). Consequently, they increase 
stroke volume 
Intravenous vasodilators should be considered for symptomatic relief in AHF with SBP >90 mmHg 
(and without symptomatic hypotension). Symptoms and blood pressure should be monitored 
frequently during administration of intravenous vasodilators. In patients with hypertensive AHF, 
intravenous vasodilators should be considered as initial therapy to improve symptoms and reduce 
congestion. Intravenous vasodilators for treating AHF are described in table 20.4. 
Note 
Vasodilators should be used with caution in patients with significant mitral or aortic stenosis. 
Consider oral vasodilators in case intravenous vasodilator not available or unavailability of intensive 
care or high dependent unit care. 
C: isosorbide dinitrate (PO) 10–20mg 12hourly 
OR 
B: hydralazine (PO) 25mg 6–8hourly. Maximum dose: 200 mg 24hourly 
Inotropes (Inotropic agents): Indicated in patients with hypotension (SBP <90 mmHg or mean 
arterial BP < 60mmHg) and peripheral hypoperfusion. Dosage see table 20.5 below. 

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Vasopressor (norepinephrine preferably):Indicated in patients with cardiogenic shock, despite 
treatment with another inotrope, to increase blood pressure and vital organ perfusion. Dosage see 
table 20.5 below 
Indication: Patients with cardiogenic shock, despite treatment with another inotrope, to increase 
blood pressure and vital organ perfusion. 
Table 20.5: Positive inotropes and/or vasopressors for treat acute heart failure. 
Inotropes 
/ 
Vasopressors 
Bolus 
Infusion rate 
Dobutamine 
No 
2–20µg/kg/min(beta+) 
Dopamine 
No 
3–5 µg/kg/min; inotropic(beta+) 
>5 µg/kg/min:(beta+), vasopressor(alpha+)
Norepinephrine 
No 
0.2–1.0µg/kg/min 
Epinephrine 
Bolus:1mg can be given iv during 
resuscitation, 
Repeated every3–5 min 
0.05–0.5µg/kg/min 
Other Inotropes & inodilators: 
D: digoxin injection (IV) 0.25 mg/mlin 2 ml injection 
OR 
D: digoxin (PO) 0.125mg / 0.25mg 
Special pharmacological treatment consideration: 
Add ACEI 
B: captopril (PO) 6.25–25mg 8hourly 
OR 
C: enalapril (PO) 5–20mg 12hourly 
OR 
C: lisinopril (PO) 5mg – 10mg 24hourly (When patient is out of congestive state) 
Add Beta-blocker  
C: carvedilol (PO) 6.25–25mg 12hourly a day especially in heart failure with reduced 
systolic function  
Thrombo–embolism prophylaxis 
In Thrombo–embolism prophylaxis, Low Molecular Weight Heparin (LMWH) is recommended in 
patients not already anticoagulated and with no contra indication to anticoagulation, to reduce the risk 
of deep venous thrombosis and pulmonary embolism. 
B: unfractionated heparin (SC) 5,000IU 12hourly  
OR 
S: Low molecular weight heparin (SC) 40mg–80mg 12hourly 
OR 
S: Rivaroxaban (PO) 15mg/20mg 24hourly 
Note 
All patients with AHF should be treated at centre/hospital where at least can perform 
Echocardiographic assessment and Intensive Care Units (ICU) or High care dependent Units 
(HDUs) are available. 
20.10   Chronic Heart Failure 
Patients who have had HF as defined above for some time are often said to have ‘Chronic Heart 
Failure’. A treated patient with symptoms and signs that have remained generally unchanged for at 
least 1 month is said to be ‘Stable chronic heart failure’ 
Diagnostic Criteria  
The diagnosis of chronic heart failure requires the following features: 
•
Symptoms of heart failure, typically breathlessness or fatigue, at rest or during exertion
•
Objective evidence of cardiac dysfunction preferably by Echocardiography (Systolic and/or
Diastolic)
•
A clinical response to treatment is supportive but not sufficient for diagnosis.

457!
Hence diagnosis and management of CHF should be sought at referral centres where at least 
echocardiography assessment can be performed. 
Treatment of Systolic Heart Failure (LVEF< 45–50%) 
Goals of treatment 
•
Prevention of disease leading to cardiac dysfunction and heart failure eg hypertension,
coronary artery disease, valve disease etc.
•
To achieve maintenance or improvement in quality of life and improve survival
Non-pharmacological Treatment 
•
Avoid excessive fluid intake in severe HF Limit fluid intake to 1–1.5 L/day if fluid overloaded
despite diuretic therapy.
•
Regular exercise within limits of symptoms and other lifestyle modification (refer to table
20.2).
Note 
Sexual counselling regarding the risk of pregnancy and the use of oral contraceptives and 
phosphodiesterase-5 inhibitors (e.g sildenafil) are not recommended in advanced HF, if used 
nitrates should be avoided <24–48hours of nitrate intakes. 
Medicines to avoid or to be used with caution. 
•
NSAIDs & COXIBS
•
Class I anti–arrhythmic
•
Calcium antagonists
•
Lithium
•
Tricyclic antidepressants
•
Corticosteroid
Pharmacological Treatment (Approach combination therapy) 
Diuretics  
B: furosemide (PO) 40–80mg 12hourly 
OR 
S: torsemide (PO) 5–20mg 24hourly 
AND  
Mineralocorticoid (Aldosterone) Receptor Antagonists: 
C: spironolactone (PO) 25–50mg 24hourly 
OR 
S: eplerenone (PO) 25–50mg 24hourly 
Thiazide 
D: hydrochlorothiazide (PO) 12.5–25mg 24hourly 
OR 
S: metolazone (PO) 0.1–10mg 12hourly  
Angiotensin Receptor Inhibitors ACEI or Angiotensin Receptor Blockers (ARB) 
B: captopril (PO) 6.25–25mg 8hourly 
OR 
C: enalapril (PO) 5–20mg12hourly 
Angiotensin Receptor Blocker–ARB (*Do not combine with ACEI, Indicated in patient sensitive to 
ACEIs) 
C: losartan (PO) 50mg 24hourly 
OR 
S: candesartan (PO) 4–16mg 24hourly 
Beta blocker (Carvedilol–improve Morbidity & Mortality in CHF). 
C: carvedilol (PO) 6.25–25mg twice a day especially in heart failure with reduced systolic 
function
Note 
Beta Blockers is contraindication to patients with Bronchial Asthma or Severe Pulmonary Disease 
Symptomatic bradycardia or hypotension 

457!
Heart failure in Type 2 Diabetes Mellitus and Non-DM: 
S: empagliflozin (PO) 10mg/ 25mg 24hourly 
Add on therapy in patient in NYHA class III/IV.  
Vasodilator agents: The combination of hydralazine/nitrate 
C: isosorbide dinitrate (PO) 10–20mg 12hourly 
AND   
B: hydralazine (PO) 25 mg 6–8hourly. Maximum dose: 200 mg/day 
Cardiac Glycosides–Digoxin, give with caution as has narrow therapeutic index see below under 
section of Cardiac Glycosides 
D: digoxin (PO) 0.125mg–0.25mg 24hourly 
Note 
Patients at high risk of digoxin toxicity are: Elderly, patients with poor renal function, 
hypokalaemia and low body weight 
Anti–thrombotic agents. 
Heparin &/or warfarin – firmly indicated on congestive heart hailure with atrial fibrillation, previous 
thromboembolic events or a mobile LV thrombus Heparin for DVT prophylaxis for patients admitted to 
hospital, unless contraindicated: 
B: unfractionated heparin (SC) 5000 units 8hourly 
OR 
S: low molecular weight heparin (IV) 40-60mg/ml 24hourly 
OR 
C: warfarin (PO) 5 mg 24hourly (Monitor INR to therapeutic range (2.0–2.5) 
OR 
S: rivaroxaban (PO) 15-20mg 24hourly 
Antidote for heparin 
B: protamine (IV) 10ml/ml in 5mls Ampoule/vial. 
1mg of protamine sulphate neutralizes approximately 100units of heparin. 
Thiamine Supplement: Consider in all unexplained heart failure 
Note 
•
Ideally all patients with CHF should be managed in dedicated HF clinics/units with devoted HF
expert staffs (nurses & doctors) for further evaluation and Device therapy including CRT, CRT-
D and ICD. The following category of patients should be referred for specialized care
o
Severe HF class III/IV
o
HF of unknown origin
•
Relative contraindication: asymptomatic bradycardia, low blood pressure, Intolerance to low
doses, Previous use of ß –blockers and discontinuation because of symptoms, Bronchial
asthma, or severe pulmonary disease.
20.11 Pulmonary Oedema 
Diagnostic Criteria 
Common cause of pulmonary oedema is cardiac/fluid overload, and the common causes 
•
Systolic heart failure complicating fluid overload
•
Renal failure complicating fluid overload
•
Iatrogenic fluid overload
Other Cause of pulmonary oedema 
•
Increased capillary permeability Acute Respiratory Distress Syndrome (ARDS); many causes
include Systemic sepsis–gram negative infection, pancreatitis, head injury, aspiration of gastric
contents, amniotic embolus.
Non-pharmacological Treatment 
Initial management 
•
Maintain airway, bed rest in Fowler`s position except if hypotensive or comatose.
•
Administer oxygen to keep PO2> 60 mmHg (O2 saturation > 90%)

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•
Correct base–acid & electrolyte disorders, determine and correct arrhythmias,
Pharmacological Treatment 
Cardiac failure 
B: furosemide (IV) 20mg–80mg may be repeated in 10–15 minutes, If symptoms persist, 
C: morphine (IV) 1–3mg diluted form,  
•
Inotropic support if hypotensive SBP <90mmHg,
S: dobutamine (IV) 2–20 µg/kg/min
•
Intravenous vasodilator nitroglyceride if SBP > 100mmHg
Non–cardiac (ARDS) 
•
Treat the underlying conditions
•
Ventilate with PEEP – if RF
•
Inotropic support if SBP<90mmHg
•
Dialysis if renal failure
Note 
•
All patients suspected with pulmonary oedema should be referred to high level of
care where hospital resourced with high care dependent unit or intensive care unit.
•
Patient should be stabilized first at low level of care before referral to the high level
of care.
20.12 Infective Endocarditis (IE) 
The infective process of endocardial layer of the heart can involve native or prosthetic valve and 
congenital defects/shunts. Alpha–haemolytic streptococci are the most common causes of native 
valve endocarditis but Staphylococcus aureus is more likely if the disease is rapidly progressive with 
high fever or is related to a prosthetic valve (Staphylococcus epidermidis). 
Diagnostic Criteria  
Use Modified Dukes Criteria below and consult microbiologist where possible. Three sets of blood 
cultures should be taken before starting treatment. 
Modified Dukes Criteria 
Major Criteria 
•
Positive blood cultures of typical organism for IE from at least two separate blood cultures
•
Evidence of endocardial involvement by echocardiogram (Trans–thoracic Echo/Trans–
oesophageal Echo)
Minor Criteria 
•
Fever > 38ºC
•
Presence of Rheumatic heart disease, congenital heart disease
•
Vascular phenomena; Major arterial emboli, septic pulmonary infarcts, mycotic aneurysm,
intracranial haemorrhage, conjuctival hemorrhage, Janeway lesions
•
Immunological phenomena; glomerulonephritis, Osler`s nodes, Roth`s spots,
•
Rheumatoid factor.
•
Serologic evidence of active infective endocarditis or blood culture not meeting major
criterion.
Definition of infective endocarditis according to the modified Duke criteria: 
Definitive diagnosis of IE 
Pathological criteria  
•
Microorganisms demonstrated by culture or on histological examination of a vegetation, a
vegetation that has embolized, or an intracardiac abscess specimen
OR
•
Pathological lesions: vegetation or intracardiac abscess confirmed by histological
examination showing active endocarditis.
Clinical criteria 
•
Two major criteria OR
•
One major and three minor criteria OR
•
Five minor criteria

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Possible Diagnosis of IE 
•
One major and one minor OR
•
Three minor criteria
Rejected IE 
Firm alternate diagnosis. 
•
Resolution of symptoms suggesting IE with antibiotic therapy for ≤4 days; or
•
No pathological evidence of IE at surgery or autopsy, with antibiotic therapy for ≤4 days;
OR
•
Does not meet criteria for possible IE, as above.
Note 
•
Positive blood cultures remain the cornerstone of diagnosis and provide live bacteria for both
identification and susceptibility testing.
•
To improve yield of culturing bacteria at least three blood sample sets are taken at 30
minutes apart each containing 10mL of blood and should be incubated in both aerobic and
anaerobic atmospheres.
•
Sampling should be obtained from a peripheral vein using a meticulous sterile technique.
Pharmacological Treatment 
Empirical Treatment 
Consider for negative blood culture or if risk delaying treatment for blood culture outweigh the befit of 
starting treatment early  
Treatment for native valves: 
A: benzyl penicillin G (IV) 18–24milllion Units/24hours 4hourly in equally divided dose 4–
6weeks 
OR 
B: ceftriaxone (IV) 2g 24hourly 4–6weeks 
AND 
B: cloxacillin (IV) 2g 6hourly 4–6 weeks 
AND 
A: gentamicin (IV) 1–1.5mg/kg 8 hourly for at least 2weeks 
OR 
If methicillin–resistant staphylococci anaerobes (MRSA) 
S: vancomycin (IV) 30mg/kg 24 hourly in two equally divided dose, not to exceed 2gm in 
24hours unless serum levels are monitored 4–6weeks. 
Note 
It is important to assay serum gentamicin levels every 3–4days. One–hour peak concentration 
should not exceed 10mg/l and trough concentration (2–hour pre– dose) should be less than 2mg/l. 
Prosthetic valve empirical treatment 
A: benzyl penicillin G (X–Pen) (IV) 18 –24 milllion Units 4 hourly for 24hours in equally 
divided dose 6 – 8 weeks 
OR 
B: ceftriaxone (IV) 2g 24hourly >6 weeks 
AND 
B: cloxacillin (IV) 2g 6 hourly >6 weeks 
AND 
A: rifampicin 300 –600mg (IV) 8hourly >6 weeks 
AND 
A: gentamicin 1mg/kg (IV) 8hourly 2 weeks. 
Note 
•
It is important to assay serum gentamicin levels every 3–4days. One–hour peak concentration
should not exceed 10mg/l and trough concentration (2–hour pre– dose) should be less than
2mg/L.
•
Gentamycin in renal failure should be given based on CrCl.
•
Patients with complicated IE should be evaluated and managed in high level of care or centre,
with immediate surgical facilities and the presence of a multidisciplinary including an Infectious
Disease specialist, a microbiologist, cardiologist, imaging specialists, and cardiac surgeons

460!
Infective Endocarditis Prophylaxis 
•
Antibiotic prophylaxis should be considered for patients at highest risk for IE:
•
Patients with any prosthetic valve, including a trans catheter valve, or those in whom any
prosthetic material was used for cardiac valve repair.
•
Patients with a previous episode of IE.
•
Patients with Congenital Heart Disease (CHD):
I.
Any type of cyanotic CHD.
II.
Any type of CHD repaired with a prosthetic material, whether place surgically or by
percutaneous techniques, up to 6 months after the procedure or lifelong if residual
shunt or valvular regurgitation remains.
Note 
Antibiotic prophylaxis is not recommended in other forms of valvular or CHD. 
Prophylaxis of Endocarditis Infective 
•
To reduce the risk of bacterial endocarditis, antibiotic prophylaxis should be given to patients
undergoing dental procedures requiring manipulation of the gingival or periapical region of the
teeth or perforation of the oral mucosa.
Antibiotic prophylaxis is not recommended for, 
•
Respiratory tract procedures including bronchoscopy or laryngoscopy, or trans nasal or
endotracheal intubation
•
Gastrointestinal or urogenital procedures or Trans–oesophageal Echocardiogram, gastroscopy,
colonoscopy, cystoscopy, vaginal or caesarean delivery.
•
Skin and soft tissue procedures
  Table 20.6: Recommended prophylaxis for high–risk dental procedures in high-risk patient 
Situation 
Antibiotic 
Single–dose 30–60 minutes before procedure 
Adults 
Children 
No allergy to penicillin or 
ampicillin 
amoxicillin or 
ampicillin* 
2g (PO/IV) 
50 mg/kg (PO/IV) 
Allergy to penicillin or ampicillin 
clindamycin 
600 mg (PO/IV) 
20 mg/kg (PO/IV) 
*Alternatively, B: ceftriaxone (IV) 1g for adults or 50 mg/kg for children. Cephalosporins should not be
used in patients with anaphylaxis, angio–oedema, or urticaria after intake of penicillin or ampicillin
due to cross–sensitivity.
20.13 Acute Rheumatic Fever 
It is a non–suppurative sequela of a group A ß haemolytic streptococcal (GABHS) pharyngeal 
infection. 
Diagnostic Criteria Jones See table 20.7 below 
Definitive Diagnosis 
•
Two major criteria or
•
One major criterion with two minor criteria, with evidence of antecedent streptococcal
infection
Table 20.7: Criteria for Acute Rheumatic Fever Diagnosis 
Major Criteria 
Minor Criteria 
1.
Carditis 
2.
Migratory polyarthritis 
3.
Sydenham’s chorea 
4.
Erythema Marginatum 
1.
Clinical 
•
Fever 
•
Arthralgia 
2.
Laboratory 
•
Elevated Acute Phase Reactants eg CRP 
•
Prolonged PR interval
Plus 
Supporting evidence of recent group, A streptococcal infection e.g. positive throat culture or antigen 
detection and/or elevated streptococcal antibody tests* 
*anti –streptolysin O, anti –deoxyribonuclease B

461!
Non–pharmacological Treatment 
Acute stage: 
•
Bed rest and supportive care until all evidence of active carditis has resolved
•
Patient education.
•
Intensive health education for prevention of sore throats.
Pharmacological Treatment 
Treatment of acute attack for eradication of streptococci in throat: Regardless of the presence or 
absence of pharyngitis at the time of diagnosis. 
A: benzathine penicillin (IM) 1.2MU stat  
Paediatric> 5 years 0.3MU, 5–10 years 0.6 MU > 10 years 1.2 MU stat 
OR 
A: penicillin V (PO) 500mg 8-12 hourly 24 hourly for 10days 
Children > 10years 500mg, 5–10 years 250mg, < 5years 125mg (PO) 8-12 hourly for 10 
days 
Patients allergic to penicillin 
A: erythromycin (PO) 500mg or 40mg/kg 6hourly for 10days. 
Treatment of Acute Arthritis and Carditis: 
A: acetylsalicyclic acid (PO) 25mg/kg 6hourly 24hourly as required. 
Acetylsalicyclic acid should be continued until fever, all signs of joint inflammation and 
the ESR have returned to normal and then tapered gradually over 2 weeks. If symptoms 
recur, full doses should be restarted. *dose should be reduced if tinnitus or other toxic 
symptoms develop 
In severe carditis with development of increasing heart failure or failure of response to aspirin, Add
A: prednisolone (PO) 1–2mg/kg 24hourly for 3–4weeks 
Then review and gradual reduction and discontinuation of prednisolone may be started after 3–4 
weeks when there has been a substantial reduction in clinical disease. 
Heart failure should be managed in the usual way (see Heart Failure Section 20.9). 
Treatment of Sydenham’s chorea: 
B: haloperidol(PO) 1.5–3mg 8hourly for 24 hours as required (Adult). 
Paediatrics 50µg/kg for 24 hours in 2 divided doses. 
Referral: Ideally all patients should be referred to high level of care a specialized hospital care, 
where surgery is contemplated 
Antibiotic prophylaxis after rheumatic fever 
Prophylaxis should be given to all patients with a history of acute rheumatic fever and to those with 
rheumatic heart valve lesions. The optimum duration of prophylaxis should be up to at least 21years 
of age. 
Note 
Specific situations requiring prophylaxis for longer periods (up to 30years as a guide): 
•
definitive carditis in previous attacks
•
high risk of exposure to streptococcal infection at home or work (crowded conditions,
high exposure to children)
Medicine of choice 
A: benzathine penicillin (IM) 2.4MU monthly or every three weeks*  
Paediatrics <12yrs 1.2MU every 4 weeks or 3 weeks* up to 21–30yrs 
OR 
A: phenoxymethylpenicillin (PO) 250mg 12hourly Adult  
Paediatric<12yr 125–250mg 12hourly for 24hours up to 21–30years 
OR 
A: erythromycin (PO) 250mg 12hourly for 24hours Adult 

462!
Paediatric <12yr 125–250mg 12hourlyfor 24hours up to 21–30yrs*every 3week regimen is 
more effective 
Valvular Heart Disease and Congenital Structural Heart Disease 
Valvular Heart Disease are chronic acquired sequelae of Acute Rheumatic Fever or Acute Sequelae 
of Infective Endorcaditis or Ischaemic Heart Disease, consisting of valvular damage, usually left heart 
valves, with varied progression of severity and complications. 
Congenital Heart Disease is a congenital chamber defects or vessel wall anomalies  
Valvular Heart Disease and Congenital Structural Heart Disease may be complicated by: 
•
Heart failure
•
Infective endocarditis
•
Atrial fibrillation
•
Systemic embolism eg Stroke
General measures 
•
Advise all patients with a heart murmur regarding the need for prophylaxis treatment prior
to undergoing certain medical and dental procedures.
•
Advise patients to inform health care providers of the presence of the heart murmur when
reporting for medical or dental treatment
Referral: Should be considered from low level of care to high level of care where specialized 
(physician`s care) or super–specialized care (Cardiologist`s care) can be offered  
20.14 Pulmonary Embolism 
20.14.1   Acute Pulmonary Embolism 
Clinical Spectrum less than two weeks 
•
Sudden onset of dyspnoea often with unexplained anxiety (most common)
•
Pleuritic chest pain and haemoptysis
•
Massive embolism: pleuritic chest pain, cyanosis, right heart failure and shock. Minor
emboli or pulmonary infarction may herald massive embolism and must be treated
vigorously
•
About 90% of emboli are from proximal leg deep vein thromboses (DVTs) or pelvic vein
thromboses. DVTs are at risk for dislodging and migrating to the lung circulation. Thus,
termed as venous thromboembolism (VTE).
Diagnostic Criteria  
Determination pre-test probability of PE 
Use validated scoring system: Wells Score 
•
Score > 6.0–High clinical probability proceeds with imaging test to confirm PE and treat,
•
Score 2.0 to 6.0–Moderate clinical probability; negative D–dimer, PE is excluded and D–
dimer positive, obtain imaging tests to confirm based on result treat.
•
Score < 2.0–Low clinical probability negative D–dimer, PE is excluded. Positive D–dimer
obtain imaging tests to confirm or rule out and based on result treat
Alternatively 
•
Score > 4–PE likely, d–dimer positive proceeds with diagnostic imaging to confirm and treat
PE.
•
Score 4 or less–PE unlikely, consider d–dimer to rule out PE.
Table 20.8: Wells Score 
Variable 
Score 
Clinically suspected DVT 
3.0 points 
alternative diagnosis is less likely than PE 
3.0 points 
Tachycardia (heart rate > 100) 
1.5 points 
Immobilization (≥ 3d)/surgery in previous four weeks 
1.5 points 
History of DVT or PE 
1.5 points 
Hemoptysis 
1.0 points 
Malignancy (with treatment within six months) or palliative 
1.0 points 

463!
•
ECG – Not reliable test for diagnosis may be normal. However,
•
Sinus tachycardia most common feature, acute right ventricular strain – i.e. right axis shift,
S1Q3T3 occurs in small percentage of cases, may develop acute bundle branch block –
right or left, may simulate right ventricular infarction, may develop arrhythmias – eg atrial
fibrillation
•
Arterial blood gases; not diagnostic, the pO2 decreased <60mmHg due ventilation/perfusion
mismatch. pCO2 decreased due to hyperventilation, pH increased but may decrease in
shocked patient
•
D–dimer test – very sensitive blood test, but not specific. A negative test d–dimer test
excludes an embolus in majority of cases (best exclusive test to rule out PE when is
negative)
•
Chest X–ray – Not very reliable usually normal, diaphragm may be raised on affected area,
atelectasis may occur, peripheral wedge–shaped shadow & plural effusion
•
Cardiac Echocardiography: Useful in diagnosis, features suggestive or support
•
evidence of massive embolus acute right ventricular strain
•
Computer Tomography Pulmonary Angiogram Scan (CTPA); Useful can demonstrate the
presence and extent of proximal pulmonary emboli
•
Ventilation/Perfusion Scan; Useful in stable patient to confirm the diagnosis. The presence
of a perfusion defect with normal ventilation not corresponding to an x–ray abnormality is
characteristic
•
Pulmonary Angiography: Still gold standard investigation, may be necessary to establish
•
Diagnosis and catheter-based embolectomy in the catheterization lab.
Non-pharmacological Treatment 
•
Administer O2 – maintain pO2 > 60mmHg,
•
Treat shock
•
Correct electrolyte & acid base abnormalities and arrhythmias
•
Ventilate if patient in respiratory failure
Pharmacological Treatment 
Anticoagulation 
B: unfractionated heparin (UFH) (IV) 10,000units then maintenance infusion starts with 
6,000U over 6 hours to keep PTT or clotting time 2–3times above baseline. PTT should 
be performed 12hourly per lab instruction. 
OR 
S: low molecular weight heparin (SC) 1mg/kg 12hourly for 24hours 
Start warfarin after 24hours of heparin and continue post discharge for long–term. If the aetiology 
unknown may be for life, if aetiology is established at least for six months. Maintain INR 2.0–3.0 
Thrombolytic (Fibrinolysis) 
Indicated in proximal massive pulmonary emboli and haemodynamically unstable if no 
contraindication exists 
S: streptokinase (IV)250,000IU over 30minutes, then 100,000IU per hour for 24hours 
OR 
S: alteplase (rtPA) (IV) 100mg over 2hours 
Referral: All cases suspected of pulmonary embolus should be referred to a high level of care – 
specialized hospital care with HCDU/ICU 
20.14.2 Chronic Pulmonary Embolism 
Chronic pulmonary embolism is mainly a consequence of incomplete resolution of acute pulmonary 
thromboembolism. Clinically symptoms and signs may be preceded by Acute Pulmonary Embolism 
for more than 2weeks.  
Pharmacological Treatment 
Long-term oral anticoagulation 
C:warfarin(PO) 2–10mg 24hourly 
OR 
S: rivaroxaban (PO) 15-20mg 24hourly 

464!
Maintain INR 2.0–3.0 for warfarin use individuals. 
Referral: All cases suspected of pulmonary embolism should be referred to a high level of care 
20.15   Cardiac Arrhythmias/ Dysrhythmias 
Always exclude underlying structural cardiac disease in all patients with cardiac dysrhythmias as well 
as performing Holter ECG monitoring aiding at detecting type of arrhythmia.  
20.15.1 Tachyarrythmias 
20.15.1.1 Narrow QRS Complex Tachyarrythmias (SVTs) 
Definition Sustained (> 30 seconds) or non–sustained narrow QRS (≤ 0.1 seconds) tachycardias. 
Atrial Fibrillation 
Acute onset (< 48 hours) 
•
Assess clinically, e.g. heart failure, mitral stenosis, thyrotoxicosis, hypertension, age and
other medical conditions.
•
Consider anticoagulation with heparin or warfarin.
•
Synchronized DC cardioversion is occasionally necessary in emergency especially
haemodynamic instability or consider if is the first episode.
Non-acute/chronic (> 48 hours) 
•
As above, but not immediate DC cardioversion is indicated, unless in hypotensive
emergency cases. Anticoagulation with oral warfarin 2-5mg orally once a day for at least a
month, then perform elective cardioversion at specialized hospital.
Atrial flutter 
•
P waves visible before QRS, commonly occurs, usually 2:1. (150 per minute). P waves,
usually negative in Lead II precede QRS, blocked P in ST segment or hidden by QRS.
•
Vagal stimulation with ECG may reveal blocked P waves.
AV Junctional Re-Entry Tachycardias 
Usually paroxysmal, often young with normal heart. 
•
AV nodal re-entry or WPW syndrome. P waves usually not visible (hidden by QRS).
Non-pharmacological Treatment 
Electrical Cardioversion. 
Synchronized DC cardioversion, 200 J, after sedation with: 
A: diazepam (IV)10–20 mg stat 
If flutter has been present longer than 48hours, defer cardioversion for 4weeks after anticoagulation 
with warfarin, unless severe symptoms or heart failure requires urgent cardioversion. 
Pharmacological Treatment 
None is nearly as effective as DC cardioversion. 
Consider anticoagulants if Atrial flutter sustained. 
Long term treatment: Recurrent atrial flutter is an indication for referral. Many can be cured by 
radiofrequency catheter ablation. 
Atrial tachycardias 
•
Rare, often incessant P before QRS (often long PR) or hidden in T
•
May cause heart failure (tachycardia cardiomyopathy).
Atrial fibrillation 
I.
With fast ventricular response without abberant conduction.
Pharmacological Treatment, Initial: 
Anticoagulation with warfarin 
OR 
S: rivaroxaban (PO)15-20mg 24hourly (in Non-valvular AF) 
Rate control (Control the ventricular rate with one of the following): 
D: digoxin (IV) Initial dose: 0.25-0.5mg; then 0.25mg 4-6hourly to maximum of 1mg; 
Maintenance dose: 0.125-0.25mg 24hourly (IV) or (PO) (Digoxin0.25mg (PO) daily; use 
only in heart failure).  

465!
OR 
B: atenolol (PO) 50–100mg 24hourly (contraindicated in asthmatics). 
OR 
D: diltiazem (IV) initial dose: 15-20mg over 2minutes; may repeat in 15 minutes, 
Maintenance dose: 5-15mg hourly by continuous IV infusion  
OR 
S: verapamil (IV) 5 to 10 mg over 2minutes; may repeat in 30minutes 
DC cardioversion in selected cases, after 4weeks of anticoagulation 
Digoxin only controls rate at rest and is insufficient on its own. If used for long-term, combine with β –
blocker: 
D: digoxin (PO) 0.125-0.25mg 24hourly 
In the elderly and patients with renal impairment: Adjust dosages according to trough levels within the 
therapeutic range. Do levels only if the patient has been on the drug for at least 10 days. 
AND / OR 
B: atenolol (PO) 50–100 mg 24hourly 
OR 
S: bisoprolol (PO) 2.5mg – 10mg 24hourly 
OR  
C: metoprolol (PO) 25mg -50mg 24hourly 
OR 
S: sotalol (PO) 80mg – 160mg 12hourly 
Note 
Avoid use of Digoxin in patients with Accessory pathway. 
II.
With fast ventricular response with Aberrant conduction (eg: Wolff-Parkinson-White
syndrome, WPW)
Catheter ablation of the accessory pathway in symptomatic patients with preexcited AF, especially if 
the accessory pathway has a short refractory period that allows rapid antegrade conduction.  
Long – term 
•
Continue warfarin anticoagulation long-term, unless contraindicated:
C:warfarin (PO) 5mg 24hourly
OR
S: rivaroxaban (PO) maintance dose; 15mg / 20mg 24hourly
OR
Left atrial appendage occlusion (LAAO).
Note 
•
INR monitoring in patients on warfarin. Maintain therapeutic Range INR 2–3: Stable patients
check 3 monthly. If INR < 1.5 or > 3.5: do monthly monitoring.
•
Left atrial appendage occlusion (LAAO) is indicated in Atrial Fibrillation patients who can not
tolerate long-term Anticoagulantion or contraindicated to OACs (Oral anticoagulants) and
have thrombo-embolic risk (CHA2DS2-VASc score ≥2), increased risk of bleeding (HASBLED
score ≥ 3) and thrombo-embolic events despite adequate OAC after excluding other
plausible causes (eg carotid disease).
20.15.2   AV Junctional Re-Entry Tachycardias 
 
Non-pharmacological Treatment 
Vagal manoeuvres: Valsalva or carotid sinus massage. The patient should be supine and as relaxed 
as possible, to avoid competing sympathetic reflex 
Pharmacological Treatment 
If vagal manoeuvres fail: 
S:adenosine (IV) 6mg over 1-3 seconds (maybe given IO) followed by rapid flush with 
20mL NS, if no conversion within 1-2minutes give 12mg, repeat a second time if necessary 
(30mg total) 
If none of the above is effective, and patient is hypotensive, consider DC shock 

466!
Prevention of recurrent paroxysmal atrial fibrillation 
Only in patients with severe symptoms despite the above measures: 
S: amiodarone (PO) 200mg 8hourly for 1week, followed by 200mg 12hourly for one 
week and thereafter 200mg 24hourly. Specialist initiated. 
Precautions: 
•
Halve dosage of warfarin and monitor INR closely if patient on warfarin, until stable
•
Avoid concomitant digoxin use.
Note 
Verapamil and digoxin are contraindicated in WPW syndrome. 
Long-term treatment: Teach the patient to perform vagal manoeuvres, Valsalva is the most 
effective. For infrequent, non–incapacitating symptoms: 
ß –Blockers 
B: atenolol (PO) 50–100mg 24hourly (If asthmatic) 
OR 
S: verapamil (PO) 80–120mg 8hourly for 24hours (Normal heart) 
Referral: Refer to Cardiac specialized center for Mapping and Radiofrequency Ablation (RFA) 
20.15.3   Wide QRS (Ventricular) Tachyarrhythmias (VTs) 
Sustained (> 30 seconds) or non-sustained wide QRS (> 0.12 seconds) tachycardias 
Regular Wide QRS Tachycardias 
These are ventricular tachycardias until proved otherwise. Regular wide QRS supraventricular 
tachycardias are uncommon. 
Non-pharmacological Treatment  
Refer all cases after resuscitation and stabilization. Emergency DC cardioversion is mandatory with a 
full protocol of Cardiopulmonary Resuscitation (CPR) 
•
If no cardiac arrest: DC cardioversion, 200J, after sedation with: Diazepam, I.V, 10–20mg If
200J fails, use 360J.
•
If cardiac arrest: Defibrillate (not synchronized).
Pharmacological Treatment 
DC cardioversion is first line therapy for regular wide QRS tachycardias.  
Medicines are needed if VT recurs after cardioversion or if spontaneous termination/recurrence. 
S: amiodarone (IV) 5mg/kg (150-300mg) infused over 30minutes then continue with 
maintenance dose to total dose of 1200mg/24hours  
OR  
S: amiodarone (PO)800 mg 24hourly for 7days, 600mg/day for 3days followed by a 
maintenance dose of 200–400mg/day  
Amiodarone may cause serious long-term side effects due to long half-life. Therefore, patients 
require regular monitoring by specialist. 
A: lidocaine (IV) 50–100mg (1–2mg/kg) initially and at 5minute intervals if required to a total 
of 200–300mg,   
Thereafter, for recurrent ventricular tachycardia only 
A: lidocaine (IV)1–3mg/minute for 24–30hours. lidocaine will only terminate ± 30% of 
sustained ventricular tachycardias, and may cause hypotension, heart block or convulsions. 
Note 
•
Never give verapamil IV to patients with a wide QRS tachycardia.
•
For emergency treatment of ventricular tachycardia, DC cardioversion is first–line therapy,
even if stable.
Sustained (> 30 Sec) Irregular Wide QRS Tachycardias 
They are usually due to atrial fibrillation with bundle branch block, or pre-excitation (WPW syndrome). 

467!
Non-pharmacological/Pharmacological Treatment 
•
If the QRS complexes have a pattern of typical right or left bundle branch block, with a rate
< less than 170/minute, treat as for atrial fibrillation. See the section on atrial fibrillation.
•
If the rate is > 170 per minute, and/or the complexes are atypical or variable, the likely
diagnosis is WPW syndrome with atrial fibrillation, conducting via the bypass tract, DC
conversion.
Referral: Refer patient to high care centre for further management including arrhythmia mapping and 
RFA 
Non-Sustained (< 30 Sec) Irregular Wide QRS Tachycardias 
They are usually ventricular, commonly in acute myocardial infarction. In acute myocardial infarction, 
only treat non–sustained ventricular tachycardia if causes significant haemodynamic compromise. 
Ensure the serum potassium level is above 4 mmol/L. 
Pharmacological Treatment 
Medicines are needed if VT recurs after cardioversion or if spontaneous termination/recurrence. 
S: amiodarone (IV) 5 mg/kg (150-300mg) over 30minutes then continue with maintenance 
dose to total dose of 1200mg for24hours  
OR  
S: amiodarone (PO) 800mg 24hourly for 7days, followed by 600mg 24hourly for 3 days 
then a maintenance dose of 200–400mg 24hourly 
Only in a haemodynamically stable patient: 
A: lidocaine (IV) 50–100mg (1–2mg/kg) initially and at 5minute intervals if required to a total 
of 200–300mg 
Thereafter, for recurrent ventricular tachycardia only: 
A: lidocaine (IV) 1–3mg/minute for 24–30hours 
In the absence of acute ischaemia or infarction, consider torsade’s de pointes. 
Torsade’s De Pointes Ventricular Tachycardia (VT) 
•
Has a twisting pattern to the QRS complexes and a prolonged QT interval in sinus rhythm,
it is usually due to a QT–prolonging drug, ± hypokalaemia.
Non-pharmacological Treatment 
•
Cardioversion/defibrillation, as necessary.
•
Torsade’s complicating bradycardia: temporary pacing
Pharmacological Treatment 
Stop all QT-prolonging drugs. Correct serum potassium. 
A: magnesium sulphate (IV) 2g over 5–10minutes 
If recurrent episodes after initial dose of magnesium sulphate: 
A: magnesium sulphate (IV) 2g over 24hours 
Torsade’s complicating bradycardia: temporary pacing. 
A: adrenaline infusion to raise heart rate to >100 per minute 
(if temporary pacing unavailable). 
Referral: Refer all cases of wide QRS tachycardia, after resuscitation and stabilization for possible 
arrhythmia mapping and RFA. 
20.16 Heart Block (Second and Third Degree) 
Most cases occur in patients over 60 years and is idiopathic. Acute, reversible AV block commonly 
complicated by inferior myocardial infarction, here temporary Pacemaker used as bridge therapy. 
The condition may also be induced by medicines, metabolic and electrolyte derrangments. 
Non-pharmacological Treatment 
•
Emergency cardio-pulmonary resuscitation.
•
External pacemaker should be available in all secondary hospitals and must be preceded
by appropriate analgesia.
 Pharmacological Treatment 
Analgesia if external pacemaker: 

468!
C: morphine (IM)10–15mg 3–6hourly 
For Temporary treatment of complete AV block before referral for pacemaker: 
A: atropine (IV) bolus 0.6–1.2mg every 3 – 5min (max 3mg) may be repeated until a 
temporary or permanent pacemaker is inserted.  
(Use in an Inferior Infarct patients, hypotension, and second-degree AV block). 
For resuscitation of asystole: 
A: adrenaline (IV) 1:10000, slow 5mL (0.5mg) 
Referral 
•
All cases with a heart rate below 40 beats/minute after resuscitation and stabilization to
high level of care where permanent pacemaker implantation can be performed.
•
All cases of second or third-degree AV block, whether myocardial infarct or other reversible
cause is suspected, and whether the patient is thought to be symptomatic.
Note 
Complete Heart Block Is a Medical Emergency Refer Urgently 
20.17 Sinus Bradycardia & Sinus Arrest 
This rhythm does not require treatment, unless they are causing symptoms, i.e. syncope, dizziness, 
tiredness, and poor effort tolerance. Sinus bradycardia <50/minute or sinus arrest with slow escape 
rhythm, accompanied by hypotension, strongly suggests a treatable underlying cause: 
•
Acute inferior myocardial infarct
•
Hyperkalaemia, especially if wide QRS and/or peaked T waves
•
Drugs, especially combination of verapamil and ß –blocker or digoxin
•
Hypothermia
•
Hypoxia
Treat the cause. Consider atropine if inferior infarct. 
Note 
•
Refer the patient After stabilization to the Cardiac Specialized centre for thorough
evaluation 
and 
Pacemaker 
Implantation 
[Temporary/Permanent 
Pacemaker
Implantation (single or Dual chamber) depending on the underlying cause], prepare
Vancomycin injection for sterilization of Permanent Pacemaker pouch.

469!
CHAPTER TWENTY-ONE 
KIDNEY AND UROLOGICAL DISORDERS 
These are disorders resulting from structural malformation or function of the genitourinary system that 
may lead to kidney impairment. These disorders include diseases originating from the kidney and 
systemic diseases, which result in complications affecting the kidney. Hypertension and diabetes 
mellitus are the commonest conditions causing complications in the kidney, therefore all patients with 
hypertension and diabetes mellitus should be regularly screened for kidney complications.  
21.1 Chronic Kidney Diseases (CKD) 
It is structural or functional kidney damage present for >3months, with or without a decreased 
glomerular filtration rate (GFR). Early screening in high-risk groups [hypertension, Diabetes and 
glomerular diseases] is crucial in improving outcome of CKD. Once cause and plan for care has been 
established, adults with early CKD stages 0-3 can be managed at primary care level. 
Clinical Presentation 
Clinical features depend on the stage of kidney disease. In advance stage includes: 
•
Anorexia
•
Malaise
•
Vomiting
•
Oliguria/anuria
Investigations 
•
Kidney function tests (serum creatinine and urea) - at diagnosis check every month for
3months. If active sediment/proteinuria, provider may check more frequently
•
FBC (HB)
•
Urinalysis (Protein, red blood cells and cast cells) then quantify the amount of protein in
urine by Esbach test or Urine albumin-creatinine ration or Urine protein-creatinine ratio
•
Kidney-Ureter-Bladder (KUB) ultrasound
•
CXR
•
ECG
•
Serum electrolytes Potassium, Calcium Phosphate and Sodium [CKD stage 3-5: Check
monthly]
•
Serum albumin (for corrected calcium)
•
Serum bicarbonate levels (venous) [CKD stage 3-5: Check monthly]
•
Parathyroid hormone levels, Serum Phosphate and Alkaline phosphatase (ALP) [CKD
stage 5 on dialysis]
Note 
Cause of CKD should be determined and addressed. Especially when thinking of kidney 
transplantation 
The general management of the patient with chronic kidney disease involves the following issues  
•
Treatment of reversible causes of kidney dysfunction
•
Preventing or slowing the progression of kidney disease
•
Treatment of the complications of kidney dysfunction
•
Identification and adequate preparation of the patient in whom kidney replacement therapy
will be required
Table 21.1: Staging of kidney disease for adequate management of CKD stage/glomerular 
filtration rate (GFR*) (ml/minute/1.73) 
Stage 
Description 
Action Includes actions from preceding 
stages 
Stage 0 or GFR 
>90
Increased risks for CKD e.g. 
•
Diabetes mellitus
•
Hypertension
•
Glomerular disease
•
HIV
Screening for advanced CKD and CVD 
disease  
CKD risk reduction i.e. treat hypertension, 
diabetes and HIV  
•
Check creatinine/BUN every month for 3
months then yearly if stable

470!
•
Hepatitis B/C
Stage 1 or GFR 
>90
Kidney damage with normal GFR 
Diagnose and treat comorbid conditions See 
for Stage 0  
Stage 2 or GFR 60-
89  
Kidney 
damage 
with 
mild 
GFR 
reduction 
Refer to determine cause and develop care 
plan  
While on the care plan, monitor the GFR in 
these patients and make sure kidney 
function is not worsening rapidly and watch 
for stage 3  
Stage 3 or GFR 30-
59  
Moderate GFR reduction 
Refer to physician/nephrologist 
Monitor and manage complication 
Check creatinine/BUN every 3months 
Stage 4 or GFR 15-
9  
Severe GFR reduction 
Refer to nephrologist 
Prepare for kidney replacement therapy 
Stage 5 or GFR 
<15  
Kidney 
failure 
requiring 
kidney 
replacement therapy End stage kidney 
disease  
Refer to nephrologist 
* Use CKD-EPI formula without the ethnicity factor. This calculator is available freely online.
Laboratories in Tanzania should report as eGFR.(Delanaye and Mariat, 2013)[1, 2]
Non-pharmacological Treatment 
•
Reduce salt intake.
•
Low protein diet (not exceed 1g/kg per day) is indicated in the presence of CKD stage 4
and 5. (Evidence)
•
Reduce cardiovascular disease risk factors – See section: Prevention of ischaemic heart
disease and atherosclerosis.
•
Treat underlying conditions.
•
Decrease significant proteinuria, if present.
Significant proteinuria = more than +2 protein on urinalysis OR spot urine protein creatinine ratio of > 
0.1 g/mmol OR ACR (albumin-creatinine ratio) > 100 g/mol, confirm as positive if raised on at least 2 
of 3 occasions, in the absence of infection, cardiac failure and menstruation.  
Proteinuria 
•
In established chronic kidney disease, decrease proteinuria, irrespective of presence or
absence of systemic hypertension.
•
Monitor kidney function and potassium especially with impaired kidney function.
•
If volume depleted, first rehydrate before commencing ACE-inhibitor.
•
ACE-inhibitor are contraindicated in:
ü
Hyperkalaemia
ü
known allergy to ACE-inhibitor
Begin with low dosage of ACE-inhibitor and titrate up ensuring blood pressure remains in normal 
range and no side effects are present, up to the maximum dose or until the proteinuria disappears – 
whichever comes first.  
Pharmacological Treatment 
Adults  
C: enalapril (PO) 10–20mg 12hourly 
OR 
C: lisinopril (PO) 5-10mg 24hourly (titrate max 40mg 24hourly) 
Also see other ACEI in hypertension treatment (Cardiovascular Chapter) 
Hyperlipidaemia 
If hyperlipidaemia is a co-existent risk factor manage according to section 
21.1.1Diabetic Kidney Disease 
This is a clinical diagnosis based on the presence of albuminuria, decreased estimated glomerular 
filtration rate (eGFR) or both in diabetes. This diagnosis includes diabetic nephropathy which has 

471!
microalbuminuria (30-300mg/g) and retinopathy in its defining characteristics. In diabetics, optimise 
control according to section 9.6: Diabetes mellitus type 2, in adults.  
Investigations 
•
Urinalysis (Dipstick biochemistry + microscopy)
•
Kidney biopsy with the following indications – if cause not apparent
o
Albuminuria >300mg/g within 5years of DMt1 onset
o
RBC cell cast, dysmorphic RBC or WBC casts in urine sediment
o
Presence of other systemic illness eg SLE
o
Rapid decline (per year) of eGFR>5mL/min/1.73m2
•
Ultrasonography kidney ureter and bladder (KUB)
Table 21.2: Pharmacological Treatment of CKD patients with Diabetes mellitus  
[3-5, 20-25) (Saisho, no date; Wanner et al., 2016; V. Perkovic et al., 2019; Vlado Perkovic et al., 
2019; Zou et al., 2019)] 
Non-dialysis CKD Adults (Titrate carefully) 
eGFR 
Medication 
Considerations 
>90
Stage 1
89-60
Stage 2
As in treatment of non-CKD Diabetes: see 
Diabetes Mellitus Chapter 
For type-2 DM with high cardiovascular risk (an 
add on) 
S: empagliflozin (PO) 10mg 24hourly 
OR 
S: stagliptin (PO) 50mg 24hourly 
Strong consideration of including 
SGLT2-Inhibitors 
59-30
Stage 3
A: gliclazide (PO) 40–80mg 12hourly if not 
available use  
OR 
C: glimepiride (PO) 1-8mg 24hourly +/- 
S: empagliflozin (PO) 10 mg 24hourly 
Caution on Metformin and long 
acting sulphonyl urea 
Titrate carefully 
29-15
Stage 4
C: gliclazide (PO) 40 – 80mg 12hourly 
OR  
C: glimepiride (PO) 1-8mg 24hourly +/- 
S: sitagliptin 25mg 24hourly 
If on insulin, dose reduction is 
needed 
< 15 
Stage 5 
OR 
On dialysis 
Insulin preferred. Reduce dosage with decreasing 
eGFR 
D: pioglitazone (PO)15-30mg 24hourly 
fluid control 
21.1.2 Hypertension and CKD 
Treat if present. See Cardiovascular chapter 
The target blood pressure for CKD patients without proteinuria should be <140/90 and 
for those with proteinuria should be <130/80.  
Investigation 
•
Ambulatory blood pressure monitoring
•
As for CKD section
•
R/o secondary causes and control
Non-pharmacological Treatment 
•
Salt restriction (low sodium diet)
•
Cardiovascular risk reduction as per Hypertension/CVD section

