MSF Paediatric Care 2024

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Paediatric care

Clinical and therapeutic guidelines

Practical guide for doctors, nurses and


other healthcare professionals managing
common paediatric conditions

Internal document
2024 edition
Acknowledgements
The Paediatric care: clinical and therapeutic guidelines, 1st edition (2023) have been
developed by Médecins Sans Frontières (MSF) under the supervision of the International
Paediatric Working Group, and in close collaboration with other relevant working groups.
These are the first international paediatric guidelines to be produced by MSF and are
partly based on the previous OCP-OCG, and OCBA Paediatric Guidelines originally written
by Marianne Sutton, which they now replace. We also thank Marie-Claude Bottineau and
Myrto Schaefer for their contributions to, and coordination of, the previous guidelines.

MSF would like to express its sincere gratitude to everyone who has contributed to the
development of these guidelines:
International Paediatric Working Group:
Jordan Amor-Robertson, Inma Carreras, Manuel Dewez, Anja Gao, Laurent Hiffler,
Sophie Janet, Hans-Jörg Lang, Jaap Karsten, Daniel Martinez Garcia, Nikola Morton,
Oluwakemi Ogundipe, Roberta Petrucci (Coordinator), Harriet Roggeveen, Neal Russell,
Jiske Steensma, Johanna Thomson, Lisa Umphrey, Ana Victoria Valori.
Other contributors:
Gabriel Alcoba, Haydar Alwash, Mohana Amirtharajah, Valentina Burzio, Roberta Caboclo,
Cristina Carreno, Esther Casas, Arlene Chua, Ana de la Osada, Lynette Dominguez,
Teresa Gadsden, Kerstin Hanson, Christian Heck, Patrick Hérard, Cathy Hewison,
Melissa Hozjan, Rupa Kanapathipillai, Amin Lamrous, John Lawrence, James Lee,
Ian Maconochie, Kathryn Maitland, Mignon McCulloch, Juno Min, Laura Moreto,
Caroline Mwangi, Carolina Nanclares, Lynne Nield, Maura Pedrini, Erwan Piriou,
Anne Pittet, Kirrily de Polnay, Ian Proudfoot, Amulya Reddy, Koert Ritmeijer, Cliff Roberson,
Carla Schwanfelder, Saschveen Singh, Martin Sosa, Esther Sterk, Elisabeth Szumilin,
Malcolm Townsend, Vicky Treacy-Wong, Alejandro Vargas Pieck, Joana van Holthe,
Blandine Vasseur, Cedric Yoshimoto.
International Guidelines Publication team:
Author-coordinators: Nadia Lafferty, Clara van Gulik
Medical Editor: Elisabeth Le Saout
Language editor: Carolina López Vázquez
Lay-out designer: Evelyne Laissu

Published by
Médecins sans Frontières

© Médecins sans Frontières, 2024


All rights reserved for all countries. No reproduction, translation and adaptation may be
done without the prior permission of the Copyright owner.

Médecins Sans Frontières. Paediatric care: clinical and therapeutic guidelines. 2024 edition.
Ref. L010PEDM05E-P
Introduction

Despite a significant reduction in childhood mortality over the last 30 years, under-5 mortality
remains unacceptably high. In 2021, 5 million children under the age of 5 died, almost half of
whom were neonates, representing a global under-5 mortality rate of 38 deaths per 1000 live
births1. If current trends continue, 54 countries will fail to meet the Sustainable Development
Goal target 3.2, which aims to end preventable newborn and child deaths, and to reduce
the under-5 mortality rate to less than 25 deaths per 1000 live births by 20302. Though
data on mortality trends among older children are more limited, each year approximately
800 000 children 5-14 years old die worldwide1. The significance of this for MSF’s work is
evident - more than 80% of under-5 deaths occur in the Sahel and southern Asia1, while over
55% of deaths in the 5–14-year age group occur in sub-Saharan Africa alone3.
The leading causes of death among young children worldwide remain unchanged – pneumonia,
diarrhoea and malaria together accounted for over 1.6 million deaths of children under 5 in
20194, despite the availability of simple and effective treatments for these diseases. In the
older paediatric age groups, global data on cause of death is not reported, but individual
country data implicates the same 3 top killers as for the under-5 age group, with the addition
of injuries, as the leading causes of death in the 5-14-year age group3. An unacceptably large
proportion of childhood deaths could be prevented by access to timely and appropriate
medical care, vaccination and adequate nutrition.
These guidelines have been developed to ensure that children seen in MSF facilities receive
prompt, high-quality care to reduce child mortality. They provide clear, evidence-based clinical
guidance for common paediatric conditions and promote consistency of practice across MSF
facilities. Best practice guidance has been adapted and tailored to ensure alignment with the
medications and equipment that are available in MSF projects.
These guidelines will be updated regularly online as new evidence and guidance becomes
available. As such, new printed editions will be released when necessary. Comments and
feedback should be addressed to the Paediatric Working Group at DL-MSF-PediatricWorkingG
roupInternational@geneva.msf.org.

References
1. The Global Health Observatory. Child mortality and causes of death. The Global Health
Observatory. Accessed November 30, 2023.
https://www.who.int/data/gho/data/themes/topics/topic-details/GHO/child-mortality-
and-causes-of-death
2. Sustainable Development Goal 3 | Department of Economic and Social Affairs. United
Nations. Accessed November 30, 2023.
https://sdgs.un.org/goals/goal3
3. Masquelier B, Hug L, Sharrow D, et al. Global, regional, and national mortality trends in older
children and young adolescents (5–14 years) from 1990 to 2016: an analysis of empirical
data. Lancet Glob Health. 2018;6(10):e1087-e1099.
https://doi.org/10.1016/S2214-109X(18)30353-X
4. Diarrhoea. UNICEF DATA. Accessed November 30, 2023.
https://data.unicef.org/topic/child-health/diarrhoeal-disease/

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About these guidelines

This is the first international edition of the MSF Paediatric care guidelines. It is the result of the
collective work of numerous internal paediatric guidelines and protocols produced over the
years by dedicated paediatricians and paediatric nurses working in MSF Medical departments,
Operational cells and projects. These guidelines have been developed by the International
Guidelines Publication (IGP) team, in close collaboration with the International Paediatric
Working Group (IPWG) and other relevant working groups.

Objective
The objective of these guidelines is to improve the clinical care of a sick or injured child.
Although predominantly focused on hospital care, they are designed for use in any inpatient
or outpatient healthcare facility with a major paediatric care component. The primary target
audience of these guidelines is general clinicians/physicians and clinical officers with little or
no experience in paediatric care, but they can be used as a support for all healthcare workers
involved in the delivery of medical care for children.

Age range
The Convention on the Rights of the Child defines a child as any human being below the age
of 18 years, however acknowledging that the specific needs of adolescents over 15 years are
complex and require specific expertise, the age range covered in these guidelines is 1 month
to 15 years inclusive.

Definitions
The following WHO definitions for adults, adolescents, children and infants are used in these
guidelinesa:
- A neonate is an infant younger than 4 weeks of age.
- An infant is a child younger than 1 year of age.
- A child is a person 1 to 9 years of age.
- An adolescent is a person 10 to 19 years of age.
- An adult is a person older than 19 years of age.

Antibiotic recommendations
Antimicrobial resistance caused by inappropriate use of antibiotics is a global health problem
and antibiotic stewardship is essential in all contexts. Antibiotic choices are therefore aligned
with the WHO AWaRe (Access, Watch, Reserve) antibiotic handbook1 wherever possible.

Children with severe acute malnutrition


General medical complications and their management in children with severe acute
malnutrition (SAM) are integrated throughout these guidelines. Where treatment for children
with SAM differs from that of children without SAM, it is explicitly outlined in the relevant
chapter. For medical complications that are specific to children with SAM and are not relevant
to children without SAM e.g. refeeding syndrome, there is a dedicated chapter.

a Note that countries may have other definitions under their respective national laws.

4
HIV and tuberculosis in children
Paediatric HIV and tuberculosis are included only briefly in these guidelines as comprehensive
guidance is available in disease-specific MSF guidelines.

Illustrations
All illustrations in these guidelines have been redrawn for consistency or are original drawings.
The majority have been redrawn with permission by Anthony Calvert, from source material
primarily from WHO Hospital Care for Children, MSF publications and from images provided by
David Watson. Figure 8.1 - Dorsal slit procedure and Figure 9.1 - Two bag method for delivery
of IV fluids in DKA are original drawings by Sarah Imani.

References
1. The WHO AWaRe (Access, Watch, Reserve) Antibiotic Book. World Health Organization;
2022. Accessed November 30, 2023.
https://www.who.int/publications-detail-redirect/9789240062382

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Table of contents

Introduction.............................................................................................................................. 3
About these guidelines............................................................................................................. 4
Abbreviations and acronyms.................................................................................................. 15

Chapter 1: Paediatric history and clinical examination


1.1 Introduction...................................................................................................................... 19
1.2 Taking a paediatric history............................................................................................... 20
1.3 Clinical examination......................................................................................................... 22

Chapter 2: Emergencies
2.1 Resuscitation..................................................................................................................... 27
2.1.1 Basic life support...................................................................................................... 27
2.1.2 Advanced life support.............................................................................................. 32
2.2 Circulatory impairment and shock................................................................................... 35
2.2.1 Classification of circulatory impairment and shock................................................. 35
2.2.2 Clinical features........................................................................................................ 36
2.2.3 Immediate management......................................................................................... 36
2.2.4 Monitoring and further management..................................................................... 38
2.2.5 Further critical care management when intensive care is available........................ 40
2.3 Choking............................................................................................................................. 42
2.4 Anaphylaxis....................................................................................................................... 46
2.4.1 Clinical features and diagnostic criteria................................................................... 46
2.4.2 Management........................................................................................................... 46
2.5 Haemorrhagic shock......................................................................................................... 49
2.5.1 Investigations........................................................................................................... 49
2.5.2 Management........................................................................................................... 49
2.6 Drowning.......................................................................................................................... 50
2.6.1 Pathophysiology....................................................................................................... 50
2.6.2 Management........................................................................................................... 50
2.6.3 Investigations........................................................................................................... 52
2.6.4 Post resuscitation management.............................................................................. 52
2.7 Trauma.............................................................................................................................. 53
2.7.1 Primary survey......................................................................................................... 53
2.7.2 Secondary survey..................................................................................................... 56
2.7.3 Specific injuries........................................................................................................ 57
2.8 Head injury........................................................................................................................ 59
2.8.1 Assessment and initial management....................................................................... 59
2.8.2 Management........................................................................................................... 62
2.8.3 Raised intracranial pressure..................................................................................... 63
2.8.4 Discharge criteria..................................................................................................... 63

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2.9 Poisoning........................................................................................................................... 64
2.9.1 Diagnosis and approach to the suspected poisoned child....................................... 64
2.9.2 Initial management and approach........................................................................... 65
2.9.3 Toxic agent not known: the toxidromic approach.................................................... 66
2.9.4 Decontamination..................................................................................................... 68
2.9.5 Toxic agent known: specific treatment.................................................................... 69
2.9.6 Prevention................................................................................................................ 71

Chapter 3: Acute febrile illness


3.1 Approach to a child with fever......................................................................................... 77
3.1.1 Identifying underlying cause.................................................................................... 77
3.1.2 Investigations and management.............................................................................. 79
3.1.3 Management of fever.............................................................................................. 83
3.2 Severe bacterial infection or sepsis.................................................................................. 85
3.2.1 Clinical features........................................................................................................ 85
3.2.2 Initial management.................................................................................................. 85
3.2.3 Investigations........................................................................................................... 86
3.2.4 Ongoing management............................................................................................. 86
3.3 Meningitis and encephalitis............................................................................................. 88
3.3.1 Clinical features........................................................................................................ 88
3.3.2 Initial management.................................................................................................. 89
3.3.3 Investigations........................................................................................................... 90
3.3.4 Ongoing management............................................................................................. 92
3.3.5 Steroid therapy........................................................................................................ 93
3.3.6 Complications.......................................................................................................... 93
3.3.7 Chemoprophylaxis and prevention.......................................................................... 94
3.4 Malaria.............................................................................................................................. 95
3.4.1 Clinical features........................................................................................................ 95
3.4.2 Investigations........................................................................................................... 96
3.4.3 Management........................................................................................................... 96
3.4.4 Prognosis................................................................................................................ 102
3.4.5 Prevention.............................................................................................................. 103
3.5 Tetanus............................................................................................................................ 104
3.5.1 Clinical features...................................................................................................... 104
3.5.2 Management......................................................................................................... 105
3.5.3 Prevention.............................................................................................................. 108
3.6 Enteric (typhoid and paratyphoid) fever........................................................................ 109
3.6.1 Clinical features...................................................................................................... 109
3.6.2 Diagnosis................................................................................................................ 110
3.6.3 Management......................................................................................................... 110
3.6.4 Prevention.............................................................................................................. 112
3.7 Measles........................................................................................................................... 113
3.7.1 Clinical features...................................................................................................... 113
3.7.2 Management......................................................................................................... 114
3.7.3 Prevention.............................................................................................................. 116
3.8 Orbital and peri-orbital cellulitis.................................................................................... 117
3.8.1 Clinical features...................................................................................................... 117
3.8.2 Management......................................................................................................... 118