472!
Table 21.3: Pharmacological Treatment of Hypertension and CKD 
eGFR 
STAGE 
Medication 
*At least one medication be taken at bedtime
Considerations 
>90
Stage1
And 
89-60
Stage2
With Proteinuria >500mg/day 
C: enalapril (PO) 10–20mg 12hourly  
OR 
C:lisinopril) 5-10mg 24hourly (titrate 
max 40mg 24hourly) 
OR 
S: irbesartan (PO) 150-300mg 24hourly 
If not available, use another ARB as in 
Hypertension treatment 
If poorly response + oedema 
Diuretics as in section on fluid overload 
+/- 
D: diltiazem (PO) 60-120mg 12hourly  
OR 
S: verapamil (PO) 40–80mg 8hourly 
Check K+ level 
Consider repeat creatinine 
after 
5-7days 
of 
starting 
ACE-Inhibitor 
With no Proteinuria <500mg/day 
If has oedema  
Diuretics See section on fluid overload 
 PLUS 
ACE-Inhibitors/ARB as above 
ADD if not controlled 
D: diltiazem (PO) 60-120mg 12hourly 
OR 
S: verapamil (PO) 40–80mg 8hourly 
Other medications If above fails 
C: spironolactone  
OR 
S: eplerenone as in Hypertension 
treatment/Portal hypertension +/- 
B: hydralazine (PO)12.5 mg – 50 mg +/- 
B: nifedipine (PO) 20-40mg 12hourly  
OR 
C: amlodipine 5-10mg 24hourly +/- 
B: atenolol (PO)25–00mg 24hourly 
If not available or intolerable use below 
C: 
carvedilol 
(PO)6.25mg-25mg 
12hourly  
OR 
S: bisoprolol (PO) 2.5-5 mg 24hourly +/- 
S: doxazosin (PO) 1mg 24hourly (titrate 
max 16mg) 
OR 
A: 
methyldopa 
(PO)250-1000mg 
8hourly 
59-30
Stage 3
As above 
Dose adjustment 
C: lisinopril (PO) 5-10mg 24hourly 
Monitor 
potassium 
more 
frequency 
29-15
Stage 4
< 15 
Stage 5 
OR 
On dialysis 
DO NOT USE ACE inhibitor OR angiotensin 
receptor blocker. Treatment as above 
Dose reduction for 
S: bisoprolol (PO)2.5mg 24hourly 
A: methyldopa (PO)250mg – 1 g 24hourly  
S: doxazosin (PO) 1mg 24hourly (titrate max 
16mg 24hourly 
Fluid control may be more 
important 
*Diuretics
*Salt restriction
*Ultrafiltration volume in
dialysis

473!
Fluid overload  
Treat fluid overload if present and refer. Exclude other causes of oedema as part of management. 
Adults 
B: furosemide (slow I.V, PO) 40–80mg 12hourly. 
OR 
D: torsemide (PO) 10-20mg 24hourly (titrate max 200mg/day) 
If poor response, repeat after 1hour. 
If diuresis is inadequate and there is no hypokalemia a combination therapy with thiazide or thiazide-
like diuretics could be used 
B: furosemide (maximal 600mg/day) slow infusion rather than boluses +/- 
D: hydrochlorothiazide (PO) 25-50mg 12hourly  
OR 
S: metolazone (PO) 2.5–20mg 24hourly 
Note 
Do not give I.V fluids – use heparin lock or similar I.V access. 
Referral to nephrologist 
•
All cases of suspected chronic kidney disease stages 3–5 for assessment and planning
•
All children
•
All cases of CKD with:
o
haematuria,
o
proteinuria
o
raised blood urea or creatinine initially for assessment and planning
•
Uncontrolled hypertension/fluid overload
•
CKD associated with hyperlipidaemia
•
No resolution of proteinuria with ACE-I therapy
Note 
Patients who might qualify for dialysis and transplantation or who have complications should be 
referred early to ensure improved outcome and survival on dialysis, i.e. as soon as GFR drops 
below 30 mL/min/1.73m2, or as soon as diagnosis is made/suspected 
21.1.3 Dialysis 
Refer to the National guidelines for Dialysis services from the MOHCDGEC for the detailed 
indications, procedures and management of patients on dialysis (Haemodialys or Peritoneal dialysis) 
21.1.4 CKD Associated Metabolic Acidosis 
(serum bicarbonate below 22mmol/l)  
S: sodium bicarbonate (PO) 650mg 12hourly. Titrate to serum bicarbonate levels 23-
29mmol/l 
OR 
S: calcium carbonate (PO) 500mg 12hourly. 
21.1.5. Hyperkalaemia 
Refers to an elevation in potassium concentration ≥5.5 mmol/l. Kidney failure and use of 
medications use are common causes. Severity of hyperkalaemia may be mild (5.5-6), moderate 6.1-
6.5 and Severe >6.5. Severity grading increases once there is ECG changes.  
Clinical Presentation 
•
Muscle weakness (ascending)
•
Muscle fasciculation
•
Paralysis
•
Cardiac conduction abnormalities
•
Cardiac
arrhythmias
Investigation 
•
Serum 
potassium 
– 
frequent
reassessment 0hr, 1hr, 3hr
•
ECG (decreased size of p waves, T
wave changes, prolonged PR and
widening QRS)
•
Serum bicarbonate
•
Full blood picture
•
Serum creatinine

474!
•
Lipid levels – Total cholesterol and
LDL
•
Uric acid
•
Blood glucose
Non-pharmacological Treatment 
•
Avoid foods rich in potassium; which include potatoes, bananas, green vegetables
•
Stop offending medication Renin-angiotensin-aldosterone system inhibitors. NSAIDS and
potassium sparing diuretics
Pharmacological Treatment 
Cellular membrane stabilization – All patients with potassium >6.5mmol/l or with ECG changes 
Adults 
A: calcium gluconate (IV) 10% 10-30mls stat 
Reserve for ICU through a central line. 
D: 10% calcium chloride (IV) 10mls stat 
-may repeat again if ECG abnormal within 5-10minutes
-do not give together with sodium bicarbonate
Potassium shift to the intracellular compartment (repeated dosing of insulin may be 
necessary) 
Adults 
 
A: insulin short acting 5-10IU +50mls of 50% Glucose iv injection. Only give glucose if 
RBG is <11 
•
Monitor RBG for hypoglycaemia
•
Repeat insulin short acting /glucose every 4-6 hours
Children 
A: insulin short acting 0.1IU/kg + dextrose 0.5g/kg for 30min 
AND 
Adults 
C: salbutamol nebulized 2.5-10mg every 4-6hours 
OR 
If has metabolic acidosis and not overloaded 
Adults and Children 
C: sodium bicarbonate (IV) 1mEg/kg over 15minutes 
Removal of Potassium from the body 
D: calcium (or sodium) polystyrene sulphonate 15-30g 8hourly for 3days. (Caution: Bowel 
perforation risk). Can be given 3time a week chronically 
AND 
B: furosemide (PO/slow I.V) 40–80mg 12hourly +/- haemodialysis 
If above is not available 
C: lactulose (PO)10-30ml hourly until rapid laxation then 30mls 8hourly per 24hours 
21.1.6 CKD Associated Anaemia 
Patients with CKD present with anaemia, which may be contributed by several factors including 
inability to produce erythropoietin, frequent, blood loss (form gastritis, dialysis therapy and poor 
appetite.  [Refer to the national guidelines for dialysis]  
Investigations for anaemia for patients with CKD stage 3-5 
•
Peripheral smear
•
Reticulocyte count
•
Full blood count
•
Iron studies; serum iron, transferrin saturation and serum ferritin
•
Stool for occult blood

475!
Patients with CKD stage 3 and below with anaemia should be given erythrocyte stimulating agents 
(ESA) when Haemoglobin is < 10 g/dL and interrupt or reduce once Haemoglobin level reaches 
11g/dL.  
S: erythropoietin alfa (IV) 50-100 units/kg 3times a week as approximate starting dose, 
May be given with IV iron supplimentation 
Patients with CKD stage 3 and below with iron deficiency indicated by transferrin saturation <30% or 
serum ferritin <500ng/ml should be given iron supplementation; 
D: Iron sucrose (IV) 100mg with each dialysis for 10doses 
Note 
IV Iron is preferred to oral iron and can be given with ESA among patients on dialysis. 
21.1.7 Mineral Bone Disease (MBD) 
Mineral bone diseases are common among patients with CKD including those undergoing 
maintenance haemodialysis and these diseases contribute cardiovascular complication and 
mortality. Clinical features of these disorders include Bone pain, Convulsions, Tetany, Tissue 
calcification, Fractures. The following investigations should be carried out to identify these disorders 
among patients with CKD stage 3 and below;  
•
Serum calcium,
•
Albumin (for correction of calcium)
•
Phosphate
•
Parathyroid hormone (intact)
•
Vitamin D Levels
•
Lumbar-X-ray (lateral)
•
DEXA scan (those suspected)
Non-pharmacological Treatment 
•
Nutritional consultation: Low phosphate diet and high calcium diet
Pharmacological Treatment  
Hyperphosphataemia treatment 
S: calcium carbonate (PO) 500-1500mg 8hourly with meals [For patients with 
hypocalcaemia] 
21.1.8 Haemodialysis (HD) Catheter Related Blood Stream Infection 
A common life-threatening complication which needs prompt recognition and response in the 
dialysis unit. 
Clinical Presentation 
•
Chills and/or fever ≥ 37.8 oC
•
Tunnel or exit site purulence
•
Rigors
Investigations 
•
Blood culture
•
FBP
•
Investigate for metastatic infection when indicated
Non-pharmacological Treatment 
•
Refer to management of sepsis if in shock
•
Removal of catheter if there is non-response to therapy, exit site infection, tunnel infection,
metastatic infection or hemodynamic instability
Pharmacological Treatment 
Usual 14-21days of treatment 
•
Empirical (while waiting for microbiological results)
Children 
C: flucloxacillin (IV) 25-50mg/kg/day in 3 divided doses
AND 

476!
D: ceftazidime (IV) 50mg/kg/dose every 48hourly, give after dialysis or on dialysis days 
Adults 
C: flucloxacillin (IV) 1-6g/d in 3 divided doses 
AND 
D: ceftazidime (IV) 1gstat immediately after HD and 1g after subsequent HD session 
OR 
Adult 
S: vancomycin (IV)20mg/kg loading over last 1 hour then 1g during the last hour of 
subsequent HD sessions 
AND 
D: ceftazidime (IV) 1gm STAT immediately after HD and 1g after subsequent HD session 
Children 
S: vancomycin (IV) 10mg/kg/dose (consider checking serum levels) 
AND 
D: ceftazidime 50mg/kg/dose 48hourly, give after dialysis or on dialysis days 
•
Tailored
o
According to bacteriological results
o
If negative continue with empirical treatment showing clinical improvement
Note 
In case all above mentioned antibiotics are not available, patients should be treated empirically with 
antibiotics favouring both gram negatives and gram positives. 
Catheter lock (during treatment) 
D: gentamicin lock  
D: vancomycin lock 
21.2 Acute Kidney Disease 
Acute kidney disease is a sudden decline in the glomerular filtration rate (GFR) resulting elevation of 
serum blood urea, creatinine and other waste products. Practically AKI is recognized when there is 
urine output of less than 0.5ml/kg/hour for >6 hours. Causes of AKI are classified as pre-renal, renal 
and post-renal causes and usually result in reversible kidney failure, these causes include; 
Table 21.4:  Causes of acute kidney injury 
Category  
Examples  
Intervention  
Pre-renal: loss of effective 
blood flow to the kidneys  
Low blood volume 
• 
Diarrhea, 
burn, 
acute blood loss 
Heart failure 
Hepatic failure  
Restore blood volume 
•
IV fluids
Low blood pressure 
•
Use of inotropes
Renal: caused by intrinsic 
kidney insult  
-Glomerulonephritis
-Nephrotoxic medications
-Rhabdomyolysis
-Tumor lysis syndrome
Treatment of specific  
Glomerular disorders 
Omit offending nephrotoxic drugs 
Post renal: occurs as a 
consequence 
of 
urinary obstruction 
-BPH
-Urinary stones
-Obstructed urinary catheters
-Bladder stones
Relief of obstruction 
-Urinary catheterization
-Nephrostomy
Clinical Presentation 
•
Oedema
•
Oluguria/anuria
•
Convulsions in children
Investigation 
Early disease 
•
Creatinine [increase of ≥ 26micromol/l within 48hrs or ≥ 50% increase within 7 days
defines AKI]
•
Urea

477!
•
Ultrasound KUB
•
Urinalysis (Dipstick and microscopy)
Advanced disease defined by urine output of less than 0.5ml/kg/hour for >12 hours. 
•
Serum electrolytes [potassium, chloride, bicarbonate, Sodium phosphate and calcium]
•
Arterial Blood Gases
•
Uric acid
•
Urine electrolytes – Fractional excretion of Sodium
•
Chest X-ray
•
ECG
•
Kidney biopsy if cause not obvious clinically
•
Creatine kinase if Rhabdomyolysis is suspected
Non-pharmacological Treatment 
•
Give oxygen, and nurse in semi-Fowlers’ position if patient has respiratory distress.
•
Stop intake of all salt and potassium containing foods and fluids
•
Restrict fluid intake to 10 mL/kg/day daily plus visible fluid losses
•
Remove nephrotoxic medications
•
Adequate nutritional support: sufficient amounts of energy and adequate protein. Consider
enteric/parenteral nutrition
Pharmacological Treatment 
Treat underlying cause 
Adults  
If dehydrated, 
A: 0.9% sodium chloride (PO/IV) while monitoring urine output 
If diastolic blood pressure is greater than 100 mmHg or systolic blood pressure is above 150 
mmHg:  
C: amlodipine (PO) 5 mg 
If there is respiratory distress (rapid respiration, orthopnoea) and is fluid overloaded [chest crackles 
and raised JVP]:  
B: furosemide (IV bolus) 80mg. (higher doses may be tried once) 
If there is respiratory distress (laboured breathing with low serum bicarbonate=metabolic acidosis) 
C: sodium bicarbonate (IV) 150mEq in 1L of 5%Dextrose  
Consider Proton pump inhibitors to reduce risk of gastrointestinal bleeding 
C: pantoprazole (IV/PO) 40mg 24hourly 
Treat Hyperkalaemia as in CKD 
Haemodialysis or Peritoneal dialysis when indicated 
Note 
•
Indications for dialysis include pulmonary oedema, Hyperkalaemia, metabolic acidosis
not responding to medical therapy and uremic encephalopathy or pericarditis. Acute
poisoning with a dialysable substance is another indication.
•
Patients with AKD will be followed regularly to monitor and prevent CKD. A weekly
kidney assessment (creatinine and/or urinalysis) for one month and then monthly for 2
months and then 6-monthly thereafter is a suggested regime when there is no CKD.
•
Do not put up a drip and do not give a fluid infusion if the patient is fluid overloaded or
urine does not increase with iv. fluids
Referral 
All cases where adequate laboratory and clinical resources exists, management according to the 
hospital level guidelines may be instituted. Referral to the nephrologist should occur in the 
following:-  
•
Glomerulonephritis is a strong possibility – haematuria and proteinuria.
•
Worsening despite initial treatment.
21.3 Glomerular Diseases (GD) 
Glomerular diseases include a broad array of clinicopathological syndromes which progress to 
glomerulosclerosis and eventually end stage kidney disease. Glomerular disease may be a result of 
a primary condition of the kidney or may be secondary to a systemic disorder. 

478!
Clinical Presentation 
•
Proteinuria
•
Reduced GFR (and its effects)
•
Haematuria
•
Hypertension
•
Oedema.
21.3.1 Glomerular disease - Nephritic syndrome 
A non-infectious inflammatory process that involves the nephron. History and examination should 
exclude secondary causes. 
Clinical Presentation: 
•
Painless macroscopic turbid, bloody or brownish urine
•
Peripheral and facial oedema
•
Difficulty in breathing
•
Hypertension encephalopathy with impaired level of consciousness or convulsions
•
Little or no urine excretion
Investigations 
•
Serum Creatinine
•
Blood urea nitrogen/Urea
•
Urinalysis (Dipstick + microscopy)
•
confirm proteinuria by Urine albumin-creatinine ratio (UACR) or Urine protein-creatinine
ratio (UPCR)
•
Urine culture
•
Complete blood count
•
Kidney biopsy and histology
•
Others on tertiary hospital e.g. ANA, dsDNA, RF, , complements, Syphillis tests (VDRL or
RPR)
Non-pharmacological Treatment 
•
Give oxygen, and nurse in semi-Fowlers position if patient has respiratory distress.
•
Restrict intake of all salt
•
Restrict potassium containing foods and fluids
•
Restrict fluid intake to 10 mL/kg/day daily plus visible fluid losses
Pharmacological Treatment 
Adults  
Fluid overload  
B: furosemide (IV bolus) 80mg  
If hypertension  
If diastolic blood pressure is greater than 100mmHg or systolic blood pressure is above 150mmHg: 
C: amlodipine (PO) 5mg stat before referral to higher facility 
Continue with other medications as in hypertension section (caution contraindications) 
Note 
 The definitive treatment of nephritis depends on the cause – an assumption of acute post 
streptococcal nephritis or any other disease cannot be made without specific investigation, which 
may include kidney biopsy. 
21.3.2 Nephrotic syndrome 
It is a kidney disorder characterized by urinary protein loss leading to generalized body swelling. It 
is severe proteinuria defined as: Adults: 3.5 g/day,  
Clinical Presentation 
•
Oedema
•
Hypoalbuminaemia
•
Hyperlipidaemia
Note 
•
Diagnosis of nephrotic syndrome requires a kidney biopsy, however in children (1year-18
years) biopsy is indicated for children with steroid resistant nephrotic syndrome
•
Children (1-18 years) should be given treatment with steroid, they should be referred for
renal biopsy if there is no response.

479!
Non-pharmacological Treatment 
Adequate calories and adequate protein 1g/kg/d 
No added salt to limit fluid overload 
Pharmacological Treatment 
The management of glomerular disease depends on the type/cause of the disease and is 
individualized guided by a specialist according to the histology results obtained after renal biopsy.  
Note 
 Referral to nephrologist may include treatment using immunosuppressant such as prednisolone, 
mycophenolate mofetil, cyclophosphamide, angiotensin blockade etc 
Table 21.5 Histology based treatment of Glomerular diseases 
S/N 
Histological 
Pattern 
Treatment Regime 
Special considerations 
1 
Minimal 
change 
disease 
Children 
Steroid Sensitive  
Initial: A: prednisolone 60mg/m2/d] or 2mg/kg/d 
[max 60mg/d] for 6 weeks [complete 6weeks of 
initial treatment if remission is attained at 
4weeks) 
Continue: 
A: 
prednisolone 
40mg/m2 
or 
1.5mg/kg for 6weeks, if the patient has attained 
remission by 4weeks of initial treatment, after 
6weeks of alternate days’ therapy taper and 
stop within 6weeks (taper by 5-10mg a week) 
Relapsing 
Steroid 
Sensitive 
0.9% 
sodium 
chloride 
A: prednisolone 60mg/m2 or 2mg/kg [max 
60mg/d] until in complete remission for 3 days,  
THEN 
A: prednisolone single dose on alternate days 
(40mg/m2 per dose or 1.5mg/kg per dose: 
maximum 40 mg on alternate days) for at least 4 
weeks. 
S: levamisole (PO) 2.5mg/kg on alternate days 
for 12months 
Frequent relapse steroid dependent 
S: cyclophosphamide 2mg/kg/d 10-12 weeks 
[max 168mg/kg cumulative dose] OR 
S: cyclosporine 4-5mg/kg/d (starting dose) OR 
S: tacrolimus 0.1mg/kg/d (starting dose) OR 
S: everolimus 0.5-2mg 12hourly OR 
S: sirolimus 1-3mg 12hourly OR 
S: mycophenolate mofetil 1200mg/m2/d in two 
divided doses 
S: rituximab 375-1000mg/m2 
Steroid resistant Nephrotic syndrome 
S: mycophenolate mofetil 1200mg/m2/d in two 
divided doses OR 
S: mycophenolate sodium AND 
A: prednisolone high dose 
In children biopsy is 
indicated for 
1.
Children with
steroid
resistant NS
2.
Late failure to
respond
following initial
response
3.
Decreasing
kidney
function
Monitor calcineurin 
inhibitor toxicity/levels 
Adults 
D: 
prednisolone 
(PO) 
1mg/kg 
24hourly 
(maximum 80 mg) OR 
alternate-day single dose of 2 mg/kg (maximum 
120 mg – 4-week if remission, continue to 16 
weeks if complete remission not achieved 
Frequent relapse/steroid dependent/resistant 
Slow 
taper 
after 
remission over 6 months 
Check HBA1c monthly 
Screen osteoporosis  

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2 
Focal 
segmental 
glomerulos
clerosis 
for idiopathic only 
D: prednisolone (PO) 1mg/kg [max 80mg] daily 
or alternate day dose 2mg/kg [max 120mg] 4-
16weeks 
OR 
Intolerance for steroids or steroid resistant 
S: cyclosporine 3.5-5mg/kg/d in 2divided doses 
OR 
S: tacrolimus 0.1mg/kg/day in 2 divided doses 
(then titrate) 
Exclude secondary 
Slow 
taper 
after 
remission over 6months 
Monitor levels 
3 
Membrano
us 
nephropath
y 
For idiopathic membranous nephropathy only 
Children 
Alternating 
monthly 
treatment 
with 
Methyl 
prednisolone + Prednisolone (month 1, 3 & 5) 
and oral Cyclophosphamide (month 2, 4 & 6)  
D: methylprednisolone 10mg/kg for 3days, 
prednisolone 0.5mg/kg for 27 days 
S: cyclophosphamide 2mg/kg for 30 days 
 Alternative regimes 
S: cyclosporine 3.5-5mg/kg in two divided doses 
with prednisolone 0.15 mg/kg/day for 6 months  
S: tacrolimus 0.2mg/kg in two divided doses 
without prednisolone 
Adults 
S: cyclophosphamide 
A: prednisolone 1mg/kg/day 
D: methylprednisolone IV monthly 
Alternative regimes 
S: tacrolimus 0.1mg/kg/day in 2 divided doses 
for 6 months OR 
S: cyclosporine 3.5-5mg/kg/d in 2 divided doses 
If albumin is less than 25g/l + thrombosis risk 
C: 
warfarin 
5mg 
PO 
[refer 
to 
DVT 
anticoagulation] 
Exclude secondary 
Monitor for 6 months 
before initiation unless 
life 
threatening 
symptoms OR 
Raising creatinine 
-Do 
not 
use 
serum
creatinine 
>309
micromol/l [CKD patient]
Kidney biopsy might be 
repeated 
4 
Membrano
proliferative 
S: cyclophosphamide OR 
S: mycophenolate mofetil 1200mg/m2/d in two 
divided doses 
OR 
S: mycophenolate sodium 
AND 
A: prednisolone 
5 
Immunoglo
bin 
A 
Nephropath
y 
Initial supportive care for 3-6 month 
C: enalapril (PO)10-20mg  24hourly OR 
C: lisinopril (PO)2.5-10mg 24hourly 
For those persistent proteinuria 1g/d for 6 
months 
Adults and children 
A: prednisolone (PO) 1mg/day for 6 months 
Note 
Other registered ACEI 
or ARBs may be used 
as 
in 
Hypertension 
section 
6 
Lupus 
nephritis 
Adult 
All patients 
S: 
hydroxychloroquine 
(PO) 
6mg/kg/day 
maintenance 
Class II with proteinuria >3g/day 
Treat as in Minimal change disease above 

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Class III and class IV 
Initial 6 months 
D: methylprednisolone (IV slow) 250mg-1000mg 
30min 3days monthly 
AND 
S: 
cyclophosphamide 
(IV) 
500-1000mg/m2 
monthly  
OR  
S: mycophenolate mofetil (PO) 0.5-1g 12hourly 
titrating (PO) 1.5g 12hourly if tolerated OR 
S: mycophenolate sodium  
Maintenance 
S: azathioprine (PO) 1.5-2.5mg/kg/d  
OR 
S: mycophenolate mofetil (PO) 0.5-1g 12hourly 
OR 
S: mycophenolate sodium OR 
S: cyclosporine 4-5mg/kg/d (starting dose) 6 
months OR 
S: tacrolimus 0.1mg/kg/d (starting dose) 
Oral prednisolone less 
effective 60mg/day may 
be given 
Open to use a shorter 
more frequent regime 
EURO 
lupus 
Cyclophosphamide 
500mg every two weeks 
x 6doses 
Class V + persistent nephrotic range proteinuria 
As clas II and IV 
7 
Pauci-
Immune 
focal 
and 
segmental 
necrotizing 
glomerulon
ephritis 
Initial 
S: cyclophosphamide (IV) 15mg/kg every 2 
weeks x3 doses then every three weeks for 3-6 
months OR 
S: cyclophosphamide oral 1.5-2mg/kg daily 3-6 
months 
AND 
D: methylprednisolone (IV) 250mg-1000mg slow 
30min 3days as induction then  
Prednisolone 1mg/kg then taper to 30mg in one 
week then taper down to 5mg by 4-6months 
Severe disease 
S: rituximab 1g followed by 14 days later 
another 1g  
OR 
S: rituximab 375 mg/m2 per week for 4 weeks 
AND 
D: methylprednisolone (IV) 250-1000mg slow 
30min 3days as induction then  
A: prednisolone 1mg/kg then taper to 30mg in 
one week then taper down to 5mg by 4-6months 
Maintenance therapy  
S: azathioprine (PO) 1-2mg/kg/d 18months 
OR 
S: mycophenolate mofetil 1g 12hourly OR 
S: mycophenolate sodium 
S: Haemodialysis 
S: Plasmapheresis 
In special indications 
21.4 Kidney Transplantation 
Kidney transplantation is one of the kidney replacement therapies with good outcomes in morbidity 
and mortality. A Kidney Transplant recipient (KTR) is a fully rehabilitated individual who is capable of 
contributing to the society. 
21.4.1: Transplant Donor Evaluation 
General principles of preparing a live Kidney Transplant Donor will be outline in this subsection. Risk 
assessment and communication to ensure the donor candidate is able to decide without undue 
pressure is one of the early steps in evaluation. The transplant program policies of concerned centre 

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should be the basis for decision. Post decision for both accepted or excluded, follow up care should 
be formulated. 
Clinical presentation 
A complete history and physical examination should be documented. 
Investigations 
Investigations will be based on the following :- 
Adults aged 18years and above should be considered for live related donation. Pre-donation 
evaluation should include  
•
Psychosocial assessment
•
Surgical assessment for suitability
o
Obesity
o
Anticoagulation
o
Vascular anatomy and native kidneys in polycystic kidney disease
o
Urology
•
Diabetes screening
•
Cancer screening this should proceed even after transplantation.
o
Imaging, cystoscopy even colonoscopy for candidates with specific increased
risks
o
Do not exclude patients with cured malignancy. Waiting time will depend on
malignancy
•
Pulmonary disease assessment
•
Cardiovascular disease assessment
o
ECG and ECHO
o
Stress ECG
o
Dobutamine ECHO if above 40 years/ has risk of myocardial arterial disease.
•
Peripheral arterial disease
o
All candidates by history and physical examination. Imaging may be necessary.
Consult vascular surgeon prior to transplantation.
•
Neurological disease screening
o
Wait for 6 months after a stroke or TIA
o
Screen for intracranial aneurysms in high risk autosomal dominant polycystic
kidney disease
•
Gastrointestinal and Liver disease
o
History and physical examination to exclude active PUD, Diverticulitis,
Pancreatitis Cholelithiasis Inflammatory bowel disease and liver disease
§
Specific investigations may be necessary
•
Haematological
o
Screen for thrombophilia and antiphospholipid antibodies in high risk individuals
o
Need for anticoagulation is not a contraindication for transplantation
•
Immunological assessment
o
Document and communicate all sensitizing events (blood transfusion &
miscarriage)
o
Perform HLA antibody testing at transplant evaluation
•
Infection screening
o
Hepatitis B/C
o
HIV
o
CMV
•
Compatibility testing
o
ABO blood typing
o
Human leukocyte typing for MHC and Class I, II in both donor and recepients
o
Donor specific anti-HLA antibodies in recipients
•
Pre-donation Kidney function
o
Serial Serum creatinine, eGFR
o
Measured creatinine clearance
o
OR measured GFR
o
In special situations single kidney GFR (using radio labelled agents eg TC-DTPA
- technetium 99mTc-diethylenetriamine pentaacetic acid (DTPA)

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21.4.2: Transplant Candidate 
All patients with CKD stage 4-5 should be informed of, educated about and considered for kidney 
transplantation regardless of socioeconomic status, sex, or ethnicity. Pre-emptive transplantation 
referral should be 6-12 months before anticipated RRT initiation. Active diseases should be 
controlled first before transplantation. 
The following are not recommended for kidney alone transplant 
•
Multiple myeloma and AL amyloidosis
•
Decompensated cirrhosis
•
Severe irreversible obstructive or restrictive lung disease
•
Severe uncorrectable and symptomatic cardiac disease
•
Progressive central neurodegenerative disease
Transplant candidate assessment should include the following 
•
Psychosocial assessment, Adherence to therapy and Tobacco use avoidance
•
Surgical assessment for suitability
o
Obesity
o
Anticoagulation
o
Vascular anatomy and native kidneys in polycystic kidney disease
o
Urology
•
Diabetes screening
•
Cancer screening this should proceed even after transplantation.
o
Imaging, cystoscopy even colonoscopy for candidates with specific increased
risks
o
Do not exclude patients with cured malignancy. Waiting time will depend on
malignancy
•
Pulmonary disease assessment
•
Cardiovascular disease assessment
o
ECG and ECHO
o
Stress ECHO
o
Dobutamine ECHO if above 40 years/ has risk of myocardial arterial disease.
•
Peripheral arterial disease
o
All candidates by history and physical examination. Imaging may be necessary.
Consult vascular surgeon prior to transplantation.
•
Neurological disease screening
o
Wait for 6 months after a stroke or TIA
o
Screen for intracranial aneurysms in high risk autosomal dominant polycystic
kidney disease
•
Gastrointestinal and Liver disease
o
History and physical examination to exclude active PUD, Diverticulitis,
Pancreatitis Cholelithiasis Inflammatory bowel disease and liver disease
§
Specific investigations may be necessary
•
Haematological
o
Screen for thrombophilia and antiphospholipid antibodies in high risk individuals
o
Need for anticoagulation is not a contraindication for transplantation
•
Immunological assessment
o
Document and communicate all sensitizing events (blood transfusion &
miscarriage)
o
Perform HLA antibody testing at transplant evaluation
•
Infection screening
o
Hepatitis b/c
o
HIV
o
CMV
21.4.3 Transplant Recipient 
This section will cover the management of kidney transplant recipients (KTRs). It includes initial and 
maintenance immunosuppression, monitoring and management of special conditions. Enhanced 
investigations and treatment in this group is paramount to ensure kidney graft survival. 

484!
21.4.4.1 Induction Therapy 
There is a choice of Interlukin 2 receptor blockers and lymphocyte depleting agents. Patients with 
high immunologic risk for acute graft rejection should receive lymphocyte-depleting agents instead 
of IL2-RA. The following factors favor using lymphocyte-depleting agents. 
•
One or more human leukocyte antigen (HLA) mismatches
•
Younger recipient and older donor age
•
Panel reactive antibody (PRA) greater than 0 percent
•
Presence of a donor-specific antibody (DSA)
•
Blood group incompatibility
•
Delayed onset of graft function
•
Cold ischemia time greater than 24 hours
For low risk patients 
Adults 
S: basiliximab 20mg (IV) stat within 2hours before transplant and (IV) 20mg stat on day 4 
OR (high risk patients) 
S: rabbit anti-thymocyte globulin 1.5 mg/kg/day for 4 to 7 days; the first dose prior to 
transplant (Intra OP) 
OR 
S: Antithymocyte globulin ATG (horse) 
Children 
For children above 35kg use same dose as adults. 
Below 35kg use below 
S: basiliximab (IV) 10mg stat within 2hours before transplant and 10mg IV stat on 
day 4 
OR (high risk patients) 
S: horset anti-thymocyte globulin 1.5mg/kg/day for 4 to 7days; the first dose prior 
to transplant 
21.4.4.2 Maintenance Immunosuppressive Medication 
A combination of immunosuppressive medication which include a calcineurin inhibitor (CNI) and an 
antiproliferative agent with or without corticosteroids is recommended at this stage. Except for when 
mammalian target of rapamycin inhibitors (mTORi) is used, it is recommended to start 
immunosuppression before or during transplantation without waiting for graft function establishment.  
Monthly investigations 
•
Serum creatinine and Blood urea nitrogen
•
Urinalysis
•
Urine biochemistry (Urine dipstick)
•
Serum Tacrolimus (12-h trough) or cyclosporin (12-h trough or 2-h post dose) levels
according to patient’s regime
Pharmacological Treatment 
 Adults 
S: tacrolimus initial 0.1-0.2mg/kg/day in 2divided doses titrate to planned serum levels 
(immediate release) 
OR 
If tacrolimus is not available 
Adults and Children 
S: cyclosporin (modified) 7-12mg/kg/day in 2divided doses (titrate to serum levels) 

485!
In special indications (eg. with Kaposi Sarcoma) or mostly low risk KTRs 
Adults 
S: sirolimus loading dose: 15mg loading dose on day 1. Maintenance: 5mg/day (trough 
concentration 5-7ng/mL 
AND 
S: mycophenolate mofetil (PO) 1-1.5g 12hourly 
OR 
S: mycophenolate sodium 360-1080mg 12hourly 
OR 
S: azathioprine Initial following transplant IV/PO 2-5mg/kg stat. Maintenance (PO) 1-
3mg/kg 24hourly 
AND 
Glucocorticoids as part of triple-agent immunosuppressive regime 
Initial 
D: methylprednisolone 7mg/kg (maximum of 500mg) IV stat intra (OP) –operation 
OR 
A: prednisolone 1mg/kg/day (max 80mg) for first 3 days’ post-transplant 
Maintenance 
A: prednisolone 20mg/day 7 days then taper by 5mg weekly maintain at 5mg/kg 
After 4months post transplantation efforts to decrease dose of immunosuppression if there has been 
no acute rejection. Do not stop steroids or CNIs  
Note 
•
Use of a non-dihydropyridine CCB to minimize CNI dosage may be economical.
•
Assessment for medication adherence is crucial. So education for all KTRs and family
members is important.
21.4. 4. 3 Monitoring schedule for the Kidney Transplant Recipients (Routine)  
Kidney transplant recipients have high risk of getting complications including surgical complications 
(first 3 months), frequent infections (first six months) and complication related to immunosuppressive 
medications including diabetic mellitus. Some of the immunosuppressive medications have a narrow 
therapeutic window and have toxic effects including nephrotoxicity. Therefor these patients need 
regular and frequent follow up as indicated in the table below. 
Table 21.6: Monitoring schedule for the Kidney Transplant Recipients (Routine 
Test 
Screening intervals by time after transplantation 
1week 
1month 
2-3months 
4-6months
7-
12month
s 
>12months
Creatinine 
+ 
eGFR 
Daily 
2-3 per week
Weekly 
Every 
2 
weeks 
Monthly 
Every 
2-3 
mo 
Urine protein 
(UACR/UPCR
) 
Once 
Every 3 months 
Annually 
Complete 
blood count 
Daily 
2-3/week
Weekly 
Monthly 
Annually 

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21.4.5. Acute Kidney Graft Rejection 
An acute rejection is clinically suspected in patients with increased serum creatinine, after the 
exclusion of other causes of graft dysfunction. Other causes are generally excluded with a biopsy. 
Acute rejection should be treated after kidney biopsy unless this will substantially delay treatment.  
Clinical presentation 
•
Occur within the first six months
after transplantation
•
Fever
•
Malaise
•
Oliguria
•
Graft pain and/or tenderness
•
Worsening
hypertension
Investigations 
•
Kidney 
biopsy 
which 
may 
be
repeated if there is failure of
treatment
•
Serum creatinine and Blood Urea
nitrogen
•
Kidney Ultrasound and dopper US
of the kidney
•
Nuclear medicine renal scans
•
Urinalysis – urine biochemistry and
microscopy
•
BK polyomavirus
•
CMV
Acute cellular rejection (Use Banff classification in treatment) 
D: methylprednisolone (IV) 300-500mg 24hourly for 3-5days followed by prednisolone 
taper. 
If corticosteroids have failed 
OR/AND 
S: rabbit Anti-thymocyte globulin 1.5 mg/kg/day for 4 to 7days 
OR 
S: anti-thymocyte globulin (ATGam) Children and Adolescents: IV: 10 to 15mg/kg/dose 
once daily for 14days, then if needed, may administer every other day up to a total of 21 
doses in 28 days 
Antibody-mediated acute rejection (Histology of injury + vascular endothelium c4d staining + 
serologic evidence) 
D: methylprednisolone (IV) 300-500mg daily for 3-5days 
AND 
S: plasma exchange 24hourly or alt. day until serum creatinine within 30% of previous 
(max 5sessions) 
OR 
S: rituximab 200 to 375 mg/m2 after completion of plasmapheresis and IVIG 
OR 
S: rabbit Anti-thymocyte globulin 1.5 mg/kg/day for 4-7days 
OR 
S: anti-thymocyte globulin (ATGam) Children and Adolescents: IV: 10 to 15 mg/kg/dose 
24hourly for 14days, (up to 21 doses in alternate days sometimes)
Diabetes 
Weekly 
Every 3 months 
Annually 
Lipid profile 
- 
- 
Once 
- 
- 
Annually 
BKV 
Nucleic 
acid testing 
monthly 
Every 3 months 
- 
EBV 
Nucleic 
acid testing 
Once 
Monthly 
Every 3 months 
- 
BP/pulse/weig
ht/height 
Each clinic visit 

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21.4. 6 Other Conditions in Transplantation and their Managements 
Table: 21.6 Other Common Conditions That Are Encountered Among Transplant Recipients 
and Their Management 
Diagnosis/Conditions 
Evaluation 
Treatment 
Recurrent Kidney Disease 
Urine protein 
Serum creatinine 
Kidney biopsy 
+/- ANCA 
+/- Anti-GBM antibodies 
CBC, LDH 
+/- Plasmapheresis 
+/- Cyclophosphamide and corticosteroids 
-/+ ACE-Inhibitor or ARBs 
Vaccinations 
Check Hepatitis B surface 
antibodies 
12weeks 
after 
completing vaccination 
All inactivated vaccines (unless not approved) are okay 
HBV vaccination before transplant 
Avoid vaccinations in the first 6/12 
Influenza vaccine may be given in the first 6months. 
AVOID live vaccines 
Pneumococcus 
Viral diseases 
BK polyoma virus (BKV) 
Kidney biopsy 
BKV Nucleic acid testing 
Reduce immunosuppression 
Cytomegalovirus 
CMV 
serologies 
pre-
transplant both donor and 
recipient 
CMV plasma Nucleic acid 
testing is used for diagnosis 
and montoring treatment 
Prophylaxis for 3 months 
S: valganciclovir (PO) 900mg 24hourly 
For treatment of life-threatening disease 
S: ganciclovir (IV) 6mg/kg 12hourly until clinical response 
Then continue with  
S: valganciclovir (PO) 900mg bid until symptom resolution 
Epstein-Barr Virus and Post-
Transplant 
Lymphoproliferative disease 
EBV by nucleic acid testing 
Reduce immunosuppressive medication with patients who 
have raising EBV loads 
EBV disease and post-transplant lymphoproliferative 
disease 
Herpes simplex virus 1,2 
and varicella zoster virus 
Superficial disease 
Oral acyclovir /valacyclovir until lesions have resolved 
Systemic disease 
1.
Reduce immunosuppressive medication
2.
Iv. Acyclovir
Frequent attacks 
Give prophylactic antivirals 
Pneumocystis 
jirovecii 
pneumonia 
Diagnosis 
by 
bronchial 
alveolar lavage and/or lung 
biopsy 
-Prophylaxis for 3-6 months with
A: trimethoprim+sulfamethoxazole
-After treatment for acute rejection (6 weeks)
-Add corticosteroids for moderate to severe disease
Candida 
Prophylaxis with oral clotrimazole lozenges, nystatin or 
fluconazole 
Cardiovascular 
diseases 
CVD 
New onset diabetes after 
transplantation (NODAT) 
Fasting 
plasma 
glucose 
and/or 
HbA1c and/or 
Glucose tolerance testing 
See above schedule or after 
starting 
or 
changing 
medication 
Adult 
A: acetylsalicylic acid 75mg PO (Balance risk/benefit)- 
maintenance 
Oral – check section on DM management in CKD patients. 
Atherosclerotic CVD 
A: acetylsalicylic acid (PO)75mg per 24hours maintenance 
Malignancy 
All malignancies 
Education 
on 
self-
examination and Health care 
directed screening 
See relevant chapter on management 
Kaposi Sarcoma 
Change to mTOR Inhibitors 

488!
21.5 Cystic Kidney Disease 
Acquired or hereditary disorders of the kidneys. Autosomal dominant polycystic kidney disease is a 
common cause of end stage kidney disease. It is progressive and incurable condition. 
Clinical presentation 
•
Kidney
o
Nocturia, polyuria and frequency due to concentration defect
o
Hypertension
o
Pain syndrome (infection, bleeding, stones, rupture or compression)
o
Uremic manifestations
•
Extra-kidney manifestations
o
Polycystic liver disease
o
Intracranial aneurysms
o
Cardiac – valvular heart disease
Diagnostic ultrasonographic criteria 
15-39 -years
≥3 cysts, unilateral or bilateral
40-59 years
≥2 cysts in each kidney
≥60 years
≥4 cysts in each kidney
Investigations
•
Ultrasonography – KUB
•
Serum creatinine
•
Urinalysis – biochemistry and microscopy
•
Genetic testing for those who want.to be donor (family history)
•
CT scan – contrast enhanced has better sensitivity
•
ALT, AST and bilirubin if using Tolvaptan
Non-pharmacological Treatment 
•
Increase fluid intake >3 L if has no fluid retention (eGFR <30mL/min/1.73m2)
•
Kidney transplantation when indicated
o
Might need pretransplant native nephrectomy
Pharmacological Treatment 
S: tolvaptan (PO) 45mg in the morning and 15mg 8hours later (titrate to 90mg am and 
30mg pm) 
o
pm dose should be taken before 4pm
21.6 Renal artery stenosis 
Renal artery stenosis is narrowing of the one or both renal arteries. Atherosclerosis or fibromuscular 
dysplasia are the commonest causes. Progression to chronic kidney disease and end-stage disease 
may be prevented or slowed. 
Clinical presentation 
•
Hypertension, which is resistant, refractory to therapy with three or more drugs.
•
Young onset hypertension with no family history
•
An acute rise in serum creatinine >30% after ACE-inhibitor or ARB use
•
Episodes of flash pulmonary oedema
•
Asymmetrical kidneys.
•
Unexplained hypokalaemia

!
!
489!
Investigations 
• 
Serum creatinine/BUN 
• 
Urine protein creatinine ratio 
• 
Urinalysis 
• 
Duplex Doppler ultrasonography 
• 
Computer tomography angiography 
• 
Magnetic resonance angiography 
• 
ACE-inhibitor Scintigraphy 
• 
Conventional arteriography
 
Non-pharmacological Treatment 
Revascularization (when >80% stenosis) 
Pharmacological 
A: acetyl salicylic acid (PO) 75mg 24hourly 
ACE-Inhibitors or ARBs as in the section of Hypertension 
A pathological description characterized by thrombocytopenia, microangiopathic hemolytic anemia 
and organ injury. AKI is a common manifestation in the kidney due to the glomerular circulation 
damage and occlusion. Early recognition is important. 
Clinical presentation 
• 
Haemolysis 
• 
Ischemic organ dysfunction 
• 
AKI 
• 
Extrarenal manifestations include 
o 
Pancreatitis and Hepatitis 
o 
Seizures 
o 
Diarrhoea/vomiting and abdominal pain 
o 
Digital gangrene 
 
Investigations 
• 
ADAMTS13 activity (>10% excludes TTP) 
• 
Bacterial culture/serology 
o 
HIV serology 
• 
ANA, anti-ds DNA, anti-phospholipids, anti Scl70 
• 
Kidney biopsy 
 
Pharmacological Treatment 
Identify and treat the underlying cause. Primary thrombotic microangiopathies includes complement 
mediated aHUS and Thrombotic thrombocytopenic purpura with decreased ADAMTS13. 
S: plasma exchange (until ADAMTS13 to exclude TTP) +/- immunosuppression 
21.8 Reflux nephropathy 
A type of chronic interstitial nephritis associated with vesico-ureteric reflux (VUR) in early life with the 
appearance of scars in the kidney as demonstrated by various imaging modalities. May be 
associated with renal dysplasia and other congenital abnormalities of the urinary tract. Including 
urethral valves. 
Clinical presentation 
• 
Usually asymptomatic 
• 
Hypertension 
• 
Frequency of micturition 
• 
Dysuria 
• 
Aching lumbar pain 
• 
Urinalysis shows leucocytes 
 
Investigations 
• 
Ultrasonography – KUB 
• 
Radionuclide DMSA scans 
• 
Serial imaging by Magnetic 
Resonance Imaging – MRI 
• 
Renal biopsy 

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• 
MCUG- micturating 
cystourethrography 
• 
Urine analysis – 
dipstick/biochemistry/microscopy 
• 
Serum creatinine 
• 
Urine culture
 
Non-pharmacological Treatment 
• 
If recurrent pyelonephritis occurs in an abnormal kidney with minimal function – 
Nephrectomy 
• 
Hypertension may be cured by removal of a diseased kidney 
• 
Severe reflux may be managed by ureteric reimplantation or sub trigonal injection of 
Teflon/polysaccharide 
 
Pharmacological Treatment 
Treat UTI as in section with Urinary tract infection. 
 
21.9 Contrast Induced Nephropathy (CIN) 
Contrast induced nephropathy (CIN), which is also known as Contrast Induced Acute Kidney Injury 
may occur after administration of iodinated contrast material, which is called contrast-induced 
nephropathy. Common contrast based studies resulting in CIN include CT scan, MRI and coronary 
angiography. Contrast induced acute kidney injury is usually characterized by rapid recovery of renal 
function. 
Clinical features  
Major clinical manifestations of CIN include  
• 
Early mild increase in serum creatinine that is generally observed within 24-48 hours after 
the iodinated contrast exposure and that is usually mild. Serum creatinine starts to decline 
within 3-7days of exposure 
• 
Nonoliguria, patients with CIN are passing urine normally and if it occurs develop 
immediately. 
o 
Oliguria and more severe elevation of creatinine may develop in patients with 
moderate to severe CKD.  
• 
Urinalysis may show sediments consistent with acute tubular necrosis. 
• 
Other 
manifestations 
of 
reduced 
GFR 
including 
hyperkalaemia, 
acidosis 
and 
hyperphosphataemia  
 
Investigations 
• 
All patients scheduled for contrast studies should have serum creatinine performed before 
the study and 24-48hours after contrast study  
• 
For patients with raised creatinine 
o 
Serial creatinine should be performed until 7 days 
o 
Potassium, sodium, phosphorus, calcium and urinalysis  
o 
Kidney ureters and bladder ultrasound 
 
Treatment and prevention of CIN  
Non-pharmacologic Treatment  
• 
Identify all at risk patients; diabetic mellitus, heart failure, patients with CKD 
• 
Stop NSAID 24-48 hours prior to contrast study  
• 
Encourage adequate hydration prior to study  
• 
Use lower possible dose of contrast (<125 ml)   
• 
Use low osmolar (iohexol, ioversol) or iso-osmolar (iodixanol) contrast media 
 
Pharmacologic Treatment 
• 
Fluid administration should be used if there are no contra-indications. Normal saline should 
be administered before and continued for few hours after the study 
o 
Outpatients: 3mL/kg over one-hour pre-procedure and 1-1.5mL/kg/hour during 
and for four to six hours’ post-procedure, with administration of at least 6mL/kg 
post-procedure 

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o 
Inpatients; 1mL/kg/hour for 6-12hours pre-procedure, intra-procedure, and for 6-
12hours post-procedure 
Note 
Patient with severe CIN may need to undergo haemodialysis if there is no improvement within 
7days. 
 
 
21.10 Urinary Tract Infection (UTI) 
Urinary tract infections may involve the upper or lower urinary tract. Infections may be complicated 
or uncomplicated. Uncomplicated cystitis is a lower UTI in a non-pregnant woman of reproductive 
age and who has a normal urinary tract. All other UTIs should be regarded as complicated. The 
commonest causative pathogens for UTIs irrespective of the group of patients involved in Tanzania 
are Escherichia coli, Klebsiella pneumonia, Proteus spp. and Staphlococcus aureus. 
 
Note  
• 
Differentiation of upper from lower urinary tract infection in young children is not possible 
on clinical grounds 
• 
Upper UTI is a more serious condition and requires longer and sometimes intravenous 
antimicrobial treatment.  
• 
Special considerations should be given in the following groups of patients: children, 
pregnant women, elderly (>60 years) and other individuals with functional or structural 
abnormalities in the urinary tract. 
 
Clinical presentations of lower UTI (cystitis) 
• 
Suprapubic pain/tenderness, dysuria, frequency, and urgency 
• 
Pyuria and occasionally haematuria 
• 
Temperature 380C or higher  
 
Clinical presentations of upper UTI (pyelonephritis)  
• 
Flank pain/tenderness  
• 
Pyuria and occasionally haematuria 
• 
Temperature 380C or higher  
• 
Vomiting 
 
Clinical presentations of catheter associated UTI (CAUTI) 
• 
Presence of symptoms and signs of UTIs (as stated in cystitis or pyelonephritis above) 
occurring in a person whose urinary tract is currently catheterized or has had a catheter in 
place within the past 48 hours. 
 