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Chapter 4: Respiratory conditions
4.1 Approach to a child with a respiratory complaint......................................................... 125
4.1.1 Respiratory symptoms and signs........................................................................... 125
4.1.2 Management......................................................................................................... 129
4.1.3 Respiratory support............................................................................................... 129
4.2 Croup (laryngotracheitis and laryngotracheobronchitis)............................................................132
4.2.1 Clinical features...................................................................................................... 132
4.2.2 Management......................................................................................................... 132
4.3 Epiglottitis....................................................................................................................... 136
4.3.1 Clinical features...................................................................................................... 136
4.3.2 Management......................................................................................................... 136
4.3.3 Prevention.............................................................................................................. 138
4.4 Bacterial tracheitis.......................................................................................................... 139
4.4.1 Clinical features...................................................................................................... 139
4.4.2 Management......................................................................................................... 139
4.5 Pneumonia...................................................................................................................... 141
4.5.1 Clinical features...................................................................................................... 141
4.5.2 Investigations......................................................................................................... 142
4.5.3 Management......................................................................................................... 143
4.6 Empyema........................................................................................................................ 146
4.6.1 Clinical features...................................................................................................... 146
4.6.2 Management......................................................................................................... 147
4.7 Bronchiolitis.................................................................................................................... 148
4.7.1 Clinical features...................................................................................................... 148
4.7.2 Management......................................................................................................... 148
4.8 Diphtheria....................................................................................................................... 151
4.8.1 Clinical features...................................................................................................... 151
4.8.2 Management......................................................................................................... 152
4.8.3 Prevention.............................................................................................................. 153
4.9 Pertussis (whooping cough)........................................................................................... 154
4.9.1 Clinical features...................................................................................................... 154
4.9.2 Management......................................................................................................... 154
4.9.3 Post-exposure prophylaxis..................................................................................... 156
4.9.4 Prevention.............................................................................................................. 156
4.10 Asthma.......................................................................................................................... 157
4.10.1 Acute exacerbation of asthma............................................................................. 157
4.10.2 General management of asthma......................................................................... 161
4.10.3 Asthma education and action plan...................................................................... 164
4.11 Tuberculosis.................................................................................................................. 166
4.11.1 Stages of infection............................................................................................... 166
4.11.2 Clinical features.................................................................................................... 166
4.11.3 Diagnostic approach............................................................................................ 168
4.11.4 Investigations....................................................................................................... 169
4.11.5 Paediatric diagnostic algorithms.......................................................................... 170
4.11.6 Management....................................................................................................... 173
4.11.7 Prevention and screening.................................................................................... 175

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4.12 Mastoiditis.................................................................................................................... 177
4.12.1 Clinical features.................................................................................................... 177
4.12.2 Management....................................................................................................... 177

Chapter 5: Gastrointestinal conditions


5.1 Vomiting.......................................................................................................................... 187
5.1.1 Assessment............................................................................................................ 187
5.1.2 Management......................................................................................................... 188
5.2 Diarrhoea........................................................................................................................ 189
5.2.1 Acute diarrhoea..................................................................................................... 189
5.2.2 Specific considerations for children with malnutrition.......................................... 192
5.2.3 Persistent diarrhoea............................................................................................... 192
5.3 Dehydration.................................................................................................................... 194
5.3.1 Non-malnourished children................................................................................... 194
5.3.2 Children with severe acute malnutrition (SAM).................................................... 198
5.4 Approach to a child with acute abdominal pain............................................................ 202
5.4.1 Identifying underlying cause.................................................................................. 202
5.4.2 Initial management................................................................................................ 204
5.5 Intussusception............................................................................................................... 205
5.5.1 Clinical features...................................................................................................... 205
5.5.2 Management......................................................................................................... 206
5.6 Acute appendicitis.......................................................................................................... 207
5.6.1 Clinical features...................................................................................................... 207
5.6.2 Management......................................................................................................... 207
5.7 Bowel Obstruction.......................................................................................................... 209
5.7.1 Clinical features...................................................................................................... 209
5.7.2 Causes of acute bowel obstruction........................................................................ 210
5.8 Pyloric stenosis............................................................................................................... 213
5.8.1 Clinical features...................................................................................................... 213
5.8.2 Management......................................................................................................... 213

Chapter 6: Cardiology
6.1 Introduction.................................................................................................................... 221
6.2 Cardiac failure................................................................................................................. 222
6.2.1 Clinical signs and assessment................................................................................ 222
6.2.2 Investigations......................................................................................................... 222
6.2.3 Management......................................................................................................... 223
6.2.4 Follow-up............................................................................................................... 224
6.2.5 Treatment of any reversible causes....................................................................... 224
6.3 Acute rheumatic fever.................................................................................................... 225
6.3.1 Diagnosis................................................................................................................ 225
6.3.2 Management......................................................................................................... 226
6.3.3 Prevention.............................................................................................................. 226
6.4 Infantile beriberi............................................................................................................. 227

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Chapter 7: Neurological disorders
7.1 Neurological assessment................................................................................................ 231
7.2 Acute symptomatic seizures........................................................................................... 233
7.2.1 Terminology........................................................................................................... 233
7.2.2 Clinical features...................................................................................................... 233
7.2.3 Management......................................................................................................... 234
7.2.4 Management if acute seizures resume.................................................................. 238
7.2.5 Management of post-ictal state............................................................................. 238
7.2.6 Follow-up............................................................................................................... 238
7.3 Febrile seizures............................................................................................................... 240
7.3.1 Diagnosis................................................................................................................ 240
7.3.2 Management......................................................................................................... 240
7.4 Epilepsy........................................................................................................................... 241
7.4.1 Assessment and diagnosis..................................................................................... 241
7.4.2 Classification of seizures........................................................................................ 241
7.4.3 Management......................................................................................................... 242
7.4.4 Follow-up and monitoring..................................................................................... 244
7.5 Altered level of consciousness....................................................................................... 245
7.5.1 Clinical features and assessment........................................................................... 245
7.5.2 Management......................................................................................................... 246

Chapter 8: Renal and genitourinary tract


8.1 Upper urinary tract infection (pyelonephritis).............................................................. 255
8.1.1 Clinical features...................................................................................................... 255
8.1.2 Investigations......................................................................................................... 256
8.1.3 Management......................................................................................................... 257
8.1.4 Follow-up............................................................................................................... 258
8.2 Post-infectious glomerulonephritis................................................................................ 259
8.2.1 Clinical features...................................................................................................... 259
8.2.2 Investigations......................................................................................................... 259
8.2.3 Management......................................................................................................... 259
8.3 Nephrotic syndrome....................................................................................................... 261
8.3.1 Clinical features...................................................................................................... 261
8.3.2 Investigations......................................................................................................... 262
8.3.3 Management......................................................................................................... 262
8.3.4 Prognosis................................................................................................................ 264
8.4 Acute kidney injury......................................................................................................... 265
8.4.1 Classification and causes........................................................................................ 265
8.4.2 Clinical features...................................................................................................... 266
8.4.3 Investigations......................................................................................................... 266
8.4.4 Management......................................................................................................... 267
8.4.5 Prognosis................................................................................................................ 269
8.5 Acute painful scrotum.................................................................................................... 270
8.5.1 Clinical features...................................................................................................... 270
8.5.2 Investigations......................................................................................................... 272
8.5.3 Management......................................................................................................... 272

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8.6 Paraphimosis................................................................................................................... 273
8.6.1 Clinical features...................................................................................................... 273
8.6.2 Management......................................................................................................... 273

Chapter 9: Endocrinology
9.1 Diabetes mellitus (type 1).............................................................................................. 281
9.1.1 Diagnosis................................................................................................................ 281
9.1.2 Management......................................................................................................... 282
9.2 Diabetic ketoacidosis...................................................................................................... 283
9.2.1 Diagnosis................................................................................................................ 283
9.2.2 Management......................................................................................................... 284
9.2.3 Management of complications.............................................................................. 289
9.2.4 Resolution of DKA and transition to subcutaneous (SC) insulin............................. 291
9.2.5 Discharge criteria and follow-up............................................................................ 293
9.3 Hypoglycaemia............................................................................................................... 294
9.3.1 Clinical features and assessment........................................................................... 294
9.3.2 Management......................................................................................................... 295

Chapter 10: Haematology


10.1 Anaemia........................................................................................................................ 299
10.1.1 Clinical features and history................................................................................. 300
10.1.2 Management....................................................................................................... 301
10.1.3 Specific considerations in children with SAM...................................................... 303
10.2 Sickle cell disease.......................................................................................................... 304
10.2.1 Clinical features.................................................................................................... 304
10.2.2 Acute painful or vaso-occlusive crisis (VOC)........................................................ 305
10.2.3 Febrile illness....................................................................................................... 306
10.2.4 Acute chest syndrome (ACS)................................................................................ 307
10.2.5 Acute anaemia in SCD.......................................................................................... 307
10.2.6 Splenic sequestration........................................................................................... 308
10.2.7 Aplastic crisis........................................................................................................ 309
10.2.8 Stroke................................................................................................................... 309
10.2.9 Priapism............................................................................................................... 310
10.2.10 Prevention of complications.............................................................................. 310

Chapter 11: Bone and joint problems


11.1 Introduction.................................................................................................................. 317
11.2 Approach to a child presenting with a limp................................................................. 318
11.2.1 Identifying underlying cause................................................................................ 318
11.2.2 Specific common causes of limp.......................................................................... 319
11.3 Pulled elbow................................................................................................................. 321
11.4 Osteomyelitis................................................................................................................ 322
11.4.1 Clinical features.................................................................................................... 322
11.4.2 Management....................................................................................................... 323
11.4.3 Chronic osteomyelitis........................................................................................... 324

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11.5 Septic arthritis............................................................................................................... 326
11.5.1 Clinical features.................................................................................................... 326
11.5.2 Management....................................................................................................... 327

Chapter 12: Medical complications specific to children with severe acute malnutrition (SAM)
12.1 Introduction.................................................................................................................. 333
12.2 Re-nutrition (osmotic) diarrhoea................................................................................. 334
12.2.1 Clinical features and assessment......................................................................... 334
12.2.2 Management....................................................................................................... 334
12.3 Refeeding syndrome..................................................................................................... 336
12.3.1 Clinical features and assessment......................................................................... 336
12.3.2 Management....................................................................................................... 337
12.3.3 Prognosis.............................................................................................................. 337
12.4 Paralytic ileus (acute abdominal distension)............................................................... 338
12.4.1 Clinical features and assessment......................................................................... 338
12.4.2 Management....................................................................................................... 338
12.4.3 Monitoring........................................................................................................... 339
12.5 Persistent oedema........................................................................................................ 340
12.5.1 Clinical features and assessment......................................................................... 340
12.5.2 Management....................................................................................................... 340
12.6 Kwashiorkor skin lesions.............................................................................................. 342
12.6.1 Management....................................................................................................... 342
12.6.2 Antibiotics for infected lesions............................................................................. 344

Chapter 13: HIV Infection


13.1 Introduction.................................................................................................................. 349
13.2 Key recommendations.................................................................................................. 350
13.3 Diagnosis....................................................................................................................... 351
13.4 Management................................................................................................................. 352
13.4.1 Initial management.............................................................................................. 352
13.4.2 Start antiretroviral treatment.............................................................................. 357
13.4.3 HIV and tuberculosis co-infection........................................................................ 358
13.4.4 Co-trimoxazole prophylaxis.................................................................................. 358
13.5 Prevention of Mother to Child Transmission (PMTCT)..............................................................360
13.6 Prior to discharge.......................................................................................................... 361

Chapter 14: Fever of unknown origin (FUO) and neglected tropical diseases (NTDs)
14.1 Fever of unknown origin (FUO).................................................................................... 365
14.1.1 Causes.................................................................................................................. 365
14.1.2 Clinical features.................................................................................................... 365
14.1.3 Investigations....................................................................................................... 366
14.1.4 Management....................................................................................................... 366

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14.2 Leishmaniasis................................................................................................................ 372
14.2.1 Visceral leishmaniasis (kala-azar)......................................................................... 372
14.2.2 Cutaneous leishmaniasis...................................................................................... 374
14.2.3 Post-kala-azar dermal leishmaniasis (PKDL)......................................................... 377
14.3 Noma (cancrum oris).................................................................................................... 378
14.3.1 Clinical features.................................................................................................... 378
14.3.2 Management....................................................................................................... 379
14.3.3 Prognosis.............................................................................................................. 382
14.3.4 Prevention............................................................................................................ 382

Chapter 15: Supportive care in hospital


15.1 Oxygen therapy............................................................................................................. 387
15.1.1 Modes of delivery................................................................................................ 387
15.1.2 Monitoring........................................................................................................... 389
15.1.3 Weaning............................................................................................................... 390
15.2 Parenteral fluids............................................................................................................ 391
15.2.1 Maintenance fluid composition........................................................................... 391
15.2.2 Calculating maintenance fluid rate...................................................................... 391
15.2.3 Potassium in maintenance fluids......................................................................... 393
15.2.4 Monitoring........................................................................................................... 395
15.3 Electrolyte abnormalities............................................................................................. 396
15.3.1 Normal electrolyte ranges................................................................................... 396
15.3.2 Sodium disorders................................................................................................. 397
15.3.3 Potassium disorders............................................................................................. 401
15.3.4 Calcium disorders................................................................................................. 403
15.4 Pain management......................................................................................................... 405
15.4.1 Assessment.......................................................................................................... 405
15.4.2 Management....................................................................................................... 407
15.4.3 Chronic pain......................................................................................................... 411
15.4.4 Considerations for children with severe acute malnutrition (SAM)..................... 411
15.4.5 Neuropathic pain................................................................................................. 412
15.4.6 Sedation or analgesia before a painful procedure............................................... 412
15.5 Nutritional support for the critically unwell child....................................................... 414
15.5.1 Indications for enteral nutrition........................................................................... 414
15.5.2 Enteral nutrition products.................................................................................... 415
15.5.3 Daily fluid requirements...................................................................................... 416
15.5.4 Energy requirements in critical illness................................................................. 416
15.5.5 Calculating target daily enteral feed volumes in the acute phase of
critical illness........................................................................................................ 417
15.5.6 Administration of enteral feeds........................................................................... 418
15.5.7 Advancing enteral feeds....................................................................................... 419
15.6 Palliative care................................................................................................................ 420
15.6.1 Symptom management....................................................................................... 420
15.6.2 Communication.................................................................................................... 422
15.6.3 Psychosocial support........................................................................................... 423

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Appendices
1. Developmental milestones................................................................................................ 429
2. WHO growth charts for children....................................................................................... 432
3. Paediatric vital signs.......................................................................................................... 436
4. Oropharyngeal airway insertion........................................................................................ 438
5. Intraosseous needle insertion........................................................................................... 439
6. Performing a lumbar puncture.......................................................................................... 443
7. Clinical Respiratory Score (CRS)......................................................................................... 446
8. Asthma action plan............................................................................................................ 447
9. How to make a spacer with a plastic bottle....................................................................... 448
10. Inhaler technique using a spacer..................................................................................... 449
11. Sputum specimen collection in children......................................................................... 451
12. WHO rehydration plans A, B and C.................................................................................. 453
13. Glasgow and Blantyre Coma Scales................................................................................. 454
14. Urinary collection procedures......................................................................................... 457
15. Suprapubic aspiration of urine........................................................................................ 463
16. Body surface area estimation in children........................................................................ 466
17. Blood pressure centiles for age....................................................................................... 467
18. F-75 feed volumes in Phase 1.......................................................................................... 468
19. ARV prophylaxis in PMTCT............................................................................................... 469
20. Causes of fever of unknown origin (FUO)........................................................................ 471
21. EVENDOL chart................................................................................................................ 477
22. Daily enteral feed volumes and administration in critically unwell children................... 478

14
Abbreviations and acronyms

ADH Antidiuretic hormone


AIDS Acquired immune-deficiency syndrome
AKI Acute kidney injury
ALS Advanced life support
AP Anterior-Posterior
ATN Acute tubular necrosis
AXR Abdominal x-ray
BC Blood culture
BGL Blood glucose level
BLS Basic life support
BMI Body mass index
BMR Basal metabolic rate
BP Blood pressure
BSA Body surface area
BUN Blood urea nitrogen
CCAM Congenital cystic adenomatoid malformation
CSF Cerebrospinal fluid
CHD Congenital heart disease
CMV Cytomegalovirus
CPR Cardiopulmonary resuscitation
CRP C-reactive protein
CRT Capillary refill time
CSF Cerebrospinal fluid
CT Computed tomography
CXR Chest x-ray
DD Developmental delay
DKA Diabetic ketoacidosis
DR-TB Drug-resistant tuberculosis
DS-TB Drug-sensitive tuberculosis
ECG Electrocardiogram
EFAST Extended focused assessment with sonography in trauma
ENT Ear, Nose and Throat
EPI Expanded Programme on Immunisation
ESR Erythrocyte sedimentation rate
FBC Full blood count
FR Frequent relapses
FSGS Focal segmental glomerulosclerosis

15
G5% Glucose (dextrose) 5%
GCS Glasgow Coma Scale
GFR/eGFR Glomerular filtration rate/estimated GFR
Hb Haemoglobin
HIV Human immunodeficiency virus
HR Heart rate
HUS Haemolytic uraemic syndrome
ICU Intensive care unit
IPD Inpatient department
ITFC Inpatient therapeutic feeding centre
IUGR Intrauterine growth retardation
LOC Level of consciousness
LUS Lung ultrasound
MCD Minimal change disease
MUAC Mid-upper arm circumference
MVA Motor vehicle accident
NaCl Sodium chloride
NBM Nil by mouth
NGT Nasogastric tube
NSAID Non-steroidal anti-inflammatory
OGT Orogastric tube
OPD Outpatient department
ORS Oral rehydration salts
PCR Polymerase chain reaction
PIGN Post-infectious glomerulonephritis
POCUS Point-of-care ultrasound
PRBC Packed red blood cells
ReSoMal Rehydration solution for malnutrition
RL Ringer lactate
RR Respiratory rate
SDNS Steroid-dependent nephrotic syndrome
SPA Suprapubic aspirate
SpO2 Oxygen saturation
SRNS Steroid-resistant nephrotic syndrome
SSNS Steroid-sensitive nephrotic syndrome
T1DM Type 1 diabetes mellitus
TB Tuberculosis
US Ultrasound
UTI Urinary tract infection
WBC White blood cells

16
1

Chapter 1:
Paediatric history and clinical examination

1.1 Introduction............................................................................................................. 19
1.2 Taking a paediatric history...................................................................................... 20
1.3 Clinical examination................................................................................................ 22
Chapter 1: Paediatric history and clinical examination
1

1.1 Introduction

This chapter outlines how to take a comprehensive paediatric history and perform a full clinical
examination in a child. It is not always necessary to take a complete history, the scope and
detail are determined by the nature of the presenting complaint and/or the child’s age. For
example, birth and developmental history may provide important information to support the
correct diagnosis and management of a young child, while social and past medical history may
be more relevant in older children. For adolescents, consider that they may prefer to provide
their history or be examined without the presence of their parents/carers.

19
Chapter 1: Paediatric history and clinical examination

1.2 Taking a paediatric history

Patient profile
– Age (in months for children < 2 years)
– Gender
– Relationship to accompanying adult

Presenting complaint
– Main problem or symptoms
– If child was referred from another facility, note main reason for referral

History of presenting complaint


– When and how symptoms started. If several symptoms, order of onset
– Previous episodes
– Siblings or other household members with similar illness
– In infants and younger children, ask about:
• Feeding (any changes to pattern, volume)
• Bowel movements, wet nappies
• Sleeping pattern, alertness, activity
• Weight gain or loss

Past medical history


– Previous illnesses, major injuries, hospital admissions
– Vaccination status (ask for vaccination card if available); note missing vaccinations for age

Medication history
– Current or recent medications
– Traditional treatments used (medicines or procedures, e.g. uvula excision, scarification,
circumcision)
– Known allergies

Birth history
– Maternal age
– Obstetric history:
• Total number of pregnancies and their outcomes
• Complications during pregnancy
• HIV status: if maternal HIV status is positive, note whether adequate prophylaxis for
prevention of mother-to-child transmission (PMTCT) received; if early infant diagnosis
(EID) done, including available results
• Tuberculosis: if maternal tuberculosis or any household TB contacts, note whether
isoniazid prophylaxis was taken and completed
• Malaria
• Nutritional status
• Supplements: folic acid, vitamin D, multivitamins

20
Chapter 1: Paediatric history and clinical examination
1

– Delivery:
• Assisted: by a skilled (or traditional) birth attendant, midwife and/or obstetrician
• Location: at a health facility or at home
– Any problems during delivery:
• Foetal distress
• Use of instruments (e.g. forceps, vacuum)
• Breech, footling breech
• Caesarean section
– Gestational age, birth weight, and Apgar score (if available)
– Any problems with breathing or injuries at birth:
• Admission to neonatal care unit
• Jaundice
• Infection
• Feeding problems

Developmental history
– Age when key milestones achieved and current developmental stage (see Appendix 1)
– School-age child: any specific problems (academically, physically, socially with peers)
– Behavioural concerns for age: aggression, isolation, self-harm, addictions

Family history
– Any illnesses, diseases or conditions in the family, especially amongst children
– Directly ask about: tuberculosis, sickle cell disease, severe anaemia, thalassaemia, epilepsy,
diabetes, hypertension, asthma

Social history
– Ask about the child’s living situation and conditions
– Family structure: primary carer, number of siblings
– School attendance (includes religious school)
– Concerns with safety or food security
– Context: refugee or internally displaced persons (IDP) camp or settlement; area affected by
conflict, epidemic, isolation; part of neglected or targeted population (based on religion,
location, tribe, ethnic group, political affiliation).

21
Chapter 1: Paediatric history and clinical examination

1.3 Clinical examination

Tips
– Observe the child and their interaction with parents/carers.
– Get down to the child’s level as much as possible; avoid towering over them.
– Try to gain the child’s trust.
– Avoid fully undressing the child – undress partially to expose the area to be examined.
– If the child is calm and not distressed, take the opportunity to examine the cardiac, respiratory
and neurological systems first.
– Leave examinations that can upset the child (e.g. ear, nose, throat and mouth) and
examination of any painful areas until last.
– Examine young children (6 months to 3 years) as much as possible on the parent’s/carer’s
lap.
– Use toys to distract the child during the examination.
– Communicate directly with the child: children 5 to 12 years will usually be co-operative if
they are informed about what is going to be examined and how.
– Respect privacy: adolescents may prefer not to be examined in front of their parents/carers;
ask them their preference.
– Respect local cultural norms regarding gender of patient and clinician performing
examination.
– Be honest: if something is going to hurt, tell the child in a calm fashion.

General appearance
– Note obvious features: well/unwell, active/lethargic, uncomfortable, irritable, distressed, in
pain, malnourished.
– Observe for obvious difficulty breathing, e.g. sitting upright and holding self-up with
extended arms.
– Note any jaundice, anaemia, cyanosis, clubbing, oedema, lymphadenopathy.
– Specifically look for rashes, petechiae, skin turgor (pinch test for dehydration).

Vital sign measurements


– Measure weight and height and plot on centile chart (see Appendix 2).
– Measure head circumference if < 3 years and plot on centile chart (see Appendix 2).
– Measure and document heart rate, respiratory rate, oxygen saturation (SpO2) and axillary
temperature, comparing to normal for age (see below and Appendix 3):
Respiratory rate Heart rate
Age
normal range (breaths/min) normal range (beats/min)
< 2 months 30-60 100-160
2 to 11 months 30-50 90-160
1 to 5 years 25-40 80-140
6 to 12 years 20-30 70-120
> 12 years 14-20 60-100

22
Chapter 1: Paediatric history and clinical examination
1

– Evaluate nutritional status (select relevant parameter):

Parameter Indication

Weight-for-height or -length (W/H or L) Wasting, overweight

Height-for-age (H/A) Stunting

Weight-for-age (W/A) Underweight

Body Mass Index (BMI) Under- or overweight

Mid-upper arm circumference (MUAC) Wasting

Head and neck


– Children < 24 months: check anterior fontanelle with child in upright position. Persistent
bulging or tense fontanelle can indicate raised intracranial pressure. Sunken fontanelle may
indicate dehydration or malnutrition.
– Hair: check for signs of kwashiorkor (loss of colour, fragile, dry and brittle).
– Neck: palpate thyroid, check for any cysts or lymphadenopathy.
– Eyes/conjunctivae: note any abnormalities or signs of infection, PERLA (pupils equal and
reactive to light and accommodation).
– Ears: check tympanic membranes with otoscope.
– Nose: check nostrils (any foreign bodies, visible polyps, septal deviation).
– Throat: check tonsils (size, colour, presence of exudate) and back of throat (clear airway).
– Mouth: check for cleft palate, palpate for retro-auricular and submandibular
lymphadenopathies, and check teeth (number and general hygiene).

Cardiovascular
– Measure: Heart rate (HR), blood pressure (BP), capillary refill time (CRT).
– Pulses: brachial in infants, femoral or radial in older children.
– Palpate: location of apex beat, character of apex beat (heaving/thrusting, hyperdynamic,
tapping).
– Auscultate: heart sounds, rhythm, any murmurs.

Respiratory
– Measure: Respiratory rate (RR), oxygen saturation (SpO2), presence of cyanosis.
– Breathing effort: tracheal tug, use of accessory muscles, chest indrawing, nasal flaring.
– Percussion: dullness may indicate consolidation (pneumonia, empyema, pleural effusion);
hyper-resonance may indicate pneumothorax.
– Auscultation: equal/unequal breath sounds; presence of rales, crepitations, stridor (indicates
upper airway obstruction), wheeze or rhonchi; transmitted upper airway noises or voice
sounds.