Clinical presentations of urosepsis  
• 
Any of the above features of cystitis or pyelonephritis plus two or more of the following: (1) 
Temperature >38° C or <36° C; (2) tachycardia >90 beats per minute; (3) tachypnoea 
>20/minute, (3) WBC count>12,000/mm3  or <4000/mm3; confusion, hypotension or any 
other evidence of organ dysfunction as a sequelae of UTI complications. 
 
Investigations 
• 
Quantitative or semi-quantitative urinalysis (high protein, low sugar, nitrites positive, 
leucocyte esterase positive, and low pH) and Urine microscopy (>8–10 WBC/HPF) may be 
suggestive of UTIs. 
• 
Quantitative urine culture (growth of at least 104 or 105 colony forming units of bacteria/ml 
of urine) and antimicrobial sensitivity testing. Concomitant urine and blood cultures are 
indicated in case of urosepsis. 
• 
Urinary LAMM – in patients with suspected to have genitourinary TB 
• 
Ultrasound (kidney and pelvis) to exclude stones or structural abnormalities in patients with 
recurrent UTI 
 
Note 
Positive WBC counts on urinalysis or urine microscopy + compatible 2 or more clinical presentations 
supported by urine culture in centers where this test is available. 
 
Non-pharmacological Treatment, 
• 
Ensure adequate hydration 

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• 
Voiding of urine whenever an urge to micturate occurs; or after sexual intercourse in 
adults. 
• 
Removal of indwelling bladder catheter (where indicated) 
 
Pharmacological Treatment  
Analgesics in severe dysuria and flank pain  
Adult:  
A: paracetamol (PO) 500-100mg every 6-8hours.  
Children: 
 
A: paracetamol (PO) 15 mg/kg/dose 4–6hourly when required to a maximum of 4doses 
per 24hours; 
 
Uncomplicated cystitis  
 
Adults:  
A: nitrofurantoin (PO) 100mg 12hourly for 5days 
 
 
OR 
B: flucloxacillin + amoxicillin (FDC) (PO) 500mg 8hourly for 5days 
 
Complicated cystitis  
Adults:  
A: ciprofloxacin (PO) 500mg 12hourly for 7days 
 
 
OR 
B: amoxicillin+ clavulanic acid (FDC) (PO) 625mg 12hourly for 7days 
 
For pregnant women and adolescents 
A: nitrofurantoin (PO) 100mg 12hourly for 5days 
 
 
OR 
B: amoxicillin + clavulanic acid (FDC) (PO) 625mg 12hourly for 7days 
 
For children 
A: nitrofurantoin (PO) 50mg 12hourly for 5days (Do not give Nitrofurantoin if the child has 
G6PG deficiency or porphyria) 
 
 
OR 
B: amoxicillin + clavulanic acid (FDC) (PO) 40mg/kg/day of amoxicillin in 3divided doses 
(maximum 2000 mg amoxicillin) for 7days 
 
Acute Pyelonephritis  
Outpatient therapy is only indicated for women of reproductive age, who do not have any of the 
danger signs – see referral criteria. All other patients should be referred.  
A: ciprofloxacin (PO) 500mg 12hourly for 10days 
 
 
OR  
B: ceftriaxone (IV) 1g [For a child ceftriaxone (80 mg/kg I.V or I.M)] 24hourly for 5days  
 
Catheter associated UTI (CAUTI) 
Patients with indwelling or suprapubic catheters and nephrostomy tubes invariably become carriers 
of potential bacterial pathogens and routine antimicrobial treatment is not indicated. However, 
judicious evidence from clinical and laboratory evidence is critical to warranty antimicrobial 
therapies.  
A: ciprofloxacin (PO) 500mg 12hourly for 7days  
 
 Urosepsis 
A: gentamicin (I.V/I.M) 120mg [For children 7.5mg/kg] 24hourly for 5days (completion of 
10days treatment to be guided by culture results)  
AND  
D: ceftriaxone + sulbactam (FDC) (IV) 1g [For children 80 mg/kg I.V or I.M] 24hourly for 
5days  
 
Alternatively; 
A: gentamicin (I.V/I.M) 120mg [For children 7.5mg/kg] 24hourly for 5days (completion of 
10 days’ treatment to be guided by culture results)  
 
 
AND  
S: piperacillin + tazobactam (FDC)(IV) 4.5g 6-8hourly for 5–7days 

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OR 
S: Meropenem (IV) 250–500mg 8hry for 5–7days  
 
Once results for urine and blood cultures are available change the antibiotic treatment options 
accordingly. 
 
Referral  
Refer the patient urgently to the next facility with adequate expertise and facilities if: - 
 
Acute pyelonephritis with:  
o 
Vomiting  
o 
Features of suggestive of urosepsis  
o 
Diabetes mellitus  
 Acute pyelonephritis in:  
o 
Pregnant women  
o 
Women beyond reproductive age  
o 
Men  
 
21.10 Urology Disorders 
Are diseases that affect urinary system including urinary incontinence, urolithiasis, benign prostatic 
hyperplasia, prostate cancer. 
21.10.1 Prostatitis 
It is an inflammation of the prostate usually secondary to bacterial infection caused by urinary or STI 
pathogens.  
 
Clinical Presentation 
• 
Perineal, sacral or suprapubic pain  
• 
Dysuria and frequency  
• 
Varying degrees of obstructive 
symptoms which may lead to 
urinary retention  
• 
Sometimes fever
 
Investigations  
• 
Urine analysis 
• 
Urine culture 
 
Pharmacological Treatment  
Acute bacterial prostatitis  
In men < 35 years or if there are features of associated urethritis (STI regimen):  
S: cefixime (PO) 400mg as a single dose  
 
Followed by:  
A: doxycycline (PO) 100mg 12hourly for 7days  
 
In men > 35 years or if there is associated cystitis:  
A: ciprofloxacin (PO) 500 mg 12hourly for 14days 
 
Referral to Urologist if 
• 
No response to treatment  
• 
Urinary retention  
• 
High fever  
• 
Chronic/relapsing prostatitis  
 
21.10. 2 Benign Prostatic Hyperplasia (BPH) 
Benign prostatic hyperplasia is a noncancerous (benign) growth of the prostate gland. Management 
of BPH depends on severity of symptoms according to International Prostate Symptom Score (IPSS) 
 
Clinical Presentation 
• 
Obstructive symptoms: weak, intermittent stream and urinary hesitancy   
• 
Irritative (frequency, nocturia and urgency) voiding symptoms.  
• 
Digital Rectal Examination reveals a uniform enlargement of the prostate with smooth 
surface and firm in consistence. The median sulcus is also palpable 

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• 
Urinary retention with a distended bladder may be present in the absence of severe 
symptoms, therefore it is important to palpate for an enlarged bladder during examination.  
• 
Pelvic or transrectal USS confirms the prostate enlargement 
• 
Prostatic specific antigen levels are within normal range 
• 
Symptoms should be graded by the IPSS – international prostate symptom score into mild, 
moderate and severe 
 
Non-pharmacological Treatment  
• 
Patients with mild symptoms should be put under watchful waiting (change of lifestyle and 
regular follow up) 
o 
Reduce fluid intake especially in the evening, avoid caffeinated drinks 
• 
Patients with severe symptoms should undergo surgery, transurethral resection of the 
prostate for prostate weighing up to 75g and those weighing more than 75g should 
undergo open prostatectomy 
• 
For patients presenting with urinary retention, insert a urethral catheter as a temporary 
measure while patient is transferred to hospital  
• 
Remove drugs that prevent urinary outflow e.g. tricyclics and neuroleptics.  
 
Pharmacological Treatment 
Patients with moderate symptoms according to IPSS should be put under medical therapy unless 
opt for surgery. 
Medical treatment of BPH includes alpha-adrenergic blocker or 5 alpha- reductase inhibitor or a 
combination of both 
 
Adrenergic Alpha Blockers: 
 
D: tamsulosin (PO) 0.4mg 24hourly 
OR 
 
D: alfuzosin (PO) 10mg 24hourly 
 
5-alpha Reductase Inhibitors 
 
D: finasteride (PO) 5mg 24hourly 
 
 
 
OR 
S: dutasteride (PO) 0.5mg 24hourly 
Anticholinergics 
 
S: oxybutynin (PO) 5mg 8hourly for patients with persistent urgency despite above 
medications 
 
Note 
All patients with BPH and associated complications like recurrent UTI, Haematuria, Kidney 
insufficiency, hernia and urinary stones need surgery and should be referred to centres where 
specialized care can be offered.  
 
21.10. 3 Prostate Cancer 
Usually occurs in men over 50years and is most often asymptomatic. Systemic symptoms, i.e. 
weight loss, bone pain, etc. occurs in 20% of patients. Obstructive voiding symptoms and urinary 
retention are uncommon in the early stages of the disease. 
 
Clinical Presentation 
• 
The prostate gland is hard and may be nodular with obliterated median sulcus on digital 
rectal examination and/or PSA elevation 
• 
Verification of prostate cancer is by prostate core biopsy 
• 
As the axial skeleton is the most common site of metastases, patients may present with 
back pain or    pathological fractures. 
• 
Lymph node metastases can lead to lower limb lymphoedema. 
• 
Serum prostate specific antigen (PSA) is generally elevated and may be markedly so in 
metastatic disease. 
 
Note 
Interpretation of PSA should be interpreted careful, PSA has a low sensitivity therefore some 
patients may have low PSA value (<4.0ng/mL) and have prostate cancer. There false positivity 
where PSA is raised in the absence of prostatic cancer 
 
 

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Non-pharmacological Treatment 
• 
Watchful waiting- low risk patients with short life expectancy 
• 
Active surveillance-lowest risk of cancer progression and more than 10years life 
expectancy 
• 
Radical prostatectomy- patients with localized cancer and life expectancy more than 
10years 
• 
Surgical Androgen deprivation therapy (bilateral orchidectomy) for advanced prostate 
cancer 
 
Pharmacological Treatment 
Medical androgen Deprivation Therapy is offered in patients with advanced disease, PSA levels 
more than 50ng/ml, poorly differentiated tumour and in those who cannot receive any form of local 
treatment. 
 
For early disease 
• 
Watchful waiting – low risk patients with short life expectancy 
• 
Active surveillance – lowest risk for cancer progression and more than 10 years life 
expectancy 
• 
Radical prostatectomy – patients with localized cancer and life expectancy more than 10 
years 
 
Late disease 
Luitenising hormone releasing hormone (LHRH) Agonists 
S: goserelin (subcutaneous) 3.6mg every week or 10.8mg every 12weeks 
OR 
S: bicalutamide (PO) 50–150mg 24hourly 
 
 
OR 
S: Both LHRH and bicalutamide 50mg 24hourly if above options fail 
 
 
OR 
Castrate resistant prostate cancer 
S: docetaxel 75mg/m2 every 3weeks 
 
 
Referral for oncologist: All patients with suspected cancer (For more detail refer to the Malignant 
diseases section) 
21.10.4 Urolithiasis 
Stones formed in the urinary tract are a result of urine, which is supersaturated with respect to a 
stone-forming salt. Kidney stones have been associated with an increased risk for chronic kidney 
disease, end-stage kidney failure, and cardiovascular diseases. 
 
Clinical Presentation 
• 
Sudden onset of acute colic, localized to the flank, causing the patient to move constantly.  
• 
Sweating, pallor, nausea and vomiting and blood in urine  
• 
Referred pain to the scrotum or labium (L1) on the same side as the stone moves down 
the ureter  
• 
Urinalysis with features of infection or microscopic haematuria 
• 
Ultrasound with an acoustic shadow with features of obstructive uropathy eg. Hudroureter 
or hydronephrosis 
• 
Plain x-ray can pick up to 90% of calculi as they are radio-opaque 
• 
Conventional intravenous urogram or CT urography confirms upper urinary tract lithiasis. 
 
Investigations 
• 
Plain abdominal X-ray 
• 
Non-contrast CT-Scan of the Kidney Ureter and Bladder (CTKUB) – GOLD STANDARD 
• 
Ultrasonography – Kidney Ureter and Bladder (KUB) 
• 
Chemical composition of the stone – most valuable test 
• 
Urinalysis – Dipstick biochemistry +Microscopy 
 
For First Stone 
• 
Serum Calcium, magnesium, phosphate, uric acid, urea, K, Na, Cl, HCO3 
 

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Recurrent Stone 
• 
Parathyroid hormone 
• 
Urine dipstick – biochemistry 
• 
24-HR Urea, creatinine clearance, sodium, calcium, oxalate and uric acid 
 
 
Table 21.7: Non-Pharmacological Treatment 
 
• 
Surgical intervention is indicated (uteroscopy, percutaneous nephrolithotomy and 
extracorporeal shockwave lithotripsy) for  
o 
obstructive uropathy  
o 
infection,  
o 
urgent intervention (surgical or otherwise) if a patient has a solitary kidney 
emergency decompression is indicated by percutaneous nephrostomy placement 
or ureteric DJ Stenting 
• 
Stone 
fragmentation 
with 
ureteroscopy 
stone 
fragmentation/ 
ultrasonic 
disaggregate/extracorporeal shock wave lithotripsy 
 
Pharmacological Treatment  
Analgesia for pain, if needed:  
A: ibuprofen (PO) 400mg 8hourly for 3 days 
OR 
A: diclofenac (IM) 75mg stat then continue (PO) 50mg 8hourly 
OR 
B: tramadol (IV) 100mg stat then continue with (PO) 50mg 8hourly 
 
 
OR 
B: pethidine (IM) 100mg stat 
Other management e.g. antiemetic for vomiting may be needed or IV fluids 
 
For distal ureteric calculi less than 7mm  
D: tamsulosin (PO) 0.4mg 24hourly for a month may be prescribed for spontaneous stone 
expulsion.  
OR 
B: nifedipine (PO)10mg 24hourly for 30days (monitor blood pressure) 
 
For prevention of stone 
 
Thiazide diuretics for calcium stones ANY of the following  
 
A: bendrofluazide (PO) 5mg 24hourly 
OR 
D: hydrochlorothiazide (PO) 12.5-50mg 24hourly 
 
For low uric acid levels 
 
 
AND 
 
B: allopurinol (PO) 50-100mg 24hourly  
21.10.5 Obstructive uropathy 
Obstructive uropathy contribute to the burden of CKD, obstruction may occur anywhere along the 
urinary tract. Causes of obstruction vary based on the location of obstruction 
• 
Obstruction within the kidney causing dilatation of individual calyces  
Type of stone 
Prevention strategy 
All stones 
Increase water intake to have at least 2L of urine/day 
Hyperoxaluria 
Low oxalate diet + increase dietary calcium intake 
Limit vitamin C supplementation 
Calcium stones 
Reduce salt intake, Restriction of animal protein (less meat, fish 
and poultry) 
Increase intake of fruits and vegetables 
Calcium oxalate, cystine and 
uric acid 
Diet high in fruits and vegetables, Prescription citrate,  
Uric acid 
Control gout 
Calcium phosphate and struvite  
Acidify urine 

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• 
Obstruction at or distal to the renal pelvis causes diffuse caliectasis of hydronephrosis. 
Ureteral obstruction may result from stones, tumors, enlarged lymph nodes and 
retroperitoneal fibrosis 
• 
Bladder tumors can obstruct one or both ureters or ureteric orifices 
 
Clinical Presentation 
Generally, patients present one or more of the following symptoms  
• 
Pain  
• 
Change in urine output 
• 
Hypertension  
• 
Hematuria  
• 
Increased serum creatinine  
 
Investigations  
• 
Urinalysis 
• 
Full blood count  
• 
Serum creatinine   
• 
KUB ultrasound  
• 
Intravenous pyelography  
• 
CT IVU 
• 
MRI 
• 
Examination under anaesthesia 
 
Non-pharmacological treatment 
Measures to reduce recurrence risk 
• 
Taking adequate fluids 2L/day for patients with renal stones  
 
Pharmacological Treatment 
• 
Relief of pain 
C: diclofenac (PO) 100mg as initial dose followed by 50mg 6-8hourly  
OR 
C: morphine (IV/SC) 1-4mg 1-4hourly (may increase up to 10mg 4hourly as needed for 
acute pain) 
 
Referral of the patients   
• 
The patient should be referred to the urologist for definitive treatment of the cause of 
obstruction  
• 
Patient may need long term follow up if there is impaired renal function 
 
21.11 Sexual Dysfunction 
21.11.1 Female Sexual Dysfunction 
Sexual dysfunction in women refers to sexual problems associated with personal distress and may 
take different forms including lack of sexual drive, impaired arousal, failure to achieve orgasm or 
dyspareunia. Diagnostic criteria are reached when a sexual problem is recurrent/ persistent and 
result in personal distress.  
 
The causes of sexual dysfunction are multifactorial and may include psychological problem 
(depression or anxiety), relationship conflicts, fatigue, stress, prior physical or sexual abuse, 
medications or physical problems that make sexual activity uncomfortable (endometriosis, 
genitourinary symptoms of menopause). 
 

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Non-pharmacological Treatment 
Correction of contributing factor (genital lesion, systemic or hormonal factors and drugs e.g. SSRIs) 
Psychological therapies 
Use of antidepressants 
 
21.11.2 Male sexual dysfunction 
It is inability to attain and maintain an erect penis with sufficient rigidity for vaginal penetration and 
ability to ejaculate. Organic causes include neurogenic, vasculogenic, endocrinological as well as 
many systemic diseases and medications.  
 
Non Pharmacological Treatment 
• 
Education counselling  
• 
Consider the removal of drugs that may be associated with the problem.  
• 
A change in lifestyle or medications may resolve the problem, e.g. advise cessation of 
smoking and alcohol abuse.  
 
Pharmacological Treatment  
• 
Treat the underlying condition.  
• 
If persist refer the patient  
 
Note 
The use of medication like sildenafil may result to serious problem. 
 
 
 
 
 

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CHAPTER TWENTY-TWO 
MALIGNANT DISEASE CONDITIONS 
 
22.1 Cancer Prevention, Screening and Early Detection 
Cancer represents a unique public health opportunity, unlike other Non-Communicable disease, it is 
possible to prevent most of cancers prevails in Sub-Saharan Countries including Tanzania by 
intervening at both Primary and secondary levels of the natural history of the disease. 
 
Primary prevention is mainly based on educating the public to modify their life styles to avoid risk 
factors for cancer as well as ensure the availability and affordability of prophylactic vaccines, the 
secondary prevention focus on the availability of effective screening programs that allow for 
reducing incidence and downstage cancer.  
 
Early detection detects (or diagnoses) the disease at an early stage, when it has a high potential for 
cure (e.g. cervical or breast cancer) reduce morbidity, improve quality of life as well as increase 
survival due to good outcome following treatment. 
 
Key interventions in Cancer Prevention Primary Prevention 
This is the most efficient and cost-effective form of cancer control it involves prevention interventions 
that keeps a cancerous process from developing which can be through behavior change by health 
counseling, education and environmental controls or through a biological mechanism, such as 
Vaccination. 
 
Among the most important modifiable risk factors for cancer are: tobacco use; overweight, and 
obesity; harmful alcohol use; sexually transmitted human papilloma virus (HPV) infection, HIV/AIDS; 
air pollution, both outdoor and indoor; and occupational carcinogens. 
 
Public health education and promotion: Public Awareness raising on risk factors for cancer and 
providing education on ways of avoiding as well as reducing exposure through behavior change is 
essential. However, this is a long term intervention and may be difficult to quantify. Community 
education should also focus raise awareness and knowledge on the benefits of early diagnosis, 
ways of detection and screening. These preventive measures should be highly promoted by also 
raise awareness of warning symptoms and signs of cancer and taking prompt action, by the general 
public as well as physicians, nurses and other health care providers, can have a great impact on the 
disease through early diagnosis and hence more effective management. 
 
Vaccination 
Human papillomaviruses (HPVs) is among the most important infections associated with cancers, 
which can cause most cervical and anal cancers as well as a fraction of oral cancers; hepatitis B 
virus (HBV) and hepatitis C virus (HCV), which can cause liver cancer; and Helicobacter pylori, 
which is a bacterium that can cause cancer of the stomach.  
 
Highly effective vaccines against HBV have been available for several decades and most countries 
include HBV vaccination in their childhood immunization programs; vaccination is also highly 
effective in preventing infection with the HPV types that cause the majority of cervical cancers.  
 
Hepatitis Vaccination is recommended to general population and the high risk group such as health 
care workers, and can be done at all levels. The Vaccine is given in 3 doses in 6 months. Second 
dose should be given after 1 month after 1st dose and 3rd dose 6 months after the first dose. 
 
HPV vaccination is recommended to girls between the age of 9 to 14 years. HPV vaccine is given in 
two doses at 6 months apart.   
 
Secondary Prevention: Early detection and Cancer Screening 
The main aim of cancer screening is to prevent death from cancer. Screening can also make it 
possible to use less severe treatment methods if the cancer is detected early enough. Cervical, 
breast, skin, Prostate and bowel cancer, screening can actually prevent the cancer from developing. 
However only cervical cancer screening is offered as part of an organized program with adequate 
resources for high quality.  
 

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Breast Cancer: Screening for breast cancer includes breast self-examination (BSE), clinical breast 
examination (CBE) and breast imaging (mammogram and/or ultrasound scanning). BSE is 
recommended at day 10 of the menstrual cycle. For post-menopausal women, a monthly BSE 
schedule should be established.  
 
All patients with clinical suspicious lesions should have imaging as part of early detection. 
Mammogram is recommended for women over 40 years, while ultrasound is the imaging of choice 
for younger women. MRI may be used where possible for screening and early detection in patients 
at high risk of breast cancer such as those with BRCA1 & 2 gene mutations. 
 
For prevention and early detection, all women aged 25 years and above should be taught on breast 
self–examination and should be advised to have regular physical check with a heath provider and 
have a regular annual Mammography. They should also be encouraged on physical excise and 
proper diet. 
Skin Cancer: Prevention or early detection is through frequent self–health check–up or screening 
exercise and prompt treatment of early skin lesions. For light skinned people–avoid UV light 
especially people with Albinism. 
Colon: colorectal cancers are usually asymptomatic until advanced stage hence regular screening 
with annual digital rectal examination, stool for occult blood + colonoscopy and are recommended 
starting at 50 years of age. 
Prostate: Routine screening not recommended, but when done should begin with PSA and digital 
rectal examination at age 50 if life expectancy is >10 years. It is recommended that screening of 
high risk group should take place starting at age 45. 
22.2 Gynecological Malignancies 
22.2.1 Cancer of the Uterine Cervix 
 
It is caused by persistent infection with human papilloma Virus (HPV). Risk factors include early 
coitus and childbirth, multiple sexual partners, smoking and HIV infection. It is preventable through 
avoiding risk factors, screening and vaccination. When detected early, it is curable by surgery or 
radiotherapy hence regular screening is required for all women. 
 
Diagnostic Criteria 
• 
Asymptomatic in early stages of the disease.  
• 
Majority present with abnormal vaginal bleeding (post coital, inter-menstrual or 
postmenopausal vaginal bleeding).  
• 
Foul smelling discharge, pain and incontinence (VVF or RVF) are symptoms of late 
disease    
 
Investigations 
• 
FBC, LFT, RFT and HIV test.  
• 
CXR.  
• 
Abdomen and Pelvis USS.  
• 
Pelvic MRI, CT Scan of the abdomen and pelvis.  
• 
PET/CT 
• 
Bimanual Examination under Anesthesia (EUA) and Biospy.   
 
Table 22.1 Management of Cervical cancer by disease stage. 
Stage 
Management 
Stage IA1: 
Simple hysterectomy or if patient desires fertility consider conization 
Stage IA2–IB2 
Consider Wertheim Hysterectomy plus bilateral pelvic lymph node 
dissection. RT may be given post operation or alone. No benefit of 
adjuvant chemotherapy 
Stage IB2; IIA and IIB 
2.0Gy/Per Fraction to 50Gy external beam + 8.0 Gy x 3 Fractions HDR 
+/– Chemotherapy depending on renal function 
Stage IIIA and IIIB 
If stage by CT or MRI and no distant metastasis and good renal function: 
2.0Gy to 50 Gy external beam + 8.0 Gy x 3 Fractions HDR 
Stage lll A and lll B 
2.5 Gy to 50 Gy external beam only no HDR nor chemotherapy if poor 
renal function 
Stage lV A + good general 
Can be given curative dose of 50 Gy external beam 

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condition, no VVF or RVF: 
+ Brachytherapy or palliative dose of 20Gy/5 Fractions or 30 Gy/10 
Fractions or 10Gy Single Fraction monthly X 2 Fractions 
Stage lll B advanced/stage 
lV B with bad general 
condition 
Palliative care / supportive care 
 
Pharmacological Treatment 
Chemotherapy is given as a radiotherapy sensitizer or on palliative intent.  
S: cisplatin (IV) 40 mg/m2 to max of 70 mg is given weekly during radiation therapy. 
• 
If patient is HIV positive or has mild renal impairment consider 30 mg/m2 to max of 60 mg 
weekly. 
• 
Available and preferred palliative chemotherapy drugs for metastatic, recurrent or 
persistent cancer after RT, given in single or combination regimen include: cisplatin, 
paclitaxel, bevacizumab, carboplatin, docetaxel and gemcitabine. 
• 
Do FBC, urea and creatinine before each cycle of chemotherapy. 
 
 
Follow up: 
First visit at 4–6 weeks post treatment then 3–6 months in the first 2 years, there after yearly.  
 
*This follow-up schedule applies to all malignancies with few exceptions* 
Note 
• 
All patients suspected or confirmed to have cervical cancer should be 
referred to cancer specialized centers for definitive management.      
• 
All women aged 25 years and above are advised to have regular cervical 
screening with VIA and VILI or Pap smear                                                                                   
 
22.2.2 Endometrial Cancer 
This is predominantly a disease of old women. Adenocarcinoma is the commonest histological type. 
Risk factors for endometrial carcinoma include obesity, diabetes, high fat diet, early age at 
menarche, nulliparity and late age at menopause, old age and use of tamoxifen. 
 
Diagnostic Criteria 
• 
 Abnormal Uterine Bleeding for women in the post-menopausal period. 
• 
For Pre-menopausal women; may present with irregular bleeding, intramenstrual bleeding, 
vaginal discharge, pain during intercourse and unexpected weight loss. 
 
Investigations 
• 
FBC, LFT, Urea, Creatinine   
• 
Cancer Antigen 125 (CA 125)  
• 
CXR 
• 
Abdomen and Pelvis USS 
• 
Abdomen and Pelvic CT scan and/or Pelvic MRI 
• 
Endometrial biopsy to confirm the diagnosis 
• 
PET/CT 
 
Staging:  FIGO and TNM 
 
Table 22.2 Management of Endometrial cancer by Stage 
Stage 
Management 
All Patients 
Medically operable patients should undergo Surgery.  
Perform TAH and BSO or radical hysterectomy if cervical stromal involvement 
and obtain peritoneal cytology. Consider selective pelvic and paraaortic LN 
dissection for myometrial invasion or if grade 2–3, and include nodes from 
paraaortic, common iliac, external iliac, internal iliac, and obturator chains. 
 
Stage 1A/1B 
Grade 1 - Observation; Grade 2-3 or presence of other adverse features: Offer 
Vaginal Brachytherapy (VBT) 7Gy x 3 fractions 
Stage IA, IB, II 
clear cell or 
serous 
Offer Adjuvant Chemotherapy + Vaginal Brachytherapy  7Gy x 3 fractions Or 
Pelvic External Beam Radiation Therapy alone (46Gy) 

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carcinoma, IB 
High Grade 
Stage III 
Adjuvant Chemotherapy + Radiotherapy (High Risk Disease: EBRT (46Gy) + 
VBT 7Gy x 3 fractions ) 
Stage IV 
Chemotherapy 
 
 
Note 
• 
For inoperable disease stage llb – lVA, radiotherapy and or chemotherapy can be offered 
as neo-adjuvant prior to surgery 
 
 
Pharmacological Treatment 
Cytotoxic therapy for inoperable, metastatic or recurrent disease is given with palliative intent.  
Recommended regimens are; 
S: doxorubicin (IV) 60 mg/m2 over 30 minutes AND cisplatin (IV) 50 mg/m2 1 hour(IV) 
infusion on day 1; repeat every 21days for 4 – 6 cycles 
 
 
 
OR 
S: cisplatin (IV) 50 mg/m21-hour infusion on day 1 AND doxorubicin(IV) 45 mg/m2 over 20 
minutes on day 2 AND paclitaxel (IV) 160 mg/m2 over 3hours on day 2 AND   filgrastim 
(SC) 5 µg/kg on days 3–12; repeat every 21days for 4-6 cycles 
 
 
 
OR 
S: carboplatin (IV) AUC 5–6 1-hour infusion day 1 AND paclitaxel (IV) 175 mg/m2 over 
3hours on day 1 repeat every 21 days for 4-6 cycles 
Note 
• 
All patients should be referred to a gynecologist for evaluation and surgical management 
• 
All surgical specimens should be sent for histopathology diagnosis and staging. 
• 
After surgery and histopathology report, all patients should be referred to cancer 
specialized center for management and follow up. 
 
22.2.3 Cancer of the Vulva 
Vulva cancer is predominantly a disease of older women. Squamous cell carcinoma is the 
commonest histological type, usually arising from premalignant lesions–vulva intraepithelial 
neoplasia (VIN). Risk factors contributing to development of VIN and later vulva cancer include HPV 
infection, infection with HIV, and cigarette smoking.  
 
Diagnostic Criteria 
• 
A lump or vulva mass 
• 
Presence of leukoplakia and other dystrophic changes on the vulva  
• 
Itching is a common manifestation and may become ulcerative (“non-healing ulcers”) 
 
Investigations 
• 
FBC, LFT, Urea, Creatinine, HIV test 
• 
CXR 
• 
Ultrasonography or CT scan of Abdomen and Pelvis 
• 
Colposcopy to determine presence of other lesions in the vagina and cervix 
• 
Biopsy from the vulvar lesion to confirm the diagnosis 
• 
PET/CT 
 
Staging: FIGO and TNM. 
Management: 
Treatment is individualized, taking into considerations of histological type, disease stage and patient 
factors 
 
Primary treatment is surgery. Wide Local Excision (Radical Vulvectomy) plus Groin Lymphnode 
dissection.   
 
Radiotherapy is indicated in the following conditions: 
• 
As primary therapy for patient with small primary tumors particularly young patients in 
whom surgical resection would have significant psychological consequences. 
• 
For patients with locally advanced disease where resection is not possible. 

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• 
After surgery to treat the pelvic and groin nodes. 
• 
After surgery in patients with positive surgical margins. 
• 
In palliation (Pain, Bleeding etc) 
 
Pharmacological Treatment: As for cervical cancer 
 
22.2.4.    Gestational Trophoblastic Disease 
22.2.4.1 Hydatidiform mole 
Two types; complete and partial hydatidiform mole. Treatment is suction curettage or hysterectomy. 
Careful risk assessment is needed to determine patients who require chemotherapy after surgery. 
Patient with high risk hydatidiform mole will have to reserve single agent chemotherapy; 
methotrexate or actinomycin D    
Note: Patient should be followed up with weekly serum β–hCG after surgery until it is undetectable. 
22.2.4.2 Choriocarcinoma  
Choriocarcinoma is extremely chemo sensitive; cure is possible even in metastatic disease. All 
patients with choriocarcinoma should undergo a careful pre-treatment evaluation for proper staging 
and risk stratification. 
 
Investigations: 
• 
Serum β-hCG level 
• 
LFT, RFT, TSH, T3, T3 
• 
CXR and or CT Scan chest 
• 
Abdomen and Pelvis USS or CT Scan 
• 
Brain MRI 
• 
Tissue sample for histology 
• 
CSF hCG level 
• 
PET/CT 
Clinical presentation: 
• 
Persistently raising or plateau BhCG postmolar pregnancy. 
 
Staging: FIGO Staging  
 
Stage I – Persistently elevated human chorionic gonadotropin (hCG) levels; tumor confined to the 
uterine corpus 
Stage II – Tumors extending to the adnexa or to the vagina, but limited to the genital structures 
Stage III – Pulmonary metastases on chest radiograph, with or without uterine,pelvic, or vaginal 
involvement 
Stage IV – Metastatic disease outside of the lungs and pelvis and/or vagina 
 
Table 22.3 Prognostic Factors required for Stage grouping and Risk score 
 
Risk Score 
Prognotic Factor 
0 
1 
2 
4 
Factor 
score 
Age (years) 
<40 
>40 
 
 
 
Antecedent pregnancy 
Hydratidiform 
mole 
Abortion 
Term 
pregnancy 
 
 
Interval months from index 
Pregnancy 
<4 
4-6 
7-12 
>12 
 
Pretreatment hCG (IU/mL) 
<103 
103 to 
<104 
104 to 105 
>105 
 
Largest tumor size, 
including uterus (cm) 
<3 
3-5 
>5 
 
 
Site of metastasis 
Lung 
Spleen, 
kidney 
Gastrointestinal 
tract 
Brain, 
liver 
 
Number of metastasis 
identified  
 
1-4 
5-8 
>8 
 
Previous failed 
chemotherapy 
 
 
Single 
medicine 
Two or 
more 
medicines  
 
Total Risk Score 
 
 
 
 
 

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Table 22.4 Risk Stratification (FIGO) and Treatment recommendation 
Stage / Score 
Recommendation 
Low risk: Stage I – III with 
WHO risk score below VI 
Single agent: methotrexate (IV) or actinomycin D (IV) 
High risk: Stage IV or II 
and III with WHO risk 
score above VI 
Combination therapy: 
1. 
EMACO (etoposide, methotrexate, actinomycin D, 
cyclophosphamide, vincristine) (IV) 
2. 
APE ( actinomycin D, cisplatin, etoposide) (IV) 
Brain metastasis 
methotrexate, dexamethasone and prophylactic anti epileptic to 
control seizures Or High dose EMACO plus intrathecal 
methotrexate and leucovorin. 
Concomitant whole brain radiation: 20-30 Gy in 2Gy daily fraction 
concurrently with high dose chemotherapy(MTX) 
 
Note 
Do serial measurement of BhCG at start of treatment and weekly during therapy. 
 
Table 22.5 Recommended Chemotherapy regimens for Single agent 
Single Agent 
1 
S: actinomycin D (IV) 12µg/Kg daily for 5 days 
With response: Repeat same dose 
Without response: add 2µg/Kg to the initial dose or switch to methotrexate protocol 
2 
S: methotrexate (IV) or (IM) 0.4mg/Kg daily for 5 days 
With response: Repeat same dose 
Without response: add 0.6mg/Kg to the initial dose or switch to actinomycin D protocol 
Note:  
• 
Do serial measurement of BhCG at start of treatment and weekly during therapy. 
• 
Do FBC, Platelet count, LFT daily. 
• 
If no response to single agent , give combination drugs. 
 
Table 22.6 Recommended Chemotherapy regimens for Combination therapy 
Combination Therapy (EMACO – Regimen) 
Course 
1 
(EMA) 
Day 1 
S: VP – 16 (etoposide) (IV) 100mg/m2 infusion over 30 minutes AND actinomycin 
D (IV) 0.5mg bolus AND methotrexate (IV) 100mg/m2 bolus, followed by a 
200mg/m2 IV infusion over 12 hours 
Day 2 
S: VP – 16 (etoposide) (IV) 100mg/m2 infusion in 200ml of saline over 30 minutes 
AND actinomycin D (IV) 0.5mg bolus 
folinic acid (IM) 15mg OR orally every 12 hours for 4 doses beginning 24 hours 
after start of methotrexate (IV) 
Course 
2 
(CO) 
Day 8 
S: vincristine (IV) 1mg/m2 (IV) bolus AND cyclophosphamide 600mg/m2 1 hour 
(IV) infusion.  
 
Note 
• 
Cycles are repeated after every 14 days until β–hCG is normal 
 
 
 

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Follow-up 
• 
Weekly measurement of hcg level until they are normal for 3 consecutive weeks 
• 
Monthly hcg levels until levels are normal for 12 consecutive months 
• 
Effective contraception during the entire period of hormonal follow–up 
 
22.2.5 Cancer of the Ovary 
Epithelial tumours comprise 90% of all ovarian malignancies. Due to anatomical location, most 
patients present with advanced disease. 
 
Diagnostic Criteria 
• 
Minimal or no symptoms in early stage 
• 
Abdominal distension with palpable mass, pain and ascites are all late signs 
 
Investigations: 
• 
Inspection and bimanual examination under anesthesia (EUA) recto–vagina are mandatory 
to exclude primary disease or extension from other sites such as cancer of the cervix 
• 
FBC, RFT, LFT, CA 125 & CEA 
• 
CXR 
• 
Abdomen and Pelvis CT Scan or USS 
• 
Histology of Oophorectomy specimen or biopsy obtained at laparotomy 
• 
Ascitic fluid/peritoneal and pelvic washing cytology 
 
Staging: Is based on surgical diagnosis (laparotomy): FIGO: IA, IB, IC, IIA, IIB, IIC, IIIA, IIIB, IIIC, 
IVA and IVB. 
 
Table 22.7: Management: Surgery 
Stage 1 and 2 
Total hysterectomy with Bilateral Salpingo –Oophorectomy (TAH+BSO) and 
omentectomy should be performed in resectable tumor.  
 
If total tumor removal is not possible, then maximum debulking (Cyto –
reductive) surgery is done. This is followed by adjuvant Chemotherapy. 
Unilateral salpingo-oophorectomy is only justified for stage IA tumour with 
favourable histology. 
Stage 3 
Neoadjuvant chemotherapy followed by Surgery and then Adjuvant 
Chemotherapy. 
Stage 4 
As stage 3 +/- Palliative care. 
 
Pharmacological Treatment  
Adjuvant chemotherapy 
Indicated in all patients at high risk i.e. stage IC or II, high grade or clear cell cancers of any stage. 
Recommended regimens is; 
S: carboplatin (IV) AUC 6  1 hour infusion Day 1 AND  paclitaxel (IV) 175 mg/m2 over 3 
hours day1; repeat every 21days for 6 cycles. 
 
 
For recurrent disease: give same regimen if tumor is platinum sensitive (recurrence after 6 months 
since last chemotherapy cycle) 
For platinum resistant disease give gemcitabine or bevacizumab as single agent or in combination 
with taxanes. When available, liposomal doxorubicin is active and indicated in recurrent disease. 
 
S: gemcitabine (IV) 1000 mg/m2  30 minutes infusion Day 1, Day 8 and Day 15;  
     Repeat every 4 weeks for 6 Courses  
S: bevacuzimab (IV) 15 mg/kg 1-hour infusion Day1, every 3 weeks until  
     disease progression  
 
Endocrine therapy is indicated in selected cases with recurrent disease.  
S: tamoxifen (PO) 20mg every 12 hourly,daily AND goserelin (SC) 3.6 mg 
    every 4 weeks or 10.8mg every 12 weeks  
 
Note 
All patients must be referred to a gynecologist and cancer specialized center for evaluation and 
proper management 

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22.3 Breast Cancer 
The etiology of breast cancer is so far unknown, however, age, nulliparity, not breastfeeding, first 
pregnancy age 35years, previous radiation exposure, family history of breast cancer, smoking and 
alcohol consumption, are the risks associated with breast cancer. 
 
Screening for breast cancer includes breast self-examination (BSE), clinical breast examination 
(CBE) and breast imaging (mammogram and/or ultrasound scanning and or MRI Breast). All 
patients with clinical suspicious lesions should have imaging as part of early detection.  
 
Diagnostic criteria 
A solitary hard lumps or mass in the breast that may be associated with 
• 
Changes of breast skin appearance or ulceration 
• 
Nipple retraction 
• 
Presence of axillary lymphadenopathy or elsewhere 
• 
Attachment/fixed to chest wall muscles 
 
Other symptoms and signs include cough, bone pain/fracture, or neurological symptoms depending 
on site of metastasis 
 
Investigations 
• 
FBC, LFT, Urea, Creatinine 
• 
ECHO Mammogram/MUGA (Baseline Ejection Fraction and follow up) 
• 
 Bilateral Mammography, Breast Ultrasound as necessary 
• 
CXR 
• 
Abdominen and Pelvic USS 
• 
Bone scan 
• 
CT scan and or PET/ CT where indicated 
• 
Open biopsy for histopathology and Immunohistochemistry (IHC) 
• 
A core needle biopsy done manually, or preferably by ultrasound or stereotactic guidance 
is recommended. 
• 
Immuniohistochemistry (IHC) – ER, PR and Her 2 
• 
FISH/CISH for Equivocal Her 2 for Confirmation of Her 2 OverExpression 
• 
Breast MRI may be of value in select group of women who have had equivocal 
mammogram/ ultrasound.  
 
Staging: TNM 
Management: Includes surgery, chemotherapy, radiotherapy, hormonal therapy and targeted 
therapy 
 
Surgery 
Optimal management includes multidisplinary evaluation by clinical oncologist and breast surgeon.  
 
Options for surgical management include:  
• 
Breast conserving surgery with lumpectomy/quadrantectomy 
• 
Modified radical mastectomy 
• 
Toilet Mastectomy 
 
As described above, all surgical approaches should include surgical axillary staging with axillary 
lymph node dissection to level 1 and 2 nodes (>10 lymph nodes dissected). 
 
Surgical approaches aimed at breast conservation should only take place in cases that allow for 
multi-disciplinary management with access to radiotherapy. If radiotherapy access is limited, 
mainstay of surgical care should be modified radical mastectomy. 
 
Radiotherapy is strongly indicated in the following conditions: 
• 
After BCS 
• 
T3–4 tumor 
• 
Positive surgical margin 
• 
If ≥ 4 sampled lymphnodes are positive 
• 
Palliation for fungating and bleeding tumor, mets to bones, brain etc. 
 

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Radiotherapy dose: 50Gy/25 Fractions given in 5 weeks or Hypofractionation 40.05Gy/15 
Fractions. For palliative intent usually 30Gy/10 Fractions in 2 weeks 
 
Pharmacological Treatment 
Chemotherapy is indicated for almost all patients as neo-adjuvant, adjuvant or palliative. Patients, 
who are planned for surgery and have ≥ T3 tumors, should receive neo-adjuvant chemotherapy 
before operation.  
 
Table 22.8 Recommended chemotherapy regimens for Breast cancer 
Dosing schedules for combinations for HER 2 negative disease:  
 
1 
Dose-dense doxorubicin (IV) AND cyclophosphamide(IV) followed by weekly paclitaxel (IV) 
 
S: doxorubicin (IV) 60 mg/m2 over 30 minutes’ day 1 AND cyclophosphamide (IV) 600 mg/m21-hour 
infusion day 1 given every 14 days for 4 cycles  
 
Followed by  
 
S: paclitaxel (IV) 80 mg/m2 by 1-hour infusion weekly for 12 weeks. 
 
2 
Dose-dense adriamycin AND cyclophosphamide followed by 3 weekly taxanes 
 
S: doxorubicin 60 mg/m2 (IV) over 30 minutes on day 1 PLUS cyclophosphamide 600 mg/m2 1 hour 
(IV) infusion day 1 given every 21 days for 4 cycles then 
 
Followed by  
 
S: paclitaxel (IV) 175 mg/m2 3 hours infusion day 1, given every 21days for 4 cycles 
OR 
S: docetaxel (IV) 100 mg/m2 3 hours infusion day 1 given every 21days for 4 cycles.  
 
3 
TAC (IV) chemotherapy regimen 
 
S: docetaxel (IV) 75 mg/m2 3 hours’ infusion day 1 AND doxorubicin (IV) 50 mg/m2 30 minutes’ day 
1 AND cyclophosphamide (IV) 500 mg/m2 1-hour infusion day 1 given every 21 days for 6 cycles. 
 
 
Dosing schedule for combinations for HER2-Positive disease: 
 
1 
S:  doxorubicin (IV) 60 mg/m2 30 minutes’ day 1 AND cyclophosphamide (IV) 600 mg/m2 1-hour 
infusion day 1 given every 21 days for 4 cycles followed by paclitaxel (IV) 80 mg/m2 1-hour infusion 
weekly for 12 weeks  
                                                        AND 
S:  trastuzumab (IV) 4 mg/kg with first dose of paclitaxel (IV) followed by trastuzumab (IV) 2 mg/kg 
weekly to complete 1 year of treatment. 
 
2 
As an alternative, trastuzumab (IV) 6 mg/kg (IV) every 21 days may be used following the 
completion of paclitaxel (IV) and given to complete 1 year of trastuzumab (IV) treatment. 
 
Note 
• 
All cycles are with myeloid growth factor support. 
• 
FBC, RFT, LFT before each cycle. 
• 
 Cardiac monitoring at baseline, 3, 6, and 9 months. 
 
Other Regimens are:  
S: CAF (cyclophosphamide, adriamycin and 5-flourouracil)/  
S: CEF (cyclophosphamide, epirubicin and 5-fluorouracil) and  
S: CMF (cyclophosphamide, methotrexate and 5-fluorouracil) (for elderly patients>65 yrs 
with poor cardiac function) 
 
 

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For Metastatic Breast Cancer (Stage 4):   
Chemotherapy regimens for either combinations ie  
S: CAF, CEF, gemcitabine/paclitaxel,  
S: trastuzumab+paclitaxel/carboplatin or trastuzumab+paclitaxel or trastuzumab + 
docetaxel or trastuzumab+capecitabine; or single agent  
S: trastuzumab, taxane or capecitabine or gemcitabine. 
 
Endocrine therapy  
Premenopausal ER/PR Positive 
S: tamoxifen (PO) 20 mg daily for 5 years 
 
Post-menopausal ER/ PR Positive 
S: anastrazole (PO) 1 mg daily for 5 years  
OR 
S: tamoxifen (PO) 20 mg daily for 2 years followed anastrazole (PO) 1 mg daily for 3 
years. 
 
Note 
● All patients must be referred to a specialized oncology center for proper management 
22.4 Cancer of The Skin 
Skin cancers are classified into non melanoma and malignant melanoma. 
22.4.1 Non-melanoma Skin Cancers 
Basal cell carcinoma (BCC) and squamous cell (SCC) are the most common non melanoma skin 
cancers. SCC is more aggressive than BCC and has the potential to metastasis.  The main cause of 
these skin cancers is overexposure to Ultraviolet radiation. Risk factors include light-coloured skin 
(e.g albinism), previous burn and immunosuppression eg after transplant or HIV infection  
 
Prevention or early detection; is through frequent self–health check–up or screening exercise and 
prompt treatment of early skin lesions. For light skinned people–avoid UV light especially people 
with Albinism. 
 
Diagnostic Criteria 
The most common warning sign of skin cancer is a change in the appearance on exposed areas of 
the skin, such as a new growth or a sore that will not heal. Occasionally, such changes may appear 
on an old burn area. 
 
 
Investigations 
• 
None if lesion is small 
• 
Local X-ray if bone involvement is suspected 
• 
CXR  
• 
Biopsy – preferably excisional biopsy where possible for histology 
• 
CT or MRI for suspected Nodal and bone involvement. 
• 
PET/CT when indicated 
 
Management  
Surgery is the primary treatment. Wide local excision that achieves negative surgical margins is 
adequate. Skin grafting may be required after surgery. Amputation sometimes is done for palliation. 
Locally destructive methods such as curetting or cryotherapy may be employed 
Radiotherapy 
Indication: Positive margin, high grade disease or inoperable tumour.   
Dose: 60-66Gy/ in 30-33 Fractions EBRT for Radical Treatment, 30Gy in 10 Fractions for palliative 
treatment  
 
Pharmacological Treatment 
S: 5-fluorouracil topical cream apply every after 12 -24 hours, for very superficial lesions or 
carcinoma in situ  
Systemic chemotherapy is given for palliation in advanced stage or as radio sensitizer. 

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22.4.2 Malignant Melanoma 
 
Diagnostic criteria 
History of a pre-existing naves which has changed recently –itching, colour change, increase in size, 
satellite lesions, elevated surface, ulceration and/or oozing. 
 