Abdomen
– Check for distension, visible masses, peristalsis, hernias.
– Palpate abdomen: superficial palpation then deep palpation, noting tenderness (avoid any
known tender area until the end of the exam), rebound tenderness or guarding. If pain
is significant, lightly percuss the abdomen rather than palpating – percussion tenderness
indicates peritonitis.
– Feel for liver and spleen: note any hepatomegaly or splenomegaly and any tenderness.

23
Chapter 1: Paediatric history and clinical examination

– Feel for kidneys: palpate the flank area to check for a renal mass; tap gently with the ulnar
part of your hand to examine for signs of pyelonephritis.
– Auscultate for bowel sounds: overactive bowel sounds are present with gastroenteritis;
bowel sounds are often decreased in appendicitis; absent or tinkling bowel sounds indicate
intestinal obstruction.
– Check for ascites (if clinically relevant): ask the child to lie flat on their back and percuss
from periphery of abdomen towards the umbilicus. If ascites is present, it will be dull to
percussion initially, becoming tympanic towards the umbilicus. Note the level of ascites,
that corresponds to the change in percussion note. Another technique for ascites detection
is to ask the patient or parent/carer to place a hand in the midline of their abdomen, while
the examiner taps one flank side of the abdomen with the palm of their other hand resting
on the opposite flank area; a fluid wave will be felt in the palm of their hand if ascites is
present.

Musculoskeletal
– Ask child to walk and observe gait and any limp.
– Where relevant, examine: the back for kyphosis, lordosis or scoliosis; extremities for any
muscle atrophy; affected joints (range of motion, stability, any swelling or tenderness).

Neurological
– Note level of consciousness (AVPU, see Appendix 3), neck stiffness (nuchal rigidity).
– Tone: check for hypotonia or hypertonia. For infants over 6 months, pull gently by the arms
to a sitting position and check for head lag, too weak to sit or any stiffness.
– Reflexes: test patellar reflex by tapping the patellar tendon with a reflex hammer.
– Ask the child to walk, walk heel-to-toe, and stand on one leg. Note any abnormalities.
– If any neurologic or neuromuscular abnormalities are detected or suspected, perform a full
neurological examination (Chapter 7, Section 7.1) and developmental assessment (compare
to milestones in Appendix 1).

External genitalia
– Check for any hernias, hydroceles (accumulation of fluids inside scrotum) or cryptorchidism
(absence of one or both testes from the scrotum).
– In girls, check and note any scarring or signs of female genital mutilation (be discreet and
sensitive to the context).
– Rectal examination should only be done when there is a specific indication.

24
Chapter 2: 2
Emergencies

2.1 Resuscitation............................................................................................................ 27
2.1.1 Basic life support.............................................................................................. 27
2.1.2 Advanced life support...................................................................................... 32
2.2 Circulatory impairment and shock.......................................................................... 35
2.2.1 Classification of circulatory impairment and shock.........................................35
2.2.2 Clinical features............................................................................................... 36
2.2.3 Immediate management................................................................................. 36
2.2.4 Monitoring and further management.............................................................38
2.2.5 Further critical care management when intensive care is available................40
2.3 Choking.................................................................................................................... 42
2.4 Anaphylaxis.............................................................................................................. 46
2.4.1 Clinical features and diagnostic criteria...........................................................46
2.4.2 Management................................................................................................... 46
2.5 Haemorrhagic shock................................................................................................ 49
2.5.1 Investigations................................................................................................... 49
2.5.2 Management................................................................................................... 49
2.6 Drowning................................................................................................................. 50
2.6.1 Pathophysiology............................................................................................... 50
2.6.2 Management................................................................................................... 50
2.6.3 Investigations................................................................................................... 52
2.6.4 Post resuscitation management...................................................................... 52
2.7 Trauma..................................................................................................................... 53
2.7.1 Primary survey................................................................................................. 53
2.7.2 Secondary survey............................................................................................. 56
2.7.3 Specific injuries................................................................................................ 57
2.8 Head injury............................................................................................................... 59
2.8.1 Assessment and initial management...............................................................59
2.8.2 Management................................................................................................... 62
2.8.3 Raised intracranial pressure............................................................................ 63
2.8.4 Discharge criteria............................................................................................. 63
2.9 Poisoning.................................................................................................................. 64
2.9.1 Diagnosis and approach to the suspected poisoned child...............................64
2.9.2 Initial management and approach.................................................................. 65
2.9.3 Toxic agent not known: the toxidromic approach............................................66
2.9.4 Decontamination............................................................................................. 68
2.9.5 Toxic agent known: specific treatment............................................................69
2.9.6 Prevention........................................................................................................ 71
References Chapter 2..................................................................................................... 72
Chapter 2: Emergencies

2.1 Resuscitation 2

Cardiopulmonary arrest in children usually has a very poor outcome. Paediatric cardiopulmonary
arrest occurs most commonly secondary to respiratory or circulatory failure, and less frequently
due to a primary cardiac cause such as an arrhythmia1, unlike in adults. Primary respiratory
arrest may occur with drowning or poisoning. To optimize survival, imminent cardiopulmonary
arrest can be prevented in a seriously ill or injured child with early and effective resuscitation
by providing basic and/or advanced life support.
Basic life support (BLS) can be performed by any healthcare worker in any setting. The objective
is to rapidly assess for signs of respiratory or circulatory problems and to take immediate steps
to support the airway (A), breathing (B) and circulation (C). Advanced life support (ALS) should
be performed in hospitals and emergency departments with adequate staffing and training.

2.1.1 Basic life support


Based on European Resuscitation Council Guidelines 20211, see Figure 2.4 page 31 for
algorithm.
Before approaching the child, briefly check that the area is safe and shout for help from
bystanders.

Is the child responsive?


Stimulate the child and ask loudly if they are ok.
– Yes, child responds, cries or moves:
• Evaluate their condition and request help.
• Monitor closely.
– No, child does not respond:
• If there is more than one rescuer, call for advanced support as soon as unconsciousness is
recognised.
• Turn the child carefully onto their back (immobilise cervical spine first if likely spinal injury,
see Section 2.7.1, though this should not take priority over resuscitation).
• Open airway: simultaneously tilt the head back gently by placing one hand on the
forehead, and lift the chin by placing the fingertips of the other hand under the chin (see
Figure 2.1a). Be careful, especially in infants, not to push down on the soft tissues of the
neck.
• If unable to open airway this way, try a two-handed jaw thrust: standing at the child’s
head, place thumbs gently on the child’s cheeks and put first two fingers of each hand
behind the angle of the jaw to push mandible forwards (see Figure 2.1b).
• Maintain the airway in a neutral position for infants (< 1 year), using a small roll under
shoulder blades if necessary due to their prominent occiput, and in slight extension
(‘sniffing position’) for children (see Figure 2.1c and Figure 2.1d). Avoid hyperextending
the neck as this may obstruct the airway.

27
Chapter 2: Emergencies

Figures 2.1 - Airway manoeuvres for paediatric BLS


2.1a - Head tilt-chin lift 2.1b - Jaw thrust

2.1c - Neutral airway position (< 1 year) 2.1d - Sniffing position (≥ 1 year old)

Is the child breathing?


Keeping the airway open (as above), put your face close to the child’s face so that your cheek
and ear are directly above the nose and mouth of the child, looking towards their chest. Then
look, listen and feel for maximum 10 seconds: look for chest movement; listen for breath
sounds; feel for air movement against your cheek.
– Yes, breathing normally:
• Place into recovery position
• Call for help
• Monitor breathing.
– No, not breathing normally:
• Remove any obvious and/or visible airway obstruction carefully. Take caution not to push
objects deeper or damage the airway during attempts for removal.
• Give 5 rescue breaths (see below for details).
Rescue breaths
Bag-mask ventilation (with self-inflating bag):
– Choose the correct size and shape of face mask to get a good seal around the mouth and
nose. The mask should cover the mouth and nose without pressing down on either, and
without covering the eyes. If the child is between sizes, the larger size is usually better.

28
Chapter 2: Emergencies

– Choose the correct ventilation bag size according to weight: 2


• < 10 kg: neonatal (volume 320 mL)
• 10 to 30 kg: paediatric (volume 600-700 mL)
• ≥ 30 kg: adult (volume > 1000 mL)
– Use the E-C clamp technique (Figure 2.2) to lift the jaw against the mask, pressing and sealing
the mask on the face:
• Position the third, fourth and fifth fingers of one hand (forming an “E” shape) along the
jaw to lift it upwards.
• Next, use the thumb and index finger of the same hand (forming a “C” shape) to hold the
mask onto the face, ensuring a good seal.
• Avoid pressure on the soft tissues underneath the chin because this can push the tongue
into the posterior pharynx, resulting in airway compression and obstruction.
– With the other hand, squeeze the ventilation bag until the chest rises. Deliver each breath
over 1 second, making sure the chest rises with each breath. Avoid excessive ventilation,
aiming to deliver one ventilation breath every 2-3 seconds.
– In older children, it may be difficult to achieve a good seal with one hand therefore a two-
handed technique can be used when there are two rescuers available. Use the E-C clamp
technique with both hands to hold the mask onto the face, while a second rescuer squeezes
the ventilation bag.

Figure 2.2 - E-C clamp technique for bag-mask ventilation

Are there signs of life?


Clear signs of life: Any movement, coughing, breathing (gasping or infrequent irregular breaths
are not normal breathing).
– Yes, clear signs of life:
• Continue to give rescue breaths at a rate of approximately one breath every 2-3 seconds
until child breathing well.
• Monitor carefully.

29
Chapter 2: Emergencies

– No, no clear signs of lifea:


• Immediately start cardiopulmonary resuscitation (CPR):
▹ Give 15 chest compressions (see below for details) followed by 2 rescue breaths.
▹ Continue providing CPR with chest compressions and breaths at a ratio of 15:2 until
child shows signs of life (waking up, moving, opening eyes, breathing normally).

High Quality CPR


• Rate 100-120 compressions/min for both infants and children.
• Compression depth to at least 1/3 of the anterior-posterior diameter of chest, being
sure not to exceed the adult limit of 6 cm in larger children.
• Allow complete chest recoil after each compression and avoid leaning on the chest.
• Minimise interruptions in chest compressions.
• Avoid excessive ventilation.
• Ideally perform chest compressions on a firm surface.

Chest compressions
– In all infants and children, chest compressions are done on the lower half of the sternum:
• In infants: chest compressions are given just below the inter-nipple line. If one rescuer,
use two fingertips to compress the chest (Figure 2.3a); if two rescuers, use two thumbs by
encircling hands around chest to do compressions (Figure 2.3b). Compress to at least 1/3
of anterior-posterior depth of chest.
• In children: trace the lowest ribs to the middle of the chest to locate the xiphisternum.
Place the heel of one hand on the sternum one finger breadth above the xiphisternum,
ensuring that the fingers are lifted off the chest to avoid restricting chest movement.
Position yourself directly above the child’s chest and, keeping the arm straight, compress
the chest. For larger children, both hands with fingers interlocked can be used.
– Depress sternum by at least 1/3 of anterior-posterior depth of chest (maximum 6 cm1) with
each compression, then release pressure completely. Continue at a rate of 100-120/minute.
– After 15 compressions, repeat head tilt-chin lift and give 2 breaths. If there are two rescuers,
one should remain focused on the airway to maintain the correct position, while the other
carries out chest compressions (and squeezes the ventilation bag if a two-handed ventilation
technique is used).
Figures 2.3 - Hand positions for chest compressions in infants
2.3a - One rescuer technique 2.3b -Two rescuers technique

a New ERC guidance no longer recommends checking for a pulse before starting chest compressions.

30
Chapter 2: Emergencies

Figure 2.4 - Paediatric basic life support algorithm, European Resuscitation Council (ERC)b 2

b Reprinted from European Resuscitation Council Guidelines 2021: Paediatric Life Support, with permission from
European Resuscitation Council. Copyright European Resuscitation Council – www.erc.edu – 2023_NGL_008.

31
Chapter 2: Emergencies

2.1.2 Advanced life support


This section applies to settings where paediatric emergency care and resources are available.
– In any seriously ill or injured child, approach emergency management based on the principles
of ABCDE, where A is airway, B is breathing, C is circulation, D is disability, and E is exposure.
– The aim is to support vital functions (respiratory, circulatory, neurological) and stabilise the
patient. Without treatment, decompensation of respiratory or circulatory failure will lead to
cardiopulmonary arrest.
– In emergency care settings, a team leaderc should be pre-identified to coordinate the
management, ensure treatment sequence and rapidly identify changes in the child’s
condition (improvement or deterioration).
If the child is unresponsive, follow the BLS algorithm (Section 2.1.1) to determine the need for
CPR before doing an advanced ABCDE assessment. Otherwise assess and manage ABCDE in
any seriously unwell or injured child as follows:

Assess A (airway) and B (breathing)


– Check airway patency.
– Check respiratory rate (RR) and oxygen saturation (SpO2).
– Assess for signs of respiratory distress or failure:
• Increased respiratory effort: nasal flaring, retractions (subcostal, substernal, intercostal),
head bobbing, grunting (infants).
• Abnormal RR: too fast or too slow (see Chapter 1, Section 1.3 and Appendix 3).
• Inefficient breathing: shallow breathing, irregular breathing, decreased chest expansion.
• Decreased air entry on auscultation.
• Hypoxia: visible cyanosis or SpO2 < 94%.