Investigations 
• 
CXR 
• 
Abdomen and Pelvic CT Scan or USS 
• 
PET CT  
• 
Excisional biopsy of suspicious lesion for histopathology 
 
Staging: Clark’s or Breslow classifications are used. Tumour size closely correlates with prognosis. 
Detection/ prevention: Frequent self –check up or screening exercise and prompt treatment of naves 
 
Management: Surgery is the primary treatment. 
• 
Wide local excision and graft 
• 
Amputation sometimes for advanced useless limb 
 
Pharmacological Treatment 
 
S: cisplatin (IV) 20mg/m2/day 30 minutes’ infusion day 1-4 AND vinblastine (IV) 
1.6mg/m2/day bolus day 1-5 AND dacarbazine (IV) 800mg/m2 30minutes infusion day 1 
repeat every 21 days for 6 cycles 
OR 
S: dacarbazine (IV) 250mg/m2 30 minutes’ infusion Day1–Day 5 every 21 days  
for 4 cycles  
 
 
 
OR 
S: temozolomide (PO) 200mg/m2 Day 1–Day 5 every 28 days 
 
Radiotherapy used for palliation if: 
• 
Lesion is inoperable. May use large fractions: 30Gy/6Fractions/1 week 
• 
Excision margins are involved or very close 
• 
Palliative intent 30Gy in 10 Fractions/ 20Gy in 5 Fractions (brain mets, fungation or profuse 
bleeding, bone pain etc) 
 
22.4.3 Kaposi’s sarcoma (KS) 
It is a malignant tumour of angio–formative cells usually starting from the skin but occasionally 
involving many other organs of the body. Kaposi sarcoma can be primarily categorized into four 
types: epidemic of AIDS–related, immunocompromised, classic or sporadic, and endemic (African). 
Here we have Non AIDS related (endemic) KS and AIDS related (epidemic) KS where the late is 
more common 80–85%. 
Diagnostic criteria 
• 
KS presents as a firm, dark brown nodules or plaque in the skin. Usually more on the limbs 
• 
In young children and those with immunodeficiency it presents as wide spread 
lymphadenopathy with or without skin lesions.  
• 
Presence of B symptoms (fever, sweating and weight loss) is commonly associated with 
epidemic type.  
 
Investigations 
• 
FBC, LFT, Urea & Creatinine, HIV test (if positive CD4 count and viral load) 
• 
CXR 
• 
Abdomen and Pelvis ultrasound or CT scan 
• 
 Chest Scan CT 
• 
Bronchoscopy and Endoscopy 
• 
Skin biopsy for histological confirmation 
 
Staging of KS: Epidemic Kaposi sarcoma use AIDS clinical trials group (ACTG) system and for 
endemic/classical Kaposi sarcoma use Mitsuyasu classification system. 
 

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Management: 
• 
Treatment is palliative irrespective of type and stage hence careful assessment and 
decision is required to choose the best palliative treatment.  
• 
ARVs should be initiated in epidemic KS patients who have not started the treatment.  
• 
Choice of palliation depends on clinical presentation and patient general condition. 
 
Radiotherapy: Is the best palliative treatment in symptomatic patient with local or extensive 
disease. 
• 
8Gy single fraction for disease on limbs or lower half body  
• 
6Gy single fraction for upper half body 
• 
Dose of 9Gy/3Fractions or 22Gy/11 Fractions can be prescribed for lesions elsewhere. 
 
Pharmacological Treatment 
Palliative chemotherapy is usually given in patient with generalized disease.  
 
Recommended regimens are: 
 
S: doxorubicin (IV) 25 mg/m2 over 30 minutes day1 AND bleomycin (IV) 10 IU/m2 over 10 
minutes’ day 1 PLUS vincristine (IV) 1.4mg/m2 over 10 minutes (max.2mg) day1 given 
every 21 days for 6 –8 cycles  
OR 
S: paclitaxel (IV) 100mg/m2 day 1 every 14days   
OR 
S: docetaxel (IV) 75mg/m2 day 1 every 21days is given for persistent or recurrent after 
ABV. 
 
22.5 Head and Neck Cancers 
Cancer of the head and neck include the following: The oral cavity, pharynx, larynx, nasal cavity, 
para nasal sinuses, salivary glands, and thyroid.   
 
These tumours may present with a neck mass due to lymph node metastases, with or without 
findings from the primary disease site. Important etiological factors are smoking, excessive alcohol, 
viral infections (eg HPV and EBV), genetic predisposition, previous exposure to radiation and 
industrial chemicals. Squamous cell carcinoma is the commonest histological type for the 
malignancies but salivary gland tumors are mostly adenocarcinoma. 
 
22.5.1 Nasopharyngeal Cancer 
Nasopharyngeal carcinoma is the predominant tumor type arising in the epithelium of the 
nasopharynx. 
 
Diagnostic Criteria 
• 
Neck mass, unilateral hearing loss, tinnitus, nasal obstruction, epistaxis, and cranial nerve 
palsies 
 
Investigations: 
• 
FBC, RFT, LFT and HIV 
• 
CXR 
• 
Abdominal ultrasound 
• 
CT scan and/or MRI of the nasopharynx, skull base, and neck 
• 
Nasopharyngoscopy 
• 
Endoscopic guided biopsy of the primary tumor for histology 
• 
PET CT 
• 
Immunohistochemistry to further confirm the diagnosis 
 
Staging: TNM staging system 
 
Management 
Due to deep location of nasopharynx, and anatomic proximity to critical structures, radical surgery is 
typically not used. Role of surgery is initially for biopsy for histological confirmation. It may also be 
used for management of the neck for persistently enlarged lymph node. 
 

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Nasopharyngeal cancer is mainly treated by radiotherapy either alone or in combination with 
chemotherapy. 
 
Table 22.9 Management of Nasopharyngeal cancer by Stage 
Stage 
Management 
Stage I 
Radiotherapy alone to primary disease and neck 
Stage II–IVB 
Concurrent chemotherapy and radiation to the primary disease and neck 
Stage IVC 
palliative care (which may include chemotherapy and radiotherapy) 
Induction 
chemotherapy 
can be considered for 
stage III–IVB 
If delays are anticipated in initiation of concurrent chemotherapy and 
radiation. 
Local recurrence 
Chemotherapy, surgery or re-irradiation 
 
22.5.2 Laryngeal Cancer 
 
Laryngeal cancer is one of the most common cancers of head and neck. It is predominantly found in 
men and mostly in those with history of tobacco smoking and alcohol intake. It is divided into three 
major anatomic regions; supraglottis, glottis and subglottic. 
 
Diagnostic Criteria 
• 
Hoarseness, stridor, difficulty in breathing, neck mass, odynophagia, cough. 
 
Investigations: 
• 
FBC, RFT and LFT 
• 
CXR 
• 
CT scan and/or MRI of the Head and Neck 
• 
Laryngoscopy 
• 
Pathology: Definitive diagnosis is confirmed by laryngoscopy-guided biopsy of the primary 
tumor 
 
Staging: TNM Staging system 
 
Table: 22.10 Management of Laryngeal Cancer by Stage 
Stage 
Management 
Stage I and II 
Primary site: Partial or Total laryngectomy OR Radiotherapy alone. 
Stage III–IVB 
Concurrent Chemoradiation or Total Laryngectomy and neck dissection 
followed by Adjuvant Radiotherapy or Chemo radiotherapy 
Stage IVC 
Palliative care 
 
22.5.3 Hypopharyngeal Cancers: 
Hypopharyngeal cancer includes tumors arising from the pyriform sinus, posterior pharyngeal wall, 
postcricoid region. It is associated with tobacco use, alcohol consumption, and Plummer–Vinson 
syndrome.  
 
Diagnostic Criteria: 
• 
Dysphagia, odynophagia, change in speech (dysarthria), neck mass, referred otalgia, 
throat pain, weight loss, sensation of mass in throat and hoarseness of voice. 
 
Investigations 
• 
FBC, RFT and LFT 
• 
Hypopharyngoscopy and biopsy for histopathology 
• 
CXR 
• 
CT scan and/or MRI of the Head and Neck 
 
Staging: TNM staging system. 
 
Management  
Radiation therapy is the mainstay of first-line local treatment for early stage hypopharyngeal 
carcinoma. For more advanced disease, concurrent chemoradiation reduces the rate of distant 
metastasis, and improves local control.  

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22.5.4 Salivary Gland Cancer 
Salivary gland cancers arise from major or minor salivary glands in the head and neck region. The 
most 
common 
malignant 
salivary 
gland 
tumors 
are 
mucoepidermoid 
carcinoma 
and 
adenocarcinoma 
 
Presentation: Depends on primary site involved. 
• 
Mass, pain, nerve palsies, neck mass 
 
Investigations: 
• 
FBC, LFT, and RFT 
• 
CXR 
• 
CT scan and/or MRI of Head and Neck 
• 
Biopsy of the primary tumor for histology.  
 
Staging: TNM staging system:  
Treatment: 
• 
Complete surgical resection with adjuvant radiotherapy if adverse features are present 
• 
If disease is not resectable, definitive radiotherapy or concurrent chemoradiotherapy is 
indicated 
• 
Neck dissection is indicated for high-grade tumors or clinically positive neck disease  
 
22.5.5 Nasal Cavity and Paranasal Sinus Cancer 
These are tumors arising from nasal cavity and the four paired paranasal sinuses (frontal, ethmoid, 
maxillary, and sphenoid). 
 
Diagnostic Criteria: 
Nasal obstruction, epistaxis, proptosis, double vision, cheek mass, loss of sensation of the cheek 
and loosening or pain of the teeth 
 
Investigations: 
• 
FBC, RFT and LFT 
• 
CXR 
• 
Abdominal Ultrasound 
• 
CT scan and/or MRI of the Para nasal sinuses and neck 
• 
Direct fibre-optic endoscopy 
• 
Endoscopic guided biopsy of the primary tumor for histopathology 
 
Staging: TNM Staging system 
Treatment: 
• 
Treatment is by surgery and or radiotherapy with or without chemotherapy. 
• 
Surgical resection of the primary tumor and neck dissection followed by radiotherapy can 
be done in early disease stages. It may also be used for management persistently 
enlarged lymph nodes, persistent or recurrent disease after radiotherapy.  
• 
Stage I–IINO: Complete surgical resection followed by radiotherapy alternatively definitive 
radiotherapy.  
• 
Radiotherapy can be given as an alternative definitive treatment, either alone or in 
combination with chemotherapy. It is used in palliative care for advanced diseases 
• 
Chemotherapy is used in induction, concurrent or adjuvant therapy.   
 
22.5.6 Oral Cavity Cancer 
Oral cavity consists of the upper and lower lips, gingivobuccal sulcus, buccal mucosa, upper and 
lower gingiva, retromolar trigone, hard palate, floor of mouth, and anterior two–third of the tongue. 
Risk factors include smoking, excessive consumption of alcohol, poor oral hygiene, prolonged focal 
denture irritation, betel nut chewing, and syphilis. 
 
Diagnostic Criteria: 
• 
Non-healing ulcer, speech difficulty, hypersalivation, neck mass, dysphagia and otalgia 
 
 
 

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Investigations:  
• 
FBC, LFT, RFT and HIV   
• 
CXR 
• 
CT Scan and/or MRI of the Head and Neck  
• 
Mirror and fibre-optic endoscopic examination 
• 
Biopsy for histologic confirmation 
 
Management:  
 
Surgery is the mainstay treatment modality for cancer of the oral cavity. Single modality treatment 
with surgery or radiation therapy is preferred for early-stage oral cavity cancer.  
 
Definitive radiation with concurrent chemotherapy is the current standard for unresectable locally 
advanced disease. Radiotherapy can be given as palliative treatment to primary or metastatic area. 
Chemotherapy may also be given as palliative care in a very advanced disease. 
 
22.5.7 Oropharyngeal Cancer 
Oropharynx is located between the soft palate superiorly and the hyoid bone inferiorly. The 
oropharynx has four walls; soft palate, tonsillar region, base of tongue, and pharyngeal wall. It is 
associated with tobacco use and alcohol consumption and HPV. Tonsillar and pharyngeal tongue 
tumors frequently are initially recognized by nodal metastases. 
 
Clinical Presentation 
• 
Sore throat, non-healing oropharyngeal ulcers, dysphagia, referred otalgia, hoarseness 
(with larynx invasion), odynophagia, hot potato voice and impaired tongue movement, 
including protrusion. 
 
Investigations:  
• 
FBC, LFT, RFT and HIV   
• 
CXR 
• 
CT Scan and/or MRI of the Head and Neck  
• 
Mirror and fibre-optic endoscopic examination 
• 
Biopsy for histologic confirmation 
 
Management: 
Oropharyngeal cancers are mainly treated by Radiotherapy in combination with chemotherapy. 
Surgery can be used in selected cases.  
 
Table 22.11 Recommended Radiotherapy and Chemotherapy treatment for Head and Neck 
tumours 
Curative radiotherapy 
Radiotherapy dose for head and neck cancers is 66–70Gy given at 
conventional fraction of 1.8–2Gy/fractions. 
Concurrent Chemotherapy 
S: cisplatin (IV) 40mg/m2 1hour infusion weekly during Radiotherapy  
                                      OR  
S: cisplatin (IV) 75mg/m2 1 hour infusion day 1 repeat every 21 days 
during radiotherapy. 
Induction Chemotherapy 
For patients with Advanced Head and Neck Cancers - PF or TPF (taxane, 
platinum and 5 FU) for 3 – 6 cycles.  
S: carboplatin (IV) AUC 5 1hour infusion day 1 AND 5-flourouracil (IV) 
400mg/m2 bolus day 1 AND paclitaxel (IV) 175mg/m2 3 hour infusion day 
1 repeat every 21 days for 3-6 cycles. 
Adjuvant Chemotherapy: 
In curative intent concurrent chemoradiotherapy is indicated with 
cisplatin/5FU (IV) If induction chemotherapy was not given then adjuvant 
chemotherapy is recommended. Alone or in combination with cetuximab. 
S: carboplatin (IV) AUC 5 1hour infusion day 1AND 5-flourouracil (IV) 
400mg/m2 bolus day 1 AND Cetuximab (IV) 400mg/m2 2 hours infusion 
day 1 (to be administered 1 hour before cisplatin/5-Fu) (IV) every 21 days 
for 3-6 cycles. 
Treatment of Recurrent or 
Metastatic disease 
Combination therapy cisplatin or carboplatin/docetaxel or paclitaxel. 
paclitaxel/ cisplatin/ 5-FU cisplatin/ gemcitabine, gemcitabine/ vinorelbine, 
carboplatin, cetuximab (IV). 
Single agents cisplatin, carboplatin, paclitaxel, docetaxel, 5-FU, 
methotrexate, gemcitabine and capecitabine (IV) 

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Note 
• 
Head and neck tumour patients must be referred to cancer specialized centers for 
evaluation and definitive management. Follow up visits: 1st visit at 4–6weeks then after 
each 3–4 months in the 1st year, 6 monthly in the 2nd year thereafter yearly.   
 
22.5.8 Thyroid Carcinoma 
Thyroid cancer is a commonest endocrine malignancy in Tanzania. It accounts approximately 0.8-
1% of all malignancies seen at Ocean Road cancer institute annually. Histological types are 
medullary, anaplastic and well differentiated thyroid cancer.  
 
Majority of these cases are differentiated thyroid cancer, the commonest being follicular subtype 
followed by papillary subtype and rare ones being Hurthle cell, follicular variant of papillary thyroid 
carcinoma, tall cell, columnar, solid and clear cell. Female are mostly affected, the male to female 
ratio being 3:1 
 
Diagnostic Criteria 
• 
Thyroid mass (Anterior neck mass), Obstructive symptoms (Stridor, hoarseness), laryngeal 
nerve palsy, dysphagia 
• 
Metastatic symptoms such as weight loss, difficulty in breathing, bone pain/pathological 
fractures 
 
Investigations: 
• 
Thyroid function tests (T3, T4, TSH), FBC, LFTs, Urea & Creatinine, Serum calcitonin, 
Serum thyroglobulin levels 
• 
Thyroid Scan 
• 
CXR 
• 
Isotope bone scan 
• 
CT Scan of the neck 
• 
Biopsy or Fine needle aspiration cytology (FNAC) of a thyroid lesion 
 
Staging: TNM Staging system 
Treatment:  
Surgery is the mainstay of treatment; lobectomy, total or near total thyroidectomy. Radiotherapy is 
indicated in all cases of anaplastic carcinoma. 
 
Pharmacological Treatment 
• 
Radioactive iodine I-131 sodiumor potassium iodide ablation is indicated in all patients with 
well differentiated thyroid cancer after surgery. 
• 
Post ablation; Thyroid-stimulating hormone (TSH) suppression therapy (levothyroxine) is 
indicated in all patients post ablation and post-lobectomy.  Aim is to keep TSH <0.1mU/L. 
• 
Tumor recurrence or metastasis: Local reccurence should be managed surgically. Local 
reccurence or distant metastases not suitable for surgery that are iodine avid are treated 
with I-131.  
• 
Palliative chemotherapy is indicated for patients with visceral metastatic diseases not 
responding to I-131. Recommended regimen is: 
 
                   S: pacliataxel (IV) 175mg/m2  3 hours infusion day 1 AND doxorubicin (IV) 
                       60mg/m2 bolus day1 every 3 weeks up to 6 cycles. 
 
• 
Radiotherapy is indicated for Adjuvant treastment to the thyroid bed post surgery with 
macro/microspopic residual disease, in unresectable and local reccurence that does not 
take up I-131 and palliation of bone and brain metastasis. Palliative dose: 30Gy in 10 
Fractions. 
• 
For anaplastic carcinoma radiation is indicated and dose recommended 50-60Gy in 20-30 
Fractions. 
• 
Medullary Thyroid Tumor (MTC) is primarily managed by surgery, Radiotherapy  
• 
Anaplastic Thyroid Cancer (ATC) is aggressive disease. A Total thyroidectomy followed by 
adjuvant radiotherapy is indicated to resectable disease. If unresectable ATC palliative 
radiotherapy 
and 
combination 
chemotherapy 
is 
indicated. 
The 
recommended 
chemotherapy regimen is as above in metastatic disease.  
Note: All patients must be referred to a cancer specialized center for proper management. 

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22.6 Gastrointestinal Malignancies 
22.6.1 Esophageal Cancer 
Histologically there are two types; SCC and adenocarcinoma. Tobacco and alcohol abuse are major 
risk factors for SCC whereas obesity, gastroesophageal reflux disease (GERD) and Barrett’s 
esophagus are the major risk factors for adenocarcinoma.   
 
Diagnostic Criteria 
• 
Difficult in swallowing (dysphagia) is the commonest symptom which is associated with 
weight loss and poor performance status. 
 
Investigation 
• 
FBC, LFT, Urea, Creatinine 
• 
Barium swallow and meal 
• 
Chest and Abdominal CT scan 
• 
Abdominal USS 
• 
Rigid oesophagoscopy or oesophagoduodenoscopy (OGD) and biopsy for histology 
 
Staging: TNM Staging system 
Management: Surgery and radiotherapy 
Surgery is a major component of treatment for resectable disease. Surgery and or radiotherapy may 
be curative in early diseases. However, most patients present in late stages, hence the goal of 
treatment is to prolong survival and relieve symptoms. Radiation (alone or in combination with 
chemotherapy) is given as a definitive, preoperative, postoperative therapy or palliative setting.  
 
Chemotherapy 
 
Table 22.12 Recommended chemotherapy regimens for neo-adjuvant, adjuvant or palliative 
for Esophageal cancer 
Neoadjuvant Chemotherapy 
S: paclitaxel (IV) 175 mg/m
2 3hours’ infusion day 1 AND cisplatin (IV) 
75 mg/m
2 1-hour infusion day 1 OR carboplatin (IV) AUC 5 1-hour 
infusion day 1 given every 21 days for 6 cycles 
                                  OR 
S: docetaxel (IV) 75mg/m
2 3hours’ infusion day 1 AND cisplatin (IV) 
75mg/m
2 1-hour infusion day 1 every 3 21 days for 6 cycles  
 
Adjuvant Chemotherapy 
S: 5–FU (IV) 1000 mg/m
2  (IV) bolus day 1–day 5 AND  cisplatin (IV) 
75 mg/m
2  1 hour  infusion day1 given every 21 days for 6 cycles             
Palliative Chemotherapy 
S: capecitabine (PO) 1000mg/m
2 12 hourly on day 1–14, cycled every 
21 days for 6 cycles or until disease progression or intolerable toxicity 
 
 
Note 
• 
All patients should be referred to cancer specialized centers for proper management               
Stenting, gastrostomy tube and parenteral nutrition are employed to provide feeding 
when there is total dysphagia. 
 
22.6.2 Gastric Cancer 
Gastric cancer is often diagnosed at an advanced stage. Among the risk factors include age, 
gender, genetic factors, smoking, smoke or salt preserved food, diet less of fruits and vegetables, 
infection with H. Pylori and Epstein Barr Virus. About 90–95% of the tumors are adenocarcinoma.  
 
Diagnostic Criteria: 
• 
Epigastric pain worsened by food intake, early satiety 
• 
Distal tumours may present with obstructive symptoms 
• 
Occult of manifest bleeding may be a feature 
• 
Other symptoms include epigastric mass, pallor, weight loss, supraclavicular nodes, 
hepatomegaly, periumbilical nodes 
 
 
 

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Investigations: 
• 
FBC, LFT, RFT 
• 
Stool for occult blood 
• 
Carcinoembryonic antigen (CEA)_ 
• 
IHC – Her 2 Status  
• 
CXR 
• 
Barium meal (double contrast)  
• 
Abdomen and pelvis CT scan or USS 
• 
Endoscopy and biopsy for histology 
 
Staging: TNM staging system 
Management: 
Surgery is the primary treatment for early stage gastric cancer. Total or partial gastrectomy is 
performed together with lymph node dissection. By pass surgery is done to relieve obstructive 
symptoms. Surgery is usually preceeded by Chemotherapy (Perioperative) or adjuvant 
chemoradiotherapy. 
 
Pharmacological Treatment 
Table 22.13 Recommended chemotherapy regimens for Gastric cancer 
Perioperative 
chemotherapy 
S: 5-fluorouracil (IV) 500mg/m2 bolus day 1 AND epirubicin (IV) 50mg/m2 30 
minutes’ infusion day 1 AND cisplatin (IV) 60mg/m2 1-hour infusion day 1, cycled 
every 21 days for 6 cycles.  
                                    OR 
S: capecitabine (PO) 625mg/m2 12 hourly daily for 21 days AND epirubicin (IV) 
50mg/m2 30 minutes’ infusion day 1 AND cisplatin (IV) 60mg/m2 1-hour infusion day 
1, cycled every 21 days for 6  
cycles.  
                                   OR 
S: 5-fluorouracil (IV) 200mg/m2/day Continous infusion day 1-4 AND epirubicin (IV) 
50mg/m2 30 minutes’ infusion day 1 AND cisplatin (IV) 60mg/m2 1-hour infusion day 
1, cycled every 21 days for 6 cycles.  
 
locally advanced 
and metastatic 
gastric 
adenocarcinoma. 
S: paclitaxel (IV) 175mg/m
2 3hours’ infusion AND carboplatin (IV) AUC 5 1-hour 
infusion on day 1, cycled every 21 days for 6 cycles AND/OR trastuzumab (IV) 
6mg/m2 2hours loading dose day1, and then 4mg/m2 every 14 days (For Her 2 + 
Patients). 
OR 
S: docetaxel (IV) 60mg/m
2 2 hours’ infusion day 1 AND cisplatin (IV) 60mg/m
2 1 1 
hourday1 + 5–FU (IV) 750mg/m
2 continuous infusion over 24 hours on day1–4, 
cycled every 21 days for 6 cycles AND/OR trastuzumab (IV) 6mg/m2 2hours’ 
infusion loading dose day1, and then 4mg/m2 every 14 days (For Her 2 + Patients). 
 
Palliative setting 
 
S: capecitabine (PO) 1000mg/m
2 12 hourly on day 1–14, cycled every 3 weeks, 6 
cycles or until disease progression or intolerable toxicity. 
 
 
 
Note 
• 
Concurrent Chemo radiotherapy with 3DCRT may be used as adjuvant post surgery. 
• 
Radiotherapy can also be used in palliative setting to control bleeding and pain.  
• 
Gastric (MALT) lymphoma are associated with Chronic H. pylori inflammation. They are 
managed by H. pylori eradication and Chemoradiotherapy (see details in Lymphoma 
section). 
• 
Patients with CD 117 positive gastro intestinal stromal tumor (GIST) respond well to 
imatinib. 
 
22.6.3 Hepatocellular Carcinoma 
Associated with chronic Hepatitis B/C infection 
 
Diagnostic criteria 
• 
An arterial bruit and ascites may be present 
• 
Right upper abdominal swelling and pain often associated with weight loss, fever, jaundice 
 

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Investigation 
• 
FBC, LFT, RFT, Biochemistry, Serum alpha feto protein, HBsAg, HBcore antibody, partial 
thromboplastin time (PTT) 
• 
CXR 
• 
Abdomen and Pelvis USS  
• 
3 Phase Liver Protocol CT/MRI Scan with IV Contrast 
• 
PET/CT 
• 
Biopsy or FNAC of the liver 
 
Staging:  TNM staging system  
 
Table 22.14 Child Pugh Score 
Parameter 
Points for increasing abnormality 
 
I 
II 
III 
Encephalopathy 
(grade) 
None 
1-2 
3-4 
Ascites 
None 
Slight 
Moderate 
Albumin 
>3.5 
2.8-3.5 
<2.8 
Prothrombin time (s) 
1-4 
4-6 
>6 
Bilirubin (mg/dl) For 
primary biliary 
cirrhosis 
1-2 
1-4 
2-3 
4-10 
>3 
>10 
 
Management  
Table 22.15 Treatment Recommendations 
Presentation 
Recommended treatment 
Resectable 
Partial hepatectomy 
Unresectable, 
medically 
operable 
Liver transplant 
 
Unresectable, 
medically 
inoperable 
Conformal Radiotherapy +/- Chemotherapy 
Systemic therapy alone 
Supportive care 
Palliative  
Radiotherapy for Bone and Brain metastases 
 
Flow Chart 22.1 Management of Hepatocellular cancer by Stage and Child Pugh Score  
 
 
 
Pharmacological Treatment  
Recommended systemic regimen used for palliation 
 
S: doxorubicin (IV) 60 mg/m2 over 30 minutes day1 given every 3 weeks for 4–6 cycles. 
S: sorafenib (PO) 400mg daily until disease progression or unacceptable  
    toxicity. 

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Prevention: Vaccination for Hepatitis B/C 
22.6.4 Rectal Cancer 
Risk factors include: inherited genetic syndromes, diet high in red and processed meat, smoking and 
alcohol abuse, having inflammatory bowel disease, type ll diabetes and obesity. Histology; 
commonest is adenocarcinoma 95%.  
Diagnostic Criteria: 
•
Change in bowel habit eg constipation or diarrhea, sense of incomplete bowel emptying.
•
Rectal bleeding or blood in stool.
•
Abdominal mass with or without obstructive symptoms
•
Unexplained weight loss and other symptoms of advanced disease.
Investigations: 
•
FBC, RFT, LFT, CEA
•
Stool for occult blood
•
CXR
•
Barium enema (double contrast)
•
Abdomen and Pelvis USS
•
Digital rectal examination
•
Sigmoidoscopy or Colonoscopy with Biopsy of the lession
•
Abdomen and Pelvis CT Scan
Staging: TNM staging system 
Management 
Surgery is the primary treatment for early disease. Hemicolectomy with lymphnode dissection is 
commonly performed in colon cancer. Give preoperative chemotherapy for locally advanced disease 
to shrink the tumor. Radiotherapy plays a role in rectal tumor as neo–adjuvant, adjuvant or palliative.  
Pharmacological management: 
Management of locally advanced and metastatic colorectal cancer involves various active 
chemotherapy drugs, either in combination or as single agents: 5–FU, leucovorin, capecitabine, 
oxaliplatine, irinotectecan and bevacizumab are available for various combination regimens and 
schedules. 
Table 22.16 Recommended Chemotherapy regimens for Rectal cancer 
Neo-adjuvant chemo radiotherapy 
S: 5–FU (IV) 350 mg/m
2 over 30 minutes AND leucovorin (IV) 20 
mg/m
2 infusion over 30 minutes’ day 1–day 5 given on 1
st and 5
th 
weeks of RT, concurrent with RT: 45 Gy/25#/5weeks followed by 
surgery in 4–10 weeks.  
3–10 weeks after surgery continue with chemo as below: 
S: 5–FU (IV) 50 mg/m
2 over 30 min day 1–day 5 PLUS leucovorin 
(IV) 20 mg/m
2 30 minutes infusion day1–day5 every 21 days for 4
cycles
Adjuvant chemo Radiotherapy 
3–10 weeks after surgery 
S: 5–FU (IV) 500 mg/m
2 over 30 minutes’ day 1–5 & day 29–33, 
concurrent with RT:45 Gy/25#/5 weeks. 
Four weeks after completion of chemo radiation; continue with 
chemo: 5–FU (IV) 450 mg/m
2 bolus day 1–day 5, Every 4 weeks for 
2 cycles 
OR 
S: capecitabine (PO) 825mg/m2 12 hourly during Radiotherapy. 
Management of Metastatic disease 
As colon 

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22.6.5 Colon Cancer 
Investigations 
• 
FBC, RFT, LFT, CEA 
• 
Stool for occult blood 
• 
CXR 
• 
Barium enema (double contrast) 
• 
Abdomen and Pelvis USS. 
• 
Digital rectal examination 
• 
Sigmoidoscopy or Colonoscopy with Biopsy of the lession 
• 
Abdomen and Pelvis CT Scan 
 
Staging: TNM staging system 
Management 
• 
Management of Non-metastatic disease: Surgery then Adjuvant Post Op 
Chemotherapy. 
• 
Management of Metastatic disease: Single or Combination Chemotherapy. 
 
Table 22.17 Recommended Chemotherapy regimens for Colon cancer 
Adjuvant Chemotherapy 
S: oxaliplatin (IV) 85mg/m2 2 hours’ infusion day 1 AND leucovorin(IV) 
400mg/m2 over 20 minutes day1 AND 5-fluorouracil (IV) 400mg/m2 
bolus day1, then 1200mg/m2/day X 2 days (IV) Continous infusion (USE 
INFUSION PUMP) repeat after every 14 days for 6-12 cycles.  
OR 
S: oxaliplatin (IV) 130mg/m2 2hours’ infusion AND capecitabine (PO) 
1000mg/m2 12 hourly for 14 days, 21 days’ cycles for 4-8 cycles. 
OR 
S: capecitabine (PO) 1000mg/m2 12 hourly daily for 14 days, 21 days 
cycle for 6 cycles.  
 
Metastatic disease 
 
S: oxaliplatin (IV) 85mg/m2  2 hours infusion day 1 AND leucovorin (IV)  
400mg/m2 infusion over 20 minutes day1 AND 5- fluorouracil (IV) 
400mg/m2 bolus day1, then 1200mg/m2/day X 2 days  (IV) Continous 
infusion (USE INFUSION PUMP) repeat after every 14 days for 6-12 
cycles. With/without bevacizumab (IV) 5mg/kd  1 hour infusion day 1 or 
cetuximab (IV) 500mg/m2 infusion over 2 hours day 1 
                              OR 
S: oxaliplatin (IV) 130mg/m2 2hours’ infusion AND capecitabine (PO) 
1000mg/m2 12 hourly daily for 14 days, 21 days’ cycles for 4-8 cycles. 
With/without bevacizumab (IV) 5mg/kg 1-hourinfusion day 1 
                               OR 
S: capecitabine (PO) 1000mg/m2 12 hourly daily for 14 days, 21 days 
cycle for 6 cycles.  
 
 
 
Note 
• 
Colorectal cancers are usually asymptomatic until advanced stage hence regular 
• 
Screening with annual digital rectal examination, stool for occult blood + colonoscopy 
and is recommended starting at 50 years of age. 
 
22.6.6 Anal Cancer 
Investigations 
• 
FBC, RFT, LFT, HIV/CD4 
• 
CXR 
• 
Abdomen and Pelvis USS. 
• 
Digital rectal examination 
• 
Sigmoidoscopy or Colonoscopy with Biopsy of the lession 
• 
Abdomen and Pelvis CT scan 
 
Staging: TNM Staging system 
 

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Management 
• 
For resectable Good Performance status: Surgery (APR) then Adjuvant 
Chemoradiotherapy (45Gy-50Gy) 
• 
For Unresectable Good Performance status: Neoadjuvant Chemoradiotherapy (45Gy-
50Gy) then Surgery (APR) 
• 
For Inoperable and Poor Performance statu: Palliative Radiotherapy 
 
Pharmacological Management 
Concurrent Chemoradiotherapy:  
 
S: mitomycin C (IV) 10mg/m2 bolus day 1 and 29 AND 5-flourouracil (IV) 1000mg/m2 
Continous infusion day 1-4 and 29-32. (USE INFUSION PUMP).  
OR 
S: capecitabine (PO) 825mg/m2 12 hourly a day during radiotherapy (5 days    a week) 
AND 5- fluorouracil (IV) 1000mg/m2 Continous infusion day 1-4 and 29-32. (USE 
INFUSION PUMP).  
 
Metastatic disease 
As Rectum 
22.7 Lung Cancer 
Worldwide lung cancer is the leading cause of cancer-related death. Approximately 85 %–90% of 
lung cancer cases are caused by cigarette smoking. There are 2 main types of lung cancer; Non-
small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). These 2 types have different 
prognosis and management approach. 
 
22.7.1 Non-small cell lung Cancer 
Accounts for approximately 85% of all lung cancer cases 
 
 Diagnostic Criteria 
• 
Chronic chest symptoms in a smoker 
• 
Haemoptysis 
• 
May present with superior vena cava obstruction (SVCO) syndrome 
• 
Cough in patient exposed to asbestos 
• 
Findings of chest symptoms, weight loss, poor karnofsky performance scale (KPS) 
 
Investigations: 
• 
FBC, LFT, Urea, Creatinine 
• 
CXR PA & lateral views  
• 
CT Scan of Thorax and Abdomen 
• 
Abdominal USS 
• 
Bronchoscopy and Biopsy for histopathology 
• 
Cytology of sputum or bronchial aspirate examination 
 
Staging: TNM staging system 
Management: Surgery (pneumonectomy or lobectomy) is curative for stage I and some stage II 
disease. 
 
Pharmacological Treatment: 
Recommended Chemotherapy regimens for adjuvant, unresectable or recurrent and metastatic 
disease are;  
 
S: carboplatin (IV) AUC 1-hour infusion 6 day1 AND paclitaxel (IV) 175 mg/m2 3 hours’ 
infusion day 1 every 21 days for 6 cycles 
 
Radiotherapy  
With advanced radiotherapy machine and treatment technic, RT may be given for neo–adjuvant or 
adjuvant to surgery.  Palliative Radiotherapy is frequently used in metastatic disease to bone, spinal 
cord compression, brain, liver and in case of superior vena cava obstruction (SVCO), atelectasis, 
obstructive pneumonitis and fungating masses. Dose of 30GY/10 Fractions/2weeks gives good 
symptom relief. 

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22.7.2 Small cell lung cancer 
SCLC is characterized by early development of widespread of metastases. It is highly sensitive to 
initial chemotherapy and radiotherapy; however, most patients eventually die of recurrent disease.   
 
Diagnostic criteria and investigations: As in non – small cell lung cancer (NSCLC) however brain 
scan and bone marrow aspirate are necessary 
 
Staging: Limited disease versus extensive disease 
 
Pharmacological Treatment 
Aim is for local control and palliation. Cure rate is low 
 
Platinum + Etoposide are the major drugs for which the tumor is sensitive.  
 
S: cisplatin (IV) 60 mg/m2 1-hour infusion Day 1 AND etoposide (IV) 100 mg/m2 over 30 
minutes Day1–3, Every 21 days for 4 –6 cycles  
OR 
S: carboplatin (IV) AUC 5 1-hour infusion Day 1 AND etoposide 100 mg/m2 30 minutes (IV) 
infusion Day1–3, every 21 days for 4–6 cycles 
 
Other recommended chemotherapeutic drugs are irinotecan and gemcitabine 
 
Radiotherapy: 
Consolidation to primary site and mediastinum: 50Gy/25Fractions/5weeeks 
• 
Prophylactic brain irradiation in complete responders 
• 
Palliative treatment for symptoms relief in respiratory, bone or CNS symptoms: 
30Gy/10Fractions/2wks 
 
22.8 Genitourinary Malignancies 
22.8.1 Carcinoma of the Prostate 
The most common type of prostate cancer is adenocarcinoma (95 %). Tumours are stratified by T 
stage, Gleason score (GS), and PSA into three prognostic groups of low, intermediate and high risk.  
• 
Low risk: T1–T2a and PSA < 10 ng/ml and GS ≤ 6 
• 
Intermediate risk: T2b or PSA 10 – 20 ng/ml or GS 7 
• 
High risk: T2c–T4 or PSA > 20ng/ml or GS 8–10 
 
Patient can be offered appropriate treatment options according to stage of disease, prognostic risk 
group and estimated survival taking into account performance status and comorbidity.  
 
Diagnostic Criteria 
• 
May be asymptomatic in early stages of the disease 
• 
May present incidentally following examination for benign prostatic hypertrophy or elevated 
serum prostatic specific antigen (PSA) 
• 
Prostatic symptoms are associated with advanced stages of the disease, which include: 
reduced potency, urinary frequency and nocturnal, poor stream, hesitancy and terminal 
dribbling 
• 
Very often patients may present with bone pain including backache or pathological fracture 
• 
Digital Rectal Examination (DRE) typically reveals a hard, irregular prostate. TURP is 
carried out to both confirm the diagnosis and also as part of the treatment (to relieve 
obstruction). 
 
Screening for prostate cancer 
Routine screening not recommended, but when done should begin with PSA and digital rectal 
examination at age 50 if life expectancy is >10 years. It is recommended that screening of high risk 
group should take place starting at age 45 . 
 
Investigations 
• 
FBC, LFT, Urea, Creatinine, Serum PSA, ALP, Testosterone 
• 
X-rays of the painful bone or spine 
• 
CXR 

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• 
Abdomen and Pelvis USS and or CT Scan 
• 
Pelvic MRI in early-stage disease 
• 
PET/CT 
• 
Bone scan 
• 
Biopsy for histopathology 
 
Staging: TNM staging system 
 
Treatment: 
Treatment depends on disease profile (Risk stratification) and patient factors as noted above. 
Options include: 
• 
Watchful waiting 
• 
Active surveillance 
• 
Surgery (curative or palliative) 
• 
Radiotherapy (curative or palliative) 
• 
Hormonal therapy (chemical vs surgical castration) 
• 
Chemotherapy 
 
Surgery 
Early stages (Low and Interediate risk groups) can be treated with either radical prostatectomy or 
radical Radiotherapy with cure intent. However, surgery may cause postoperative impotence and 
impaired urinary control. TURP is carried out to both confirm the diagnosis and also as part of 
relieving obstruction.  
 
Radiotherapy 
Radical Radiotherapy for Adjuvant and definitive, EBRT up to 74 Gy/37 Fractions can be given using 
3DCRT or IMRT Techniques. Palliative radiotherapy is valuable to bone metastases, massive 
hematuria, spinal cord compression and brain mets,  
 
Hormonal Therapy 
Hormonal manipulation is by surgical or medical castration. It is carried out in patients with locally 
advanced or metastatic disease. Bilateral orchydectomy is a surgical hormonal manipulation and 
should not be regarded curative surgery.  
 
Pharmacological Treatment:  
   S: goserelin (SC) 3.6 mg every 4 weeks or 10.8mg every 12 weeks with/ without oral 
bicalutamide (PO) 50mg once daily 
 
Note 
• 
Goserelin is not required after orchydectomy but patient may receive Bicalutamide. 
• 
Treatment with goserelin and bicalutamide may be given up to 2 years depending on 
patient condition and Prostate Specific Antigen (PSA) levels 
 
Chemotherapy  
Recommended chemotherapy regimens for hormonal refractory prostate cancer are: 
 
S: doctetaxel (IV) 75mg/m2 2 hours’ infusion day 1 given every 21 days for 6 cycles. It is 
mainly reserved in hormonal refractory prostate cancer. 
 
For Bone metastases/osteolytic/tumour induced hypercalcemia are:  
 
S: zolendronic acid (IV) 4mg over 15min given 4 Weekly 
 
Metastatic disease  
Life long ADT ± palliative RT ± bisphosphonates for hormone refractory disease. docetaxel and 
prednisone for androgen independent disease can add Carboplatin if docetaxel not working to 
Castrate resistant prostate cancer patients.  
 
Evaluation every 3 months (Check PSA level) Castrate resistant patients with rising PSA zoledronic 
acid should be given monthly. These are given together with Ca2+ and Vitamin D supplements.  
 

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In Castrate resistant patients which did not respond to Docetaxel plus carboplatin and 
prednisolone, patients Abberaterone acetate with prednisolone is an option (500mg OD taken with 
food is highly recommended) 
 
S: abberaterone acetate (PO) 500mg one a day (Taken with food) 
OR 
S: enzalutamide (PO) 160mg daily   
 
22.8.2 Urinary Bladder Cancer 
Urinary bladder cancers are malignant tumors that commonly arise from the inner lining of the 
bladder or its connective tissue. Common pathologies include transition cell carcinoma, squamous 
cell carcinoma, adenocarcinoma, sarcomas and secondary deposits.  
 
Risk factors for bladder cancer include chronic irritation (schistosomiasis, irradiation, and 
catheterization), chemicals (aromatic amines, aniline dyes, tobacco, analgesics) and genetic 
predisposition. Symptoms include blood in the urine, dysuria, Lower urinary tract symptoms (LUTS), 
and low back pain.  
 
Diagnostic Criteria 
• 
Symptoms include blood in the urine, pain with urination, and low back pain. 
 
Investigations  
• 
FBC, RFT, LFT, Alkaline phosphatase 
• 
Urinalysis, Urine culture and sensitivity, Urine for cytology 
• 
CXR and /or CT chest 
• 
Bone scan 
• 
Abdomimen and Pelvis USS or CT scan 
• 
PET/CT 
• 
Cystoscopy with bladder mapping & Biopsy 
• 
EUA 
• 
Bimanual examination 
• 
TURBT with random biopsies of normal appearing mucosa to exclude CIS. (If trigone 
involved, biopsy prostatic urethra) 
 
Staging: TNM staging system 
Management  
Treatment of Urinary bladder cancer depends on how deeply the tumor invades into the bladder 
wall. 
 
Surgery: Several modalities that may extend from bladder preserving surgery–TURB; to radical 
cystectomy with urine diversion depending bladder muscle invasion. Post operation patient may 
receive adjuvant chemo and/or radiotherapy  
 
Chemotherapy: chemotherapy in bladder cancer may be offered before surgery or after surgery. It 
may also be given concurrent with radiotherapy or as palliative in inoperative tumor.  
 
Recommended chemotherapy regimens for locally advanced and meatasatic disease are;   
 
S: gemcitabine (IV) 1000mg/m2 infusion over 30minutes day 1, 8 & 15 AND cisplatin (IV) 
70mg/m2 infusionAND over 30mins day 2 given every 28 days for 6 cycles 
OR 
MVAC regimen 
S: methotrexate (IV) 30mg/m2 over 5 minutes day1, 15 & 22 
AND 
S: vinblastine (IV) 3mg/m2 over 10 minutes day2, 15 & 22 
AND 
S: doxorubicin (IV) 30mg/m2 over 15 minutes day2 
AND 
S: cisplatin (IV) 70mg/m2 over 30mins day2 
 
 

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Radiotherapy  
Radiotherapy may be given after bladder preserving surgery or alone in small lesions with a dose up 
to 66Gy/33Fractions concurrent with cisplatin. It is also commonly used as palliative therapy to 
control bleeding and or pain locally advanced and metastatic disease. Palliative dose 
30Gy/10Fractions or 20Gy/5Fractions   
 
22.9 Haematological Malignancies 
22.9.1 Lymphomas 
World Health Organization broadly classifies lymphomas into Hodgkin lymphoma (HL) and non-
Hodgkin lymphoma (NHL). 
 
22.9.1.1 Non-Hodgkin’s lymphoma 
NHLs are a heterogeneous group of diseases which are mainly linked by their origin within the 
lymphoid system and its different cellular components. They are sub classified based on the stage of 
maturation (immature vs. mature) and cell of origin [B cell, T cell, or natural killer cell (NK) cell]. 
 
Diagnostic Criteria 
• 
Peripheral Lymph node enlargement (commonest site-neck) 
• 
Hepatomegally and/or splenomegally in advanced stages 
• 
B-symptoms: Unexplained weight loss, fever, drenching night sweats 
• 
Coughing, trouble breathing, or chest pain in case of Superior vena cava obstruction 
(SVCO) 
 
Investigations: 
• 
CXR 
• 
Chest and abdominopelvic CT Scan 
• 
PET/CT 
• 
FBC, differential and film 
• 
Bone marrow aspirate and trephine 
• 
Immunohistochemistry (IHC) 
• 
LDH, Urea and Electrolyte, Creatinine, Albumin, Aspartate transaminase (AST), Bilirubin, 
Alkaline phosphatase, Serum calcium, Uric acid 
• 
Pregnancy test in females of child–bearing age 
• 
Hepatitis B and C 
• 
HIV status 
• 
Tissue Biopsy for histopathology 
• 
MUGA scan/ ECHO 
 
Note: Lumbar puncture and CSF cytology if there is CNS involvement of in NHL associated with a 
high risk of CNS relapse eg. Testicular, paranasal sinuses, extradural/paraspinal mass. 
 
Staging: Ann Arbor classification. 
 
Management: 
NHL diseases are sensitive to both chemotherapy and radiotherapy 
 
Indolent lymphoma 
They include Indolent B-cell lymphomas such as Follicular lymphoma, MALT lymphoma, nodal 
marginal zone lymphoma, splenic marginal zone lymphoma and small lymphocytic lymphoma, 
and Indolent T-cell lymphomas such as mycosis fungoides. 
 
Treatment  
Stage 1 and 2 can be treated with involved node radiotherapy or R_CHOP / R-CVP followed by 
radiotherapy. 
 
R-CHOP regimen: 
S: rituximab (IV) 375 mg/m2 3 hours’ infusion day 1 AND cyclophosphamide day1 750 
mg/m2 1-hour infusion AND doxorubicin (IV) 50 mg/m2 15 minutes’infusion day 1 AND 
vincristine (IV) 1.4 mg/m2 over 10 minutes (maximum 2mg) day1 AND prednisolone 
(PO) 100mg once a day, day 1–5, every 21 days for 6–8 cycles.  

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Aggressive lymphoma with CD 20 positive 
These include Diffuse Large B-cell lymphoma (DLBCL), primary CNS lymphoma, adult Burkitt 
lymphoma, mantle cell lymphoma and aggressive T-cell lymphomas. 
 
Treatment: R–CHOP 
     S: rituximab (IV) 375 mg/m2 3 hours’ infusion day1 AND cyclophosphamide (IV) day1 
750 mg/m2 1-hour infusion AND doxorubicin (IV) 50 mg/m2 15 minutes’ infusion day 1 
AND vincristine (IV) 1.4 mg/m2 over 10 minutes (maximum 2mg) day1 AND 
prednisolone (PO) 100mg once a day, day 1–5, every 21 days for 6–8 cycles.  
 
Radiotherapy 
• 
Radiotherapy is directed to genuinely stage IA and IIA Disease 
• 
Mantle or inverted Y: 40Gy/20 Fractions/4weeks with shielding of the critical organs. 
• 
Involved field RT (IFRT): 46Gy/23 Fractions/4.5weeks 
Primary CNS Lymphoma 
Standard chemotherapy regimens like CHOP are not effective possibly due to poor penetration of 
the blood-brain-barrier (BBB).  
 
S: methotrexate (IV) 8mg/m2/day twice a week until remission is achieved 
 
Burkitt Lymphoma (BL) 
Recommended chemotherapy regimens are:  
S: CODOX-M AND IVAC (Magrath regimen- cyclophosphamide, vincristine, doxorubicin, 
methotrexate/ifosfamide, etoposide, cytarabine) (IV) 
OR 
S: CALGB 9251 (cyclophosphamide, prednisolone, ifosfamide, mesna, methotrexate, 
leucovorin, vincristine, cytarabine, etoposide, dexamethasone and doxorubicin) (IV) 
OR 
S: Hyper CVAD (cyclophosphamide, vincristine, doxorubicin and dexamethasone, 
methotrexate, cytarabine, leucovorin, methylprednisolone and 6-mercaptopurine) (IV) 
OR 
S: Dose-adjusted CHOP+Etoposide (IV) 
 
Aggressive T-cell lymphomas 
Rare and more aggressive than DLBCL. First line therapy is usually  
S: CHOP with Etoposide (CHEOP) (IV) 
OR 
S: cyclophosphamide (IV) day1 750 mg/m2   1-hour infusion AND doxorubicin (IV)   50 
mg/m2 15 minutes’ infusion day 1 AND vincristine (IV) 1.4 mg/m2 over 10 minutes 
(maximum 2mg) day1 AND prednisolone (PO) 100mg once a day, day 1–5 AND etoposide 
100mg/m2 (IV) day 1-day 3; repeat every 21 days for 6–8 cycles. 
Note 
• 
For MALT lymphoma, eradication of Helicobacter pylori is essential.Splenectomy is 
recommended in splenic marginal zone lymphoma.  
• 
Topical corticosteroids are indicated for localized or generalized skin involvement in 
mycosis fungoides. Systemic therapy indicated for non responders and Sezary 
syndrome.  
 