Manage A (airway) and B (breathing)


– Open and clear the airway (see BLS guidance (Section 2.1.1) for more details). Remove any
obvious airway obstruction carefully.
– Insert an airway adjunct to maintain a patent airway if necessary. Use an oropharyngeal
airway in an unconscious child with no gag reflex (see Appendix 4 for insertion method).
– Administer high-flow oxygen (> 6 L/min) via mask (use non-rebreathing mask if available),
aiming for SpO2 > 94%.
– Assist ventilation and oxygenation with bag-mask ventilation if needed.
– Identify and treat any critical conditions immediately.

Assess C (circulation)
– Check heart rate (HR); capillary refill time (CRT); blood pressure (BP, only if capacity to be
done quickly and accurately); character of pulse.
– Look for signs of circulatory impairment:
• Weak radial pulse, or severe tachycardiad
• Lower limb temperature gradiente
• CRT of 3 or more seconds.
All 3 signs of circulatory impairment present: the child is in shock.
Slow HR and low BP: the child is decompensating; start BLS.

c If HR capacity is limited, the team leader should be involved in the resuscitation, but preferably only in minor
tasks so as to keep an overview of the resuscitation.
d Severe tachycardia is HR > 180 bpm in children < 12 months, > 160 bpm in children 1 to 5 years, > 140 bpm in
children > 5 years.
e The temperature gradient is assessed by running the back of hand from the toe to the knee; a positive
temperature gradient is defined as a notable temperature change from cold (dorsum of foot) to warm (knee).

32
Chapter 2: Emergencies

– Assess for active bleeding, pallor and dehydration. 2


– Assess for signs of inadequate perfusion to other organs:
• Altered level of consciousness
• Signs of respiratory distress (common in children with severe anaemia)
• Decreased urine output (based on history from parents/carers including fewer wet nappies).

Manage C (circulation)
– Obtain vascular access (IV/IO). If unable to get IV access after 3 attempts or maximum
90 seconds, insert IO needle (see MSF Manual of Nursing Care Procedures, Procedure:
Peripheral intravenous catheter for details on gaining IV access and MSF Manual of Nursing
Care Procedures, Procedure: Intraosseous needle, and Appendix 5 for IO access).
– Stop any active bleeding (see Section 2.5).
– Perform rapid tests for haemoglobin (Hb), blood glucose level (BGL), and malaria (in endemic
malaria contexts).
– Check electrolytes, if available.
– Promptly administer fluids and/or blood to improve circulatory volume and perfusion,
depending on underlying cause:
• Circulatory failure or shock: see Section 2.2.
• Anaphylaxis: see Section 2.4.
• Severe bleeding: see Section 2.5.
• Trauma: see Section 2.7.
– Reassess ABC every 15 minutes and monitor and record vital signs frequently (or continuously
if possible) using an early warning system (see MSF Manual of Nursing Care Procedures,
Assessment and vital signs, Charts: Vital sign charts) while identifying underlying diagnosis.

Assess and manage D (disability)


– Perform a brief examination of neurological function:
• Examine the pupils: size, symmetry, reaction to light.
• Assess level of consciousness using AVPU:
▹ Alert
▹ Voice: responds to vocal stimuli
▹ Pain: responds to painful stimulif
▹ Unresponsive
– Treat hypoglycaemia (BGL < 3.3 mmol/L or < 60 mg/dL) with 2 mL/kg of glucose (dextrose)
10% IV/IO over 2-3 minutes, or 10 mL/kg via nasogastric tube (NGT). See Chapter 9,
Section 9.3 for further detail.
– If seizures, see Chapter 7, Section 7.2.3 for management.
– If reduced level of consciousness, nurse in lateral position if airway not protected and continue
oxygen via mask. Once ABC are stable, try to identify the underlying cause and manage
accordingly. See Chapter 7, Section 7.5 for further detail on altered level of consciousness.
– Check for possible drug-induced cause and give antidote where appropriate, e.g. naloxone
for opioid toxicity (see Section 2.9).

Assess and manage E (exposure)


– Expose the child fully to complete the initial examination. Note to respect dignity and limit
heat loss.
– Rapidly assess for malnutrition using mid upper arm circumference (MUAC) and oedema
criteria.

f A painful stimulus can be given by applying supra-orbital pressure at the supraorbital notch or by applying
pressure to the nailbed.

33
Chapter 2: Emergencies

– Check temperature and look for any skin eruptions, rash, purpura, or trauma.
– Complete a focused medical history using SAMPLE:
• Signs and symptoms
• Allergies
• Medication
• Past medical history
• Last meal
• Events leading to presentation.

Cardiopulmonary arrest
If child deteriorates and becomes unresponsive, is not breathing (gasping or intermittent
breaths), and no pulse is felt within 10 seconds (or pulse < 60 beats/min with signs of poor
perfusion), start CPR (see Section 2.1.1 for more details):
– Give 5 initial rescue breaths and begin CPR with a ratio of 15 chest compressions: 2 breaths.
– Continue CPR in the absence of signs of life (moving, coughing, breathing) and concomitantly
obtain IV/IO access. Attach cardiac monitor, if available.
– Administer epinephrine IV/IO: 10 micrograms/kgg every 3 to 5 minutes (see MSF Paediatric
Injectables Handbook and MSF Vasopressor Therapy – Adrenaline protocol for more
detailed administration guidance) without interruption to chest compressions until infant/
child meets criteria to stop resuscitation (see below).
– If cardiac monitoring in place, stop chest compressions briefly to check for electrical activity
every 2 minutes. If there is electrical activity, check briefly for a pulse, minimising any
interruption to chest compressions.
– Treat reversible causes: hypovolaemia, hypoxia, hypoglycaemia, hypothermia, hypo- or
hyperkalaemia, tension pneumothorax.
If there are obvious signs of life or if pulse returns, stop CPR and:
– Follow ABCDE approach to assess and manage the child further.
– Assist ventilation and oxygenation, as necessary.
– Treat precipitating or underlying cause.
– Avoid hypothermia (wrap in blankets, cover head of infants).
When to stop CPR if no response:
– After 10 minutes if still no signs of life, confirmed by the absence of a pulse.
– After 30 minutes if pulse is present but no breathing and no reversible cause has been
identified.

Communication
Communication with family during resuscitation is extremely important and where possible it
is useful to have someone dedicated to keeping the family up to date and explaining what is
happening throughout the resuscitation. This will both reassure the family and allow them to
understand what the medical team is doing.
Effective team work also involves good communication, ensuring clarity of roles and
responsibilities and maintaining a calm, low-stress atmosphere. Closed loop communicationh
is useful in emergencies to avoid misunderstandings. After the resuscitation, it is important
to carefully record the events and any medications that were administered (if not recorded in
real time).

g Solution of 100 micrograms/mL (1:10 000) i.e. dilute 1 mL of adrenaline 1:1000 with 9 mL sodium chloride
0.9%.
h Closed loop communication is when the person receiving the message repeats it back to the person who gave
the message to ensure that it has been correctly understood. It reduces error from ambiguous messages.

34
Chapter 2: Emergencies

2.2 Circulatory impairment and shock 2

Impaired circulation can occur in any severely ill or injured child. Early recognition of
circulatory impairment, identification of the underlying cause and prompt treatment can
prevent progression to shock and be life-saving. Shock is a clinical condition in which there
is inadequate oxygen delivered to the vital organs and tissue, and, if prolonged, results in
irreversible multi-organ failure and death. Mortality in children with shock is extremely high.
In clinical practice, differentiation between circulatory impairment and shock can be difficult.
In addition, the proportion of children with true shock among all those with evidence of
circulatory impairment, is very small2. Evidence has shown that children with circulatory
impairment who do not meet the definition of shock benefit from the same treatment as
those in shock2. Therefore, for the purposes of this chapter, treatment of children is the same
for both circulatory impairment and shock. This chapter does not apply to children in diabetic
ketoacidosis (DKA) (see Chapter 9, Section 9.2), children with circulatory impairment due to
massive haemorrhage (see Section 2.5) or trauma (see Section 2.7) as they have a specific
pathophysiology and different management requirements.

2.2.1 Classification of circulatory impairment and shock


Shock in children can be classified according to the pathophysiology associated with the
underlying cause (see Table 2.1).
Table 2.1 - Classification and causes of shock in children3
Classification Pathophysiology Causes

Gastroenteritis,
Fluid loss, inadequate fluid
dehydration, diabetic
intake
ketoacidosis
Intravascular
Hypovolaemic
volume loss Trauma, splenic rupture,
Blood loss/haemorrhage
viral haemorrhagic fevers
Capillary leak Burns, bowel obstruction
Increased capillary
permeability, decreased Sepsis, anaphylaxis
Intravascular vasomotor tone
Distributive
volume shift
Loss of sympathetic tone
Spinal cord injury
leads to vasodilation
Congenital heart
Reduced disease, cardiomyopathy,
Cardiogenic Intrinsic pump failure
cardiac output myocarditis, valvular
disease, arrhythmias
Tension pneumothorax,
Obstructed Extracardiac obstruction of cardiac tamponade,
Obstructive
cardiac output blood flow pulmonary embolism,
coarctation of aorta

35
Chapter 2: Emergencies

The most common causes of circulatory impairment/shock in children which will be covered in
this section are severe dehydration (most often due to diarrhoea), sepsis, and severe anaemia,
and management is tailored to the underlying cause. Severely unwell children may have multiple
potential causes, and management must take into account the different possible underlying
conditions. Careful monitoring during and after stabilisation (or acute management) is vital to
ensure optimal survival and a positive outcome for the child.
Refer to relevant sections for further management of DKA (Chapter 9, Section 9.2) severe
haemorrhage (Section 2.5), trauma (Section 2.7), anaphylaxis (Section 2.4) and underlying
cardiac conditions (Chapter 6, Section 6.2).

2.2.2 Clinical features


Children are critically unwell with any one of the following signs of impaired circulation:
– Weak radial pulse, or severe tachycardiaa
– Lower limb temperature gradientb
– CRT of 3 or more seconds.
If all 3 signs of circulatory impairment are present, the child is in shock.
Blood pressure may remain normal even if a child is in shock.
The diagnosis of circulatory impairment is not always easy and requires good clinical judgement.
Children must be critically unwell to make a diagnosis of circulatory impairment based on
a single sign. Each of the individual signs above can also be found in non-critically unwell
children, e.g. a child may have cold feet, but if the child is otherwise well, they do not have
circulatory impairment.
The following signs indicate decompensated shock and imminent cardiopulmonary arrest:
– Inadequate respiratory effort
– Hypotension/ weak central pulses
– Bradycardia
These children need immediate resuscitation (see Section 2.1.1 and Section 2.1.2).

2.2.3 Immediate management


This section addresses immediate management of circulatory impairment/shock to stabilise
the child, during which the underlying causes should be identified and addressed where
possible. The goal is to restore adequate perfusion and oxygenation without causing harm.
Specific management is determined by identification of the most obvious reason for circulatory
impairment:
– Sepsis or severe febrile illness
– Severe anaemia (unless due to massive haemorrhage, in which case see Section 2.5)
– Severe dehydration (unless due to DKA, in which case see Chapter 9, Section 9.2)
The use of IV fluid boluses is no longer recommended in the management of circulatory
impairment/shock due to sepsis/severe febrile illness in the absence of available advanced
supportive care (mechanical ventilation, vasopressor support)4,5.

a > 180 bpm in children < 12 months, > 160 bpm in children 1 to 5 years, > 140 bpm in children > 5 years.
b The temperature gradient is assessed by running the back of hand from the toe to the knee; a positive
temperature gradient is defined as a notable temperature change from cold (dorsum of foot) to warm (knee).

36
Chapter 2: Emergencies

Emergency management 2
– Move the child to a critical care area (emergency or intensive care) and assess rapidly while
stabilising or resuscitating:
• Take rapid history (SAMPLE) and try to determine underlying cause.
• Obtain age and weight of the child. Measure mid-upper arm circumference (MUAC) and
check for oedema as a rapid assessment for malnutrition.
– Assess and manage Airway and Breathing (see Section 2.1.1 and Section 2.1.2):
• Open airway and administer oxygen > 6 L/min via mask (use non-rebreathing mask if
available).
• Attach pulse oximetry and monitor; aim for SpO2 between 94-98%.
• Assist ventilation and oxygenation with bag-mask ventilation if needed.
– Assess and manage Circulation (see Section 2.1.2):
• Obtain IV/IO access.
• Perform rapid tests for Hb, BGL, malaria (where endemic) and send blood for culture, if
available, and blood group (see MSF Blood transfusion guideline).
• Administer parenteral fluids and/or bloodc IV/IO corresponding to specific cause of
circulatory impairment (see below: Specific management).
– Administer antimalarial treatment if malaria test positive.
– Treat hypoglycaemia (BGL < 3.3 mmol/L or < 60 mg/dL) with 2 mL/kg of glucose (dextrose)
10% IV/IO over 2-3 minutes, or 10 mL/kg via NGT. See Chapter 9, Section 9.3 for further
detail on ongoing management of hypoglycaemia.
– Administer ceftriaxone IV: 80 mg/kg (max. 4 g if < 50 kg; max. 2 g if ≥ 50 kg) single dose as
soon as possible, within 1 hour of diagnosed circulatory impairment. Revise need for further
antibiotic treatment once underlying cause identified.
Parenteral fluids must be administered with caution in children with severe febrile
illness, pneumonia, malaria, meningitis, severe acute malnutrition, severe anaemia,
underlying cardiac conditions, renal failure or diabetic ketoacidosis. Adjust rate and volume of
fluid administration in these groups of children according to respective guidance and ensure
that a paediatric infusion set is always used, if available.