These include S: retinoids, interferons and low dose methotrexate. 
S: fludarabine AND Cyclophosphamide (FC) regimen is used as a second-line therapy for 
indolent B-cell lymphoma. 
Hodgkin’s disease (HD) 
Hodgkin Lymphoma comprises about 30% of all lymphomas. The disease is characterized by 
scattered large multinucleated Reed-Sternberg or mononuclear Hodgkin’s cells in an inflammatory 
background of a lymph node biopsy section. 

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Classified into two main types: 
• 
Nodular lymphocyte predominant Hodgkin lymphoma–NLPHL  
• 
Classical Hodgkin lymphoma–CHL, which is sub–divided into: 
o 
Nodular sclerosis classical Hodgkin lymphoma–NSHL  
o 
Mixed cellularity classical Hodgkin lymphoma–MCHL 
o 
Lymphocyte–rich classical Hodgkin lymphoma–LRCHL  
o 
Lymphocyte–depleted classical Hodgkin lymphoma–LDHL 
 
Diagnostic Criteria 
• 
Enlarged painless lymph nodes in the neck or elsewhere 
• 
B symptoms (weight loss, night sweats, and fever), pruritus, alcohol induced pain, general 
condition, throat, lymph nodes (site, number, size, consistency, mobility, matting), 
respiratory system, abdomen (liver, spleen, other masses), bone tenderness 
 
Investigations: 
• 
CXR 
• 
CT Scan of neck, chest, abdomen and pelvis 
• 
PET/CT 
• 
FBC, LFT, RFT, ESR, LDH, HIV Test  
• 
Bone marrow aspirate and biopsy (Not required in Stage I or II A)        
• 
Biopsy for histological diagnosis 
• 
MUGA scan / ECHO                                                                                                                                               
 
Management: 
As it is for NHL, HL diseases are sensitive to both chemotherapy and radiotherapy. 
 
Pharmacological Treatment 
Chemotherapy aims at cure for any stage of the disease. It is indicated in Stages II–IV.  
 
Recommended chemotherapy regimen is ABVD which include combination of the following drugs: 
 
S: doxorubicin (IV) 25 mg/m2 over 30 minutes AND bleomycin (IV) 10 IU/m2 over 10 
minutes AND vinblastine (IV) 6 mg/m2 over 10 minutes AND dacarbazine (IV) 375 mg/m2 
infusion over 30 minutes all given on day 1 & 15, every 28 days for 4–8 cycles. 
 
Other recommended chemotherapy regimens that can be used as salvage regimens are DHAP, 
DHAC, IGEC, ICE and MINE-ESHAP. 
 
Radiotherapy: can either be; involved field RT or mantle or inverted Y depending on site of disease: 
1.8–2Gy/Fraction for 30–40Gy total dose.  
 
22.9.2 Leukemia 
The symptoms and signs are caused by: (i) bone marrow failure (e.g. anaemia, neutropenia, 
thrombocytopenia); and (ii) infiltration of organs (e.g. liver, spleen, lymph nodes, meninges, brain, 
skin or testes).  
 
Investigations:  
• 
FBC, LFT, RFT, Coagulation indices 
• 
Peripheral blood film 
• 
Bone marrow aspiration and trephine biopsy 
• 
Flow cytometry analysis, immunophenotyping, cytogenetic and molecular evaluation. 
• 
ECHO/ECG for Cardiac function evaluation. 
 

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22.9.2.1 Acute Myeoid Leukemia (AML) 
Classification:  WHO classification 
Table 22.18 Treatment recommendations for AML 
Induction phase 
7+3 (cytarabine + daunorubicin) regimen; 
 
S: cytarabine (IV) 100mg/m
2 24 hourly for 7days AND daunorubicin (IV) 
60mg/m
2 24hourly for 3 days 
 
Consolidation phase 
If in remission ie blast cells < 2% in bone marrow, 
 
S:  high dose cytarabine (HiDAC) (IV) regimen is used.  
 
Transplant 
S: Allogeneic hSCT is considered in some patients (high risk patients) 
 
Relapsed AML 
(FLAG-IDA) regimen is used in relapsed cases. This is followed by allogeneic 
hSCT if remission is achieved. 
 
S: fludarabine (IV) 30mg/m
2 for 4 days, ANDhigh dose cytarabine (IV) 2g/m
2 
for 4 days AND Filgastrim (SC) 300mcg/m
2 for 5days, AND idarubicin (IV) 
10mg/m
2 for 3 days. 
 
Palliative single-dose 
regimen 
 
S: Low- dose cytarabine (SC) 20mg 12 hourly for 10 days. OR azacitidine 
(SC) 75mg/m
2 /day for 7 days. Repeat after every 4-6 weeks. 
 
 
Management of acute promyelocytic leukemia (APL) 
It is a medical emergency. Treatment should be initiated as soon as diagnosis is suspected based 
on cytologic criteria, before definitive genetic, cytogenetic or immunostaining confirmation is made.  
 
All -trans - retinoic acid (ATRA) is added in all three phases of APL treatment. There is a high risk of 
developing DIC and differentiation syndrome. Differentiation syndrome is treated with;  
 
S:  dexamethasone (IV) 10mg twice a day for 3 days or until symptoms resolve. Consider 
cessation of ATRA if symptoms are severe. 
 
Table 22.19 Treatment recommendations for APL 
Induction phase 
S: ATRA (IV) 45mg/m
2/day AND Arsenic trioxide (ATO) (IV) 
0.15mg/kg/day daily until bone marrow remission. OR ATRA (IV) 
45mg/m
2/day AND daunorubicin (IV) 50mg/ m
2 for 4days PLUS/MINUS 
cytarabine (IV) 200mg/ m
2 for 7days 
cytarabine (IV) is added in patients with high risk of relapse. 
 
Consolidation phase 
S: ATRA AND ATO, OR ATRA AND daunorubicin OR ATO AND 
daunorubicin OR daunorubicin AND cytarabine 
Maintanance phase 
ATRA alone OR ATRA (IV) 45mg/m
2/day orally for 15 days after every 
3months PLUS 6-mecaptopurine (IV) 60mg/ m
2 orally once a day PLUS 
methotrexate (IV) 20mg/ m
2 orally once weekly. All given for 2 years. 
 
22.9.2.2 Acute Lymphoblastic Leukemia (ALL) 
Treatment: The treatment of ALL is complex. The recommended regimens are; 
 
S: HYPER-CVAD/MTX-ARA-C Regimen (cyclophosphamide/mesna/vincristine/ 
doxorubicin/dexamethasone/methotrexate/cytarabine/leucovorin) (IV) 
 
22.9.2.3 Chronic Myeloid Leukemia (CML) 
Investigations: similar to other leukemia, plus BCR-ABL1 analysis by PCR or FISH for Ph 
chromosome analysis 

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Treatment  
For BCR-ABL1 positive, first line treatment is Tyrosine kinase inhibitors (TKI) 
 
Chronic phase: Characterized by blast cells < 10%.  
 
S: imatinib (PO) 400mg once a day every day. 
 
Accelerated phase: blasts 10 – 19%.   
 
S: imatinib (PO) 600-800mg/day in 2 divided doses until chronic phase is reachived. 
Thereafter continue with 400mg once a day daily. 
 
Blast crisis: Blast cells > 20%. If the patient was not on TKIs, treat as in accelerated phase.  
If patient was on TKIs, treat as acute leukemia. 
S: Second line TKIs include nilotinib, dasatinib, bosutinib and ponatinib (PO) 
 
If BCR-ABL1 negative 
S: hydroxyurea (PO) 40mg/kg daily. The dose ranges between 1mg and 3mg based on the 
WBC count. 
 
 
Note 
• 
Adequate hydration should be maintained.Blood transfusion is indicated based on the 
degree of anaemia 
 
D: allopurinol (PO) 300mg 24hourly daily to prevent hyperuricemia. 
 
22.9.2.4 Chronic Lymphoid Leukemia (CLL) 
Staging: Rai and Binet staging systems. 
Treatment 
S: chlorambucil (PO) 0.1mg/kg 24hourly for 2weeks, then rest for 2 weeks, repeat until 
remission is achieved. 
OR 
S: Combination of Fludarabine, Cyclophosphamide and Rituximab (FCR) regimen (IV) 
 
B: prednisolone (PO) 1mg/kg 24 once a day for 2 weeks is added if there is evidence of 
autoimmunity (autoimmune hemolytic anaemia or autoimmune thrombocytopenia) 
 
22.9.3 Multiple myeloma 
Clinical features – CRAB: Features of hypercalcemia, renal impairment, features of anaemia, bone 
pain, reccurent infections due to impaired antibody production, and bleeding tendencies and 
hyperviscosity syndrome in rare cases. 
 
Investigations:  
• 
FBC, RFT, LFT, Serum electrolytes 
• 
Peripheral smear 
• 
Bone marrow aspiration and trephine biopsy 
• 
Serum protein electrophoresis, urine for Bence Jones protein 
• 
Skeletal survey by X-ray, CT Scan or MRI 
• 
Serum β2 microglobulin 
Staging: Revised International Staging System (RISS) Adopted by the International Myeloma 
Working Group  
 
Treatment: Radiotherapy is used for pain control of lytic lesions that are refractory to systemic 
therapy, treatment of spinal cord compression from plasmacytoma and primary treatment of solitary 
plasmacytoma.Supportive treatment with blood transfusion, antibiotic, hydration and analgesia when 
indicated. 

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Bisphosphonate therapy 
S: zoledronic acid (IV) 4mg once monthly for 2 years 
Recommended chemotherapy regimens include the following drugs in various combinations: 
Melphalan, Thalidomide, Lenalidomide, Bortezomib, Cyclophosphamide, Prednisolone and 
Dexamethasone. 
S: thalidomide (PO) 200mg 24hourly for 28days 
OR 
S: lenalidomide (PO) 25mg 24hourly for 21days, 
AND  
S: dexamethasone (PO) 40mg 24hourly on day 1, 8, 15, 22, repeats after every 4 weeks.  
OR 
S: bortezomib (IV) 1.3mg/m2 24hourly AND dexamethasone (PO) 40mg 24 hourly 
WITH/WITHOUT cyclophosphamide (PO) 300mg/m2 all on day 1,8,15,22. Repeat every 4 
weeks 
22.10 Central Nervous System Maligancies 
22.10.1 Meningiomas 
Meningiomas are the second commonest tumors of the brain and constitute 20% of all intracranial 
tumors. Commonest sites are cerebral convexity, parasagittal and sphenoid 
ridge.  
Clinical presentation 
•
Chronic headache
•
Adult onset seizures
•
Loss of vision
•
Focal neurological deficits
Investigations 
•
FBP
•
Serum electrolytes
•
CT / Brain
•
CT/MR angiography
•
Histopathology studies
Pharmacological management 
•
Seizures: Give anticonvulsants.
•
Brain edema: Give Dexamethasone
Non-pharmacological management 
Surgical management 
•
Intracranial meningiomas are best managed with total excision following the principle of
maximum safe excision (Refer to Simpson grading for intracranial meningiomas)
•
Subtotal resection is associated with inferior outcome and higher regrowth rates.
Radiotherapy 
•
Radiotherapy is indicated in unresectable tumors, postoperative incomplete resection for
WHO grade 1, and all grade 2/3 tumors.
•
Meticulous attention to operative notes is required, as well as to postoperative CT/MRI.
Follow up 
•
Follow up CT Scan/ MRI every 6 months for 1 year, then annually.
•
In older patients and small tumors managed conservatively, consider CT/MRI scan yearly.

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22.10.2 Pituitary Tumors 
Pituitary tumors constitute 10% of intracranial tumors. Morbidity is often due to mass effect and 
endocrine consequencs including hyper or hyposecretion of pituitary hormones.  
 
Clinical presentation 
• 
Chronic headache 
• 
Loss of vision 
• 
Focal neurological deficits 
 
Investigations 
• 
FBP, Serum electrolytes,  
• 
Anterior pituitary hormones 
• 
CT / MRI Brain 
• 
CT/MR angiography 
• 
Visual fields assessment 
• 
Histopathology studies 
 
Pharmacological management of functional tumors 
 
Prolactinomas 
These should be treated initially with dopamine receptor agonist: 
 Give:  
D: bromocriptine (PO) 2.5mg 8 hourly  
OR  
S: cabergoline (PO) 0.25mg once/twice a week (Titrate with prolactin levels checked 2 
weekly, aim is to maintain PRL < 30ng/ml) 
 
Cushing’s disease 
Surgical management is recommended. Consider medicines that inhibit adrenocortical function only 
when surgery is not possible: S: metyrapone 250mg once a day (can be escalated based on 
response) 
 
Acromegaly 
Somatostatin analogues may be used to treat acromegaly. Give S: octreotide SR  
Efficacy is measured using clinical response defined as basal GH levels < 2.5 ng/ml, glucose-
suppressed levels <1.5 ng/ml and normalization of serum IGF-1 levels. 
 
Surgical management of pituitary tumors 
• 
This is the primary treatment for most pituitary tumors, except for prolactinomas which may 
be managed medically. 
• 
Trans-sphenoidal approach (endoscopic or microsurgical) is preferred as it is safer and 
better tolerated.  
• 
Frequently subtotal especially in large tumors or tumors invading into 
cavernous sinuses. Hypopituitarism occurs post-operative in about 12% of patients. 
 
Radiotherapy  
Indicated post subtotal tumor resection, recurrent tumors, persistently elevated circulating hormone 
levels, and inoperable patients. 
 
Follow up MRI 3 months after surgery to assess residual tumor. 
 
Radiotherapy is very effective for control of growth of pituitary tumors (>95%), but less effective for 
decreasing circulating hormone levels in functional tumors. 
 
Common complications 
Diabetes Insipidus: is characterized by excessive urine output due to lack of ADH, usually 
immediate post-operative.  Consider  
D: desmopressin (PO) 0.05mg 12 hourly daily (titrate based on response. 
 

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SIADH is characterized by decreased urine output and hyponatremia due to excessive ADH 
secretion, usually immediate post-operative.  Manage hyponatremia and consider  
 
B: furosemide (PO) 40mg 
 
CSW: characterized by excessive urine sodium secretion and hyponatremia, usually immediate 
post-operative. Manage hyponatremia with Hypertonic 3% saline. Consider  
D: fludrocortisone (PO) 0.05-0.1mg 12hourly daily. 
Follow up  
• 
There is significant risk of pituitary hypofunction after surgery or irradiation and this risk 
may occur up to 15 years later – the patients should be warned of the symptoms and be 
tested regularly.  
• 
Patients treated with standard radiotherapy are unlikely to show an early response and 
would therefore be assessed at 12 monthly intervals in terms of hormone levels and 
pituitary function. 
 
22.10.3 Gliomas 
Gliomas constitute the most common tumors of the brain affecting all age groups, with predilection 
to the adult population.  
 
22.10.3.1 Low grade Gliomas (LGGs) 
Clinical presentation 
• 
Seizures are common  
• 
progressive neurologic symptoms depending on site of tumor 
 
Imaging 
• 
CT or MRI should be done in diagnosis of Gliomas.  
• 
MR spectroscopy 
• 
Diffusion tensor tractography (DTI) 
 
Pharmacological management 
Seizures: 
Surgical management 
Long term survival approaches 100% with complete removal. After partial 
resection, survival rates range from 80-90% at 5 years to 70-80% at 10 years 
and 50-60 % at 20 years. 
 
Repeat the scans at 6, 12, 24 months to check for growth. If this is surgically resectable then repeat 
surgery should be attempted. 
 
Radiotherapy  
• 
Dose for low grade gliomas: 1.8 Gy X 28 Fractions = 50.4 Gy (5 times per 
                   week). Concurrent and adjuvant use of Temozolomide is indicated if available, 
 
S: temozolomide (PO) 75mg/m2 daily during RT and 150-200mg/m2 day 1-5  
                     Monthly for 6 months. 
 
• 
If the hypothalamus /pituitary are in the RT field, then endocrine function should also be 
evaluated annually by T4 & TSH, testosterone or FSH/LH. 
 
Follow up  
• 
CT scan immediate postoperative to assess resection.  
• 
MRI recommended at 3months and then annually unless other clinical indications 
emergency. 
 
22.10.3.2 High Grade Gliomas (HGGs) 
Anaplastic Astrocytoma (AA) and Glioblastoma Multiforme (GBM) 
 
Clinical presentation 
seizures, progressive neurologic symptoms depending on site of tumor features of mass effect, or 
focal signs depending on location. 

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Investigations 
• 
FBP, Serum electrolytes,  
• 
Histopathology studies 
• 
Immunohistochemistry studies: IDH, 1p/19q codeletion, ATRX mutations. 
 
Imaging 
• 
CT brain scan 
• 
MRI preferred investigation 
• 
MR spectroscopy 
• 
CT/MR angiography 
• 
Functional MRI (fMRI) 
 
Pharmacological management 
Seizures: Treat as per guidelines 
 
Surgical management 
• 
Complete excision of the tumor is essential for improved survival. Preoperative and 
intraoperative techniques to improve extent of resection in a safe manner (maximum safe 
resection) including brain mapping, use of intraoperative fluorescein guidance to expand 
resection magins and neuromonitoring techniques are advocated.  
• 
Extent of resection is best assessed on post-op CT/MRI scans.  
 
Radiotherapy  
• 
Patients should be CT-planned, with contrast administration. 3mm to 5mm slices cuts from 
Vertex to Base of skull. Large volume PTV = should completely encompass enhancing 
lesion seen on pre-op T2/FLAIR scan, plus small (2cm) margin. 
• 
Dose to LARGE VOLUME = 2.00 Gy X 23 Fractions = 46.00 Gy (5 times per week). 
• 
Small volume PTV (PTV2) is based on Gd-enhanced T1 weighted image= 
enhancing lesion on pre-op scans +1- 2 cm margin. 
• 
Dose to SMALL VOLUME = 2.00 Gy X 7 Fractions = 14.00 Gy 
• 
Total dose 60Gy in 30 fractions. 
• 
Other alternative radiotherapy fractionations can be used in elderly, more 
                    than 65 years of age are Hypo fractionation; 40Gy/ 15 Fractions and 5Gy X 5  
                    Fractions 
 
Note 
• 
Imaging techniques such as MR Spectroscopy may be indicated during follow up to 
distinguish tumor recurrence from post RT changes. 
 
Chemotherapy 
Concurrent chemotherapy + RT:  
S: temozolomide (PO) 75 mg/m2 daily during RT, Then 150-200mg/m2 given D1-D5 of a 28 
day cycle for 6 cycles after RT 
Oral steroid/ Ondansetron should be taken half an hour prior to chemotherapy tablet on each 
day. Tablets must be taken 1st thing in the morning on an empty stomach. 
Prophylaxis for PCP pneumonia with co-trimoxazole (one tablet twice daily) should be given 
during daily temozolomide treatment. 
 
Recurrent disease 
• 
Surgery plays an important role in selected patients- relieves symptoms, 
improves PS and QOL and reduces steroid requirement. 
• 
Repeat radiotherapy can be considered, depending on size of lesion and 
previous dose. 
• 
Palliation Chemotherapy may be only modality available- active regimens are BCNU, PCV, 
Temozolomide and more recently, Irinotecan and Bevacizumab. 
 
Follow up  
• 
A baseline scan should be done at 4 months’ post RT as a reference.  
• 
Thereafter scans are usually done at 6 months and annually, or if clinically indicated.  
• 
High index of suspicion and testing if indicated for pituitary function. 

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22.11 Oncological Emergencies 
Important oncological emergencies include Hypercalcemia, Superior venous cava obstruction, 
Spinal cord compression and Neutropenic sepsis. 
 
22.11.1 Superior Vena Cava Syndrome (SVCS) 
Superior vena cava syndrome (SVCS) is the clinical expression for obstruction of blood flow through 
the SVC. Malignancy (90%) is the most frequent cause of SVC obstruction. SVC obstruction is a 
strong predictor of poor prognosis in patients with non–small cell lung cancer. SVC obstruction in 
cancer patients can result from  
• 
Extrinsic compression of SVC 
o 
Lung Cancer (65%) 
o 
Lymphomas (15%) 
o 
Other cancers (10%) 
• 
Intrinsic compression 
 
Diagnostic Criteria 
Common symptoms and physical findings of SVCS are: 
• 
Dyspnea  
• 
Headache  
• 
Oedema and change in colour in the areas drained by SVC (examples–face and upper 
limb)  
• 
Venous distension of neck, upper chest and arms  
• 
Cough 
• 
Pemberton’s sign (development of facial flushing, distended neck and head superficial 
veins, inspiratory stridor and elevation of the jugular venous pressure (JVP) upon raising 
both of the patient's arms above his/her head simultaneously, as high as possible 
(Pemberton's maneuver) 
 
Investigations: 
• 
CXR 
• 
CT scan Chest Abdomen and Pelvis 
• 
PET/CT 
• 
Tissue diagnosis for appropriate treatment modality 
• 
Bronchoscopy 
• 
Needle aspiration of a peripheral lymph node, or mediastinoscopy 
• 
Sputum cytology 
• 
Thoracentesis. 
 
Non-pharmacological treatment: Treatment of SVC syndrome is divided into supportive and 
definitive therapy 
Supportive measures 
• 
Head elevation–To decrease the hydrostatic pressure and thereby the edema. There are 
no data documenting the effectiveness of this manoeuvre, but it is simple and without risk. 
• 
Glucocorticoid therapy (dexamethasone, 4 mg every 6 hours) to relieve inflammation and 
oedema (to be avoided before biopsy if lymphoma is suspected as steroid induced tissue 
necrosis might obscure the diagnosis) 
• 
Loop diuretics (furosemide) are also commonly used, but it is unclear whether venous 
pressure distal to the obstruction is affected by small changes in right atrial pressure. 
 
Definitive Therapy 
• 
Radiation treatment to the malignant mass. 
• 
Chemotherapy–in chemo sensitive cancers like lymphoma, germ cell tumours or small cell 
lung cancer 
• 
SVC Stent–can be useful in cases of thrombosis and for patients not responding to cancer 
treatment 
• 
Removal of central venous device. 
 
Note 
• 
It is advisable to avoid placement of intravenous lines in the arms so that fluid is not 
injected into the already compressed SVC. 

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22.11.2 Hypercalcaemia 
Hypercalcaemia refers to elevated calcium level in blood (normal range 2.2–2.6 mmol/L) that occurs 
in 10–20% patients with advanced cancers (most commonly in cancer of the breast, kidney, lung, 
prostate, head and neck and multiple myeloma) 
 
Diagnostic Criteria 
• 
Symptoms of hypercalcaemia include nausea, vomiting, constipation, polyuria and 
disorientation 
• 
Psychiatric overtones (depression 30–40%, anxiety, cognitive dysfunction, insomnia, 
coma) 
• 
Clinical evidence of volume contraction secondary to progressive dehydration may be 
apparent. Severe hypercalcaemia (above 3.75–4.0 mmol/L) is a medical emergency and a 
poor prognostic sign 
 
Investigations include  
• 
Specific biochemistry like PTH,  
• 
ECG to detect arrhythmias and  
• 
Imaging with Bone Scan or PET–CT scan to identify metastatic bone disease. 
 
Pharmacological Treatment 
Treat the hypercalcaemia first and the cause later: 
• 
Hydration & dieresis: 1–2 litres of isotonic saline (NS) over 2 hours with 30–40 mg of 
furosemide expands intravascular volume and enhances calcium excretion.  
o 
In elderly and cardiac patients, rate of hydration needs to be slower. 
• 
Bisphosphonates–via a complex mechanism inhibit osteoclast and in turn both normal and 
pathological bone resorption. Commonly used bisphosphonates are: 
S: zolendronic acid (IV) infused as 4mg (IV)   in 100 mls of NS over 15 mins. 
Normalisation of serum calcium occurs in 4–10 days and lasts 4–6 weeks. Therefore, 
if re–treatment is required, dose is repeated after 7 days 
OR 
S: ibandronate (IV)  6 mg  over 2 hours  infusion  
 
Note 
• 
Bisphosphonates and denosumab cause increasing risk of osteonecrosis of jaw 
following extraction of teeth or oral surgical procedures. Therefore, a dental review may 
be necessary to make sure the necessary dental procedures are completed prior to 
commencing therapy 
• 
Calcitonin – a thyroid hormone given 4–8 IU/kg IM or SC every 6–8 hours can bring 
about a rapid decline in calcium levels, however tachyphylaxis limits its utility.  
 
22.11.3 Spinal–cord Compression 
Spinal cord compression threatens mobility, independence and longevity in patients with metastatic 
cancer and may be the first presentation of curable malignancy in others. It most commonly occurs 
due to an enlarging vertebral metastasis encroaching on the epidural space or due to pathologic 
fracture of a vertebra infiltrated by malignancy.  
 
Management 
• 
Immobilising the patient and obtaining urgent MRI/CT whole spine should be priorities.  
• 
Corticosteroids should be initiated on suspicion of cord compression.  
 
B: dexamethasone (IV) 16 mg immediately followed by 16 mg daily in divided doses.  
• 
Bladder catheterisation is appropriate.  
• 
Once spinal cord compression is confirmed, urgent neurosurgical opinion should be 
sought. There are potential improvements in outcomes for patients treated with surgery 
upfront, though appropriateness for this will depend upon spinal stability, patient and 
malignancy related factors. 
• 
Radiotherapy: for patients who are not candidates for upfront surgery.  
• 
Palliative dose: 8Gy Single fraction or 20Gy/5Fractions or 30Gy/10 Fractions. 
 

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Note 
• 
All patients suspicious for spinal cord compression should be referred to 
neurosurgeon and radiation oncologist as soon as possible. 
 
22.11.4 Tumor Lysis Syndrome 
The syndrome is mostly observed in cancers with a rapid proliferation index such as Burkitt’s 
lymphoma, acute lymphocytic leukemia, acute non-lymphocytic leukemia, and less frequently, solid 
tumors of small-cell type, breast cancer, and medulloblastoma. 
 
Clinical Presentation 
Clinically, the syndrome is characterized metabolically by the presence of hyperuricemia, 
hyperkalemia, hyperphosphatemia, hypocalcemia and acute renal failure. 
• 
Work Up 
• 
FBP, RFT, LFT, LDH 
• 
Serum electrolytes phosphates and calcium  
• 
Urine pH and output 
• 
ECG.  
• 
CXR 
• 
CT-Scan.  
• 
Abdomen and Pelvis USS 
 
Treatment  
• 
Frequent monitoring of electrolytes such as blood-urea-nitrogen (BUN), creatinine, uric 
acid, potassium, sodium, phosphate, calcium levels and Lactate dehydrogenase (LDH) at 
least three times per day 
• 
 Also Alkalization of urine by Sodium bicarbonate added to IV fluids at 100 mEq/L this 
should continue for 48-72 hours after start of chemotherapy. 
• 
Hydration in high risk patients must start 12-48 hours’ prior the start of chemotherapy and 
continue 48- 72 hours post chemotherapy; continuous infusion should exceed 3 L/m² daily, 
resulting in urine volumes of at least 3L/Day.  
• 
IV Allopurinol 300 mg/day daily   
• 
Patients with high potassium levels must be evaluated and monitored constantly for 
cardiac rhythm disorders, do administer calcium and exchange resins, those with 
continuously low levels calcium a calcitriol must be given. 
• 
 Empiric antibiotics can be administered for opportunistic infections, consider also 
perenteral nutrition (TPN) and GCF (neupogen) if indicated. 
20.11.5 Febrile Neutropenia 
Appllied only to the management of patients with:  
• 
Fever and neutropenia as a result of a known or suspected malignancy or the use of 
chemotherapy 
• 
Fever and neutropenia as a result of a bone marrow failure syndrome. 
• 
Fever (or evidence of infection) who are receiving chemotherapy or who have completed 
cancer therapy within 6 months even though they are not neutropenic.  
Work up  
• 
FBP, LFT, RFT  
• 
Malaria screen  
• 
Urine analysis Urine / blood / stool culture Serum Electrolytes Throat Swab  
 
Treatment  
• 
Antibiotic administration  
• 
Anti pyretics and analgesics 

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Initial (first-line) and subsequent (second-line – deteriorating patients) empiric antibiotic selection. 
Patients with no significant betalactam reactions: 
D: piperacillin+tazobactam (FDC) (IV) 4 g piperacillin / 0.5 g tazobactam given every IV 6 
hourly PLUS Gentamicin 3-6mg/kg once daily. Deteriorating patients on first line treatment 
with no history of anaphylaxis to Beta Lactams (i.e. if history of rash only, can still use 
meropenem 
OR 
D: meropenem (IV) 500mg 8 hourly AND amikacin (IV) 15mg/kg/dose in 2-3 devided dose 
(or ciprofloxacin 200– 400 mg IV 12 hourly) AND vancomycin 15 - 20mg/kg/dose 8 - 12 
hourly 
Patients with history of definite anaphylaxis to Beta Lactams  
D: ciprofloxacin (IV) as above AND metronidazole (IV) 500mg – 750mg dose 8 hourly AND 
amikacin dose as above AND vancomycin dose as above 
Culture Negative Patients 
 First 48 hours 
• 
Patient had a single spike of fever (i.e. patient’s temperature returns to normal within 4 
hours of the initial fever), antibiotics may be discontinued.  
• 
Patient had more than a single spike of fever, antibiotics must be continued for a minimum 
of 7 afebrile days. Also consider the following. 
• 
If patient develops oral herpes or severe mucositis, commence IV Aciclovir.  
• 
Obvious fungal infection – suspect candida – add fluconazole IV; suspect other fungal 
infection – add Amphoteracin B IV. 
• 
Diarrhoea and vomiting – culture stool and commence ciprofloxacin and metronidazole  
• 
Signs of skin infection – add vancomycin  
• 
No clinical focus but deteriorating rapidly or extremely unwell – consider adding 
vancomycin 
 If by day 5-7 patient remains febrile, neutropenic, consider performing a fungal work-up, prior to 
commencing empiric appropriate antifungal treatment. 
 
 
 
 
 

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CHAPTER TWENTY-THREE 
MENTAL HEALTH CONDITIONS 
23.1. Patients with Aggressive and Disruptive Behaviours 
These are agitated and acutely disturbed patients, who may or may not have a mental disorder. 
Many acute medical conditions, trauma, toxicological conditions and substance related disorders 
(especially substance induced disorders) can also present with agitation. 
 
Clinical Presentation 
• 
Agitation 
• 
Aggressive behaviours 
 
Non-Pharmacological Treatment 
• 
Ensure the safety of the patient and those caring for them. 
• 
Caution is needed with elderly and frail patients as they are vulnerable to falls and 
further injury if sedated. 
• 
The use of physical restraint should only be employed when there is a need to protect 
the patient and surrounding people in an acute setting and it should be for as short 
time as possible with a constant monitoring of patients’ safety  
• 
Assess for sign of delirium. 
 
De-escalation Techniques should be attempted first: 
• 
Calm the patient 
• 
Manage in a safe environment 
• 
Ensure the safety of all staff members 
 
Pharmacological Treatments 
For cooperative patients 
A: promethazine (PO) 25-50mg stat 
  
OR 
C: diazepam (PO)10 mg stat  
 
 
OR  
C: lorazepam PO)4 mg stat  
 
Uncooperative and severely agitated patients 
If oral treatment fails after 30–60 minutes, OR If there is significant risk to the patient and others, 
give 
Parenteral treatment as follows: 
 
B: haloperidol (IM) 2.5-5mg stat, repeat in 30-60minutes, if required. (Maximum dose: 
20mg, within 24hours)  
AND 
A: diazepam (IV/IM) 10mg stat. Repeat after 30–60minutes if needed. (maximum dose: 
60mg per 24hours) 
OR 
A: promethazine (deep IM) 25–50mg Repeat after 30–60minutes if needed  
 OR 
C: lorazepam (IM) 1-4mg stat. Repeat after 30–60minutes if needed to a maximum dose of 
12mg in 24hours  
 
 
OR 
 
D: midazolam (IV/IM) 2-10mg stat                                      
 
If haloperidol is unavailable,  
A: chlorpromazine (deep IM) 25–50mg may be repeated as necessary 4 times in 24hours 
(Maximum dose: 2000mg per 24hours).  
 
If patient is known to suffer from schizophrenia and is not neuroleptic naïve give: 
S: zuclopenthixol acetate IM) 50–150 mg (Repeat after 2–3 days, if necessary.Give a 
maximum of 3 repeat injections and should not be used for longer than 2 weeks. The 
maximum administered dose should not exceed 400mg. 
If patient develops acute dystonia give: 

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A: promethazine (deep IM) 25–50 mg. In the elderly 25 mg. 
OR 
A: atropine (IM) 0.5 -2 mg when required 
 
 
Note 
• 
Repeated doses of high potency antipsychotics may lead to the development of the life-
threatening neuroleptic malignant syndrome. If suspected, stop antipsychotic, and institute 
supportive care. 
• 
Elderly patients are at increased risk of respiratory depression and delirium from 
benzodiazepines, so they should be avoided as far as possible. 
• 
Always monitor vital signs of sedated patients 
 
 
23.2. Delirium 
Delirium or acute confusion state is a condition characterized by altered level of consciousness, 
disorientation to time, place and sometimes to person.  
 
Clinical presentation 
• 
Reduced awareness of the environment 
o 
Inability to stay focused on a topic or to switch topics 
o 
Getting stuck on an idea rather than responding to questions or 
conversation 
o 
Being easily distracted by unimportant things 
o 
Being withdrawn, with little or no activity or little response to the environment 
• 
Poor thinking skills (cognitive impairment) 
o 
Poor memory, particularly of recent events 
o 
Disorientation — for example, not knowing where you are or who you are 
o 
Difficulty speaking or recalling words 
o 
Rambling or nonsense speech 
o 
Trouble understanding speech 
o 
Difficulty reading or writing 
• 
Behavioral changes 
o 
Seeing things that don't exist (hallucinations) 
o 
Restlessness, agitation or combative behavior 
o 
Calling out, moaning or making other sounds 
o 
Being quiet and withdrawn — especially in older adults 
o 
Slowed movement or lethargy 
o 
Disturbed sleep habits 
o 
Reversal of night-day sleep-wake cycle 
• 
Emotional disturbances 
o 
Anxiety, fear or paranoia 
o 
Depression 
o 
Irritability or anger 
o 
A sense of feeling elated (euphoria) 
o 
Apathy 
o 
Rapid and unpredictable mood shifts 
o 
Personality changes 
 
Non-Pharmacological Treatment 
• 
Control the acute disturbance.  
• 
Perform proper physical assessment as well as investigations in order to rule out or 
ascertain the underlying medical condition and treat accordingly 
 
Pharmacological Treatment 
Treat the underlying medical condition, if present. And any other presentations, symptomatically 
 
Acute Management 
B: haloperidol (IM) 5mg stat repeated in 30-60 minutes when required (Maximum dose: 
20mg within 24 hours) 
 

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• 
Monitor vital signs and beware of acute dystonia and neuroleptic malignant syndrome 
• 
Dosing may vary according to clinical circumstances 
 
AND/OR 
A: diazepam (IV) 10mg. 
 
OR 
C: lorazepam (IM) 1-4mg. 
Switch to oral route once containment is achieved. 
 
Note 
• 
Benzodiazepines, especially diazepam IV, can cause respiratory depression. Monitor 
patients closely 
• 
In the frail and elderly patient or where respiratory depression is a concern, reduce the 
dose by half 
• 
The safest route of administration is oral followed by IM with the IV route having the 
highest risk of respiratory depression and arrest. Use the safest route wherever 
possible.  
• 
Monitor vital signs closely during and after administration 
• 
Use haloperidol instead of benzodiazepines in patients with respiratory insufficiency 
• 
To avoid benzodiazepines toxicity, allow at least 15-30 minutes before repeating the 
IM dose 
 
23. 3. Dementia 
It is a condition which involves progressive and cognitive deficits. Dementia usually affects memory 
first, with subsequent progression to cause dysphasia, agnosia, apraxia, diminished ability with 
executive function and eventually personality disintegration. 
 
DSM-5 diagnostic criteria 
To diagnose Dementia, the following criteria need to be met: 
• 
There must be significant cognitive decline from a previous level of performance in one or 
more of the following cognitive domains - attention, executive function, learning and 
memory, language, perceptual motor and social cognition. 
• 
These deficits affect independence in performing everyday activities.  
 
Non-pharmacological Treatment 
• 
Psychoeducation about the disorder, to the patient and family 
• 
Mini Mental Status Examination, functional and behavioural assessment should be 
performed every 6 months. 
 
Pharmacological Treatment  
Mild to moderate: 
S: donepezil (PO) 5mg initially, may increase to 10mg/24hours after 4-6weeks  
Moderate to severe:  
S: donepezil (PO) 5mg initially, may increase to 10mg /24hours after 4-6weeks; may 
further increase to 23 mg/day after 3 months  
23.4. Schizophrenia 
It is a chronic mental disorder, characterized by disturbances in thought, emotions, drive, behaviour 
and withdrawal from reality. Symptoms vary from patient to patient and from time to time.  
 
DSM-5 Diagnostic Criteria 
To diagnose Schizophrenia, the following criteria need to be met; 
• 
Presence of 2 or more of the following symptoms over a 1-month period: 
a. 
Delusions 
b. 
Hallucinations 
c. 
Disorganized speech 
d. 
Disorganized behavior 
e. 
Negative symptoms 
(at least 1 of which must be a, b or c) 
• 
Individual’s premorbid level of functioning is affected in several major domains of life. 

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• 
There must be continuous impairment over a period of at least 6 months, during which the 
individual might experience either active or residual symptoms. 
• 
These symptoms must not be due to the effects of substance usage or an underlying 
medical condition 
 
Non-Pharmacological Treatment 
• 
Family counselling and psycho-education 
• 
Cognitive Behavioural Therapy (CBT) for stabilized patients 
• 
Supportive group therapy for patients with schizophrenia 
• 
Rehabilitation may be enhanced by assertive community programs, work assessment, 
occupational therapy and bridging programs prior return to the community 
 
Pharmacological Treatment 
In acute attacks: 
Treat like under section: patients with aggressive and disruptive behaviours. 
 
For maintenance: 
B: haloperidol (PO) 3-4.5mg 12hourly, 
OR 
A: chlorpromazine (PO) 100–600mg 24hourly in divided doses  
OR 
S: olanzapine (PO) 5–10mg titrate to maximum dose 20mg/24hours  
OR 
S: risperidone (PO) 1mg 12hourly then increase by 1mg every 2–3 days to 2–3mg 12 
hourly. Maximum dose 16mg/day  
 
Note: 
• 
Titrate to maximum dose while monitoring dose-response to target symptoms against 
adverse effect 
• 
The above medicines should not be given in combination 
• 
The atypical antipsychotics have been shown to be comparatively more effective in 
treatment of negative symptoms 
 
For patients who have poor compliance to oral medications and patient preference, give 
depot antipsychotics 
C: fluphenazine decanoate (IM) 6.25-50mg 2-4weekly, and monitor dose-response to 
target symptomsagainst adverse effect, if necessary, dose may be tapered 
OR 
S: zuclopenthixol decanoate (IM) 100-600mg 2-4weekly, and monitor dose-response to 
target symptomsagainst adverse effect, if necessary, dose may be tapered 
 
OR 
S: flupenthixol decanoate (IM) 20–40 mg every 4weeks, and monitor dose-response to 
target symptomsagainst adverse effect, if necessary, dose may be tapered 
 
Note 
• 
. Give a test dose first.  This is in view of the fact that depots are known to be long acting 
• 
Giving a test dose helps to determine whether the patient is sensitive to the medication 
(either via development of EPSE or any adverse reactions to the oil base) 
• 
Commence treatment with the lowest therapeutic dose 
• 
Administer the depot at the longest possible duration 
• 
adjustment of dosages should be conducted after an adequate period of assessment 
 
Adjunct Treatment 
Antiparkinsonian medicines should only be used if extrapyramidal side effects(except tardive 
dyskinesia) occur, or at higher doses of antipsychotics likely to cause extrapyramidal side effects. 
Any of the following can be used: 
 
 
A: promethazine (PO) 25-50mg 24hourly, until symptoms/signs subside 
 
 
OR 
A: benzhexol (PO) 5mg 24hourly to12hourly, last dose before 1400 hourstoavoidinsomnia 

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Referral 
Refer to the next level in the following situations: 
• 
First psychotic episode 
• 
High suicidal risk or risk of 
harm to others 
• 
Children and adolescents 
• 
Elders 
• 
Pregnant and lactating women 
• 
No response to treatment 
• 
Intolerance to medications 
• 
Concurrent medical conditions 
or other mental disorders 
23.5. Catatonia 
Causes of catatonia: schizophrenia, severe depressive disorder, bipolar disorder, organic disorders 
e.g. CNS infections, CNS tumour, cerebrovascular accident, severe intoxication of recreational 
drugs and lethal catatonia. 
Clinical features: Ambitendency, automatic obedience, waxy flexibility / catalepsy, negativism, 
stereotypy, mannerism, echolalia and echopraxia. 
Investigations: FBP, RFT, LFT, TFT, blood glucose, CK, urine drug screen, ECG, CT, MRI, EEG, 
urine and blood culture, syphilis screen, HIV, heavy metal screen, auto-antibody screen and lumbar 
puncture. 
Non-pharmacological treatment 
Hydration, early mobilization, close monitoring, transferal to ICU if patient deteriorates. 
Pharmacological treatment 
A: diazepam (IV/IM) 10-20mg 24hourly 
 
 
OR 
C: lorazepam (IM) 1-4mg 24hourly   
Note 
• 
If benzodiazepine does not work and symptoms are severe, ECT is an option 
23.6. Schizoaffective Disorder 
DSM-5 Diagnostic criteria 
For an individual to fulfill the diagnostic criteria, there must be the presence of solely hallucinations 
or delusions for at least 2 weeks in the absence of an affective episode, throughout the whole 
duration of the psychiatric illness. There must also have an uninterrupted period where there are 
prominent affective symptoms concurrent with symptoms of schizophrenia. Individuals should have 
symptoms fulfilling the diagnosis of an affective disorder for most of the duration of the illness. 
DSM-5 has specified 2 subtypes of schizoaffective disorder, which are: 
• 
Bipolar type - Whereby a manic episode is part of the entire course of the illness 
• 
Depressive type - Whereby a major depressive episode is part of the entire course of the 
illness 
 
Non-Pharmacological  Treatment 
• 
Family counselling and psycho-education 
• 
Cognitive Behavioural Therapy (CBT) for stabilized patients 
• 
Supportive group therapy for patients  
• 
Rehabilitation may be enhanced by assertive community programs, work assessment, 
occupational therapy and bridging programmes prior return to the community 
 
Pharmacological Treatment 
For Psychotic symptoms:  
A: chlorpromazine (PO) 100-1000mg in divided doses*, per day (max. dose 1000mg, per 
24hours) 
OR  
B: haloperidol, (PO) 1.5-6mg in divided doses*, per day (max. dose 20mg)  

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For Manic subtype:  
A: carbamazepine (PO) 200-1000mg 24hourly, in divided dose*  
 
OR 
C: sodium Valproate (PO) 500-1000mg 24hourly, in divided dose* 
 
For Depressive subtype:  
A: amitriptyline (PO) 12.5-75 mg nocte   
 
OR 
S: fluoxetine (PO) 10-20 mg nocte  
 
Note 
• 
Symptoms should be monitored and medication can be tapered* divided doses: in acute 
phase 8hourly or 12hourly while in maintenance phase titrate to 12hourly or preferably 
24hourly  
 
23.7. Brief or Acute/Transient Psychotic Disorder 
DSM-5 Diagnostic criteria 
For an individual to fulfill this diagnosis; 
• 
He/she must have, for a duration of between 1 day to 1 month the following symptoms: 
o 
Delusions 
o 
Hallucinations 
o 
Disorganized speech 
o 
Grossly disorganized or catatonic behaviour 
• 
Exclude differentials like major depression or bipolar depression with psychotic features, 
schizophrenia and exclude the possibility of the symptoms being due to underlying 
substance use or medical conditions. 
 
Non-pharmacological Treatment 
Manage as Schizophrenia 
 
Pharmacological Treatment 
Manage as Schizophrenia 
23.8. Bipolar Mood Disorders 
These are lifelong mental disorders, which may have an episodic, variable courses. The presenting 
episodes may be manic, hypo manic, depressive or mixed. By definition, a diagnosis of bipolar 
disorders requires either a current or previous episode of mania or hypomania.  
 
Bipolar I Disorder Diagnostic Criteria 
DSM-5 specified that an individual need to have at least 1 manic episode in order to fulfill the 
diagnostic criteria of Bipolar I disorder. 
 
Manic Episode 
A manic episode is characterized by a period of time, of at least 1 week, during which the individual 
has persistent elevated (extreme happiness) or irritable mood and present for most of the days.  
In addition, the individual needs to have at least 3 (4 if mood is only irritable) of the following 
symptoms: 
• 
Increased self-confidence(Grandiose and/or religious delusions) 
• 
Reduction in the need for sleep 
• 
Chattier than usual, with increased pressure to talk 
• 
Racing thoughts 
• 
Easily distractible 
• 
Increase in number of activities engaged 
• 
Involvement in activities that might have a potential for serious consequences 
 
There must be marked impairments in terms of functioning with the onset of the above 
symptomatology. 
 

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Non-Pharmacological Treatment 
• 
Hospitalization may be required during acute mania 
• 
Psychotherapy, usually after the manic episode has been controlled with medication 
• 
Family therapy and psycho-education of patient and family to increase compliance and 
knowledge of the condition 
• 
In severe cases, electroconvulsive therapy may be required. 
 
Pharmacological Treatment 
For Manic or Mixed Episodes 
For agitated and acutely disturbed patient: See section on patients with aggressive and disruptive 
behaviours. 
 
Maintenance therapy 
A: carbamazepine (PO) 600mg 24hourly in 2-3 divided doses, increase by 200mg at three-
day interval up to a maximum of 2000mg 
OR 
C: sodium valproate (PO) 20 mg/kg/day in 2–3 divided doses (maximum of 2000 mg, per 
day) 
 
OR 
S: lamotrigine (PO) 600mg once a day, increase by 200mg at three-day interval up to a 
maximum of 2000mg 
 
 
Note 
• 
The option of combining two mood stabilizers at S: level should be allowed i.e. sodium 
valproate and Lithium carbonate 
 
Treatment for Severe Depressive Episodes in Bipolar Patients 
Give antidepressant in combination with mood stabilizer and antipsychotic if there is psychosis: 
 
A: amitriptyline (PO) 12.5 to 50mg nocte 
OR 
S: fluoxetine (PO) 10-20mg nocte,  
AND 
A: carbamazepine (PO) 200-400mg 12hourly, maximum 2000mg/per day 
OR 
C: sodium valproate (PO) 500-2000mg 24hourly 
AND 
A: chlorpromazine (PO) 100-1000mg 24hourly in divided doses, (max. dose 1000mg, per 
day) 
 
 
OR 
B: haloperidol (PO) 1.5mg –10mg 12hourly (if there is psychosis) and symptoms should be 
monitored, and medication to be tapered     
 
Note 
 Do not use monotherapy antidepressants in bipolar patients. 
 
Referral 
Refer to the next level in the following situations: 
• 
Mixed or rapid cycling bipolar disorder 
• 
Depressive episodes in bipolar patients not responding to treatment 
• 
Manic episodes not responding to treatment 
23.9. Major Depressive Disorder 
It is a mood disorder characterized by at least 2 weeks of depressed mood and/or diminished 
interest and pleasure in activities. It is associated with impairment in level of functioning in different 
areas including social and occupational. 
 
Diagnostic Criteria 
Psychological symptoms 
• 
Depressed mood 
• 
Feeling of worthlessness 
• 
Guilt 
• 
Diminished concentration  
• 
Thoughts of death and suicide 

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Somatic symptoms 
• 
Change in appetite 
• 
Sleep disturbances 
• 
Agitation  
• 
Retardation  
• 
Loss of energy 
 
Non-Pharmacological Treatment 
Effective psychotherapies include: 
• 
Cognitive Behavioural Therapy 
• 
Interpersonal psychotherapy 
• 
Stress management / coping skills 
• 
Marital and family issues 
• 
Sleep hygiene advice 
 
Pharmacological Treatment 
A: amitriptyline (PO) 12.5–75mg 24hourly at night, increase gradually to a maximum of 
150mg 24hourly. {Elderly: Initially 12.5–50 mg. Max. 75mg) 
 
 
 
OR 
D: citalopram (PO) 10-60mg 24hourly 
OR 
S: fluoxetine (PO) 20-60mg 24hourly (morning)   
Note 
• 
Efficacy of the treatment is gauged by amelioration of symptoms and the dose should be 
titrated according to clinical response.  
• 
Monitor all patients recently started on antidepressants closely for increased agitation and 
suicidal behaviour, especially young patients (younger than 25 years).  
• 
Some symptoms, such as sleep and appetite, may improve more quickly. 
• 
If partial response or non-response, increase the dose or switch to another antidepressant. 
The first line is an alternative SSRI. The second line is an antidepressant from a different 
class. 
 