Specific management
Sepsis or severe febrile illness
– Administer maintenance fluids with glucose (dextrose) 5%/Ringer lactate (G5%/RL) IV/IO
(or glucose (dextrose) 5%/sodium chloride 0.9% (G5%/NaCl 0.9%) if RL is unavailable). See
Chapter 15, Section 15.2.
– Monitor and record vital signs, neurological status and urine output at least every
15-30 minutes, using an early warning system (see MSF Manual of Nursing Care Procedures,
Assessment and vital signs, Charts: Vital sign charts). Monitor carefully for any signs of fluid
overload.
– If deterioration or no improvement at all after 2 hours of IV fluids and IV antibiotics (as above),
check Hbd and administer a blood transfusion (see below and Chapter 10, Section 10.1.2).
Continue IV maintenance fluids while waiting for blood and stop during transfusion. Restart
IV maintenance fluids after completion of blood transfusion.
– See Chapter 3, Section 3.2 for ongoing management after stabilisation including antibiotic
advice.

c Always ensure bedside verification of ABO compatibility immediately before transfusion using an ABO testing
card.
d Blood transfusion for unresponsive sepsis is not strictly dependent on Hb, however if Hb is above 10 g/dL
transfusion may not be beneficial and decision to transfuse should be based on the balance of potential risks
and benefits.

37
Chapter 2: Emergencies

Severe anaemia (Hb < 6 g/dL)


– Administer blood transfusione (see Chapter 10, Section 10.1.2), calculating volume according
to presence or absence of fever6 as follows:
• No fever (≤ 37.5 °C) from the time of ordering blood to the time of transfusionf: administer
30 mL/kg whole blood over 4 hours or 15 mL/kg packed red blood cells (PRBC) over
3 hours.
• Fever (> 37.5 °C) at any point from the time of ordering blood to the time of transfusionf:
administer 20 mL/kg whole blood over 4 hours or 10 mL/kg PRBC over 3 hours.
– While waiting for blood, start fluid rehydration:
• Start maintenance fluids with G5%/RL IV/IO (or G5%/NaCl 0.9% if RL is unavailable). See
Chapter 15, Section 15.2.
• Stop fluids during transfusion.
– Monitor and record vital signs, neurological status and urine output at least every
15-30 minutes using an early warning system (see MSF Manual of Nursing Care Procedures,
Assessment and vital signs, Charts: Vital sign charts). Monitor carefully for any signs of fluid
overload.
Severe dehydration
– Administer fluids according to WHO treatment plan C (for non-malnourished children) or
‘Plan C SAM’ (for malnourished children). See Chapter 5, Section 5.3 for details.
– Monitor and record vital signs, neurological status and urine output at least every
15-30 minutes using an early warning system (see MSF Manual of Nursing Care Procedures,
Assessment and vital signs, Charts: Vital sign charts). Monitor carefully for any signs of fluid
overload.
– If deterioration or no improvement at all after 2 hours of IV fluids, check Hbg and administer
a blood transfusion (see above and Chapter 10, Section 10.1.2).
– Continue IV rehydration fluids as per plan at the same time as blood transfusion using a
separate IV line.

See Figure 2.5, page 41 for full shock algorithm.

2.2.4 Monitoring and further management


– Continue monitoring every 30 minutes (vital signs, neurological status, urine output,
BGL) and continue further management of underlying cause in an intensive care facility, if
available. Record all vital signs using an early warning system (see MSF Manual of Nursing
Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– Signs indicating improvement in circulation and perfusion:
• Improved peripheral and central pulses
• Urine output > 1 ml/kg/hourh
• Improved level of consciousness

e Always ensure bedside verification of ABO compatibility immediately before transfusion using an ABO testing
card.
f Ensure temperature is checked and recorded at the time of ordering blood and immediately prior to transfusion
as a minimum.
g Blood transfusion for severe dehydration that is unresponsive to initial fluid resuscitation is not strictly
dependent on Hb, however if Hb is above 10 g/dL transfusion may not be beneficial and decision to transfuse
should be based on the balance of potential risks and benefits.
h Accurate urine output can only be measured if a urinary catheter is in situ or by weighing nappies.

38
Chapter 2: Emergencies

– Monitor continuously for signs of fluid overload, which are: 2


• Increased RR by ≥ 10 breaths/min from initial RR, or
• Increased HR by ≥ 20 beats/min from initial HR
– Plus any one of the following:
• New or worsening hypoxia (decrease in SpO2 by > 5%)
• New onset of rales and/or pulmonary oedema (fine crackles in lung fields)
• New galloping heart rhythm
• Increased liver size (liver size must have been marked with pen on arrival)
• New peripheral oedema and/or puffy eyelids.
Management if signs of fluid overload present:
– Stop fluids (or slow down transfusion).
– Administer furosemide IV: 0.5 mg/kg (repeat once if necessary).
– Place child into semi-sitting position and ensure high-flow oxygen via non-rebreathing mask,
if available.
– Monitor and record vital signs every 15 minutes using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts)
until child has been stable for at least one hour.
Management if improvement in circulation and perfusion:
– Severe dehydration: complete further treatment with WHO treatment plan C or ‘Plan C
SAM’.
– Sepsis or febrile illness:
• Continue IV maintenance fluids until stable.
• Remove any potential entry point of infection, e.g. indwelling catheter.
• Adjust antibiotic regimen according to suspected source of infection. If meningitis
suspected, increase to ceftriaxone IV: 100 mg/kg (max. 4 g) once daily.
– Severe anaemia: refer to Chapter 10, Section 10.1.

Fluid refractory shock


Management if no improvement in circulation and perfusion despite adequate management
as described above:
– Clinical signs of shock persist despite maximum fluid management and/or blood transfusion.
Further fluids can be harmful and should be avoided. Consider and investigate for another
diagnosis or underlying cause.
– For acute kidney injury (AKI): persistently low urine output (< 0.5 mL/kg/hour for more than
6 hours) despite adequate fluid management. Stop any nephrotoxic drugs and adjust fluid
management (see Chapter 8, Section 8.4).
– Consider thiamine if altered mental status and/or prolonged seizures, or if severe malnutrition
or persistent hypoglycaemia in septic, hypovolaemic or cardiogenic shock. Not useful in
anaphylactic or haemorrhagic shock.

thiamine IV/PO
– Loading dose < 15 years: 100 mg slow IV infusion over 30 minutes once daily for
48 hours.
If IV not possible: give PO/via NGT at the same dose.
– Maintenance dose to be started after 48 hours of IV treatment:
• ≤ 12 years: 25 mg PO once daily for 1 month
• > 12 years: 25 mg PO twice daily for 1 month

39
Chapter 2: Emergencies

2.2.5 Further critical care management when intensive care is available


Recommended where sufficient numbers of trained personnel, protocols, syringe pumps,
continuous monitoring and laboratory services are available:
– Non-invasive ventilation (NIV) to support breathing (see Chapter 4, Section 4.1.3).
– Inotropes: low-dose epinephrine IV infusion: starting at 0.05 micrograms/kg/min with
gradual titration (see MSF Vasopressor Therapy – Adrenaline protocol).
– If severe hypotensioni (systolic blood pressure of < 50 mm Hg in < 12 months of age,
< 60 mm Hg in 1 to 5 years of age, and < 70 mm Hg in children > 5 years of age), consider
giving a fluid bolus of Ringer lactate (RL) IV, 20 mL/kg over 15 minutes.
– Electrolyte correction (if possible to measure accurately). Treat hypocalcaemia, if present
with 10% calcium gluconate IV: 0.5 mL/kg (max. 10 mL). See Chapter 15, Section 15.3.4 for
more details.
– Hydrocortisone: consider if signs of adrenal dysfunction (e.g. persistent hypoglycaemia
despite treatment). Initial dose 2 mg/kg IV, followed by: 1 mg/kg IV every 6 hours for the
first 24 hours; then 0.5 mg/kg IV every 6 hours for the next 24-48 hours.

i Requires accurate blood pressure measurement. Weak pulse is not a reliable proxy for low blood pressure.

40
Figure 2.5 - Treatment algorithm for circulatory impairment/shock

Critically unwell child with signs of circulatory impairment or shock (one of more of the following):
Weak radial pulse or severe tachycardia*, lower limb temperature gradient, CRT ≥ 3 secs

ABCDE
• Open airways and start oxygen > 6 L/min via mask
• Get IV/IO access and check Hb
• Check BGL and treat if hypoglycaemic
• Malaria test (if endemic) and treat if positive
• Administer ceftriaxone 80 mg/kg single dose**

Likely cause of circulatory impairment

Sepsis/severe febrile illness Severe anaemia (Hb < 6 g/dL) Severe dehydration

• Give maintenance fluids • Urgent blood transfusion • Start WHO treatment plan C
• Reassess every 15 - 30 mins • Start maintenance fluids or ‘Plan C SAM’
• If no improvement after 2 while awaiting transfusion • Reassess every 15 - 30 mins
hours of IV fluids: recheck • Reassess every 15 - 30 min • If no improvement after 2
Hb and give blood hours of IV fluids: recheck
transfusion***
Hb and give blood
transfusion***

If at any point signs of fluid overload develop,


stop fluids and give furosemide 0.5 mg/kg IV

If signs of shock persist after maximum fluids and/or transfusion, see Fluid refractory shock

* > 180 bpm in < 12 months, > 160 bpm 1 to 5 years, > 140 bpm in > 5 years
** Revise necessity of further antibiotic treatment once underlying infection identified.

41
Chapter 2: Emergencies

*** If Hb is above 10 g/dL transfusion may not be beneficial and decision to transfuse should be based on the balance of potential risks and benefits.
2
Chapter 2: Emergencies

2.3 Choking

Sudden onset of respiratory distress associated with coughing, gagging or stridor.

Immediate assessment and management


Call for help.

Is the child coughing effectively?

Effective cough Ineffective cough


Crying or verbal response to questions Unable to vocalise
Loud cough Quiet or silent cough
Able to take a breath before coughing Unable to breathe
Fully responsive Cyanosis
Decreasing level of consciousness

Effective cough:
– No external manoeuvres are necessary. Encourage the child to continue coughing. Effective
cough means that air is passing in/out of the upper airways and is the most effective way to
dislodge the foreign body. Do not interfere but monitor continuously.
– If the child is stable and there is a concern of a foreign body lodged in the oesophagus or
airway, obtain an x-ray.
Seen on x-ray Not seen on x-ray
Metal (except aluminium) Aluminium
Most animal bones Most wood
Glass Most plastic
Stones Most fish bones

Ineffective cough or becoming ineffective:


– Call for help and assess if child is conscious.

Is the child conscious?


Not conscious:
– Lay child on a flat surface
– Open airway and look for any obvious foreign body. If visible, try to carefully remove with
a finger sweep (do not go blindly or repeat many times as this could push the foreign body
further into the airway).
– Start BLS with 5 rescue breaths (see Section 2.1.1).
– If no response, start CPR (see Section 2.1.1).
Conscious: use external manoeuvres to dislodge foreign body as follows1:

42
Chapter 2: Emergencies

Step 1: Give 5 back blows. 2


– Infant (< 1 year):
• Lie infant along the forearm with head facing downwards, supporting the infant’s head
with your thumb on the angle of the lower jaw and two fingers on the other side of the
jaw (see Figure 2.6). Lay the arm supporting the infant on your thigh for stability.
• Using the palm of your hand, deliver sharp back blows between the infant’s shoulder
blades.
– Child (≥ 1 year):
• Depending on the size of the child, either place child with head leaning forwards over one
knee or with support over an arm (see Figure 2.7). Using the palm of your hand, deliver
sharp back blows between the child’s shoulder blades.
Try to dislodge the foreign body with each blow. Repeat up to a total of 5 times if no obvious
foreign body has come out, then re-assess.

Figure 2.6 - Back blows in an infant Figure 2.7 - Back blows in a child

Re-assess:
– Turn the child around to face you or turn the infant to face upwards (Figure 2.8a to Figure 2.8b)
while continuing to support the body, neck and head, and look for any obvious foreign body
(if visible try to remove carefully, as above).
– Check if airway still obstructed and assess if conscious or not.
• If not conscious, start BLS (see Section 2.1.1).
• If still conscious but airway obstructed, move to Step 2 to give 5 chest thrusts (infant) or
abdominal thrusts (child).

43
Chapter 2: Emergencies

Figures 2.8 - Switching from back blows to chest thrusts in the choking infant

2.8a - Face down position 2.8b - Face up position

Step 2: Give 5 chest thrusts (infant) or abdominal thrusts (child).


– Infant (< 1 year):
• Identify landmark for chest compressions (lower half of sternum, around one finger
breadth above xiphisternum) and use 2 fingers to deliver chest thrusts (similar to chest
compressions but sharper and at a slower rate). See Figure 2.9.
– Child (≥ 1 year):
• Stand or kneel behind the child and hold the child by encircling the child with your arms
under their arms (see Figure 2.10).
• Make a fist with one hand and place it between the umbilicus and xiphisternum. Using
your other hand on top of your closed hand, pull sharply inwards and upwards.
Try to dislodge the foreign body with each thrust. Repeat up to a total of 5 times if no obvious
foreign body has come out, then re-assess.

Figure 2.9 - Two-finger chest thrusts (infant) Figure 2.10 - Abdominal thrusts (child)

44
Chapter 2: Emergencies

Re-assess: 2
– Check if airway still obstructed and assess if conscious or not.
– Repeat Steps 1 and 2 continuously, assessing the child’s responsiveness, consciousness and
breathing.
– If at any point the foreign body seems visible, remove it carefully.
– If the foreign body seems to have dislodged or child seems to restart breathing effectively,
lay the child into recovery position and observe for any respiratory distress.
– If child deteriorates or becomes unconscious, start BLS (see Section 2.1.1).
Only discharge when stable and fully alert, and if clinical examination is normal. If the child lost
consciousness at any point during the episode, observe for at least 8 hours and assess prior to
discharge.

45
Chapter 2: Emergencies

2.4 Anaphylaxis

Anaphylaxis is a potentially life-threatening, rapid onset, generalised hypersensitivity reaction.


Hallmark features include life-threatening airway, breathing or circulatory problems and
usually, but not always, associated skin and mucosal changes7. The reaction is triggered by
an allergen (usually foods, insect bites or stings, or medicines) to which a person is already
sensitive. Severity can vary; a child may rapidly develop circulatory collapse or symptoms
may resolve spontaneously8. The goal is to promptly recognise and diagnose anaphylaxis (not
always easy in children) and treat immediately with IM epinephrine.
Although global epidemiological data is limited, published data shows an increasing trend of
anaphylaxis, including in children and adolescents9,10. The most common trigger reported in
children continues to be food products7.

2.4.1 Clinical features and diagnostic criteria


Diagnosis is based on history (including exposure to, or ingestion of, potential allergen) and
clinical features (see Table 2.2).
Table 2.2 - Clinical criteria for diagnosis of anaphylaxis11

Anaphylaxis is highly likely when either of the following 2 criteria are met within hours:

1. Acute onset of an illness (minutes to several hours) with involvement of the skin, mucosal
tissue, or both (e.g. generalized urticaria, itching, flushing, swollen lips-tongue-uvula)
AND ≥ 1 of the following:
A. Respiratory symptoms (e.g. dyspnoea, wheeze or bronchospasm, stridor, hypoxia)
B. Low BP or associated symptoms of end-organ dysfunction (e.g. hypotonia, syncope,
incontinence)
C. Severe gastrointestinal symptoms (severe abdominal pain, repetitive vomiting)

OR

2. Acute onset of hypotension or bronchospasm or laryngeal involvement (stridor, vocal


changes, odynophagia) after exposure to known or highly probable allergen for that
patient.

2.4.2 Management
– Identify quickly and remove external trigger (e.g. remove bee stinger; stop drug infusion if
potential likely cause).
– Assess and manage ABCDE including specifically:
• Prepare IM epinephrine as part of A.
• Assess for airway swelling: angioedema of lips, tongue, throat (laryngeal oedema). Can
child speak or do they feel they cannot swallow?
• If not breathing or cardiopulmonary arrest, start CPR (Section 2.1.1).

46
Chapter 2: Emergencies

– Administer epinephrine IM: 0.01 mg/kg (1 mg/mL (1:1000) undiluted solution in 1 mL 2


syringe) single dose into the mid-anterolateral thigh (maximum dose of 0.3 mg for children
< 12 years12,13):

Age Dose to be administered IM

Infant < 6 months 100 to 150 micrograms (0.1 to 0.15 mL)

Child 6 month to < 6 years 150 micrograms (0.15 mL)

Child 6 to < 12 years 300 micrograms (0.3 mL)

Child ≥ 12 years* 500 micrograms (0.5 mL)


* If small or prepubertal, administer 300 micrograms (0.3 mL).
– Repeat IM epinephrine after 5 minutes if response is poor or no clinical improvement14.
– Keep child supine or at 45 degrees if difficulty breathing.
– Administer oxygen > 6 L/min via mask (use non-rebreathing mask if available).
– Get IV access and administer 10 mL/kg Ringer lactate (RL) as a rapid bolus (alternatively
sodium chloride 0.9%). Reassess after 15 minutes or earlier if needed and if signs of poor
perfusion, repeat the same fluid bolus once.
– Monitor and record vital signs, particularly RR and CRT, every 5 to 10 minutes.
– If, after 2 doses of IM epinephrine and fluids, the child shows little or no improvement,
consider, where feasiblea, starting an IV epinephrine continuous infusion (refer to MSF
Vasopressor Therapy – Adrenaline protocol). Continue to administer IM epinephrine every
5 minutes until infusion is started13.
– Ensure continuous vital sign monitoring, or if not available, monitor and record every 5 to
10 minutes. Once stabilised, monitor every 30 minutes, including level of consciousness and
urinary output. Gradually reduce the infusion once clinical condition improves.

Additional treatment
Any additional treatment should only be given after the initial emergency treatment of
anaphylaxis and should not delay continuation of adrenaline administration in refractory
anaphylaxis13.
– Administer corticosteroid if refractory anaphylaxis or ongoing asthma/shock to prevent or
shorten protracted reactions, using hydrocortisone IM or IV:

Dose to be administered 3 times daily,


Age
adjusted according to response15

1 to 5 months 25 mg

6 months to 5 years 50 mg

6 to 11 years 100 mg

12 years and above 200 mg

– Administer IV antihistamine if cutaneous manifestations of anaphylaxis are present.

a Electric syringe pump available and personnel trained in its use.

47
Chapter 2: Emergencies

– Administer nebulised epinephrine if stridor or upper airways obstruction present:


• epinephrine nebulised solution: 0.5 mg/kg (max. 5 mg) in 5 mL normal saline over
15 minutes.
• Repeat another dose as soon as nebuliser finishes (to provide continuous nebulisation)
until symptoms improve.
– Administer bronchodilator if wheezing present (see also Chapter 4, Section 4.10), using
salbutamol nebuliser solution (5 mg = 5 mL):

Dose to be administered
Age
over 20 minutes

≤ 5 years 2.5 mg (1.25 mL)

> 5 years 5 mg (2.5 mL)

Follow-up
After an anaphylactic event, provide an explanation to the child and their parents/carers on
the condition, its presentation, recognition, and immediate treatment. If a trigger has been
identified, give advice on allergen avoidance.

48
Chapter 2: Emergencies

2.5 Haemorrhagic shock 2

Shock in conjunction with clinical signs of haemorrhage (external and/or internal blood loss).
Causes include trauma, gastrointestinal bleeding, splenic rupture (due to severe sickle cell
disease, malaria or trauma) or diffuse bleeding due to haemorrhagic fever or dengue shock.
If there is ongoing significant bleeding, treat as haemorrhagic shock even if Hb ≥ 8 g/dL.
Haemoglobin may initially be normal in haemorrhagic shock as it takes time for the body to
equilibrate and for the haemoglobin level to reflect actual blood lost. Repeat Hb after 30 and
then 60 minutes if it is initially normal.

2.5.1 Investigations
– Hb, FBC, platelets, blood group and Rhesus
– BGL
– Urine dipstick (macroscopic haematuria suggests renal damage)
– Blood lactate, if available
– Electrolytes, urea nitrogen, creatinine, if available
– Prothrombin time (PT), Partial thromboplastin time (PTT), if available

2.5.2 Management
– Stop any obvious life-threatening external bleeding via compression or tourniquet. In the
case of severe trauma, refer to Section 2.7 for trauma management after stabilisation of
haemorrhagic shock.
– Ask or estimate weight of child.
– Assess and manage Airway and Breathing.
– Open airway (support airwas if necessary).
– Administer oxygen > 6 L/min via mask (use non-rebreathing mask if available) aiming for
SpO2 > 94%.
– Assist ventilation and oxygenation with bag-mask ventilation if needed.
– Check Circulation and get IV or IO access. Get blood for cross-matching, bedside ABO
compatibility, and order blood for transfusion.
– Transfuse 20 mL/kg whole blood as fast as possiblea; group O negative or cross-matched
blood, whichever is available faster. Repeat as necessary guided by clinical evolution, Hb,
platelets.
– Administer 20 mL/kg of IV Ringer lactate (or sodium chloride 0.9%) as a rapid bolus if blood is
not immediately available. Repeat bolus if necessary until blood is available for transfusion,
but be cautious as fluids may dilute coagulation factors and worsen bleeding.
– Reassess clinical condition and monitor and record vital signs every 15 minutes during
transfusion.
– Administer tranexamic acid IV: 15 mg/kg (max. 1 g).
– Warm child proactively to ensure temperature > 36.5 °C. Stop any air-conditioning and warm
all fluids and blood products.
– Insert a nasogastric tube (conical tip) open to air.
– Manage underlying cause of haemorrhage.

a Always ensure bedside verification of ABO compatibility immediately before transfusion using an ABO testing
card

49
Chapter 2: Emergencies

2.6 Drowning

Defined as “the process of experiencing respiratory impairment from submersion/immersion


in liquid”a,16. Worldwide, drowning claims approximately 372,000 lives per yearb and 91%17
of these deaths occur in low- and middle-income countries18. Globally it is one of the top
5 causes of death under 14 years of agec, with the highest drowning rates in children aged 1 to
4 years16.
Outcome is often fatal but two rapid interventions at the scene of the incident can determine
survival; how quickly the child is pulled out of the water, and how swiftly proper resuscitation
is performed3. Aggressive rescue measures are warranted, especially if submersion was in cold
water (< 10˚C) as it induces rapid hypothermia with potentially good neurological outcomes.
The diving reflex may also improve survival in infants and small childrend.
In drowning, prolonged resuscitation or respiratory support may be necessary but can have
a positive outcome. Predictors of good outcome include cold water submersion (usually
10°C) and being conscious or arousable on admission. Poor outcome predictors include CPR
> 30 minutes, delay in CPR and prolonged submersion.
This chapter will cover immediate management at the scene of the incident and emergency
management in a health facility. Preventive strategies are key to reducing death from drowning
(see WHO Preventing drowning: an implementation guide 201719) but are not within the scope
of these guidelines.

2.6.1 Pathophysiology
Even a small amount of water aspirated into the airways causes significant alveolar damage
and surfactant dysfunction, leading to a clinical picture of non-cardiogenic pulmonary oedema
if the child is rescued alive. Clinically, aspiration (and sometimes laryngospasm) leads to
hypoxaemia, which rapidly leads to loss of consciousness, anoxic brain injury and respiratory
arrest. Without immediate rescue and resuscitation, cardiac arrest may result within seconds
or minutes. Hypothermia or ice-water drowning are the exception, where this process can last
an hour20.

2.6.2 Management
Objective is to:
1. Reverse hypoxia and maintain adequate oxygenation.
2. Prevent aspiration.
3. Reverse hypothermia and stabilise body temperature.

a Definition adopted at the first World Congress on Drowning (2002).


b This figure is considered to be an underestimation of actual figures of fatal drowning cases globally as the ICD
classification does not include fatal drowning due to floods, tsunamis or boat accidents.
c In the WHO Western Pacific Region, drowning is the first cause of death in children 5 to 14 years. Drowning
death rates are the highest in Africa.
d Peripheral and splanchnic vasoconstriction preserves neurological circulation.

50
Chapter 2: Emergencies

Note: the Heimlich manoeuvre or other postural drainage techniques to ‘drain’ water from the 2
lungs lack evidence to demonstrate value and are not recommended. Rescue breaths should
not be delayed in order to carry out such manoeuvres.

Immediate management after rescue


– Rapidly assess ABCDE and start BLS if unconscious (see Section 2.1.1).
– If cardiopulmonary arrest, start CPR.
– If pulse present but breathing is inadequate or reduced level of consciousness, start
respiratory support21:
• Open airways
• Administer 100% oxygen (or highest concentration available) via face mask (use non-
rebreathing mask if available).
– Immobilise cervical spine if likely spinal injury but should not take priority over resuscitation
(see Section 2.7.1).
– Remove wet clothese and dry the child.
– Wrap with blankets or survival blanket and minimise exposure.
– Presume hypoglycaemia and, if conscious and alert enough to drink safely, give a sugar-
containing drink by mouth, such as a milk feed to infants or oral glucose (15 to 30 g) or
125 to 250 mL of a sugary drink (e.g. juice) to older children, if available.
– Transfer immediately to nearest hospital or healthcare facility.