Referral 
Refer to the next level in the following situations: 
• 
Suicidal ideation 
• 
Major depression with psychotic features 
• 
Failure to respond to available antidepressants 
• 
Patients with concomitant medical illness, e.g. heart disease, epilepsy 
• 
Poor social support systems 
• 
Pregnancy and lactation 
23.10. Suicide 
Suicide is 
the 
act 
of 
intentionally 
causing 
one's 
own death. 
Mental 
disorders—
including depression, bipolar 
disorder, autism 
spectrum 
disorders, schizophrenia, personality 
disorders, anxiety disorders, physical disorders such as chronic fatigue syndrome, and substance 
abuse—including alcoholism and the use of and withdrawal from benzodiazepines—are risk 
factors.Some suicides are impulsive acts due to stress (such as from financial or academic 
difficulties), 
relationship 
problems 
(such 
as breakups or 
deaths 
of 
close 
ones), 
or 
harassment/bullying. Those who have previously attempted suicide are at a higher risk for future 
attempts. 
Effective suicide prevention efforts include; 
• 
Limiting access to methods of suicide—such as hanging, firearms, drugs, and poisons 
• 
Treating mental disorders and substance misuse 
• 
Careful media reporting about suicide 
• 
Improving economic conditions.  
 
23.11. Generalized Anxiety Disorder 
Generalized anxiety disorder is characterized by excessive, exaggerated anxiety and worry about 
everyday life events with no obvious reasons for worry.  
 
 

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Diagnostic Criteria 
Symptoms include 
• 
Persistent worry 
• 
Disturbances in sleep 
• 
Poor concentration 
• 
Mood disturbances 
• 
Muscle tension  
• 
Tremors 
 
Non-pharmacological Treatment 
• 
Psychotherapy 
• 
Most patients can be treated as outpatients 
 
Pharmacological Treatment 
Indicated where symptoms are interfering with normal functions of daily living. Where there is 
concomitant drug/alcohol dependence or co-morbid major depressive episode, an antidepressant 
may be more appropriate.  
 
Acute management  
For an acute episode or intense prolonged anxiety: 
A: diazepam (PO) 2–5 mg stat repeat 12hourly when required 
o 
Duration of therapy: up to 2weeks, taper off to zero within 6weeks 
 
Maintenance Therapy  
A: amitriptyline (PO) 25–75mg nocte (Medication should be titrated according to symptoms 
resolution) 
OR  
D: citalopram (PO) 10–40mg 24hourly (Medication should be titrated according to 
symptoms resolution)  
OR 
D: clonazepam (PO) 0.5 – 4 mg 24hourly (Medication should be titrated according to 
symptoms resolution)                                 
OR 
S: fluoxetine (PO) 20–40mg 24hourly (Medication should be titrated according to 
symptoms resolution) 
 
 
 
 
Note: 
• 
Prolonged treatment with benzodiazepines often leads to tolerance and withdrawal 
symptoms if the medicine is discontinued abruptly 
• 
Avoid combining more than one benzodiazepine. 
 
Referral 
Refer to the next level if there is lack of improvement with treatment. 
23.12. Panic Disorder 
Panic disorder is an anxiety disorder characterized by recurrent unexpected panic attacks. A panic 
attack is characterized by an acute onset of intense anxiety accompanied by a sense of 
dread/impending threat, usually for no apparent reason.  
 
Diagnostic Criteria 
The patient will experience significant fear and emotional discomfort, typically peaking within 10 
minutes and resolving within 30 minutes. There will usually be accompanying physical symptoms 
including:  
• 
Rapid pulse/palpitations 
• 
Shortness of breath 
• 
Dizziness 
• 
Sweating 
 
Non-Pharmacological Management 
• 
Psycho-education and reassurance 
• 
Psychotherapy, e.g. cognitive-behaviour therapy 
• 
Exclude an underlying medical condition, e.g. thyrotoxicosis 
 
 

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Pharmacological Treatment 
Panic attack 
Acute management 
The initial aim is to control the panic symptoms and exclude an underlying medical cause. 
A: diazepam (PO) 5-10mg 12hourly (Medication should be titrated according to symptoms 
resolution) 
  OR 
C: lorazepam (PO) 2-4mg 12hourly (Medication should be titrated according to symptoms 
resolution) 
 
 
 
OR 
D: clonazepam (PO) 0.5-3mg 12hourly (Medication should be titrated according to 
symptoms resolution) 
 
Panic disorder 
A: amitriptyline 25–75mg (PO) nocte (Medication should be titrated according to symptoms 
resolution) 
 
 
 
OR 
D: citalopram 10–40mg (PO) 24hourly (Medication should be titrated according to 
symptoms resolution)   
OR 
S: fluoxetine 20–40mg (PO) 24hourly (Medication should be titrated according to 
symptoms resolution) 
 
Note 
• 
Initiate at low dose and gradually titrate to therapeutic dosages according to tolerability. 
• 
Duration of therapy: variable, initially 6 months–1 year. 
• 
Long term medicine treatment may be necessary. 
• 
Relapses may occur when treatment is discontinued. 
• 
Consider short term co-administration of a benzodiazepine, due to the slow onset of action 
and the potential for increased anxiety during the initial phase of treatment with 
antidepressants. 
 
Referral 
Refer to the next level in the following situations; Treatment resistance or need for benzodiazepine 
treatment beyond 6 weeks 
23.13. Obsessive-Compulsive Disorder 
This condition is characterized by the presence of persistent intrusive thoughts or concerns, and is 
usually associated with compulsions, which are mental acts or behaviours which an individual 
engages in to attempt to get rid of the obsessions and/or decrease his or her distress i.e. excessive 
hand washing. Obsessive thoughts and compulsions may interfere with daily functioning. The 
features are usually distressing to the patient. 
 
Diagnostic Criteria 
• 
A pattern of repetitive behaviours 
• 
Anxiety symptoms 
 
Non-pharmacological Treatment 
• 
Psycho-education 
• 
Psychotherapy 
• 
Behaviour therapy 
 
Pharmacological Treatment 
D: citalopram, Initial dose: (PO) 20mg. If there is no or partial response after 4-8weeks, 
increase to 40mg, if well tolerated. 
OR 
S: fluoxetine, Initial dose: (PO) 20mg. If there is no or partial response after 4-8weeks, 
increase to 40mg, if well tolerated. 
 
Referral 
Refer to the next level in the following situations: Inadequate response to treatment 

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23.14. Acute Stress Disorder and Post-Traumatic Stress   Disorder 
Acute stress and post-traumatic stress disorder arise in response to stressful events. The patient 
should have experienced the event as life threatening or as a physical threat to themselves or 
others, at which time they felt fear and helplessness.  
 
Diagnostic Criteria 
Symptoms associated with both of these conditions include:  
• 
Re-experiencing of the event, e.g. flashbacks, dreams  
• 
Avoidance of situations associated with the event 
• 
Features of anxiety or increased arousal, e.g. hyper vigilance, heightened startle 
response and insomnia  
 
The conditions are symptomatically similar but differ with regard to the duration and time of onset of 
symptoms. The symptoms of acute stress disorder arise within 4 weeks of the event and last up to 4 
weeks, whereas the symptoms post-traumatic stress disorder last longer than 4 weeks, and may 
arise more than 4 weeks after the traumatic incident.  
 
Non-pharmacological Treatment 
• 
Reassurance and support of patient and family 
• 
Psychotherapy, supportive/cognitive-behavioural therapy 
 
Pharmacological Treatment 
 
Acute stress disorder:  
For acute anxiety or agitation give: 
D: clonazepam (PO) 0.5–2 mg 24hourly to 12hourly for 2weeks  
Not for longer than 2 weeks and taper to a stop in the course of 26 weeks. The maintenance 
treatment needs antidepressants 
 
Note 
• 
Prolonged use of benzodiazepines > 1 week may be detrimental to adaptation, 
leading to higher rates of post-traumatic stress disorder 
 
Post-traumatic stress-disorder:  
A: amitriptyline (PO) 50–150mg nocte   Elderly:  25- 75mg. (PO) for 4-8weeks 
OR 
D: citalopram 20-40mg (PO) 24hourly for 4–8weeks  
OR 
S: fluoxetine (PO) 20-40 mg 24hourly morning   for 4–8weeks 
 
Note 
An adequate antidepressant trial of treatment is 8–12 weeks, before an alternative treatment should 
be considered. 
 
Referral 
Refer to the next level in the following situations: 
• 
Inadequate response to treatment 
• 
Co-morbid conditions 
 
23.15. Substance Related Disorder 
!
23.15. 1. Substance Use Disorder 
23.15.1.1. Alcohol Use Disorder 
DSM-5 diagnostic criteria 
There must be a problematic usage of alcohol that has led to significant impairments 
occurring over a total of 12 months’ duration. The problematic usage of alcohol is manifested by at 
least 2 of the following: 
• 
Increasing usage of alcohol, or over a longer period than originally intended 
• 
Repeated unsuccessful efforts to cut down or control usage, despite the desire to do so. 

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• 
Large amount of time is spent on activities to obtain alcohol, use alcohol, or recover from 
the effects of alcohol. 
• 
Presence of a strong desire or urge to use alcohol 
• 
Repeated alcohol usage resulting in a significant failure to fulfill major roles 
• 
Persistent usage of alcohol despite having recurrent social or interpersonal problems due 
to the usage of alcohol. 
• 
Important activities are given up due to the usage of alcohol 
• 
Repeated usage despite significant impairments in physical health 
• 
Continued use despite knowing that there have been physical or psychological problems 
arising from the usage of alcohol 
• 
Tolerance as defined by either (1) Need for increasing amounts of alcohol to achieve the 
same or desired effects or (2) 
• 
Reduced effects with continued use of the same amount of alcohol 
• 
Withdrawal as defined by either (1) Characteristic withdrawal symptoms or (2) Alcohol is 
being used to prevent or avoid withdrawal symptoms 
 
Non-pharmacological Treatment 
• 
Cognitive Psychotherapy – Involves assessment of the patient’s readiness for behavioural 
change using the stage of change model and also make use of motivation interviewing to 
enable patients to be empowered to change 
• 
Alcoholic Anonymous groups  
• 
A self-help group, with the sole purpose of enabling patients to quit their drinking habits. 
Their program is based on 12 core principles.                                  
 
23.15.1.2. Opioid Use Disorder 
DSM-5 diagnostic criteria 
It states that there must be problematic usage of opioid that has led to significant impairments in 
terms of functioning over a 12-month period. The rest of the criteria are similar to that of alcohol use 
disorder 
Non-pharmacological Treatment 
• 
Motivational interviewing 
• 
Therapeutic group therapy in a structured environment is helpful for helping individuals 
with their addiction. 
• 
Psycho-education with regards to their possibility of HIV transmission when using shared 
needles would be helpful 
 
Pharmacological Treatment 
Opioid substitutes   
C: methadone (PO) 10-30mg stat based on clinical assessment and UDS test then 
increase by 5-10mg every 3-5days to achieve optimal dose when opioid withdrawal 
features are well controlled.Once stability is reached, the client should be planned to 
remain on treatment for a minimum of two years. For more detail refer to national 
guidelines for comprehensive management of opioid use disorder 
 
OR 
S: buprenorphine 8-32mg (PO) 8hourly (Medication should be titrated according to 
symptoms resolution)                                
 
23.15.1.3. Nicotine Use Disorder  
For an individual with nicotine use disorder, abstinence from nicotine usually leads to withdrawal 
symptoms. Nicotine detoxification requires the use of medication to prevent the symptoms which 
could become severe and potentially lead to mortality. 
 

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Diagnostic Criteria 
Withdrawal symptoms include: 
• 
Restlessness  
• 
Tremors 
• 
Difficult in getting/maintaining 
sleep 
• 
Anxiety 
• 
Loss of appetite 
 
 
Non-Pharmacological Treatment 
• 
Support group that encourage abstinence 
• 
Inpatient rehabilitation programme where necessary 
 
23.15.2 Substance Induced Disorder 
23.15.2.1. Substance Intoxication 
Alcohol Intoxication 
DSM-5 diagnostic criteria  
It specifies that there must be recent usage of alcohol and that clinically significant behavioral or 
psychological changes have arisen during or shortly after the usage. 
 
This is characterized by at least one of the following signs or symptoms: 
• 
Slurred speech 
• 
Incoordination 
• 
Unsteady gait 
• 
Nystagmus 
• 
Impairments in attention or memory 
• 
Stupor or coma 
 
Treatment 
Symptomatically, depending on how patient presents 
Opioid Intoxication 
DSM-5 Diagnostic criteria 
• 
It states that there must be recent usage of opioid, with the presence of pupillary 
constriction (or pupillary dilation due to anoxia from severe overdose) and at least 1 of the 
following signs and symptoms: 
• 
Feeling drowsy or losing consciousness 
• 
Slurring of speech 
• 
Impairments in attention or memory 
There must also be significant problematic behavioral or psychological changes that have arisen 
during or shortly after the usage.  
 
Pharmacological Treatment 
B: naloxone (IM/IV) 0.04-15mg mg; if there is no response, the dose should be increased 
every 2 minutes  
Stimulant Intoxication 
DSM-5 diagnostic criteria 
It specifies that there must be recent usage of amphetamine-type substance, cocaine or other 
stimulant that has led to significant impairments in functioning, shortly after usage. This is 
manifested by at least 2 of the following signs and symptoms: 
• 
Increase or decrease in heart rate 
• 
Pupillary dilation 
• 
Elevated or lowered blood pressure 
• 
Perspiration or chills 
• 
Nausea or vomiting 
• 
Evidence of weight lost 
• 
Psychomotor 
agitation 
or 
retardation 
• 
Muscular 
weakness, 
respiratory 
depression, chest pain or cardiac 
arrhythmias 
• 
Confusion, seizures and coma 

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Pharmacological treatment of cocaine intoxication: 
If patient presents with agitation, refer to treatment of patient with aggressive and disruptive 
behaviors 
If patient presents with psychosis, give  
A: chlorpromazine (PO) 100-1000mg in divided doses, per day (max. dose 1000mg, per 
day) 
OR  
B: haloperidol (PO) 1.5-6mg in divided doses, per day (max. dose 20mg)                         
 
 
Note 
Treatment rendered largely targets the symptoms that individuals are experiencing 
 
Pharmacological treatment of Amphetamines intoxication:  
If patient presents with agitation, refer to treatment of patient with aggressive and disruptive 
behaviors 
If patient presents with depressive symptoms after detoxication, refer to pharmacological treatment 
with depressive symptoms 
 
Pharmacological treatment of Cannabis intoxication:  
A: chlorpromazine (PO) 100-1000mg in divided doses, per day (max. dose 1000mg, per 
day) 
OR 
A: haloperidol (PO) 1.5-6mg in divided doses, per day (max. dose 20mg)                         
 
23.15.2.2. Substance Withdrawal 
Alcohol Withdrawal 
For an individual with alcohol use disorder, abstinence from alcohol usually leads to withdraw 
symptoms. Alcohol detoxification requires the use of medication to prevent the symptoms which 
could become severe and potentially lead to mortality. 
 
Diagnosis features 
Withdrawal symptoms include: 
• 
Insomnia 
• 
Tremors 
• 
Chills 
• 
Anxiety 
 
Non-Pharmacological Treatment 
• 
Support group that encourages abstinence 
• 
Inpatient rehabilitation program where necessary 
 
Pharmacological Treatment 
C: thiamine (IM) 300mg 24 hourly 
For the CNS symptoms 
C: diazepam (PO) 10 mg every 4–6 hours on the first 24 and reduce by 20% over 5 days 
(only in inpatient care) 
 
 
OR 
C: Lorazepam (PO)  
 
Relapse prevention following detoxification 
S: naltrexone (PO) 50mg 24hourly, and should be titrated, according to response 
Alcohol Withdrawal Delirium (Delirium Tremens) 
It is an acute episode of delirium that is usually caused by withdrawal from alcohol. Although the 
typical delirium occurs 2–3 days following cessation of prolonged alcohol intake, reaching a peak at 
around 5 days, some withdrawal symptoms such as tremor may start within 12 hours. 
 

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Diagnosis Criteria 
• 
Visual hallucinations 
• 
Disorientation 
• 
Fluctuating 
level 
of 
consciousness 
• 
Agitation 
• 
Tachycardia 
• 
Hypertension 
• 
A low-grade fever may be 
present 
• 
Withdrawal 
tonic-clonic 
seizures may occur between 
24 and 48 hours following 
cessation of alcohol intake 
 
Note 
It is important to consider alternative causes, when making the diagnosis. This is especially true 
for cases with an atypical presentation. 
 
EmergencyCare 
• 
Secure airway 
• 
Ensure breathing 
• 
Circulation 
• 
Give IV fluid (Dextrose Normal Saline) to prevent hypoglycaemia and hypotension 
• 
Monitor for respiratory depression 
 
Pharmacological Treatment 
A: diazepam (IV)10mg for immediate sedative or hypnotic action. If no response gives a 
second dose. 
OR 
C: lorazepam (IM/IV) 2mg for immediate sedative or hypnotic action. If no response gives 
a second dose. 
OR 
S: chlordiazepoxide (IV) 20–60mg taper over one month 
AND 
C: thiamine (IM) 100-300mg 24hourly  
OR 
A: vitamin B Complex (IV) 1ampoule in 500ml 5% Dextrose 
 
Note:  
• 
Do not administer at a rate over 5 mg/minute 
• 
Switch to oral once containment is achieved 
 
Heroin Withdrawal 
Heroin addiction, is a chronic, relapsing brain disease that is characterized by compulsive substance 
seeking and use, despite harmful consequences. When your body has become dependent on 
heroin, a number of unpleasant withdrawal symptoms will arise when the drug hasn’t been used for 
a certain amount of time. 
 
Diagnostic features include: 
Myalgia, gooseflesh, diarrhea, rhinorrhea, lacrimation, agitation, anxiety, Insomnia, sweating, 
yawning, abdominal cramping, dilated pupils, nausea and vomiting 
Pharmacological Treatment 
To prevent repeating using of the heroin, give; 
S: methadone (PO) 30-120mg 24hourly   for a minimum of 1 year   
OR 
S: buprenorphine (PO) 2-8mg 24hourly for a minimum of 1 year 
OR 
S: naltrexone (PO) 25-50mg 24hourly    for 6 months.  
 
Symptomatic Treatment 
For difficult to get sleep, give: 
A: diazepam (PO) 5–20 mg 24hourly to a minimum of 7days  
 
 
 
OR 

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A: promethazine (PO) 50mg 24hourly at bed time (medication should be titrated according 
resolution) 
 
 
 OR 
A: Chlorpromazine (PO) 50–100mg 24hourly at bed time (medication should be titrated 
according resolution) 
 
For abdominal cramps, give:  
A: hyoscine butyl bromide (PO) 20mg 8-24 hourly (medication should be titrated according 
resolution) 
 
 
 
OR 
A: diclofenac (PO) 50mg 8hourly (medication should be titrated according resolution) 
 
For diarrhoea give 
B: loperamide 4 mg (PO) stat, then 2mg after each loose stool (medication should be 
titrated according resolution) 
 
Cocaine Withdrawal 
Non-Pharmacological Treatment 
These patients usually do not require admission, however beware of depression and assess suicide 
risk 
 
Pharmacological Treatment 
No substitute drug available for detoxification 
 
C: diazepam (PO) 5–10mg 8hourlyfor 5–7 days (medication should be titrated according 
resolution) 
 
Referral 
Refer patients to specialized clinic 
 
23.16. Psychiatric Disorders Associated with Epilepsy 
Epilepsy is a disorder of the brain characterized by an enduring predisposition to generate epileptic 
seizures and by the biologic, cognitive, psychological, and social consequences of this condition. 
This association may reflect the anatomical and neurobiological source of both epileptic seizures 
and the behavioral manifestations. 
 
Antiepileptic drugs (AEDs) can play a role in the genesis of psychiatric symptoms; on the other 
hand, some psychotropic medications can lower the seizure threshold and provoke epileptic 
seizures. 
 
The following are common psychiatric disorders in patients with epilepsy; 
• 
Major depressive disorder 
• 
Bipolar mood disorder 
• 
Anxiety disorder 
• 
Psychoses 
• 
Suicidality 
 
Treatment of Psychotic Disorders in patients with epilepsy; 
 
Non-pharmacological Treatment  
• 
Psychoeducation to the patient and the family 
• 
Family therapy 
• 
Supportive group therapy 
• 
Occupational therapy 
 
Pharmacological Treatment  
A: carbamazepine (PO) 200-1000mg, in divided doses, per day (symptoms should be 
monitored and medication titrated accordingly) 
OR 
A: phenobarbitone (PO) 30-200mg, in divided doses, per day (symptoms should be 
monitored and medication titrated accordingly) 
OR 

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C: sodium valproate (PO) 500-2000mg in divided doses, per day (symptoms should be 
monitored and medication titrated accordingly) 
 
If psychosis persists, give  
B: haloperidol (PO) 0.75-4.5mg 12hourly. Maximum dose 20mg/day 
 
 
OR 
S: olanzapine (PO) 5-10mg in divided doses, per day. Maximum dose 20mg/day 
(symptoms should be monitored and medication titrated accordingly) 
 
 
OR 
S: risperidone (PO) 0.5mg 12hourly then increase by 1mg every 2-3days to 2-3mg 
12hourly. Maximum dose 16mg/day 
 
 
 
Note 
• 
Postictal psychosis remits spontaneously even without treatment but that the use of 
effective neuroleptics may shorten the duration.  
• 
Interictal psychosis is treated with antipsychotic drugs. Medications that lower the seizure 
threshold should be avoided.  
• 
Atypical antipsychotic medications may have better profiles than typical antipsychotic 
medications. 
• 
Medications that lower the seizure threshold should be avoided. 
• 
The doses should be as minimal as possible 
 
Treatment of Depressive symptoms/signs in patients with epilepsy; 
 
Non-pharmacological Treatment 
• 
Psychoeducation to the patient and the family 
• 
Family therapy 
• 
Supportive group therapy 
• 
Occupational therapy 
 
 
Pharmacological treatment 
A: carbamazepine (PO) 200-1000mg, in divided doses, per day (symptoms should be 
monitored and medication titrated accordingly) 
 
 
OR 
A: phenobarbitone (PO) 30-200mg, in divided doses, per day (symptoms should be 
monitored and medication titrated accordingly) 
 
 
OR 
C: sodium valproate (PO) 500-2000mg in divided doses, per day (symptoms should be 
monitored and medication titrated accordingly)  
 
 
AND 
A: amitriptyline 12.5-75mg (PO), nocte (symptoms should be monitored and medication 
titrated accordingly) 
 
OR 
S: fluoxetine 1 (PO) 0-20mg in divided doses, per day (symptoms should be monitored and 
medication titrated accordingly) 
 
Note 
• 
In the treatment of epilepsy-related depression, priority should be given to optimizing 
seizure control, since improved psychosocial functioning tends to accompany seizure 
remission 
• 
Some anticonvulsant therapies, including sodium valproate, gabapentin, carbamazepine, 
and lamotrigine, also have antidepressant effects and may prove effective in treating 
depression in patients with epilepsy.  
Phenobarbital is known to produce depression. 
 
 
 

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Treatment of Mania/hypomania in patients with epilepsy; 
Non-Pharmacological Treatment  
• 
Psychoeducation to the patient and the family 
• 
Family therapy 
• 
Supportive group therapy 
• 
Occupational therapy 
 
Pharmacological Treatment 
A: carbamazepine (PO) 200-1000mg, in divided doses, per day  
OR 
A: phenobarbitone (PO) 30-200mg, in divided doses, per day  
OR 
A: sodium valproate (PO) 500-2000mg in divided doses, per day  
 
Note 
Symptoms should be monitored and medication titrated accordingly 
 
23.17. Psychiatric Disorders in Pregnancy 
In some women, pregnancy and motherhood increase their vulnerability to psychiatric conditions 
such as depression, anxiety disorders, eating disorders,panic disorder, bipolar illness, and 
psychoses. These conditions are often underdiagnosed because they are attributed to pregnancy-
related changes in maternal temperament or physiology. In addition, such conditions are often 
undertreated because of concerns about potential harmful effects of medication.  
23.17.1 Depression 
Several risk factors and psychosocial correlates have been identified as contributing to depression 
during pregnancy, like; 
• 
Previous history of depression, discontinuation of medication(s) by a woman who has a 
history of depression, a previous history of postpartum depression, and a family history of 
depression 
 
Several key psychosocial correlates may also contribute to depression during pregnancy: a negative 
attitude toward the pregnancy, a lack of social support, maternal stress associated with negative life 
events, and a partner or family member who is unhappy about the pregnancy. The relationship 
between maternal depression and early childhood problems may be part of a sequence that starts 
with depressive symptoms during pregnancy. 
 
Non-pharmacological Treatment 
• 
Psychotherapies  
o 
Cognitive behavioral therapy 
o 
Interpersonal psychotherapy 
o 
Education and support are also important, particularly as pregnancy is a unique 
experience for women, some of whom may not know what to expect.  
 
Pharmacological Treatment  
A: amitriptyline (PO) 12.5–75 mg 24hourly at night, increase gradually to a maximum of 
150 mg daily. {Elderly: Initially 12.5–50 mg. Max. 75mg) 
 
 
OR  
D: citalopram 10-60mg (PO) 24hourly morning or evening and symptoms should be 
monitored, and medication to be tapered 
OR 
S: fluoxetine 20-60mg (PO) 24hourly (morning)  
 
Note 
• 
Full disclosure of both the risk and benefits of various antidepressant medications should 
be made to the patient and, if possible, her partner prior to starting any pharmacological 
treatment. 
• 
Low doses of antidepressants should be considered when initiating medication. 
 

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12.17.2 Panic Disorder 
Some women may experience first-onset panic disorder during pregnancy. Women presenting with 
panic attacks for the first time should be screened for thyroid disorder. The correlation between 
plasma levels of cortisol in the mother and in the fetus may have implications for the developing fetal 
brain. 
 
Non-pharmacological Treatment 
• 
Cognitive behavioral therapy 
• 
Supportive psychotherapy 
• 
Relaxation techniques 
• 
Sleep hygiene 
• 
Dietary counseling 
 
Pharmacological Treatment 
Refer panic disorders 
 
Note 
• 
Full disclosure of both the risk and benefits of various antidepressant medications 
should be made to the patient and, if possible, her partner prior to starting any 
pharmacological treatment. 
• 
Low doses of antidepressants should be considered when initiating medication 
 
12.17.3 Obsessive-Compulsive Disorder 
Obsessive-compulsive disorder (OCD) is characterized by thoughts that cannot be controlled 
(obsessions) and repetitive behaviors or rituals that cannot be controlled (compulsions) in response 
to these thoughts.  
 
Non-pharmacological Treatment 
• 
Cognitive behavioral therapy 
• 
Supportive psychotherapy 
• 
Relaxation techniques 
• 
Sleep hygiene 
• 
Dietary counseling 
 
Pharmacological Treatment 
Refer to the specific section above 
 
Note 
Treatments for GAD in pregnancy are the same as those in non-pregnant adults. 
 
12.17.4 Bipolar Mood Disorder 
Non-pharmacological Treatment 
• 
Cognitive behavioral therapy 
• 
Supportive psychotherapy 
• 
Relaxation techniques 
• 
Sleep hygiene 
• 
Dietary counseling 
 
Pharmacological Treatment 
Refer to the specific section above 
Note 
• 
Decision whether to use mood stabilizers must be made following an assessment of risks 
and benefits. 
• 
Low doses of mood stabilizers should be as low as possible 
• 
Factors to consider include number and severity of previous episodes, level of insight, 
family supports, and the wishes of the woman 
• 
Careful monitoring of psychological symptoms throughout the pregnancy is of paramount 
importance 
 

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12.17.5 Schizophrenia 
Non-pharmacological Treatment 
• 
Cognitive behavioral therapy 
• 
Supportive psychotherapy 
• 
Relaxation techniques 
• 
Sleep hygiene 
• 
Dietary counseling 
 
Pharmacological Treatment 
Treat as in the treatment of schizophrenia in non-pregnant woman 
 
Note 
• 
Women with a history of psychosis require close monitoring during pregnancy 
• 
Psychosis during pregnancy can have devastating consequences for both the mother and 
her fetus, including failure to obtain proper prenatal care, negative pregnancy outcomes 
such as low birth weight and prematurity, and neonaticide or suicide 
• 
Treatment of acute psychosis in pregnancy is mandatory and includes mobilization of 
supports, pharmacotherapy, and hospitalization 
• 
Electroconvulsive therapy may be used for psychotic depression 
 
23.18. Autism Spectrum Disorder 
DSM-5 Diagnostic criteria  
It states that an individual diagnosed with Autism spectrum disorder would have marked difficulties 
in terms of communication and engagement with others across multiple social situations. These 
difficulties include: 
• 
Difficulties with demonstrating appropriate behaviours in social contexts  
• 
Difficulties associated with non-verbal communications used for social interactions  
• 
Difficulties associated with failure to initiate or adapt to social interactions 
 
In addition, the DSM-5 also requires the individuals to have characteristic repetitive behavioural 
patterns, such as 
• 
Repeated stereotypical movements or  
• 
Highly ritualized behavioural patterns. DSM-5 criteria specified that these behaviours must 
have started since the early developmental period and has resulted in marked 
impairments in terms of functioning.  
 
Non-pharmacological Treatment 
For children 
• 
Every pre-school child diagnosed with autism should have an individualised intervention 
plan that sets out the goals, type(s), frequency and intensity of intervention, in order to 
address particular developmental and educational needs 
• 
An individualised intervention plan should consist of a variety of quality programs and 
activities. This includes attendance in comprehensive early intervention programmes, 
programmes targeting specific needs and also positive engagement with parents and/or 
caregivers 
• 
Alternative-augmentative communication systems may be recommended for pre-school 
children with autism because the expanded (spoken or written) communication may 
stimulate speech acquisition in non-verbal children and enhance expression in verbal 
children. 
• 
 Visual strategies are useful interventions for children with autism because they offer 
visual support to communication, increase spontaneous imitation and socially 
communicative behaviour. 
• 
Social skills programmes depend on the functioning level of the preschool child with 
autism and may include: 
o 
Assessment and teaching of social skills interaction in natural settings. 
o 
Provision of structure, visual cues and predictability. 
o 
Making abstract concepts more “concrete”. 
o 
Activities that enable purposeful and appropriate interaction with typically 
developing peers. 
o 
Goals focusing on fostering self-appreciation and self-esteem. 
 

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For the parents 
• 
Parents and caregivers should be encouraged to discuss the need for practical emotional 
support. This enables 
 
information to be provided, referrals made and support services made available 
• 
Parents and caregivers are recommended to consult appropriate professionals when 
considering educational placement for their child with autism 
 
Pharmacological Treatment 
A: haloperidol (PO)1.5-3mg 24hourly (medications should be titrated according to 
symptoms resolution) 
OR 
A: methylphenidate (PO) 18- 54 mg 24hourly(medications should be titrated 
according to symptoms resolution 
 
23.19. Attention Deficit / Hyperactivity Disorder (ADHD) 
DSM-5 Diagnostic criteria  
It states that an individual diagnosed with attention-deficit and hyperactivity disorder would have 
difficulties in terms of functioning, mainly due to (a) inattention and/or (b) hyperactivity and 
impulsivity. 
 
The DSM-5 states that these inattentive and/or hyperactivity and impulsivity symptoms must be 
present before the age of 12 years old. In addition, these symptoms must have resulted in impaired 
functioning in at least 2 different social situations. 
The DSM-5 requires the individual to fulfill at least 6 of the following signs and symptoms of 
inattention:  
• 
 Failing to pay close attention to details  
• 
 Concentration difficulties  
• 
 Difficulties with sustaining attention at tasks  
• 
Daydreaming and does not seem to be able to follow normal conversations  
• 
Difficulties with organization of tasks  
• 
Reluctance to participate in tasks that involve much attention  
• 
Frequently loses important objects  
• 
Easily distractible  
• 
Forgetfulness about daily activities.  
 
The DSM-5 also specified that only 5 of the above signs and symptoms of inattention 
need to be fulfilled if individuals are 17 years of age and above. 
 
DSM-5 also requires the individual to fulfil at least 6 of the following signs and symptoms of 
hyperactivity and 
impulsivity:  
• 
Moving about and unable to sit still  
• 
Leaves seat even when required to remain seated  
• 
Climbs or runs about in inappropriate situations  
• 
Always having excessive energy and always on the move 
• 
Chats excessively  
• 
Impulsive and gives answers even before being asked to  
• 
Having difficulties waiting for his/her turn  
• 
Unable to carry out normal conversation due to frequent interruptions 
 
Non-pharmacological Treatment 
a) Parent-training/ education programmes 
Refer parents to educational programmes to learn about ADHD, its management and coping 
strategy. 
• For parents, the programme should include individual or group-based parent-training/education 
programmes. 
• For children and youth with ADHD, the programme should include CBT or social skill training. 
• Offer training to the teachers on behavioural interventions in the classroom to help the child to 
cope with ADHD 
 
b) Behaviour therapy 
• 
Positive reinforcement of positive behaviour including reward system and praises. The 
parents can consider using 

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a star chart to promote positive behaviour at home. 
• 
Environmental modifications aim at improving attention e.g. placing the child in the front 
row of class, 
minimising distractions etc. 
• 
Combination of behaviour therapy and medication is better than medication alone. 
 
23.20. Enuresis 
DSM-5 Diagnostic criteria  
• 
Repeated voiding of urine into bed or clothes (whether involuntary or intentional) 
• 
Behavior must be clinically significant as manifested by either a frequency of twice a week 
for at least three consecutive months or the presence of clinically significant distress or 
impairment in social, academic (occupational), or other important areas of functioning. 
• 
Chronological age is at least 5 years of age (or equivalent developmental level). 
• 
The behavior is not due exclusively to the direct physiological effect of a substance (such 
as a diuretic) or a general medical condition (such as diabetes, spina bifida, a seizure 
disorder, etc.). 
 
Non-pharmacological Treatment 
• 
Fluid restriction at night especially 1 hour before the desmopressin dose until the next 
morning, or at least 8 hours after the dose. If child wakes up during the night, limit the 
amount that he or she drinks. 
• 
Star chart: effective in one-third of cases 
• 
Alarm: Child must wake up and urinate.  
 
Pharmacological Treatment 
A: amitriptyline (PO) 25mg nocte (medications should be titrated according to symptoms 
resolution) 
 
 
OR 
C: imipramine (PO) 100mg nocte (medications should be titrated according to symptoms 
resolution) 
 
23.21. Neuroleptic Malignant Syndrome (NMS) 
Mostly is caused by the use of high dose of antipsychotics; potent antipsychotics (e.g. haloperidol) 
and antipsychotics that are given via the intravenous or intramuscular routes. 
 
Diagnostic Signs and symptoms 
• 
Muscle rigidity 
• 
Fever 
• 
Altered consciousness 
• 
Mutism 
• 
Dysphagia 
• 
Diaphoresis 
• 
Tachycardia 
• 
Labile blood pressure 
• 
Tremor 
• 
Incontinence 
• 
Leukocytosis 
• 
Laboratory evidence of muscle 
injury: increase in creatinine kinase 
levels. 
 
Pharmacological Treatment 
A: diazepam10 mg (IV) 
 
 
OR 
C: lorazepam (IM/IV) 2 mg for immediate sedative or hypnotic action. If no response gives a second 
dose 
 
 
 
OR 
C: bromocriptine (PO) 2.5 mg 8hourly   
Note 
• 
NMS is a clinical emergency, It needs ICU care 
• 
It is important to stop the antipsychotics immediately 
• 
Supportive measures such as bed rest and controlling the hyperthermia by rapid cooling 
with the help of tepid water spray and via direct fluid replacement should be started 
immediately 
• 
Consideration of ventilator support or intubation would be necessary if the patient has 
severe breathing difficulties 

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23.22. Somatic Symptom Disorder 
DSM-5 diagnostic criteria 
• 
One or more somatic symptoms that are distressing or result in significant disruption of 
daily life. 
• 
Excessive thoughts, feelings, or behaviors related to the somatic symptoms or associated 
health concerns as manifested by at least one of the following: 
o 
Disproportionate and persistent thoughts about the seriousness of one’s symptoms. 
o 
Persistently high level of anxiety about health or symptoms. 
o 
Excessive time and energy devoted to these symptoms or health concerns 
DSM-5 specified time duration of at least 6 months of the presentations. 
Non-pharmacological Treatment  
• 
Regular appointments: Patients diagnosed with somatic symptom disorder should have a 
fixed, regular physician whom they can seek help from and be seen on a regular basis. 
• 
Avoid unnecessary investigation but physical examination should be performed if new 
complaints arise. 
• 
 Offer empathy to the sufferings experienced by the patient. 
• 
Psychotherapy: 
o 
Self-help techniques 
o 
Supportive   psychotherapy 
o 
Cognitive behaviour therapy (e.g. challenge cognitive distortions, activity scheduling 
to enhance physical activities). 
• 
Increase in social and occupational functioning 
Pharmacological Treatment 
 
A: amitriptyline (PO) 25-50mg 24hourly (medications should be titrated according to 
symptoms resolution) 
 
 
OR  
C: imipramine (PO) 100mg 24hourly (medications should be titrated according to 
symptoms resolution) 
 OR 
S: fluoxetine (PO) 10-20mg 24hourly (medications should be titrated according to 
symptoms resolution)  
 
 
23.24. Conversion Disorder 
DSM-5 Diagnostic criteria  
• 
One or more symptoms of altered voluntary motor or sensory function. 
• 
Clinical findings provide evidence of incompatibility between the symptom and recognized 
neurological or medical conditions. 
• 
The symptom or deficit is not better explained by another medical or mental disorder. 
• 
The symptom or deficit causes clinically significant distress or impairment in social, 
occupational, or other important areas of functioning or warrants medical evaluation 
 
Non-pharmacological Treatment 
• 
Psycho-education 
• 
Cognitive-psychotherapy 
 
Pharmacological Treatment 
A: amitriptyline (PO) 25-50mg 24hourly (medications should be titrated according to 
symptoms resolution)  
OR  
C: imipramine100mg (PO) once a day (medications should be titrated according to 
symptoms resolution) 
 
 
OR 
S: fluoxetine (PO)10-20mg 24hourly (medications should be titrated according to 
symptoms resolution). 

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CHAPTER TWENTY-FOUR 
NUTRITION DISORDERS 
Nutrition disorders can be caused an insufficient intake of food or certain nutrients, or by inability of 
the body to absorb and use nutrients, or by over consumption of certain foods. 
24.1 Iodine Deficiency Disorders (IDD) 
Clinical presentation 
• 
Goitre enlarged thyroid gland from over activity.  
• 
Hypothyroidism - dry skin, weight gain, puffy face, frequent constipation, and lethargy from 
under-active thyroid  
• 
Hyperthyroidism - exophthalmia, rapid pulse, and weight loss from over-active thyroid  
• 
Cretinism 
 
Table 24.1: Criteria for Assessing Iodine Deficiency Using Urinary Iodine Concentration. 
Micronutrient indicators 
Urinary iodine concentration 
for determining iodine status 
in the population 
 
Median urinary iodine (µg/l) 
Iodine intake 
Iodine status 
Pregnant women 
< 150 
Insufficient 
Severe iodine deficiency 
150 – 249 
Adequate 
Adequate iodine nutrition 
250 – 499 
Above requirements   
May pose slight risk of more than 
adequate iodine intake 
> 500 
Excessive 
Risk 
of 
adverse 
health 
consequences 
Lactating womenand children < 2 years 
< 100 
Insufficient 
Severe iodine deficiency 
> 100 
Adequate 
Adequate iodine nutrition 
School age children (6 years or older)
 c 
<20 
Insufficient 
Severe iodine deficiency 
20 – 49 
Insufficient 
Moderate iodine deficiency 
50 – 99 
Insufficient 
Mild iodine deficiency 
100 – 199 
Adequate 
Adequate iodine nutrition 
200 – 299 
Above requirement 
May pose slight risk of more than 
adequate iodine intake 
> 300 
Excessive 
Risk 
of 
adverse 
health 
consequences 
 
Table 24.2: Epidemiologic criteria for assessing iodine nutrition based on median urinary 
iodine concentrations in different target groups 
 
MUIC (ug/L) 
 
 
Population group 
Insufficient 
Adequate  
Above requirement 
and excessive 
School aged children 
<100 
100-299a 
> 300a 
Adults 
(women 
reproductive 
age) 
<100 
100-299a 
> 300a 
Pregnant women 
<150 
150-249 
> 250 
Lactating women 
<100 
> 100 
 
Children < 2 years 
<100 
> 100 
 
a adjusted based on best available scientific evidence to date 
Non Pharmacological Treatment 
• 
Use of iodated salt (strategy for control of iodine deficiency worldwide) 
• 
Use of iodine rich foods like: drinking water (reflecting amount of I2 present in the soil), 
Fish, Sea weeds (Sea weeds are rich in iodine but are a rare component of the diet).  
 
 

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Pharmacological Treatment  
A: iodized oil (PO) 400mg repeated after one to two years  
AND 
B: potassium iodide solution (PO) 21mg stat  
 
24.2 Vitamin A Deficiency (VAD) 
Clinical presentation 
• 
Night blindness or inability to see in the dark 
• 
White foamy patches on the eye (Bitot’s spot) or conjunctival and corneal dryness 
• 
Keratomalacia or wrinkling and cloudiness of cornea 
• 
Corneal ulceration or the cornea becomes soft and bulges 
 
Diagnosis  
Common indicators of VAD used for population surveys/assessments 
• 
Clinical eye signs (Exophthalmia)  
• 
Serum Retinol Concentration 
 
Table 24.3 Serum Retinol Concentration 
Public Health Importance 
Serum or plasma retinol: <0.70 µmol/l in preschool-age 
children or pregnant women 
Mild 
> 2% - < 10% 
Moderate 
> 10% - < 20% 
Severe 
> 20% 
 
Non-pharmacological Measures 
Dietary consumption of vitamin-A rich foods  
 
Pharmacological Treatment 
Prophylaxis 
A: vitamin A (retinol)(PO) 4-6monthly up to the age of 5years. 
 
Table 24. 4: Administration of Vitamin A 
Age range 
Dose units 
Frequency 
Route of Administration 
Infants 
6–11 
months 
(including HIV +ve) 
100,000 IU (30 mg RE) 
vitamin A3 
Stat 
Oral 
liquid, 
oil-based 
preparation 
of 
retinol 
palmitate 
or 
retinol 
acetate 
Children 
12 
months–
59months 
(including 
HIV +ve) 
200,000 IU (60 mg RE) 
vitamin A 
4-6 monthly 
 
Treatment 
For children 6- 59months and children refer to table 24.4 
For adults (except women of reproductive age)   
A: vitamin A (retinol) (PO) 200,000 IU stat. 
 
In case of Exophthalmia and Measles: 
For infants < 6 months’ give  
A: vitamin A (retinol)(PO) 50,000IU immediately on diagnosis repeat next day and on day 14 
For infants 6-11months  
A: vitamin A (retinol)(PO) 100,000IU immediately on diagnosis repeat next day and on day 14 
For children 12-59 months 
A: vitamin A (retinol)(PO) 200,000IU immediately on diagnosis repeat next day and on day 14 
For all adults except women of reproductive age 
A: vitamin A (retinol)(PO) 200,000IU immediately on diagnosis repeat next day and on day 14 
For exophthalmia or Bitot’s sport for women of reproductive age  
A: vitamin A (retinol)(PO) 10,000IU 24hourly for 4weeks 
 
 

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Note 
Children who received a prophylactic dose within the previous month should not receive the 
treatment dose of vitamin A. 
 
Referral: All complicated cases 
 
24.3 Vitamin B Deficiencies 
24.3.1 Vitamin B1/Thiamine Deficiency (Wernicke Encephalopathy and Beriberi) 
Clinical features 
• 
confusion 
• 
short term memory loss 
• 
confusion 
• 
paralysis of one or more of the ocular muscles or ophthalmoplegia 
• 
nystagmus 
• 
ataxia 
• 
peripheral neuropathy 
• 
cardiac failure 
 
Non-pharmacological Treatment 
• 
Lifestyle adjustment including discouraging of alcohol abuse. 
• 
Increase intake of thiamine rich foods 
 
Pharmacological Treatment 
For Peripheral neuropathy and cardiac failure  
C: thiamine (PO) 100mg 24hourly 
 
24.3.2 Vitamin B3/Nicotinic Acid Deficiency (Pellagra) 
Pellagra is a condition associated with nicotinic acid deficiency. It is usually accompanied by other 
vitamin deficiencies. 
 
Clinical features 
• 
diarrhea 
• 
dementia 
• 
dermatitis with darkening of sun-exposed skin 
 
Non-pharmacological Measures 
• 
Lifestyle adjustment including discouraging of alcohol abuse. 
• 
Increase intake of vitamin nicotinic acid rich foods 
 
Pharmacological Treatment 
For severe deficiency 
Children:  
C: nicotinamide (PO) 50mg 8hourly for 7days 
Adults 
 
 
C: nicotinamide (PO) 100mg 8hourly for 7days 
 
For mild deficiency 
Children  
C: nicotinamide (PO) 50mg 24hourly for 7days 
Adults 
 
 
C: nicotinamide (PO) 100mg 24hourly for 7days. 
 
Referral: On failure to respond on above treatment. 
 
24.3.3 Vitamin B6/Pyridoxine Deficiency 
Pyridoxine deficiency is related to malnutrition and alcoholism. 
 
Clinical featurestingling sensation 
• 
burning pain or numbness of the feet 
• 
Isoniazid or combination TB therapy 
 

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Non-pharmacological measures 
• 
Increase intake of pyridoxine rich foods. 
• 
Minimize alcohol consumptions 
 
Pharmacological Treatment 
For deficiency 
Children:  
B: pyridoxine (PO) 12.5mg 24hourly for 3weeks. 
Adults: 
 
 
B: pyridoxine (PO) 25 mg 24hourly for 3weeks. 
 
For medicine-induced neuropathy 
Children  
B: pyridoxine (PO) 50mg 24hourly for 3weeks. 
Adults 
 
 
B: pyridoxine (PO) 200mg 24hourly for 3weeks. 
Then followed by: 
B: pyridoxine (PO) 25mg daily as maintenance dose (for patients on TB therapy/isoniazid) 
 
Referral 
• 
Failure to respond. 
• 
Children. 
 
24.3.4 Vitamin B12 (Cobalamin) Deficiency 
Refer Haematological Disease Conditions chapter 
24.4 Malnutrition 
Classes of malnutrition are moderate acute malnutrition (MAM) and severe acute malnutrition 
(SAM) 
MAM is identified by moderate wasting WfH<-2 z-score for children 0–59 months (or for children 6 -
59months MUAC <125mm and ≥115mm) 
SAM is defined by severe wasting WfH<-3 z-score for children 0–59 months (or for children 6-
59months, MUAC<155mm) or the presence of bilateral pitting oedema. 
 
Clinical Features 
Marasmus 
Kwashiorkor 
• 
Severe weight loss and wasting 
• 
Ribs prominent 
• 
Limbs very thin 
• 
Muscle 
wasting 
old 
man’s’ 
appearance 
• 
Extremely emaciated 
• 
Frequent infection with minimal 
signs 
• 
Electrolyte imbalance 
• 
Alert and irritable 
• 
Bilateral pitting oedema, beginning in the 
lower legs and feet; can become more 
generalized (trunk, face “moon”, hands, 
arms). 
• 
Reduced fat and muscle tissue which may 
be masked by oedema. 
• 
Skin cracked and peeling off.  
• 
Fragile skin prone to ulceration and infection. 
• 
Pale appearance. 
• 
Hair changes: blond (yellow, red, sparse, 
dry, thin). Can be pulled out easily and 
without pain (atrophy of the hair roots). Bald 
patches. 
• 
Frequent infections, e.g. URT, otitis media, 
URI 
• 
Frequent association with dehydration which 
may be masked by oedema 
• 
Generally apathetic lethargic and miserable 
when left alone. Irritable when handled. 
• 
High risk of death 
 
Diagnostic criteria  
Infants less than 6 months 
• 
Weight for Length less than <-3SD 
• 
Bilateral pitting oedema of feet 

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• 
Infant is too weak to suck effectively 
• 
The infant does not gain weight or lose more than 10% of the initial weight. 
 
Table 24.5 Summary of medical complications and danger signs 
 
 
24.4.1 Management of Severe Acute Malnutrition (SAM) 
General guidelines for management of SAM: 
Refer to IMAM guidelines 
 
Non Pharmacological Treatment 
The therapeutic diet for malnourished children consists of two formulas,  
A: F-75 initial phase of treatment  
THEN  
A: F-100  
OR 
A: Ready to use Therapeutic Food (RUTF).  
 
Note 
• 
F–100 and Ready Therapeutic food is used when appetite has returned 
• 
For children 6–59 months start with 2hourly feeds (12feeds per day), and gradually 
decrease the frequency of feeding and increase the volume of each feed until the patient 
is getting 3hourly feeds (8feeds per day) 
 
If the child is conscious and has hypoglycaemia give: 
Medicine 
Child Dose  
      Frequency 
Duration 
C: 
10% 
glucose 
solution 
        OR   
C: 
10% 
sucrose 
solution 
50ml bolus 
stat 
 
THEN F-75 
 
3ml/kg/Feed 
Every 3minutes 
2hours 
11ml/kg/Feed 
2hourly 
2days 
 
Treatment of dehydration in Severe Malnourished Children: Refer to IMCI guidelines 
 
 
 
 
Appetite 
No appetite or unable to eat 
Vomiting 
Persistent/severe 
Temperature 
Hypothermia (Axillary Temperature <35.5°C, Rectal Temperature 
<36.5 °C) High fever (≥38.5 °C) 
Respiratory 
symptoms 
and signs 
Cough and fast breathing (as per IMCI guidelines) 
Lower chest in-drawing 
Anaemia 
Severe palmar pallor and jaundice 
Dehydration 
Severe dehydration based on recent history of fluid loss (watery 
diarrhoea/vomiting) with weight loss 
Alertness 
Extremely weak and lethargic, unconscious, fitting/convulsions 
Infections 
Open skin lesions, extensive infection 
Note 
• 
All children with complicated SAM are at risk of complications or death. 
• 
Stabilize before referral. 
• 
Refer urgently. 

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Pharmacological Treatment 
Table 24.5 vitamin and mineral therapy supplementation in severe acutemalnutrition: 
Medicine 
Paed age 
Dose 
Frequency 
Duration 
A: vitamin A (PO) 
<6mnths 
50,000iu 
24hourly 
2days 
 
6–12mths 
100,000iu 
 
1-5yr 
200,000iu 
AND 
A: ferrous sulphate (PO) 
 
4-<6kg 
 
6mg Fe 
24hourly 
14days 
 
6 - <10kg 
12mg 
 
1-3yrs  
18mg 
 
3-5yrs 
24mg 
AND  
A: folic acid (PO) 
<6kg 
2.5mg 
24hourly 
14days 
 
>6kg 
5mg 
 
AND  
A: albendazole (PO) 
≥2 years    
400 mg 
stat 
On discharge from 
SC/ 
direct 
admission to OTP 
 
Children with SAM and signs of shock or severe dehydration, and who cannot be rehydrated orally 
or by nasogastric tube should be treated with intravenous fluids, either: 
A: compound sodium lactate  
OR  
A: 0.45% saline  
AND 
A: Dextrose 5% 
 
Table 24.6 Inpatient Therapeutic Feeding Recommendations Phase 1 
Phase 1 (Stabilization care) 
Phase 2 (Transition and Rehabilitation) 
Age Group 
Product and Prescription 
 
Children 
<6 
Months 
• 
Give Diluted F-100 at 130ml/kg of 
body weight per day. 
• 
Breastfed children should always 
be offered breast milk before the 
therapeutic milk, and always on 
demand 
• 
Give twice the volume offered during 
phase I 
 
 
 
Children 
6-59 
Months 
• 
Give F-75 at 130ml/kg of body 
weight per day until the patient re-
gains appetite.  
• 
Start with 2hourly feeds (12 feeds 
per day), and gradually decrease 
the frequency of feeding and 
increase the volume of each feed 
until the patient is getting 3hourly 
feeds (8 feeds per day) 
• 
Replace F75 with F-100 at 150ml/kg 
of body weight per day.  
• 
Gradually introduce RUTF in small 
amounts until the child can consume 
¾ Sachet per day 
• 
When accepted, provide RUTF at 
130kcal per kg of body weight per 
day 
 
Note 
If the child is able to swallow: 
• 
If breastfed: ask the mother to breastfeed the child, or give expressed breastmilk. 
• 
If not breastfed: give a breastmilk substitute (F-75). Give 30–50mL before the child is 
referred. 
• 
If no breastmilk substitute, and IVs available, give 30–50mL of sugar water. 
If the child is not able to swallow: 
• 
Insert a nasogastric tube and check the position of the tube. 
• 
Give 50mL of milk or sugar water by nasogastric tube (as above). 
If blood sugar <3mmol/L treat with 10% Glucose: 
• 
Nasogastric tube: 10mL/kg. 
• 
Intravenous line: 2mL/kg. 
 
 

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Table 24.7 Time frame for the inpatient management of severe acute malnutrition in children  
 
Note 
• 
In case of shock with lethargy or unconsciousness, intravenous rehydration should begin 
immediately, using 15mL/kg/h of one of the recommended fluids. 
• 
Blood transfusion should be done if a child with severe acute malnutrition presenting with 
shock does not improve after 1h of intravenous therapy, a blood transfusion (10mL/kg 
slowly over at least 3h) or presents with severe anaemia, i.e. Hb <4g/dL or <6g/dL if with 
signs of respiratory distress;  
• 
It is important that the child is carefully monitored every 5–10min for signs of over 
hydration and signs of congestive heart failure.  
• 
Treat other medical conditions as per Integrated Management of Acute Malnutrition 
(IMAM) guideline 2018 
• 
All cases require careful assessment for possible TB or HIV 
 
24.5 Growth Faltering/Failure to Thrive 
Children and infants who have either: 
• 
Unsatisfactory weight gain (growth curve flattening or weight loss) on the Road to Health 
chart/ booklet. 
OR 
• 
Low weight for age, i.e. WHZ < –2 but > –3 
Note 
• 
Babies who were premature and are growing parallel to or better than the Z-score line, 
should not be classified as having failure to thrive or not growing well. 
 
Table 24.8 Feeding recommendations for all children 
Age 
(month) 
Frequency 
(Per 
day) 
Amount of food per 
serving (in addition 
to breast milk) 
Texture 
(thickness/ 
consistency) 
Variety  
At 
6 
months  
start 
complementary 
foods 2 to 3 meals 
plus 
frequent 
breastfeeds 
2 to 3 tablespoons 
Start with ‘tastes’ 
Thick 
porridge/ 
pap 
Breast milk + Animal 
foods (local examples) + 
Legumes 
(local 
examples) 
+ 
Staples 
(porridge, 
other 
local 
examples) 
+ 
Fruits/ 
Vegetables 
(local 
examples) 
+ 
Micronutrient 
Powder 
(country specific 
From 6 up 
to 
9 
months 
2 to 3 meals plus 
frequent 
breastfeeds 1 to 2 
snacks may be 
offered 
2 to 3 table spoonful 
per 
feed 
Increase 
gradually to half (½) 
250 ml cup/bowl 
Thick 
porridge/ 
pap 
Mashed/ 
pureed 
family 
foods 
From 9 up 
3 to 4 meals plus 
Half 
(½) 
250 
ml 
Finely 
chopped 
 
Stabilization/Transition* 
Rehabilitation 
Day 1-2 
Day 3-7 
Week 2-6 
1. 
Treat/prevent hypoglycaemia 
 
 
 
2. 
Treat/prevent hypothermia 
 
 
 
3. 
Treat/prevent dehydration 
 
 
 
4. 
Correct electrolyte imbalance 
 
 
 
5. 
Treat/prevent infection 
 
 
 
6. 
Correct micronutrient deficiencies 
No iron 
No iron 
Give iron 
7. 
Start cautious feeding 
F-75 
F-100 
RUTF 
8. 
Achieve catch-up growth 
 
 
 
9. 
Provide sensory stimulation and emotional 
support 
 
 
 
10. Prepare for discharge and follow-up after 
recovery 
 
 
 

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to 
12 
months 
breastfeeds 1 to 2 
snacks may be 
offered 
cup/bowl 
family 
foods 
Finger 
foods 
Sliced foods 
From 
12 
up to 24 
months 
3 to 4 meals plus 
breastfeeds 1 to 2 
snacks may be 
offered 
Three-quarters (¾) to 
1 250 ml cup/ bowl 
Sliced 
foods, 
Family foods 
From 24-
59 Months 
Give 
3 
family 
meals a day. Give 
snacks 
in 
between meals. 
 
 
Staples (local examples) 
Animal 
foods 
(local 
examples) 
Legumes 
(local examples) Fruits 
(local 
examples) 
Vegetables 
(local 
examples) 
Note: If a 
baby is not 
breastfed 
Add 
1-2 
extra 
times 
food 
and 
snacks 
Same 
as 
above 
according 
to 
age 
group 
Same as above 
according to age 
group 
Same as above, plus 1 
to 2 cups of milk per day 
+ 2 to 3 cups of extra 
fluid especially in hot 
climates 
Responsive /Active feeding 
Be patient and actively encourage the baby to eat  
Hygiene 
• 
Feed the baby using clean cup and spoon, DO NOT use a bottle 
as this is difficult to clean and may cause the baby to get diarrhoea 
• 
Wash hands with soap and water before preparing food, before 
eating and before feeding young children.  
 
24.6 Obesity and Overweight 
Management of Obesity and Overweight 
Aim of nutritional management is to: 
• 
Achieve and maintain ideal body weight by bringing about gradual weight loss 
• 
Correct fault food habits 
Management 
• 
Control total energy intake based on individual assessment by limiting energy intake from 
total fat and simple sugars. 
• 
Put the client on a weight reduction diet regime of 30-25kcal/kg /day. 
• 
High fiber, restricted fat diets based on individual assessment is recommended 
• 
Offer nutrition education and counseling to the clients with emphasis on weight 
management, fat diets and other unhealthy practices in weight control 
• 
Recommend suitable exercise program and encourage physical activity for gradual weight 
loss 
• 
Recommend support systems for the clients who need behavior modification. 
 
Note 
• 
A maximum reduction of 1000kcal daily is required to lose about 1kg a week and a 
reduction. Drastic reduction of calorie intake is however not advisable. 
• 
Diet adjustments should be gradual as such people experience excessive appetite. Use of 
appetite suppressants is not recommended 
 
Dietary considerations in the management of obesity and overweight 
Proteins 
Give slightly higher than normal as it gives a feeling of satiety and helps to maintain a good 
nutritional status yet excess is deaminated. Provide approximately 20% of total energy from 
proteins. This should include good quality proteins, lean and whole pulses. 
Fats 
Provide 20% or less of total energy from fats. Emphasize on the use of unsaturated fats to reduce 
the risk of heart problems. Restrict or avoid fried foods 
Carbohydrates 

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Provide the rest of energy 60% from carbohydrates which should be mainly in complex form; 
starches and dietary fiber. Limit simple forms like sugars 
 
Minerals and Vitamins 
Provide adequate amount of essential nutrients like minerals and vitamins to maintain a good 
nutrition status 
 Generally, increase intake of the following food: 
• 
Vegetables such as broccoli, mushroom, zucchini, cabbage, lettuce, cucumber 
• 
Fruits such as pineapple, cherimoya, peach, grapefruit 
• 
Tubers such as sweet potatoes 
• 
Low fat milk 
• 
Diuretic foods such as celery, apples, watermelon (diuretic drugs are not 
recommended) 
24.7 Nutritional Management in TB, HIV and AIDS 
• 
Maintain and improve nutrition status of a person living with HIV/ AIDS thus delay the 
progression from HIV to AIDS related diseases. 
• 
Ensure adequate intake of all nutrients thus preventing development of nutritional 
deficiencies. 
• 
Preservation of lean body mass. 
• 
Maintain body weight and fitness. 
• 
Improve performance of immune system. 
• 
Replenishment of nutrient losses incurred during infection. 
• 
Minimizing symptoms of malabsorption. 
• 
Regeneration of glycogen stores. 
• 
Maintain laboratory values within normal limits. 
 
Note 
Control side effects due to medication and monitor drug – nutrient interaction 
 
Table 24.9: Side Effects related to TB drugs and food intake recommendations to minimize 
them. 
Drug name 
Food recommendation 
Avoid 
Possible side effects 
Rifampicin 
To be taken 1 hour before or 2 after 
food. 
I hour before antacids 
Alcohol 
Nausea, vomiting, 
appetite loss 
Isoniazid 
Taken 1 hour before or 2 hours after 
food. Give 10mg B6 daily 
Alcohol 
Interferes with 
Ethambutol 
May be taken with food 
Avoid alcohol 
 
Streptomycin 
Increase fluid intake 
 
Taste changes, taste of 
food, nausea 
Pyrazinamide 
May be taken with food 
 
 
Ethionamide 
Take with or after meals(Supplement 
with Vit B6) 
Alcohol 
Abdominal
 
discomforts, 
nausea 
Ofloxacin 
Take 2hours before or after food 
Antacids, milk 
products 
 
Kanamycin 
Can be taken without regard to food 
 
 
Capreomycin 
Increase fluid and foods intake rich in 
in potassium(bananas, avocados) 
 
 
Para-
aminosalicylic 
acid(PAS) 
Take with or immediately after food. 
Increase fluid intake 
Alcohol 
 
Cycloserine 
Supplement with vitamin B6 
Alcohol 
 

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24.7.1 Nutrient Requirements and Dietary Management in TB, HIV and AIDS 
Patients 
Energy 
Most patients with chronic tuberculosis, HIV and AIDS are malnourished, energy needs are 
increased in order to minimize weight loss and achieve a desirable weight. An additional 300- 500 
kcal (35 -40 kcal per ideal body weight) is recommended. This will help in protein sparing. 
 
Protein 
An intake of 1.2- 1.5 g of protein per kg body weight is required to generate serum albumin levels 
per day, due to tissue wasting and repair of worn out tissues. 
 
Fats/ oils 
These should provide 25-30% or less of the total energy requirements of an individual. 
 
Vitamins and minerals 
The body should be provided with liberal amounts of vitamins and minerals. In TB conversion of 
beta carotene to retinol is affected in the intestinal mucosa. The client should be supplemented with 
vitamin A (as per the National Vitamin A supplementation schedule) and encouraged to eat vitamin 
A rich food. Patients on isoniazid should ideally be supplemented with 10mg of pyridoxine B6 daily 
since the drug inhibits its absorption. Additional amounts of vitamin C is recommended in the diet to 
facilitate healing of lesions. Other antioxidants (Vit A, C, and E, folic acid, zinc and selenium) 
neutralize free radicals and prevent the production of peroxides from lipids. 
 
Water 
At least 8 glasses or more of safe drinking water per day 
24.8 Dumping Syndrome. 
It is a rapid gastric emptying occurs when food especially sugar moves from stomach into small 
bowel too quickly. 
 
Nutritional implications 
• 
Loss of nutrients 
• 
Weight loss 
 
Aims of nutrition management 
• 
Provide adequate calories and nutrients to support tissue healing 
• 
Prevent weight loss 
• 
Correct hypoglycaemia in the short term 
 
Dietary Management 
After surgery the following should be done: 
• 
All fluids and foods by mouth should be withheld for 3 to 5 days and the patient fed by 
nasogastric tube 
• 
Ice chips should be held in mouth or small, infrequent sips of water should be given. 
Some people tolerate warm water better than ice chips or cold water 
• 
Low carbohydrates, clear liquids such as soups, or diluted unsweetened fruit juices should 
be given and limited to ½ to 1 cup servings, however, at least 6 cups of fluids should be 
consumed daily to replace losses resulting from diarrhoea. Carbonated beverages and 
milk are not recommended in the initial stages of the diet 
• 
The post-gastrotomy diet then begins with gradual progression to a general diet as 
tolerated. Bland foods should be started first, but a more important priority is offering the 
patient foods he/she likes and can tolerate. By the 5th to 7th day most patients can 
tolerate solid foods 
• 
For persons near desirable body weight about 1.5g to 2g protein should be given (35Kcal 
to 45Kcal/kg) 

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• 
Pectin, a dietary fibre found in fruits and vegetables maybe helpful in treating dumping 
syndrome. Pectin delays gastric emptying, slow carbohydrate absorption and reduces 
glycemic response, though small dry meals are of more benefit 
• 
Vitamin and mineral supplementation maybe necessary depending on the extent of 
surgery and whether the symptoms of dumping syndrome persist 
• 
Generally, liquids are served between meals rather than with meals to slow the passage 
of the food mass. Limit simple carbohydrates 
• 
Lie down immediately after eating to help slow the transit of food to the intestines. Clients 
who experience reflux should not lie down after eating. Beware that lactose intolerance 
may develop and produce discomfort in relation to milk and milk products. 
 
24.9 Dietary Management in Diabetes Mellitus 
There are two main types of diabetes mellitus; Type I and Type II 
Type I 
Usually under 30 years but can present at any age, present acutely, with weight loss and ketonuria: 
treated with diet and insulin. 
Type II 
Usually over 30 years, insidious onset, frequently obese: treated with diet and oral anti-diabetic 
agents. 40% will eventually require 
insulin treatment.  
Dietary control and weight loss plays an important part in the management of diabetes mellitus. 
Many Type II diabetics are overweight. Reducing body weight through careful control of energy 
intake and physical activity like walking helps to control the symptoms. 
General eating guidance when on Insulin: 
• 
In Type I diabetes, when initiating treatment, the starting dose of insulin is 0.5-1.0units 
/kg/day. Doses should be given about 30 minutes before meals.  
• 
Ideally a “basal/bolus” regimen should be used where basal (intermediate acting) insulin 
is taken at bedtime and 6-8u of soluble insulin (bolus) taken 3 times a day before meals. 
This regimen allows more flexibility with meals as the soluble insulin dose can be varied 
according to what is to be eaten and can be given at different times.   
• 
Self-monitoring of blood glucose is recommended (range 5-7mmol/litre), and the patient 
can be taught to adjust doses appropriately based on results. 
• Insulin treatment often leads to weight gain; hence patients need to follow a healthy diet and 
it is recommended that patients should not change dietary and medicine regimens 
simultaneously. 
• 
Select an insulin schedule best suited to the individual patient’s eating pattern, physical 
activity and general lifestyle. 
Diabetic Diet 
Dietician should calculate dietary requirements for individual patients in order to reduce the 
blood sugar to normal and to maintain a constant blood sugar level. 
§ 
45-50% of energy intake should be in the form of complex carbohydrates than simple sugars 
with adequate intake of fibers. 
§ 
Carbohydrates and calories should be taken in equal portions through the day with addition of 
snacks between meals. 
§ 
Alcohol is NOT RECOMMENDED in Diabetics as it can induce low blood sugars. 
§ 
Avoid intake of sugar and sugar-containing food/drinks with the exception of patient feels faint 
or is ill and cannot eat normally. 
§ 
Encouraged exercise and a snack should be taken before and after playing sport. 
§ 
Encourage take of other balanced group of foods at right proportion as per individual patients’ 
dosage regimen. 
§ 
Encourage change of life style and regular general body check-up such eyes and oral dental 
care 

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24.10 Nutrition Care and Support in the Intensive Care 
The goal of nutrition management is to preserve lean body mass 
 
Oral Nutrition Supplement 
Oral nutritional supplements (ONS) should be used whenever possible to meet patient’s needs, 
when dietary counseling and food fortification are not sufficient to increase dietary intake and reach 
nutritional goals. 
 
Enteral and Parenteral Nutrition 
Where nutritional requirements cannot be met orally or, expected to be impossible >3 days or 
expected to be below half of energy requirements for >1 week, enteral nutrition (EN) should be 
administered. 
This should be assessed on a case-by-case basis and the long-term impact of nutrition deficit 
considered. 
 
Parenteral nutrition (PN) 
Parenteral nutrition (PN) should be considered when EN is not indicated or unable to reachtargets 
over 3-7 days despite use of appropriate management strategies, and calorie and protein delivery is 
consistently <50% of prescribed targets. 
Supplemental PN should be considered after other measures to improve EN have been attempted 
or insertion of a post-pyloric enteral feeding tube is deemed unsafe and calorie and protein intake 
remain significantly less than prescribed targets (i.e. <50% over a 3-7day period) 
 
Table 24.10 Oral Nutrition Supplements  
Drinks 
Name 
Amount 
Calorie
s  
Protein 
Indication 
Contraindications  
Fresubin 
drink 
2kcal 
200mls  
400kcal 
20g 
• 
Inadequat
e intake of 
meals  
• 
Chronic 
wasting 
• 
Liver 
disease 
 
• 
Not 
suitable 
for 
children <3yrs 
• 
Use with caution in 
children < 6yrs  
• 
Not 
suitable 
in 
patients 
with 
galactosemia 
Supporta
n drink 
200mls  
300kcal 
20g 
• 
Oncology 
• 
Cachexia  
• 
Acute 
or 
chronic 
respiratory 
conditions  
• 
Immuno 
compromi
sed 
• 
Not 
suitable 
for 
children <3yrs 
• 
Use with caution in 
children < 6yrs  
• 
Not 
suitable 
I 
patients 
with 
galactosemia 
Diben 
drink  
200mls  
300kcal 
20g 
For diabetic patients 
-Hyperglycemia  
- insulin resistance 
- Impared glucose 
tolerance 
• 
Not suitable for children 
<3yrs 
• 
Use 
with 
caution 
in 
children < 6yrs  
Not suitable in patients with 
galactosemia 
Powder formular 
Lifegain 
nutrition 
suppleme
nt 
(sachet) 
30g 
120 
15g 
For 
building 
and 
regaining strength 
Note: To be used 
with 
caution 
to 
diabetic patients 
• 
Not suitable for children 
<12yrs 
• 
Not suitable for patients 
with soy or milk protein 
allergy 
 
Maxvida 
 
30g 
122 
4 
Adults  
• 
 

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Table 24.11 Enteral feeds 
Type 
of 
enteral 
feeds 
Calories 
/ 100mls   
Protein 
/ 
100mls  
Indicatons  
Contraindications  
Supportan  
150 kcal 
10g 
• 
Cancer 
• 
Cachexia 
• 
Chronic wasting diseases 
• 
Immuno-compromised 
• 
Ventilated patients 
• 
Electrolyte abnormalities 
• 
Fluid restricions 
 
• 
Not suitable for children < 
1yrs  
• 
Use 
with 
caution 
in 
children < 6yrs  
• 
Not suitable in patients 
with galactosemia 
Survimed 
OPD HN 
133 kcal 
6.7g 
• 
Malabsorption, 
• 
Pre-operative 
preparation 
of 
patients 
who 
are 
undernourished, 
• 
Patients with proven 
inflammatory 
bowel 
disease, 
• 
Following 
total 
gastrectomy, 
• 
Haemodialysis, 
• 
Disease 
related 
malnutrition. 
• 
After 
long 
term 
parenteral nutrition 
• 
Not 
suitable 
for 
children <3yrs 
• 
Use with caution in 
children < 6yrs  
• 
Not 
suitable 
in 
patients 
with 
galactosemia 
Diben  
105 kcal 
4.5g 
• 
Impaired glucose tolerance 
• 
Insulin resistance 
• 
Diabetes mellitus 
• 
Hyperglycaemia 
 
• 
Not suitable for children 
<3yrs 
• 
Use 
with 
caution 
in 
children < 6yrs  
• 
Not suitable in patients 
with galactosemia 
Fresubin 
Original 
100kcal 
3.8g 
• 
Anorexia 
• 
Convalescence 
• 
Low residue tube feed 
• 
Jejunostomy 
• 
Not suitable for children 
<3yrs 
• 
Use 
with 
caution 
in 
children < 6yrs  
• 
Not suitable in patients 
with galactosemia 
Fresubin 
Original 
Fibre 
100 kcal 
3.8g 
• 
Long 
term 
tube 
feeding 
• 
Anorexia 
• 
Convalescence 
• 
Not 
suitable 
for 
children <3yrs 
• 
Use with caution in 
children < 6yrs  
• 
Not 
suitable 
in 
patients 
with 
galactosemia 
 
 
 
 
Groviva  
30g 
 
 
Children 2yrs and 
above 
• 
 
Vidavance  
30g 
 
 
Diabetic  
• 
 

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CHAPTER TWENTY-FIVE 
POISONING 
 
Poison is any substance (liquid, solid, gas), that is harmful to the body, when ingested, inhaled, 
injected or absorbed through the skin. There is a variability of the clinical presentation and 
poisonings vary by nature of poison, victims’ age group, intention, geographic region, and level of 
economic development. Poisons can be classified according to whether the chemical is metallic 
versus nonmetallic, organic versus inorganic, or acidic versus alkaline. 
 
25.1 Common Poisons 
 The common poisoning in our setting are:  
• 
Household agents:  
o 
Organophosphate e.g malathion (insecticide) 
o 
Pesticides - nuvan top, rat poison, hydrocarbons e.g kerosene 
o 
Disinfectants and bleach 
• 
Medicines – Acetylsalicylic Acid, Paracetamol, Anticonvulsants (carbamazepine), 
Hematinic (Iron and Vitamins),  
• 
Major tranquilizers and herbal products  
• 
Foods-eg Mushroom, infected foods 
 
25.2 General Principles of Management of Poisoning 
In managing a patient who has been exposed to toxins holistic approach should be considered. 
These include. 
 
Resuscitation and stabilization 
• 
Airway, breathing and circulation should be reassessed and treated accordingly as a 
priority. Refer Approach to patient with Emergency conditions chapter. 
 
Note 
• 
A low respiratory rate with decreased oxygen saturations may indicate hypoventilation. A 
normal saturation does not exclude hypercarbia or indeed hypoxia in carbon monoxide 
poisoning. If in any doubt, arterial blood gases should be measured. Tachypnoea can be 
seen with metabolic acidosis (e.g. tricyclics, methanol), anxiety, and stimulant drug 
overdose and as an early feature of salicylate poisoning (respiratory alkalosis). 
• 
Supplementary oxygen via facemask should be given to all patients initially, taking 
account of pulse oximetry (noting the limitations described above). 
• 
Many drugs exhibit cardiovascular toxicity hypotension and or cardiac arrhythmias in 
overdose (e.g. tricyclics, b-blockers, digoxin, lithium). ECG should be recorded, 
intravenous access established and initial fluid resuscitation given as appropriate 
• 
General examination may give corroborating evidence of significant ingestions or clues 
in unknown overdoses (SSRIs, tricyclics, phenothiazines) have serotonergic or 
anticholinergic effects with pupil dilatation, and extrapyramidal movements, whilst opioid 
type drugs will cause sedation and pin point pupils.  
• 
Temperature, blood glucose (low in b-blocker, ethanol poisoning)  
• 
 Weight is important in identifying a toxic dose against the weight and may guide 
treatment, for example in paracetamol overdose. 
• 
 Examination for injury (intentional or un-intentional self-harm) suggest appropriate 
methods for treatment, or the presence of other substances such as alcohol. 
• 
If clinical condition allows, an assessment of the patient’s mental state should be made. 
 
Use the tabulated Toxidromes to identify toxins and apply the antidotes 
 
 
 
 
 
 
 

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Table 25.1 Common Toxidromes to help identification of toxins. 
Toxidrome
s 
Mental status 
Pupils 
Vitals 
Other 
manifest
ations 
Examples 
of 
toxic 
agents 
Sympathomi
metic 
• 
Hyper 
alert, 
agitation, 
hallucination, 
paranoia, 
Anxiety 
/ 
Delirium 
 
Mydriasis 
Hyperthermia, 
tachycardia, 
hypertension, 
widened pulse 
pressure 
• 
Diaphore
sis, 
tremors, 
hyperrefle
xia, 
seizures, 
Hyperpyr
exia 
 
• 
Cocaine, 
amphetamines, 
ephedrine, 
theophylline, caffeine, 
phencyclidine 
(PCP), 
Lysergic acid (LSD) 
Withdrawal 
from 
narcotics, 
benzodiazepine, 
alcohol, 
long 
term 
beta-blocker therapy 
 Cholinergic 
Confusion, 
drowsiness, 
Comma, 
Headache, 
Insomnia, 
Giddiness,  
Miosis,  
Bradycardia, 
Hypotension 
tachypnea, 
hypotension, 
bradypnea 
Hypothemia,  
• 
Salivation 
• 
Urinary 
incontine
nce 
• 
Defaecati
on 
• 
Gastric 
cramping, 
hypermoti
lity 
Emesis, 
Diaphore
sis, 
lacrimatio
n, 
GI 
cramps, 
bronchoc
onstrictio
n, muscle 
fasciculati
ons 
and 
weakness
, seizures 
Organophosphate and 
carbamate 
insecticides, 
nerve 
agents, 
nicotine, 
physostigmine, 
edrophonium 
Anticholiner
gic 
Agitation, 
hallucinations, 
delirium, coma 
Mydriasis 
Hyperthermia, 
tachycardia, 
hypertension, 
tachypnea 
Dry flush 
skin, 
dry 
mucous 
membran
es, 
decrease
d 
bowel 
sounds, 
urinary 
retention, 
myoclonu
s 
Antihistamines, 
TCA, 
antiparkinsonism 
agents, 
atropine, 
antispasmodics 
Hallucinoge
nic 
Hallucinations, 
perceptual 
distortions, 
depersonalizati
on, agitation 
Mydriasis 
(usually) 
Hyperthermia, 
tachycardia, 
hypertension, 
tachypnea 
Nystagmu
s 
Phencyclidine, MDMA, 
MDEA 
Opioid 
CNS 
depression, 
coma 
Miosis 
Bradypnea, 
apnea 
Hyporefle
xia, 
pulmonar
y edema, 
needle 
marks 
Heroin, 
morphine, 
methadone, 
diphenoxylate 

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Sedative-
hypnotic 
CNS 
depression, 
confusion, 
stupor, coma 
Variable 
Often normal; 
hypothermia, 
bradycardia, 
hypotension, 
bradypnea, 
apnea 
Hyporefle
xia 
Benzodiazepines, 
barbiturates, alcohols, 
zolpidem 
Serotonin 
syndrome 
Confusion, 
agitation, coma 
Mydriasis 
Hyperthermi, 
tachycardia, 
hypertension, 
tachypnea 
Tremors, 
myoclonu
s, 
hyperrefle
xia, 
clonus, 
diaphores
is, 
flushing, 
trismus, 
rigidity, 
diarrhea 
MAOIs, 
SSRIs, 
meperidine, 
dextromethorphan, 
TCA 
Note:PCP, Phencyclidine; LSD Lysergic acid; TCA, tricyclic antidepressant; MDMA, 3,4-methylenedioxymethamphetamine; MDEA, 
methylenedioxymethamphetamine; CNS, central nervous system; GI, gastrointestinal; MAOI, monoamine oxidase inhibitor; SSRI, selective 
serotonin reuptake inhibitor, 
 
Table 25.2 Toxins causing Dysrhythmias  
Heart rate 
Narrow QRS 
Wide QRS 
Tachycardia 
  
Amphetamines 
Antihistamines 
Anticholinergic agents 
Cocaine 
Theophylline 
 
Propoxyphene, 
Sodium channel blockers and  
Tricyclic antidepressants 
Bradycardia 
  
  
  
  
  
α-Adrenergic lytic agents 
β-Adrenergic blocking agents 
β-Adrenergic blocking agents,  
Calcium channel antagonists,  
Cardiac glycosides,  
Class Ia antiarrhythmics 
And Sodium channel blockers 
Calcium channel antagonists 
 
 
 
Note 
• 
For patients presenting with cardiac problems, consider reading ECG and use the table 
below to interpret possible causes; 
 
25.2.1 Management Protocol of a poison (specific and non-specific antidotes) 
Investigations 
The toxidromes are created to assist diagnosis. History may be inaccurate and hence the following 
laboratory tests should usually be obtained for guidance: 
• 
Complete blood count 
• 
Liver function test 
• 
Serum lactate 
• 
Arterial blood gas 
• 
Electrocardiogram 
• 
Urine pregnancy test in all 
women 
of 
childbearing 
age  
• 
Basic serum electrolytes, 
blood 
urea 
nitrogen 
(BUN), and creatinine 
 
Sympathomimetics investigations - RBG-bedside, ECG, Serum electrolytes and Renal function test, 
Liver function test, Creatinine kinase, Clotting screen: PT/PTT/INR, Full Blood Count, Arterial blood 
gas, Serum osmolality and osmolality gap. 
Abdominal X-ray may be useful in diagnosing. 
Cholinergic investigations - Glucose, BUN, Electrolytes, Prothrombin time, Liver function test, 
Cholinesterase measurements 
 
Measurement of drug or toxin concentrations in body fluids is not required in most poisonings, but in 
some exposures, it does influence management. The list of drug concentrations that may assist 
patient assessment and management are shown here; 

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Table 25.3: List of drugs or toxins requiring measurement of drug concentrations. 
Paracetamol 
Methanol 
Carbamazepine 
Methotrexate 
Carbon monoxide 
Organophosphorus 
Digoxin 
Paraquat 
Ethanol 
Phenobarbital 
Ethylene glycol 
Phenytoin 
Iron 
Salicylate 
Lithium 
Theophylline 
Methemoglobin 
Valproic acid 
 
Table 25.4: Supportive Care 
Toxic Feature 
Methods to reach 
Diagnosis 
Immediate 
Stabilization 
Definitive Management 
Signs of  COPD 
H&P, CXR 
O2, NIPPV 
Bronchodilators, steroids 
Pulmonary edema 
H&P, CXR, pro-
BNP 
O2, NIPPV 
Nitrates, diuretics 
Pulmonary embolism 
H&P, 
d-dimer, 
chest CT 
O2 
Anticoagulation, 
thrombolysis 
(massive 
PE only) 
Acute respiratory distress 
syndrome 
H&P, CXR 
O2, NIPPV 
Ventilatory  support 
Myocardial infarction 
H&P, ECG 
O2, nitrates, aspirin, 
anticoagulation 
Revascularization 
(thrombolysis or PCI) 
Metabolic acidosis 
H&P, 
metabolic 
panel, blood gas 
O2 
Directed at underlying 
cause 
 
Psychosocial Intervention 
• 
The investigations depend on the poison ingested: 
• 
If the toxin cannot be identified, then toxidrome (signs and symptoms) can be used  
 
25.2.2 Management of Ingested Poisons 
Ingested toxins are suspected in any patient with signs and symptoms irrespective of reported dose 
ingested 
 
Clinical Presentations  
• 
General clinical features: Nausea, vomiting, drowsiness, blurred vision, and dizziness 
• 
Central Nervous System toxicity: Altered level of consciousness, convulsions, acute 
confusion and coma, 
• 
Renal Toxicity:  Acute kidney injury/failure and papillary necrosis 
• 
Metabolic derangement: Metabolic acidosis, respiratory acidosis, hypoglycemia. 
• 
Allergic reactions: Urticaria, angioedema, anaphylaxis 
• 
Haematological toxicity: Aplastic anaemia, agranulocytosis   
 
Non-pharmacological Treatment 
Gastric decontamination - practice of functionally removing an ingested toxin from the 
gastrointestinal (GI) tract in order to decrease its absorption it includes gastric evacuation (forced 
emesis or gastric lavage), intra-gastric binding (most commonly by single or multidose activated 
charcoal), or speeding transit of toxins to decrease total absorption time (whole bowel irrigation or 
cathartics).GI decontamination is most likely to benefit patients who present for care soon after 
ingestion (usually within one to two hours). 
• 
Gastric Lavage 
• 
General care: Keep the patient under observation 4–24 hours depending on the poison 
swallowed. 
 
Contraindications to Gastric Lavage: 
• 
An unprotected airway in an unconscious patient 
• 
Ingestion of corrosives or petroleum products e.g. kerosene 
• 
Bowel obstruction 

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• 
Bowel perforation 
• 
GI bleeding 
• 
Identify the specific agent and remove or adsorb it as soon as possible. 
 
Note 
 
• 
Treatment is most effective if given as quickly as possible after the poisoning event, ideally 
within 1 hour. 
• 
If the patient has swallowed kerosene, petrol, or petrol-based products (note that most 
pesticides are in petrol-based solvents) or if the patient’s mouth and throat have been 
burned (for example with bleach, toilet cleaner or battery acid) do not vomit the patient but 
give water orally? Never use salt as an emetic as this can be fatal. 
 
Pharmacological Treatment 
A: activated charcoal (PO) single dose (if available) within one hour of ingestion and do 
not induce vomiting; given by mouth or NG tube according to the dosage below: 
 
Dose:  
Children below one year: 1g/kg 
Children 1-12 years of age: 25–50g 
Adolescents and adults: 25–100g 
A: compound sodium lactate or 0.9% sodium chloride (IV) 30ml/kg 2liters for 24hours if 
Shock is present 
Note 
Toxins for which multiple doses of activated charcoal are indicated includes Carbamazepine, 
Dapsone, Digoxin, Paraquat, Phenobarbitone, Quinine, Slow-release preparations such as 
theophylline, Amanita phalloides fungus, Multiple doses may also be considered in life threatening 
overdose of other drugs (e.g. tricyclic antidepressants). 
 
Content mixing:  
• 
Mix the charcoal in 8–10 times the amount of water, e.g. 5g in 40 ml of water. 
• 
If possible, give the whole amount at once; if the child has difficulty in tolerating it, the 
charcoal dose can be divided. 
• 
If charcoal is not available, then induce vomiting but only if the patient is conscious by 
rubbing the back of the patient throat with a spatula or spoon handle;  
 
Referral: Consider transferring patient to next referral level hospital, where this can be done safely, 
if the patient is: 
• 
Unconscious 
or 
deteriorating 
conscious level 
• 
Burns to mouth and throat 
• 
Severe respiratory distress 
• 
Cyanosed 
• 
Heart failure 
 
25.2.3 Food Poisoning 
Food poisoning, also called foodborne illness, is illness caused by eating contaminated food. 
Infectious organisms — including bacteria, viruses, and parasites — or their toxins are the most 
common causes of food poisoning as listed in the table. Large intestine and small intestine have an 
intermediate incubation from about 1 to 3 days. 
 
Large intestine 
Infections of the large intestine or colon can cause bloody, mucousy diarrhea associated with 
crampy abdominal pain. 
• 
Campylobacter spp, is the common one cause of food-borne disease  
• 
Shigella spp contaminate food and water and cause dysentery (severe diarrhea often 
containing mucus and blood). 
• 
Salmonella spp infections often occur because of poorly or undercooked cooked and/or 
poor handling of the chicken and eggs. In individuals with weakened immune systems, 
including the elderly, the infection can enter the bloodstream and cause potentially life-
threatening infections. 
• 
Vibrio parahaemolyticus can contaminate saltwater shellfish and cause a watery diarrhea. 

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Small Intestine Infection 
Diarrhea due to small bowel infection tends not to be bloody, but infections may affect both the small 
and large intestine at the same time. 
• 
E. coli (enterotoxigenic) is the most common cause of traveler's diarrhea. It lacks 
symptoms such as fever or bloody diarrhea. 
• 
Vibrio cholerae, often from contaminated drinking, water produces a voluminous watery 
diarrhea resembling rice-water. 
• 
Viruses such as Norwalk, rotavirus and adenovirus tend to have other symptoms 
associated with an infection including fever, chills, headache, and vomiting. 
• 
Botulism is caused by Clostridium botulinum toxin and may present with fever, vomiting, 
mild diarrhea, numbness, and weakness leading to paralysis. 
 
Pharmacological Treatment 
Adult: 
A:  0.9% sodium chloride 30mL every 30minutes; not to exceed 8-10doses 
AND 
C: loratadine 10mg (PO) 24hourly 
Children2 to 5 years: 
A:  0.9% sodium chloride 7.5-15mL every 30minutes; not to exceed 8-10doses 
AND 
C: loratadine 5mg (PO) 24hourly 
AND 
Antibiotics based on the infection suspected.  
 
25.2.4 Herbal Poisoning 
Investigations 
• 
Basic blood count, renal function, liver function, and electrocardiogram 
• 
Heavy metal screening if suspected or if symptoms are non-specific 
• 
Analysis methods exist for some herbal toxins only—Colchicines (HPLC, GCMS), tropane 
alkaloids (GCMS, oxalate (GCMS), vinca alkaloids (HPLC), cardioactive steroids 
(immunoassay)—check with local laboratory 
 
Table25.5 Organ Toxicities and Toxidromes, and Common Dietary Supplements or Herbal 
Medicines that can cause them 
Clinical features 
Xenobiotics 
Cardiac 
Sodium channel effects—Aconitum species (widen QRS, shock) 
Digoxin-like effects—Digitalis species, bufo toads 
Central 
nervous 
system 
Seizures—strychnine, thujone, essential oils (camphor, eucalyptus) 
Sedation—Valeriana species, kava kava 
Dermatological 
Blistering—cantharidin (Chinese blister beetle) 
Hematological 
Coagulopathies—G-herbs (ginger, garlic, gingko) 
Agranulocytosis—anti-mitotic agents (colchicine, podophyllotoxin) 
Hepatotoxic 
Hepatitis—multiple agents, germander commonly reported 
Veno-occlusive 
disease—pyrrolizidine 
alkaloids 
(comfrey, Senecio species, Heliotropium species) 
Nephrotoxic 
Renal failure—Aristolochia species 
Hypertension, hyperkalemia—licorice 
Anticholinergic 
Datura metel commonly used in TCM 
Hexing 
herbs 
(Atropa species, Hyoscyamus species, Mandrago 
officinarum) common in Western herbal practice 
Sympathomimetic 
Ephedra species, Citrus aurantium (bitter orange) 
Salicylate poisoning 
Willow bark, checkerberry 
 
 

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Non-Pharmacological Treatment 
• 
Ask specifically regarding the use of such products and a matched clinical feature using 
the above Toxidrome 
• 
Secure sample for identification 
o 
Actual herbs or product used 
o 
Prescription or packaging 
• 
Good resuscitative, symptomatic, and supportive care 
• 
Instruct patients and family to stop using the product 
• 
Consider outpatient monitoring of renal function, liver function, and blood counts 
• 
Report case to regulating authority 
• 
Report unusual cases to National Poison Control Center  
 
Pharmacological Treatment 
Use antidote if appropriate, activated charcoal can be given in an acute overdose of toxic dietary 
supplements and herbal medicines if there is adequate airway protection. Give: 
A: compound sodium lactate or 0.9% sodium chloride (IV) 30ml/kg 2liters for 24hours if 
shock is present 
 
25.2.5 Management of Skin Contamination 
• 
Remove all clothing and personal effects and thoroughly flush all exposed areas with 
copious amounts of running water running for: 
o 
5-minutes for non-irritants or mild irritants 
o 
15-20 minutes for moderate to severe irritants and chemicals that cause acute 
toxicity if absorbed through the skin 
o 
30 minutes for most corrosives 
o 
60 minutes for strong alkalis (e.g., sodium, potassium or calcium hydroxide) 
• 
Use non-abrasive soapand water for oily substances 
• 
Attending staff should take care to protect themselves from secondary contamination by 
wearing gloves and apron 
• 
Removed clothing and personal effects should be stored safely in a see-through plastic 
bag that can be sealed, for later cleansing or disposal. 
 
25.2.6 Management of Eye Contamination 
Rinse the eye for with clean running water for 15-20 minutes, taking care that the run-off does not 
enter the other eye. 
• 
tetracaine hydrochloride 1-2drops into affected eye will assist irrigation. Evert the eyelids 
and ensure that all surfaces are rinsed. 
• 
In the case of an acid or alkali irrigate for 30 minutes and review for possible next 30 
minutes 
• 
Where possible, the eye should be thoroughly examined under fluorescein staining for 
signs of corneal damage.  
• 
If there is significant conjunctival or corneal damage, the patient should be seen urgently 
by an ophthalmologist.  
• 
Refer when further eye evaluation cannot be performed. 
 
25.2.7 Management of Inhaled Poisoning 
• 
Move the patient to the fresh air immediately. Victims to stay away from all toxic fumes and 
gases.  
• 
Thoroughly ventilate the involved area 
Administer supplemental oxygen if cyanosis or difficulty in breathing  
• 
Mild distress/ hypoxia gives 24–40% oxygen at a flow rate of 2–6 L/min (LPM), (nasal 
canula)  
• 
Moderate distress/ hypoxia gives 24–50% oxygen at a variable flow of 6 -10 L/min (Face 
mask / Venture mask)  
• 
Severe distress/ hypoxia gives 50–90% oxygen at 10-15L/min (Non-rebreather Mask / face 
mask with reservoir bag)  
• 
Apnea give nearly 100% oxygen at 10-15L/min (Bag valve Mask “BVM” device) 
Oxygen flow should be moderated to achieve oxygen saturation levels, based on pulse 
oximetry (with a target level of 94–96% in most, or 88–92% in people with COPD) 
 
Apply Cardiopulmonary resuscitation (CPR) if there are signs of cardiac arrest 
 

580
Inhalation of irritant gases may cause swelling and upper airway obstruction, bronchospasm and 
delayed pneumonitis.  
Intubation and provision of for bronchodilators; 
A: salbutamol 4mg (PO) 6-8hourly  
OR 
A: adrenaline B: ephedrine (SC/MI) 25-50mg or (IV)  5-25mg slowly, repeated in 5-10 
minutes, if necessary  
OR 
C: salmeterol  (inhalation)  
AND 
12  years old give,   
S: ipratropium bromide (inhalation) 250-500micrograms 6-8hourly   daily maximum dose of 
2mg. 
 
6 to 12 years give, 
S: ipratropium bromide (inhalation) 250micrograms 6-8hourly, maximum daily dose of 1mg 
 
0-5 years give, 
S: ipratropium bromide (inhalation) 125-250micrograms   6-8hourly, maximum daily dose 
1mg 
 
25.3 Specific poisons 
25.3.1 Corrosive Compounds Poisoning 
Examples — Sodium hydroxide (Soaps-drain/oven cleaners), potassium hydroxide, acids, bleaches 
or disinfectants.  
 
Non-Pharmacological Treatment 
• 
Give 1Litre of water as soon as possible, beneficial within 30minutes. 
• 
Give oxygen therapy at concentrations of 2–6litres per minute (LPM), 40–70% oxygen 
(face mask with reservoir bag) 
 
Surgical review 
• 
Arrange for surgical review to check for: 
o 
Esophageal damage/rupture, if severe. 
o 
Perforation, mediastinitis and peritonitis if suspected 
 
Note 
Do notinduce vomiting or use activated charcoal  
 
25.3.2 Petroleum Compounds Poisoning 
Examples—Kerosene, Turpentine substitutes and petrol 
 
Clinical Presentation: 
• 
GIT-abdominal pain, bloody stool, vomiting  
• 
RS-Throat swelling, pneumonitis and/or pulmonary oedema-cough, tachypnea, cyanosis, 
crepitation and rhonchi 
• 
CNS-Headache, dizziness, euphoria, restlessness, ataxia, convulsion, encephalopathy 
and coma 
 
Non-pharmacological Treatment 
• 
Remove the patient from source 
• 
Remove contaminated cloth and thoroughly wash the skin with soap and water 
• 
Give supplemental oxygen 2–6litres per minute (LPM), delivering a concentration of 24–
40% oxygen (nasal cannula) or 28–50% oxygen (face mask) 40–70% oxygen (face mask 
with reservoir bag) 
• 
Oxygen flow should be moderated to achieve oxygen saturation levels, based on pulse 
oximetry (with a target level of 94–96% in most, or 88–92% in people with COPD) 
• 
If large amount of petroleum compound has been ingested less than an hour earlier lavage 
may be considered and the patient should be intubated 
 
Note 
Do notinduce vomiting or use activated charcoal  

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Kerosene (Paraffin) Poisoning 
There is a higher risk of kerosene poisoning among children. The respiratory system is the main 
target organ affected. Pneumonia is in most cases interstitial and bilateral. Vomiting after 
hydrocarbon ingestion is related to the rate of development of pneumonia; Symptoms of CNS 
impairment correlated with hypoxemia, pneumonia, and fever. 
 
Non-pharmacological Treatment 
• 
Immediately remove the child from the source of the poisoning and ensure the airway is 
open (this is always the first priority). 
• 
Remove contaminated clothing and thoroughly wash the skin with soap and water. 
• 
If possible, perform pulse oximetry and give supplemental oxygen if indicated. Intubation 
and mechanical ventilation may be needed in a patient with severe hypoxia, respiratory 
distress or decreased consciousness.   
• 
Avoid gastric lavage because of the risk of inhalation and hence pneumonitis. If very large 
amounts of kerosene have been ingested less than an hour earlier then lavage may be 
considered if the airway can be protected by expert intubation.  
 
Pharmacological Treatment, 
A: compound sodium Lactate OR 0.9% sodium chloride (IV) 30ml/kg 2liters for 24hours if 
Shock is present 
 
Note 
There is no evidence that corticosteroids are helpful in kerosene poisoning 
 
25.3.3 Organo-Phosphorus and Carbamate Compounds Poisoning 
Organophosphates and carbamates are common insecticides that inhibit cholinesterase activity, 
causing acute muscarinic manifestations (e.g., salivation, lacrimation, urination, diarrhea, emesis, 
bronchorrhea, bronchospasm, bradycardia, miosis) and some nicotinic symptoms, including muscle 
fasciculation and weakness. 
 These can be absorbed through the skin, ingested or inhaled. Examples:  
• 
Organophosphorus – Malathion, Parathion, Tetraethyl Pyrophosphate (TEPP), mevinphos 
and  
• 
Carbamates – methiocarb and carbaryl. 
 
Clinical presentations 
• 
Vomiting, diarrhoea, blurred vision or weakness. 
• 
Signs of excess parasympathetic activation: salivation, sweating, lacrimation, slow pulse, 
small pupils, convulsions, muscle weakness/twitching, then paralysis and loss of bladder 
control, pulmonary oedema, and respiratory depression. 
 
Non-pharmacological Treatment  
• 
Remove poison by irrigating eye or washing skin (if in eye or on skin)  
• 
Give activated charcoal if ingested and within 1 hour of the ingestion. 
• 
Do not induce vomiting because most pesticides are in petrol-based solvents. 
• 
In a serious ingestion where activated charcoal cannot be given, consider careful aspiration 
of stomach contents by NG tube (the airway should be protected). 
• 
Auscultate the chest for signs of respiratory secretions and monitor respiratory rate, heart 
rate and coma score (if appropriate) 
• 
Give oxygen saturation is less than 90% 
 
Pharmacological Treatment 
If there are signs of excess parasympathetic activation (see above) give: 
A: atropine (IV) boluses of 5mg  
o 
Repeat every 10minutes until satisfactory atropinization (i.e. no chest signs of 
secretions, HR>80b/min, Systolic BP >80mmHg, pupils no longer pinpoint, Dry 
axillae)  
o 
Paediatric patient can start at 0.05mg/kg, then double the dose every five minutes, 
stop doubling the dose when parameters have improved. 
If muscle weakness gives:  
S: pralidoxime (IV) (cholinesterase reactivator) 50mg/kg diluted with 15ml water by 
infusion over 30 minutes 

582
o 
Repeated once to twice. 
o 
Followed by 10–20 mg/kg/hour, as necessary. 
 
If other organophosphates are identified, the following table can be used: 
 
Table 25.6 List of common Pesticides and Chemical Poisons with their antidotes  
Group 
Poisons 
Antidote 
Agricultural 
pesticides 
  
Organophosphates 
  
Malathion, 
Acephate, 
Dichlorvos, Dimethoate,    
Fenitrothion,   Monocrotop
hos,  Phorate, 
atropine sulfate 
A:2mg (IM) mid-lateral outer thigh 
Quinalphos  
pralidoxime 
S:1-2g IV infusion (10-20 mg/mL) over 15-30min, 
repeat in 1hr if necessary and repeat 12hourly 
thereafter PRN; 
administer 30 mg/kg IV (IM, SC if no IV access) 
over 
20 
min; 
follow 
by 
4-8 
mg/kg/hour 
maintenance IV infusion 
Carbamates; 
propoxur, Aldicarb, Carbar
yl, Carbofuran,   
Methomyl 
pralidoxime 
S:1-2g (IV) infusion (10-20 mg/mL) over 15-30min, 
repeat in 1 hour if necessary and repeat q12hr 
thereafter PRN; 
administer 30 mg/kg (IV) (IM, SC if no IV access) 
over 
20 
min; 
follow 
by 
4-8 
mg/kg/hour 
maintenance (IV) infusion 
 Organochlorines; 
Endosulfan, 
Gamma 
benzene 
hexachloride, 
Heptachlor, Chlordane  
Rodenticides 
cholestyramine 
S:  4g (PO) 12-24hourly; increase gradually over 
1month intervals 
Maintenance: 8-16 g/day (PO) divided 12hourly; 
not to exceed      24g/day 
Cholestyramine 
bromadiolone 
vitamin K 
Adults 
A:Vitamin K (PO/SC) 2.5-10mg; may be increased 
PRN to 25 mg or, rarely, to 50 mg; may be 
repeated in 12-48 hours 
Newborn 
A:Vitamin K (IM) 0.5-1mg within 1hour of birth 
  
 Industrial 
chemicals 
  
  
  
  
  
  
 
 
 
 
 
  
  
Arsenic 
D-Penicillamine 
B: Give D-penicillamine (PO) 30-40mg/kg/day 1-
6months, 2hours before or three hours after 
dimercaprol 
D:dimercaprol (IM) 3mg/kg deep 4hourly for 
48hours followed by 3mg/kg 12hourly for 10days 
  
Methyl alcohol 
Ethanol 
• 
Loading dose 600 mg/kg (IV) (i.e., 7.6mL/kg of 
10% 
EtOH 
solution) 
600-
700mg/kg oral/nasogastric (NG) 
using 
a 
95% 
solution diluted to 20% or less with water or juice. 
• 
Oral maintenance of 0.15 mL/kg/hour (IV = 1.4 
mL/kg/hour 
• 
10% ethanol. 
  
Ethylene glycol 
  
  
  
folic acid/ folinic acid 
S:folinic acid 60mg (IM) over 12-24 hours  stat, 
then 15mg  (PO)  8hourly for 48 to 72 hours 
Ethanol 
• 
Loading dose 600 mg/kg intravenous (IV) (i.e., 7.6 
mL/kg of 10% EtOH solution) 
• 
600-700 mg/kg oral/nasogastric (NG) using a 95% 
solution diluted to 20% or less with water or juice 
Oral maintenance of 0.15 mL/kg/hour (IV = 1.4 

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mL/kg/hour) 10% ethanol 
pyridoxine hydrochloride 
B:10-25 mg (PO) 8 hourly then observe in 6 hours 
folinic acid 
• 
S: Loading dose 600 mg/kg intravenous (IV) (i.e., 
7.6 mL/kg of 10% EtOH solution) 
• 
600-700 mg/kg oral/nasogastric (NG) using a 95%
solution diluted to 20% or less with water or juice
S: Oral maintenance of 0.15 mL/kg/hour (IV = 1.4
mL/kg/hour) 10% ethanol
thiamine 
C: 100 mg IV; then 50-100 mg/day IM or IV; then 
IM: 5-30 mg three times daily (if critically ill); then 
5-30 mg three times daily for 1 month
Cyanide 
hydroxocobalamin 
C: 70 mg/kg (usually 5 g) (IV) infusion over 15 
minutes; additional 5 g (IV) may be given 
depending on severity of poisoning and clinical 
response 
Methemoglobinemia 
producing agents (nitrites, 
nitrates, dapsone, copper, 
aniline, 
chlorates, 
naphthalene) 
methylene blue 
C:1 mg/kg (IV) over 5-30 minutes 
If Methemoglobin level remains >30% or if clinical 
symptoms persist, repeat dose up to 1 mg/kg 
1hour after the first dose 
Drugs 
Acetaminophen 
N-Acetylcysteine
C:140 mg/kg of N-acetyl cysteine at first, followed
by 70mg/kg every 4 hours for 3days or until
acetaminophen is no longer detected in the blood
Iron 
deferoxamine 
D:1g (IM) initially and then 500mg 8hourly for 
48hours 
Benzodiazepines 
flumazenil 
A:0.2 mg (IV) for 15seconds then 0.1mg for 
60second intervals, till consciousness is restored. 
Maintain 0.3 and 0.6 mg depending on the 
patient's characteristics and the benzodiazepine 
used 
Opioids 
naloxone 
B:0.4 mg to 2mg (PO) depending on amount of 
opioid taken, then repeat in 2 to 3minutes 
Isoniazid 
pyridoxine 
B:10-25 mg (PO) 8hourly for 48hours 
Digoxin 
digoxin-specific antibodies 
S: Each vial of DigiFab (40 mg of Fab) binds 
0.5mg digoxin. 
Equimolar dose to ingested digoxin (76/80 mg 
FAB = 1 mg digoxin) 
Environmen
tal toxins 
Datura 
physostigmine 
S:0.5-2mg slow IVP (not to exceed 1 mg/min); 
keep atropine nearby for immediate use 
If no response, repeat after 20min PRN 
If initial dose effective, may give additional 1-4mg 
q30-60min PRN 
Snake bites 
Anti-snake venom 
A: Anti–snake venom (ASV)– Polyvalent 
For Mild Degree of envenomation give 5 vials (50 
ml) 
For Moderate Degree of envenomation give 5–10 
vials (50–100 ml) 

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Fore Severe Degree of envenomation give 10–20 
vials (100–200 ml) 
Dog bite 
Anti-rabies Immunoglobulins 
A: Anti-rabies human immunoglobulin 20 IU/kg 
half the dose given parenterally and the other half 
injected into and around the wound for victims 
suspected to be infected  
Botulism 
Botulinum antitoxin 
S: Administer slowly by (IV) infusion via volumetric 
infusion pump; minimize allergic reactions by 
starting at 0.5mL/min for initial 30minutes 
25.3.4 Paracetamol Poisoning 
It is the commonest taken drug overdose. The toxic dose is highly variable. In general, the 
recommended maximum daily dose for healthy adults is 4 grams. 
Chronic excessive alcohol consumption and Isoniazid  can  induce CYP2E1, antiepileptics 
including carbamazepine, phenytoin, and barbiturates induces CYP enzymes  thus increasing the 
potential toxicity of Paracetamol.  
Clinical Presentation 
•
Phase-1: 0.5–24 hours after ingestion: asymptomatic, to nonspecific symptoms (anorexia,
nausea, vomiting and malaise). Pallor, diaphoresis
•
Phase-2: 18–72 hours after ingestion: Right upper quadrant abdominal pain, anorexia,
nausea and vomiting, Tender right upper quadrant, tachycardia, hypotension and oliguria.
•
Phase-3: 72–96 hours after ingestion: all of the above and jaundice, coagulopathy,
hypoglycemia and hepatic encephalopathy, Acute Renal failure.
•
Phase-4: 4th day to 3weeks after ingestion: patient who survive critical illness in phase 3,
have complete recovery.
Investigation 
•
Liver Function Test - Liver transaminases ALT, AST, ALP, Prothrombin Time (PT) with INR
(International Normalization Ratio)
•
Serum Glucose
•
Renal Function Test: Electrolytes, BUN, Creatinine
•
ABG-Arterial Blood Gas
Non-pharmacological Treatment 
•
Resuscitation
•
In adults, the initial treatment for paracetamol overdose is gastrointestinal decontamination.
•
Usually there is no immediate threat to the airway, breathing and circulation with
paracetamol poisoning
•
Correct hypoglycaemia (Give glucose or sugar or honey)
•
If within 1 hour of ingestion of 150mg/kg or more paracetamol give activated charcoal, if
available, or induce vomiting.
Pharmacological Treatment 
A: Activated charcoal (PO) (1gm/kg, up to 50gm) if less than 2hours.  
If more than 8hours after ingestion, or the patient cannot take oral treatment, give: 
AND 
C: n-acetylcysteine (IV) 150mg/kg in 200mls of 5% Dextrose over 20 minutes, then 
50mg/kg in in 500mls of 5% dextrose over 4 hours, then 100mg/kg in 1 liter of 5% dextrose 
over 16 hours.  
In severe poisoning a further 100mg/kg may be given over the next 24 hours 
Children <20kg 
C: n-acetylcysteine (IV)150mg/kg in 3ml/kg of 5% glucose, over 15 minutes, followed by 50 
mg/kg in 7 ml/kg of 5% glucose over 4 hours, then 100 mg/kg IV in 14 ml/kg of 5% glucose 
over 16 hours. 
For conscious and not vomiting or when there is severe reaction to N-acetylcysteine give: 
S: methionine (IV) (<6 years: 1 gram every 4 hours - 4 doses; 6 years and above: 2.5 
grams every 4 hours for 4 doses). 

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Note 
• 
Syrup of ipecac is contraindicated in inducing vomiting to control paracetamol overdose 
because the vomiting it induces delays the effective administration of activated charcoal and 
oral acetylcysteine 
 
25.3.5 Acetylsalicylic Acid and other Salicylates Poisoning. 
Clinical Presentation  
• 
Initial signs and symptoms 
o 
Tinnitus and impaired hearing, rapid breathing (acidotic-like breathing), vomiting, 
dehydration, fever, double vision and feeling faint 
• 
Late signs 
o 
Drowsiness, bizarre behavior 
o 
Unsteady walking and coma 
 
Investigations 
• 
Blood gases 
• 
pH and bicarbonates  
• 
Serum electrolytes (Calcium and 
Magnesium) 
• 
An 
ECG 
to 
evaluate 
for 
dysrhythmias 
• 
ABG,  
• 
LFTs,  
• 
Full Blood Picture (Leukocytosis and 
thrombocytopenia) 
• 
Coagulation studies (PT and PTT) 
 
Non-pharmacological Treatment 
• 
Give activated charcoal within one hour of ingestion if available. If charcoal is not available 
and a severely toxic dose has been given, then perform gastric lavage or induce vomiting 
as above 
• 
Monitor blood glucose every 6 hours and correct as necessary  
• 
Monitor urine pH hourly. 
 
Pharmacological Treatment 
C: Fluid resuscitation:  If hypokalemia, give  
A: compound sodium lactate (IV) 1litre for 24hr if CNS hypoglycemia is seen give bolus of 
20 mL 50% Dextrose then 5% Dextrose 1litre for 24hours  
AND 
C: sodium bicarbonate (IV) 1mmol/kg over 4hours to correct acidosis and to raise the pH 
of the urine to above 7.5 so that salicylate excretion is increased. 
  
AND 
C: potassium chloride (IV) 8.4mEq/ml, maintain fluids until urine output is 2-3 mL/kg per 
hour 
 
Replace fluid losses (Plasma potassium concentration should be corrected before giving sodium 
bicarbonate as hypokalaemia may complicate alkalinization of urine) Give; 
A: 0.9% sodium chloride (IV) as maintenance requirements  
OR 
Hemodialysis is required if the concentration exceeds 700mg/liter or in presence of severe metabolic 
acidosis 
 
25.3.6 Iron Poisoning 
Symptoms appear at doses greater than 20mg/kg.  Iron levels above 350–500µg/dL are considered 
toxic, and levels over 1000µg/dL indicate severe iron poisoning.Iron pills can look like candy to 
children. Intentional overdose can occur among adults, but is rare. 
 
 
Clinical Presentations  
• 
Nausea, vomiting, abdominal pain and diarrhoea.  
• 
The vomitus and stools are often grey or black.  
• 
In severe poisoning there may be gastrointestinal haemorrhage, hypotension, drowsiness, 
convulsions and metabolic acidosis. 
• 
In a child, bloody vomit or stool gastrointestinal features usually appear in the first 6 hours 
and a patient who has remained asymptomatic for this time probably does not require 
antidote treatment. 

586!
Non-pharmacological Treatment 
•
Gastric lavage if potentially toxic amounts of iron were taken.
Pharmacological Treatment 
Give antidote  
D: deferoxamine (IM) 50mg/kg up to a maximum of 1g by repeated every 12hours; if very 
ill, give (IV) infusion 15mg/kg/hour to a maximum of 80mg/kg in 24hours. 
25.3.7 Carbon-monoxide Poisoning 
Carbon monoxide is a byproduct of burning organic compounds, and may of its exposure occur in 
private residences. So its toxicity is usually due to improper use of gasoline portable generators and 
indoor use of charcoal for cooking and heating. 
Clinical Presentations 
•
Common presentations includes "flu-like" and commonly include headache, dizziness,
weakness, vomiting, chest pain,
•
Dizziness, nausea or vomiting
•
Shortness of breath, blurred vision, loss of consciousness
Large exposures can result in loss of consciousness, arrhythmias, seizures, or death 
Investigations  
•
Blood gases and serum electrolytes
Non-pharmacological Treatment 
•
Give 100% oxygen at 10-15L/min (BVM device) to accelerate removal of 50% carbon
monoxide (note patient can look pink but still be hypoxemic) until signs of hypoxia
disappear.
•
Those who are unconscious may require CPR on site.
Table 24.7 Time to remove 50% carboxyhemoglobin. 
Oxygen pressure О2 
Time 
21% oxygen at normal atmospheric pressure (fresh air) 
5 hours 20 min 
100% oxygen at normal atmospheric pressure (non-rebreather oxygen mask) 
1 hours 20 min 
100% hyperbaric oxygen (3 atmospheres absolute) 
23 in 
25.3.8 Opioid Poisoning 
Physical and mental symptoms that occur after taking too many opioids, a substance found in 
certain prescription pain medication and illegal drugs like heroin. It is caused by complications of 
substance abuse, unintentional overdose, Intentional overdose, and Therapeutic drug error any time 
from birth (Delivery/ maternal opioid usage) to terminal care. Drugs involved in substance 
abuseincludes: Codeine, Diamorphene, Di Hydrocodeine, Fentanyl, Heroin, Loperamide, 
Methadone, Morphine, opium, Tramadol (etc.) alone or in combination. 
Risk factors for Toxicity 
•
Drug users
•
Social disadvantaged
•
People who had used the drug
earlier for treatment
•
Those using alcohol and other
sedatives
Clinical Presentation 
•
Acute toxicity: drowsiness, nausea and vomiting
•
Chronic toxicity: constipation, loss of appetite± nausea and vomiting
•
Respiratory depression, tachycardia, hypotension and pin point pupils
Laboratory Investigations 
•
Full Blood Picture
•
Liver Function Test (ALAT and
ASAT) 
•
Renal 
Function 
Test 
(Serum
Creatinine 
and 
Blood 
Urea 
Nitrogen, BUN) 
•
Creatinine kinase level
•
Arterial blood gas determinations

587!
•
An ECG is recommended in all
patients 
with 
suspected 
opioid 
overdose. 
Non-pharmacological Treatment 
•
Check the airway
•
Intubate the patient who cannot protect their airway
•
Give oxygen as described above.
Pharmacological Treatment  
Antidote: Hypoventilating patient with spontaneous ventilation Naloxone 
Adults & children> 20kg: 
B: naloxone (IV) Initial dose 0.5mg titrated upward until Respiratory Rate is ≥12 
Children (<20kg): 0.01mg/kg (IV) (Maximum 2mg/dose), increase till hypoventilation resolves 
Note 
•
The starting dose of naloxone is between 0.4 to 1 mg in adults and 0.1 mg/kg in children. In
suspected chronic opiate abusers
•
Naloxone must be administered slowly at doses of 0.1 to 0.4 mg IV every 1 to 3 minutes to
ensure a more controlled reversal of the opiate effects. If the naloxone is administered
rapidly in these patients, the patient may also start to feel the pain which was being
suppressed by the opiate.
•
If the respiration is shallow, administer 100% oxygen or assisted with bag-valve ventilation
until patient becomes more alert and cooperative.
•
The onset of action of naloxone is immediate with a peak response observed within 3 to 8
minutes.
•
A repeat dose may be indicated if the patient still shows signs of opiate toxicity
Patients with apnoea: 
•
Newborn with apnoea secondary to maternal opioid: 0.01mg/kg (IV/IM) (Maximum
0.4mg/kg/dose)
•
Children: <20kg 0.1mg/kg (Maximum 2mg/dose) start then repeat doses with continuous
infusion as required.
•
Adults and children>20kg Higher dose of naloxone (0.2-1mg and titrate to clinical response
For life threatening Opioid toxicity 
•
Pediatrics (< 20kg) dosing: 0.1mg/kg/IV (Maximum 2mg/dose). Repeat dose/continuous
infusion as required
•
Adults and children (More than 20kg): 2mg IV.
o
The dose should be repeated every 3 min until improvement of Respiratory Distress
Syndrome
o
If maximal cumulative dose of 10mg is reached and the respiratory insufficiency has
not improvement, consider other pathology
Note 
Withdrawal reaction might be life threatening in neonatal period, hence low doses should be given. 
Further management of Psychiatric Management of Opioid Toxicity refer Mental Disorders Chapter 
25.3.9 Heavy Metal Poisoning 
Lead Poisoning 
Lead is a heavy metal, ubiquitous in our environment (Lead-based paint and its dust, in older 
buildings) that has no physiologic role in biological systems. Lead poisoning occurs when lead builds 
up in the body, often over months or years. Lead toxicity is a particularly insidious hazard with the 
potential of causing irreversible health effects associated with chronic toxicity. 
Clinical Presentation  
The clinical presentation varies widely, depending upon the age at exposure, the amount of 
exposure, and the duration of exposure 
•
New born: Be born prematurely, have lower birth weight, slowed growth,

588!
•
Children: Developmental delay, Learning difficulties, Irritability, Loss of appetite, Weight
loss, Sluggishness and fatigue, Abdominal pain, Vomiting, Constipation, Hearing loss,
Seizures, Eating things, such as paint chips, that aren't food (pica), lower IQ , anxiety,
depression and ADHD Like symptoms
•
Adults: High blood pressure, joint and muscle pain, difficulties with memory or
concentration, headache, abdominal pain, mood disorders, reduced sperm count and
abnormal sperm, miscarriage, stillbirth or premature birth in pregnant women, anaemia,
Fanconi’s syndrome, wrist drop
Laboratory Investigations 
•
Lead blood levels > 10 µg/dL
•
Free 
erythrocyte 
protoporphyrin
(FEP) level 
•
Erythrocyte protoporphyrin (EP) >
35µg/dL 
•
FBC
•
Liver Function Test (ALAT and
ASAT) 
•
Renal 
Function 
Test 
(Serum
Creatinine and Blood Urea Nitrogen, 
BUN) 
•
Imaging 
studies 
according 
to
presentation, 
-chest, 
bones,
abdomen 
etc 
are 
ordered 
as
appropriate.
Non-pharmacological Treatment 
•
Remove the source of lead exposure in the community
•
Closely monitor cardiovascular and mental status
•
Maintain an adequate urine output.
•
Assess renal and hepatic functions.
Pharmacological Treatment 
Blood Lead levels are 25–40 µg/dL 
D:  d-penicillamine (PO) 30-40mg/kg/day 1-6months, 2hours before or three hours after 
meals  
OR 
Blood Lead levels are 45–70 µg/dL Chelate the patient using, 
D: 2,3-dimercapto-succinic acid (IM) 10mg/kg by deep 8 hourly for 5 days, followed by 
10mg/kg 12hourly for 14 days.  
Blood Lead levels of > 70 µg/dL and/or encephalopathy 
D: dimercaprol 3mg/kg deep (IM) 4hourly for 48 hours followed by 3mg/kg 12 hourly for 10 
days 
AND 
D: ethylene diamine tetra-acetic acid (CaNa2 EDTA) 10mg/kg (IV) 8hourly for 5 days 
(calcium chelate of the disodium salt of ethylene-diamine-tetraacetic acid (EDTA)) 
Mercury Toxicity 
Mercury in any form is poisonous. Poisoning can result from mercury vapour inhalation, mercury 
injection and absorption of mercury through the skin. Methylmercury (organic mercury) poisoning is 
largely linked to eating seafood, mercury-containing fish. 
Clinical Presentation 
•
Inorganic Mercury:
o
Ash-gray mucous membrane, haematochesia, severe abdominal pain, foul breath,
hypovolaemic shock, Metallic taste, stomatitis, gingival irritation loosening of teeth
and Renal tubular necrosis.
•
Organic Mercury:
o
Visual disturbances, - Eg, scotomata, visual field constriction, ataxia, paresthesias
(early signs), hearing loss, dysarthria, mental deterioration, muscle tremor,
movement disorders, paralysis, and death (with severe exposure).
Laboratory Investigations: 
•
Blood and Urine Mercury levels
•
FBC
•
RFT
•
Hair, Toenail, and CSF mercury level
for chronic exposure
•
Plain X-ray of the abdomen

589!
Non-pharmacological Treatment: 
•
Remove from the exposure,
•
Airway Breathing and Circulation
(ABC)
•
Give oxygen
•
Copious irrigation of the skin if skin
involvement
•
Do 
gastric 
lavage 
if 
ingested
mercury 
and 
observed 
in 
the
abdominal radiographs
•
Do 
Hemodialysis 
when 
renal
function has declined.
Pharmacological Treatment 
Chelation therapy for acute inorganic mercury poisoning can be done with DMSA or 
Dimercaprol. 
 Occasionally 
2,3-dimercapto-1-propanesulfonic 
acid (DMPS), D-
penicillamine (DPCN). 
A: activated charcoal (PO) as in ingested poisons 
OR 
D: 2,3-dimercapto succinic acid (PO) (DMSA or succimer) 10 mg/kg 8 hourly  for 5 days; 
follow by 10 mg/kg/dose 12 hourly for 14 days; not to exceed 500 mg/dose 
In acute inorganic mercury poisoning: 
D: Dimercaprol: 
o
Day 1: 5mg/kg deep (IM) stat
o
Day 2–11: 2.5mg deep (IM) 12 hourly for 10 days
Surgical intervention: To remove mercury that has been logged in the intestine or colon 
25.4 Prevention of Poisoning 
Educate the patient on Dos and Don’ts of poisoning prevention. 
Do’s 
•
Keep medicines and poison in
proper containers and out of reach of
children.
•
Use containers with child resistant
caps
•
Keep all products in their original
container
•
Read medicine labels carefully to
avoid mistake
Don’ts 
•
Leave container open
•
Transfer products from their origin
•
Remove labels from the medicine
products
•
Put tablets into another container
such as purse or envelope
•
Medicine/tablets as sweet
•
Take your medicine in front of
children as they often copy
25.5 Alcohol Intoxication 
Management of alcohol intoxication see mental health conditions chapter. 
25.6 Bites and Stings 
The insect that is responsible for the majority of serious sting related reactions belong to the order 
hymenoptera. This includes bees, wasps, spiders, scorpions, ants andcentipedes.  
Diagnostic Criteria 
•
Pain, swelling, redness, and itching to the affected area
Non-pharmacological Treatment 
•
Clean the area with soap and water to remove contaminated particles left behind by some
insects
•
Refrain from scratching because this may cause the skin to break down and results to an
infection
Pharmacological Treatment 
A: ibuprofen  
Adults: 400–800mg (PO) 8hourly for 3days 
Children: 10mg/kg 8hourly maximum 400mg per day for 3days 
AND 
A: prednisolone, 2mg/kg/day (PO) in single daily not to exceed 80mg/day for 5days 
Where there is an anaphylactic reaction treat according to guideline. 

590!
AND 
A: chlorpheniramine and be ready if allergic reaction occurs. Dosage as below 
o
Children under 6years: 4mg 8hourly needed
o
6–12 years: 8mg (PO) 12hours as needed
o
>12 years and older 12mg 12hourly needed
OR 
C: loratadine (PO) 10mg 24hourly 
Usual Pediatric Dose: 
2-5years:
loratadine 
(PO) 
5mg 
24hourly 
(syrup) 
6years or older: Loratadine (PO) 10 mg24hourly (tablets, capsule, and disintegrating 
tablets) 
25.6.1 Management of Specific Bites/Stings 
25.6.1.1 Bee and Wasps Sting 
Bee Venom contains many toxins including: Haemolytic enzyme, a neurotoxic factor, histamine and 
lytic peptide. Wasp Venom contains Hyaluronidase and 5-hydroxytryptamine. 
Prevention of Complications after Bites / Sting 
•
Move victims to a safe area to avoid more bites or stings.
•
If needed, remove the stinger.
•
Wash the area with soap and water.
•
Apply a cool compression using a cloth dampened with cold water or filled with ice
•
Apply 0.5 or 1 percent hydrocortisone cream, calamine lotion or a baking soda paste to the
bite or sting several times daily until your symptoms are alleviated. 
Clinical Presentations 
•
Locally: Itching, pain, erythema, and swelling, cellulites
•
Systemic: Oedema, fatigue, nausea, vomiting, fever, unconsciousness, Anaphylaxis,
diarrhea or stool incontinence, dizziness, hypotension, haemolysis, rhabdomyosid,
haemoglobinuria and myoglobinuria
Non-pharmacological Treatment: 
•
Airway and breathing
•
Remove stingers by forceps or scrap with care
•
Elevation of the affected limb
•
Clean wound
Pharmacological Treatment 
A:  adrenaline 0.5mg (IV) (0.1Ml) of 1;1000 solution diluted in 10ml of 0.9% sodium chloride 
slowly over 30minutes 
AND 
A: chlorpheniramine (PO) 4mg 4-6 hourly; not to exceed 24 mg/day; 8mg orally 8-12hourly 
or 12mg every 12hourly; not to exceed 24mg/day 
o
Children under 2 years: Safety and efficacy not established
o
Children 2-6 years: 1 mg (PO) 4-6hourly; not to exceed 6mg/day
o
Children 6-12 years: 2mg (PO) 4-6hourly; not to exceed 12mg/day or sustained
release at bedtime.
o
Children over 12 years: 8 mg (PO) 8-12hourly or 12 mg 12hourly; not to exceed
24 mg/day
OR 
A: promethazine (PO/Rectal) 6.25 to 12.5 mg orally or rectally before meals and at 
bedtime, if necessary,  
OR 
A: promethazine 25mg orally or rectally 24hourly at bedtime 
OR 
A:  promethazine 25mg (IM or IV) stat, and may be repeated within 2hours if necessary 
OR 
C: loratadine (PO) 10mg24hourly 

Pediatric Dose: 
2-5years: loratadine (PO) 5mg 24hourly (syrup)
6 years or older: loratadine (PO) 10mg 24hourly (tablets, capsule, and disintegrating 
tablets) 
AND 
A:  0.9% sodium chloride 10–20mls/kg as a bolus 
AND  
A: paracetamol (PO) 1g for adult or 15mg/kg for children 8hourly for 48hours 
OR 
D: methylprednisolone (IV) 125mg stat inpatient with respiratory and cardiovascular 
compromised. 
Note 
•
   Patient with multiple stings: observe for 24hours 
•
Healthy adults >50stings,
•
Children 1 sting
25.6.1.2 Scorpion Sting (Envenoming) 
Scorpion stings can be very painful for days. Systemic effects of venom are much more common in 
children than adults.  
Clinical Presentations 
•
Local pain and/or paresthesia at the site of envenomation,
•
Pain and/or paresthesia remote from the site of sting,
•
Autonomic disturbances such as tachy/bradycardia, hyper/hypotension, hypersalivation and
lacrimation, urinary and faecal incontinence and pulmonary oedema. 
•
Blurred vision, roving eye movement, tongue fasculation, dysphagia, dysphonia, restless,
•
Severe involuntary shaking or jerking extremities
•
Cardiogenic shock
Deaths from scorpion stings are usually due to cardiogenic shock and pulmonary oedema. 
Grading of Envenomation 
•
Grade I involves local pain and paresthesias at the sting site. The puncture wound may not
be noticeable in this grade.
•
Grade II involves local pain and paresthesias existing at the sting site as well as proximal to
the sting site.
•
Grade III includes grade 2 classification factors with added cranial nerve (increased oral
secretions, blurry vision, rapid tongue movement, nystagmus), or skeletal neuromuscular
dysfunction (flailing of the extremities and tetanus-like arching of the back) and can also be
accompanied by autonomic dysfunction.
•
Grade IV includes both 3 and hyperthermia, up to 104 ⁰F, rhabdomyolysis, pulmonary
edema, and multiple organ failures.
Non-pharmacological Treatment 
•
Provide adequate airway, ventilation and perfusion
•
Calm the patient to lower the heart rate and blood pressure, thus limiting the spread of the
venom
•
Give oxygen as above
•
Monitor vitals: oxygen saturation, heart rate respiratory rate and blood pressure
Pharmacological Treatment 
A: Cleaning of the sting area with Normal saline 
AND 
A: compound sodium lactate (IV) 2L for 24hours 
AND 
A: adrenalin (IM) dose of 1:1000 (Repeat after 5 min if no improvement) 
591!

Children > 12 years and Adults 500 µg (0.5ml) 
Children 6-12 years 300 µg (0.3ml) 
Children < 6 years 150 µg IM (0.15ml)  
Intubation equipment should be made available before the administration of the antivenom in case of 
anaphylactic shock 
OR 
S: equine antivenom (Centruroides Scorpion) for (Grade III or IV envenomations) -
intravenous scorpion-specific F(ab’)2 equine antivenom at a maximum of three vials in 20 
to 50 mL of normal saline and infused over 30 minutes. 
Initial dose: infuse 1vial of the 3vials over 10minutes, observe for 60minutes If symptoms 
persist you may repeat the remaining 2 vials, one vial at a 30minutes interval. 
AND 
A: paracetamol (PO) or IV 1g for adult or 15mg/kg for children (PO) 8hourly for 48hours 
OR 
A:  ibuprofen 
Adults: 400–800mg (PO) 8hourly for 3days 
Children: 10mg/kg 8hourly maximum 400mg per day for 8hourly a day 
OR  
C: morphine (PO) or (IM) according to severity 
If very severe, infiltrate site with  
A: 1% lignocaine. 
25.6.1.3 Snake Bite 
A snake bite can be life-threatening if the snake is venomous. Less than 10% of 3500 snake species 
are poisonous and they include cobras and mamba’sblack mamba, king cobra, banded krait, saw-
scaled viper and rattlesnake. (Elapidac), sea snakes (hydrophidac) and the boom slang and vine 
snakes (columbidac). Clinical ccondition depends on the type of snake bite and amount of poison 
(venom) injected.   
Hence envenomation (poisoning) are: 
•
Neurotoxin in cobra, mambas and sea snakes
•
Haemotoxic in vipers and boom slang.
Snake bites should be considered in any severe pain or swelling of a limb or in any unexplained 
illness presenting with bleeding or abnormal neurological signs. Some cobras spit venom into the 
eyes of victims causing pain and inflammation.  
Table: 25.8 Various snakebites, their fatal dose, quantity of venom injected, and time to 
fatality 
Snake 
LD50 in mine 
Fatal dose 
for 
humans 
Average 
delivered 
dose 
per bite 
Average 
fatal period 
Indian cobra (Naja naja) 
0.28 mg/kg 
12 mg 
60 mg 
8 h 
Common 
krait (Bungarus 
caeruleus) 
0.09 mg/kg 
6 mg 
20 mg 
18 h 
Russell's viper (Daboia russelii) 
0.1 mg/kg 
15 mg 
63 mg 
3 days 
Saw-scaled viper (Echis carinatus) 
6.65 mg/kg 
8 mg 
13–40 mg 
41 days 
Clinical Presentations 
•
General signs include pain in the affected area, skin redness, swelling, bleeding, bruise,
•
fast heart rate, nausea, or sweating vomiting and headache
•
Shock
•
Bite for local necrosis, bleeding or tender local lymph node enlargement
592!

•
Specific signs and level of envomation are shown in the table below depending on the
venom and its effects.
Table 25.9: Assessment of severity of Snake envenomation 
Level of Intoxication 
Presentation 
No envenomation 
Absence of local or systemic reactions; fang marks (+/−) 
Mild envenomation 
Fang marks (+), moderate pain, minimal local edema (0–15 ce), erythema (+), 
ecchymosis (+/−), no systemic reactions 
Moderate 
envenomation 
Fang marks (+), severe pain, moderate local edema (15–30 cm), erythema and 
ecchymosis (+), systemic weakness, sweating, syncope, nausea, vomiting, 
anemia, or thrombocytopenia 
Severe envenomation 
Fang marks (+), severe pain, severe local edema (>30 cm), erythema and 
ecchymosis 
(+), 
hypotension, 
paresthesia, 
coma, 
pulmonary 
edema, 
respiratory failure 
Additionally, the patient may present with 
•
These include:
o
Shock
o
Local swelling that may gradually extend up the bitten limb
o
Bleeding: external from gums, wounds or sores; internal especially intracranial
o
Signs of neurotoxicity: respiratory arrest or paralysis, ptosis, bulbar palsy (difficulty
swallowing and talking), limb weakness
o
Signs of muscle breakdown: muscle pains and black urine
Note 
•
Avoid picking up the snake or try to wrap it up or kill it, as this will increase your chances of
getting bitten again. 
•
Avoid applying a tourniquet.
•
Avoid cutting into the wound at all.
•
Avoid trying to suck out the venom.
•
Avoid applying ice or use water to submerge the wound.
•
Avoid drinking alcohol.
•
Avoid drinking beverages with caffeine.
•
Avoid taking any pain-relieving medication, such as ibuprofen
Investigations 
Specific investigations  
No specific investigations, history is more useful. 
•
The 20-min whole blood clotting test (20 WBCT)
•
Enzyme linked immunosorbent assay (ELISA)
Supportive investigations may include 
•
Hemogram: Presence of neutrophilic leucocytosis signifies systemic absorption of venom.
Thrombocytopenia may be a feature of viper envenomation. 
•
Serum creatinine: This is necessary to rule out renal failure after viper and sea snake bite.
•
Serum amylase and creatinine phosphokinase (CPK): Elevated levels of these markers
suggests muscle damage (caution for renal damage). 
•
Prothrombin time (PT) and activated partial thromboplastin time (aPTT): Prolongation may
be present in viper bite. 
•
Fibrinogen and fibrin degradation products (FDPs): Low fibrinogen with elevated FDP is
present when venom interferes with the clotting mechanism. 
•
Arterial blood gas and electrolyte determinations: These test are necessary for patients with
systemic symptoms. 
•
Urine examination: Can reveal hematuria, proteinuria, hemoglobinuria, or myoglobinuria
593!

•
Electrocardiogram (ECG): Nonspecific ECG changes such as bradycardia and
atrioventricular block with ST-T changes may be seen. 
•
Electroencephalogram (EEG): Recently, EEG changes have been noted in up to 96% of
patients bitten by snakes. 
Non-pharmacological Treatment: 
•
Reassure the patient;
•
Splint the limb to reduce movement and absorption of venom.
•
If the bite was likely to have come from a snake with neurotoxin venom,
o
Clean the site with clean water to remove any poison and remove any fangs;
•
If any of the above signs, transport to hospital which has antivenom as soon as possible.
•
Paralysis of respiratory muscles can last for days and requires intubation and mechanical
ventilation or manual ventilation (with a mask or endotracheal tube and bag) by relays of
staff and/or relatives until respiratory function returns.
•
Do endotracheal intubation +/- elective tracheotomy.
•
Elevate limb if swollen
•
Monitor very closely immediately after admission, then hourly for at least 24 hours as
envenoming can develop rapidly.
Pharmacological Treatment 
Give  
A: Anti-Tetanus prophylaxis 
Treat shock, if present.  
A: 0.9% sodium chloride (IV) 10–20mls/kg bolus, repeat after 30min if still in shock 
Give fluids orally or by NG tube according to daily requirements. Keep a close record of 
fluid intake and output fluid daily requirements to be inserted 
If there are systemic signs or severe local signs (swelling of more than half of the limb or severe 
necrosis), give 
A: Anti–snake venom (IV) (ASV)are polyvalent immunoglobulins prepared to control venom 
of poisonous snakes) using indications shown below. Follow the directions given on the 
antivenom preparation. 
o
Dilute antivenom in 2–3 volumes of 0.9% Normal saline and give intravenously over 1
hour
o
Give more slowly initially and monitor closely for anaphylaxis or other serious adverse
reactions.
For mild degree of envenomation give 5 vials (50 ml) 
For moderate degree of envenomation give 5–10 vials (50–100 ml) 
Fore severe degree of envenomation gives 10–20 vials (100–200 ml) 
594!

Table 25.10: Indications for Anti-Snake Venom 
System 
Clinical features 
Cardiovascular 
Spontaneous systemic bleeding 
Whole blood clotting time >20 min 
Thrombocytopenia (platelets <100,000/mm3) 
Shock 
Arrhythmia 
Abnormal electrocardiogram 
Neurological 
Ptosis and paralysis 
Renal 
Acute renal failure 
Generalized rhabdomyolysis and muscular pains 
Hyperkalemia 
Local swelling involving more than half of the bitten limb 
Rapid extension of swelling 
Development of an enlarged lymph node draining the bitten limb 
A: adrenaline (IM) dose of 1:1000 (Repeat after 5minutes if no improvement) 
o
Children > 12 years and Adults 500 µg (0.5ml)
o
Children 6-12 years 300 µg (0.3ml)
o
Children < 6 years 150 µg IM (0.15ml)
AND 
A: chlorpheniramine and be ready if allergic reaction occurs. Dosage as below 
o
Children under 6years: 4mg 8hourly needed
o
6–12 years: 8mg (PO) 12hours as needed.
o
>12 years and older 12mg 12hourly needed
Note 
•
If itching/urticarial rash, restlessness, fever, cough or difficult breathing develop, then stop
antivenom and give
A: adrenalin 0.01 ml/kg of 1/1000 or 0.1 ml/kg of 1/10,000 solution subcutaneously and IM
or IV/SC Chlorpheniramine 250 micrograms/kg.
•
When the patient is stable, re-start antivenom infusion slowly.
•
More antivenom should be given after 6 hours if there is recurrence of blood in-coagulability
or after 1–2hour if the patient is continuing to bleed briskly or has deteriorating neurotoxin or
cardiovascular signs.
•
Blood transfusion should not be required if antivenom is given.
•
Response of abnormal neurological signs to antivenom is more variable and depends on
type of venom.
Surgical Intervention 
•
Excision of dead tissue from wound
•
Incision of facial membranes to relieve pressure in limb compartments, if necessary
•
Skin grafting, if extensive necrosis
•
Tracheotomy if paralysis of muscles involved in swallowing occurs
595!

CONTRIBUTORS 
National Medicines and Therapeutic Committee (NMTC) Members 
SN 
Name 
Membership 
1 
Prof. Abel Makubi 
Chief Medical Officer  and Chairperson NMTC 
2 
Pharm. Daudi Msasi 
Director, Pharmaceutical Services Unit- MoHCDGEC and 
Secretary NMTC 
3 
Dr. John Rwegasha 
Gastroenterologist, Muhimbili National Hospital (Member) 
4 
Dr. David Mwenesano 
Director Medical and Technical Services, National Insurance 
Fund, (Member) 
5 
Dr. 
Peter 
Masunga 
Mbelele 
Clinical Microbiologist, Kibong'oto Special Hospital 
6 
Pharm. Samiri Saitoti 
Clinical Pharmacologist,  University of Dodoma l (Member) 
7 
Dr. Delfina  Mkenda 
Gynacologist, Mbeya Zonal Referral Hospital(Member) 
8 
Dr. Deus Buma 
Clinical Pharmacist, Muhimbili National Hospital (Member) 
9 
Pharm. Silvester Maige 
Clinical Pharmacologist, Medical Store Department (Member) 
10 
Dr. John Meda 
Cardiologist, Benjamini Mkapa Zonal Referral Hospital 
(Member) 
11 
Dr. Vickfarajael  Daudi 
Pediatrician, Hydom  Lutheran Hospital (Member) 
12 
Pharm. Kauke B. Zimbwe 
Clinical Pharmacist, Benjamini Mkapa Zonal Referral Hospital 
13 
Dr. Mark Mseti 
Oncologist, Ocean Road Cancer Institute(Member ) 
14 
Pharm.Walter Ombeni 
Clinical Pharmacist, Mirembe Psychatric Hospital ( Member) 
15 
Dr. Michael Irira 
Paeditrician, Mawenzi Regional Referral Hospital ( Member) 
16 
Dr. Azma Simba 
Epidemiologist, 
Directorate 
of 
Preventive 
Services-
MoHCDGEC (Member) 
17 
Dr .Phillipina Philipo 
District Medical Officer In charge, Bahi DC (Member) 
18 
Dr. Linda Ezekiel 
Nephrologist, Directorate of Curative Services, MoHCDGEC 
(Co-opted Member) 
20 
Pharm. Cosmas Mogasa 
Principal Pharmacist, National Insurance Fund (Co-opted 
Member) 
21 
Pharm. Mary Masanja 
Principal Pharmacist, Tanzania Medicines and Medical 
Devices Authority (Co-opted Member) 
22 
Pharm. 
Regina 
J. 
Richard 
Senior Pharmacist, POLARG (Co-opted Member) 
23 
Pharm. Ibrahim Mwandu 
Pharmacist, Pharmacy Council (Co-opted Member) 
24 
Pharm.  Siana G. 
Mapunjo 
Principal 
Pharmacist, 
Pharmaceutical 
Services 
Unit-
MoHCDGEC (Secretariat) 
25 
Pharm. Noel  Mhadu 
Senior 
Pharmacist, 
Pharmaceutical 
Services 
Unit-
MoHCDGEC (Secretariat) 
26 
Pharm.  Marco Salingu 
Senior 
Pharmacist, 
Pharmaceutical 
Services 
Unit-
MoHCDGEC (Secretariat)  
27 
Pharm. Emiliana Francis 
Pharmacist I, Pharmaceutical Services Unit-MoHCDGEC 
(Secretariat) 
28 
Pharm. Aneth Wilbroad 
Pharmacist I, Pharmaceutical Services Unit-MoHCDGEC 
(Secretariat)  
29 
Pharm.  Lucy Mziray 
Pharmacist I, Directorate Curative Services-MoHCDGEC 
(Secretariat) 
596!

Lead Reviewers 
SN 
Leader Reviewrs 
Chapters 
1 
Dr. Patrick Shayo (Emergency Physician) - Muhimbili 
National Hospital 
Emergency and Critical Care 
2 
Dr. Alex Loth (Anethetics) - Muhimbili National Hospital 
Anesthesia 
3 
Dr. Mwashungi Ally (Hematologist) - Temeke Regional 
Referral Hospital 
Hematological 
Disease 
Conditions 
4 
Dr. Rogath Kishimba (Epidemiologist) - MoHCDGEC 
Notifiable Diseases 
5 
Dr. Issa Garimo, National Malaria Control Programme 
Malaria 
6 
Dr. Aneth Rwebembera, National AIDS Control Programme 
HIV/AIDS 
7 
Pharm. Jumanne  Mkumbo, TB and Leprosy  Programme 
TB and Leprosy 
8 
Dr. Raymond Makundi (Neurologist) - Muhimbili National 
Hospital (Mloganzila) 
Nervous Disease  Conditions 
9 
Dr. Jude Tarimo (Pulmonologist) - Muhimbili National 
Hospital 
Respiratory Disease Conditions 
10 
Dr. Amunga Meda (Gastroenterologist) - Muhimnbili 
National Hospital 
Gastrointestinal 
Disease 
Conditions 
11 
Dr. France Rwegoshora (Gynecologist)-Mbeya Zonal 
Referral Hospital  
Obstetrics, Gynecology  and 
Contraception 
12 
Dr. Gisenga Lija (Dermatovenereologist) - Kibaha  College 
of Health and Allied Sciences  
Sexually Transmitted Infections 
13 
Dr. Julia Wang'ari (Dermatologists) - Bombo Regional 
Referral Hospital 
Skin 
Disease 
and 
Allergic 
Reactions 
14 
Dr. Bernadetha Shilio (Opthalimologist) - Directorate of 
Curative Services, MoHCDGEC 
Eye Disease Conditions 
15 
Dr. Baraka Nzobo (Dental surgeon) - Morogoro Regional 
Referral Hospital 
Oral and Dental Conditions 
16 
Dr. Martin Elimath (ENT Specialist) - Muhimbili National 
Hospital 
Ear, Nose and Throat Diseases 
17 
Dr. Bryceson Kiwelu (Orthopedic Surgeon) - Tumbi 
Regional Referral Hospital  
Musculorskeletal Disorders 
18 
Dr. Deogratius Banuba (Orthopedic Surgeon) - Singida 
Regional Referral Hospital 
Trauma and Injuries 
19 
Prof. Andrew Swai  (Endocrinologist) - Tanzania Diabetes 
Association 
Metabolic 
and 
Endocrine 
Disease Conditions 
20 
Dr. Engerasiya Kifai (Cardiologist) - Jakaya Kikwete Heart 
Institute 
Cardiovascular 
Disease 
Conditions 
21 
Dr. Kajiru Kilonzo (Nephrologist) - Kilimanjaro Christian 
Medical Centre 
Kidney and Urological Disorders 
22 
Dr. Jerry Ndumbalo (Oncologist) - Ocean Road Cancer 
Institute 
Malignant Disease Conditions 
23 
Dr. Enock Changarawe (Psychiatrist) - Mirembe Psychiatric 
Hospital  
Mental Health Conditions 
24 
Mrs. Elizabeth Lyimo (Nutritionist) - Tanzania Food and 
Nutrition Centre 
Nutrition Disorders 
25 
Dr. Benard Mbwele (Epidermiologist) - UDSM  Mbeya 
collage of  Health and Allied Sciences 
Poisoning 
26 
Prof. Jeremiah Seni (Microbiologist) - Catholic University of 
Health and Allied Sciences 
UTI (Section) 
597!

Other Contributors 
SN 
Name 
Background 
Institution 
1 
Dr. Sirili Harya 
Neural Surgeon 
Muhimbili National Hospital 
2 
Dr. Francis Fredrick Furia 
Nephrologist 
Muhimbili National Hospital 
3 
Dr. Lugano Wilson 
Anesthetics 
Muhimbili National Hospital 
4 
Dr. Emmanuel Balandya 
Hematologist 
Muhimbili National Hospital 
5 
Dr. Jackson Ilangali 
Publi Health Specialist 
MTaPs - MSH 
6 
Mr. Machumu Miyeye 
Pharmacist 
RCHS 
Programme, 
MoHCDGEC 
7 
Ms. Fiona  Chilunda 
Advisor 
Health System Strengthening 
Project - Dodoma 
598!