Management in hospital setting


If no immediate management done prior to arrival, start ABCDE and resuscitation (Section 2.1).
Respiratory failure/hypoxia
– Administer 100% oxygen (or highest concentration available) aiming to maintain SpO2
> 94%.
– Consider bag-mask ventilation if oxygenation inadequate or signs of respiratory failure.
– If alert but remains hypoxic or in respiratory failure, transfer to an intensive care unit for
respiratory support (if available).
– If breathing spontaneously:
• Admit for observation for at least 8 hours.
• Monitor and record vital signs as often as required using an early warning system (see
MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign
charts).
• Assess respiratory effort, including pulmonary auscultation regularly.
• Administer oxygen aiming to maintain SpO2 > 94% and observe carefully.
– If child develops respiratory distress, widespread crackles on auscultation or hypoxia,
transfer to intensive care unit for further management and respiratory support.
– If signs of shock develop, treat for shock (see Section 2.2). Be cautious to avoid excess fluid
administration as there may be cerebral oedema due to anoxia. Avoid hypotonic solutions.
– Routine antibiotic treatment is not necessary. Only if signs of respiratory infection or sepsis
appear (fever, cough, dyspnoea), start appropriate antibiotic treatment (see Chapter 4,
Section 4.5 for pneumonia and Chapter 3, Section 3.2 for sepsis treatment).
Trauma
– Immobilise C-spine (if not already done) if possible injury suspected, mechanism of injury
unclear, or consciousness impaired.

e Clothes should be cut off in case of suspected spinal injury to avoid excessive movement of the neck.

51
Chapter 2: Emergencies

Prevent aspiration
– Vomiting is common following drowning and complications due to aspiration occur
frequently in children with altered consciousness.
– If reduced consciousness, insert a nasogastric tube (conical tip) to remove swallowed water
(or debris).
Hypothermia
– Remove wet clothes and dry the child (if not already done).
– Wrap with blankets or survival blanket and minimise exposure.
– If core temperature < 35.5 °C, start active warming where possible:
• Use warmed blankets, heating pads, survival blankets, etc. depending on availability.
• Administer warmed IV fluids or pass IV fluids via a warmer device, if available.
Hypoglycaemia
– Check BGL and treat hypoglycaemia if BGL < 3.3 mmol/L or < 60 mg/dL with 2 mL/kg of
glucose (dextrose) 10% IV/IO over 2-3 minutes, or 10 mL/kg via NGT.

2.6.3 Investigations
– No routine investigations required if asymptomatic and alert.
– Perform FBC, BGL and electrolytes (if available) if altered mental status persists despite
resuscitation (absence of hypoxia) or if initial cause of drowning not known, e.g. traumatic
brain injury, hypoglycaemia, another medical condition.

2.6.4 Post resuscitation management


– Monitor and record vital signs, pulse oximetry, respiratory effort and level of consciousness
as often as required using an early warning system (see MSF Manual of Nursing Care
Procedures, Assessment and vital signs, Charts: Vital sign charts).
– Monitor BGL and treat hypoglycaemia (BGL < 3.3 mmol/L or < 60 mg/dL) with 2 mL/kg
of glucose (dextrose) 10% IV/IO over 2-3 minutes, or 10 mL/kg via NGT. See Chapter 9,
Section 9.3 for further detail on ongoing management of hypoglycaemia.
– Observe for signs of complications and treat accordingly:
• Neurological injury: abnormal neurological examination, seizures, prolonged impaired
level of consciousness. Provide supportive care and control seizures. Avoid hypo- and
hyperglycaemia.
• Respiratory distress or infection: bronchospasm is common after drowning. Treat with
bronchodilators as for asthma (see Chapter 4, Section 4.10). If clinical signs of pneumonia,
treat with appropriate antibiotics (see Chapter 4, Section 4.5).
– Steroids should not be prescribed routinely as there is insufficient data to support their use
in the management of drowning.
– If child is asymptomatic, admit child for close observation for approximately 8 hours. If no
clinical deterioration and the child is well, discharge after 8 hours.
– Instruct parents/carers to return to the emergency department if any respiratory or other
problems develop.

52
Chapter 2: Emergencies

2.7 Trauma 2

Unintentional trauma, particularly road traffic injuries, falls, drowning, poisoning and burns,
are amongst the leading causes of global deaths amongst children22. Over 95% of injury related
paediatric mortality occurs in low- and middle-income countries. Road traffic injury alone is
the leading cause of death amongst 15- to 19-year-olds and the second leading cause of death
in children 5 to 14 years. Additionally, children are often victims of trauma and violence in
conflict-affected settings23. For drowning (Section 2.6), burns (see MSF Clinical Guidelines)
and poisoning (Section 2.9) refer to respective chapters.
This chapter covers the management of a child with possible multiple severe injuries due to
trauma. The aim is to assess and rapidly identify life-threatening injuries such as24:
– Airway obstruction
– Breathing difficulties with chest injuries
– Circulation problems due to severe bleeding (internal or external)
– Disabilities: head and spinal injury.

2.7.1 Primary survey


– Assess and immediately treat any life-threatening conditions25,26.
– Catastrophic bleeding - stop any obvious massive life-threatening external bleeding:
• Apply direct pressure.
• Use tourniquet, if necessary, on limbs.
• Use haemostatic gauze/agents.
• If penetrating foreign object, do not remove.
– Apply Airway, Breathing, Circulation, Disability and Exposure approach as described in
Section 2.1.2 and add protection of the cervical spine (see below).

Airway and cervical spine


– If talking or crying vigorously, airway is clear.
– Stabilise the cervical spine if likely head or neck injury associated, or if concern with
mechanism of injury. Use appropriate size neck collars or tape and sandbags or fluid bags.
– Assess airway:
• Identify any obstruction: listen for snoring, stridor, gurgling, grunting; look for blood,
vomit, teeth, objects/shrapnel, debris in mouth/nasal passage. Remove or suction any
obvious matter.
• Look for direct trauma of airways, neck, or signs of facial fractures.
• Examine neck for tracheal deviation (tension pneumothorax) and subcutaneous
emphysema (crackling sound when pressing on skin).
• If burns, check for singeing of nasal hair/eyebrows/eyelashes, burns to the face/neck,
hoarse voice, and black ash/soot in saliva, expectoration or on suctioning.
– Maintain patent airway by proper head positioning (use a towel or padding to avoid passive
flexion of the cervical spine).
– Avoid excess movement of the cervical spine, especially when performing airway manoeuvres:
if cervical spine injury is a concern, use jaw-thrust only, avoiding head-tilt or chin-lift.
– Insert oropharyngeal airway adjunct (e.g. Guedel) to keep airway patent.

53
Chapter 2: Emergencies

– Where feasible, consider the need for a definitive airway (ETT, tracheostomy).
– If not breathing, start bag-mask ventilation while continuing assessment.

Breathing
– Look, listen and feel to assess breathing (see Section 2.1.1).
– If breathing, check if efficient and adequate: assess RR, SpO2, chest movement, intercostal
or subcostal recession, tracheal deviation, air entry or additional sounds on auscultation.
– Administer oxygen > 6 L/min via mask (use non-rebreathing mask if available), aiming for
SpO2 > 94%.
– Examine chest for any bruising, injury (closed or open), and for blood (haemothorax) or air
(pneumothorax) in the pleura (see also Section 2.7.3):
• For tension pneumothorax: insert large bore needle in 2nd intercostal space mid-clavicular
line, or 5th intercostal space mid-axillary line to immediately release tension.
• For pneumothorax or haemothorax: insert a chest drain.
– Insert gastric tube to avoid gastric distension (use orogastric route in the case of head
trauma).

Circulation
– Assess HR, CRT, BP, signs of impaired circulation and shock. Note that even with significant
bleeding, children may initially have normal BP and Hb, with or without tachycardia, but
have an altered mental state indicating circulatory impairment.
– Get IV/IO accessa (use large bore cannulae, ideally 2 sites) and take blood for Group and
crossmatch, Hb and BGL.
– If in shockb, start appropriate treatment:
• Administer 20 mL/kg IV Ringer lactate (or sodium chloride 0.9%) as a rapid bolus.
• If no response or transient response to initial fluid bolus, administer blood transfusion as
for haemorrhagic shock: whole blood 20 mL/kg as rapidly as possible.
– Control any major bleeding:
• Apply direct pressure or compression to any external sites of haemorrhage. Consider
temporary use of a tourniquet or blood pressure cuff if necessary to reduce bleeding
(refer to MSF Tourniquet for Haemorrhage Control protocol).
• For suspected pelvic fracture, stabilise using a pelvic binderc or a folded wrap around the
child at the level of the greater trochanters and secured in place.
• Reduction: immobilise any obvious long-bone fractures using splintsd.
– Administer tranexamic acid IV, 15 mg/kg (max. 1 g) if within 3 hours of injury.
– Initiate surgical consultation for definitive bleeding control if required.
– Once circulation is stabilised, perform ‘Extended Focused Assessment with Sonography in
Trauma’ (EFAST) Point-of-Care Ultrasound (POCUS) exam for patients with blunt abdominal
or chest trauma, if trained (see below for more detail).

Disability
– Assess level of consciousness using AVPU or Glasgow Coma Scale (GCS, see Appendix 13),
and check pupils.
• If unconscious, insert an NGT (or orogastric tube (OGT) if concern of basal skull fracture) if
not already done. Leave on free drainage. Keep nil by mouth (NBM) until alert and stable.

a Note that all fluids or drugs that are administered via IO require application of pressure either manually or via
pump.
b Haemorrhagic shock is most common in trauma, but cardiogenic or neurogenic shock may also be associated.
c EMEQPEBI1M PELVIC BINDER, medium (SAM Sling II)
d EMEQSPLM1190 MOULDABLE SPLINT, 11 x 90 cm; EMEQSPLM1590 MOULDABLE SPLINT, 15 x 90 cm;
EMEQSPLM1145 MOULDABLE SPLINT, 11 x 45 cm

54
Chapter 2: Emergencies

– Check BGL. 2
– Check for active movement of extremities.
– Aim to minimise any further injury to the brain by ensuring adequate oxygenation and
intravascular fluid volume and pressure.
– Administer analgesia.

Exposure & environment control


– Full exposure is necessary to do a rapid head-to-toe assessment for any other life-threatening
injuries or clinical signs. Undress the child by cutting all clothes away.
– Perform a log roll to examine the back, spine and rectal tone (see footnotee for an example
of link with images of a paediatric log roll).
How to do a log roll
• A log roll is performed to examine the posterior side of a patient while keeping the
spine, especially the cervical spine, aligned in case of possible spinal injury.
• Perform with at least 4 people; one for the head, one for chest, one for pelvis and legs,
and one to examine the back. In bigger children, an extra assistant may be necessary
to hold the legs. Except for the person at the head, all assistants should stand on the
same side of the patient.
• Ensure neck has been immobilised using an appropriately sized neck collar.
• Explain to child what is being done. Ask child to cross arms across their chest with their
hands on their shoulders.
• Head: stand at head end and hold the head and shoulders securely by placing one
hand on either side of the child’s head, with the index finger resting below the jaw and
the remaining fingers supporting the neck and occiput. This person is responsible for
keeping the head aligned with the body when the child is turned to his side.
• Chest: the tallest person in the team should take this role. Leaning over the child, place
one hand on the child’s far shoulder and the other on top of the pelvis on the same
side.
• Pelvis: Place one hand on top of the iliac crest (crossing arms with the person in control
of the chest), and other hand on the underside of the far thigh/knee (depending on the
size of the child). This person is responsible for ensuring that the lower spine remains
aligned during the roll.
• Legs: If the child is bigger, this assistant supports the legs by placing one hand under
the knee of the far leg and the other hand under the ankle of the same leg.
• The person in charge of the head counts to 3 and on 3, all assistants roll the child
towards them simultaneously, keeping in time with the speed of the head being
turned. The body and head of the child should remain aligned at all times.
• When the back examination is finished, the person in charge of the head will again
count to 3 and on 3, all assistants roll the child back to the supine position, keeping
head and body aligned at all times.

– Assess temperature and take measures for aggressive hypothermia preventionf: use warming
blankets, fluids and blood warmer, warm the room.

Once the primary survey is completed and life-threatening conditions are stabilised, start
the secondary survey. Continue to assess and monitor ABCDE and if at any time the child
deteriorates, restart the primary survey.

e Example of source for log roll in images: https://www.clinicalguidelines.scot.nhs.uk/nhsggc-paediatric-


clinical-guidelines/nhsggc-guidelines/intensive-and-critical-care/moving-and-handling-the-child-with-
suspecteddiagnosed-spinal-injury-cervical-spine-log-rolling/
f Children are more susceptible to hypothermia and it is a major factor in trauma mortality.

55
Chapter 2: Emergencies

2.7.2 Secondary survey


– Take a more detailed history on how the injury or trauma occurred and any relevant medical
history:
• Use AMPLE for history:
▹ A-Allergies
▹ M-Medications
▹ P- Past medical history
▹ L- Last meal
▹ E- Events
• For handover between healthcare providers, use MIST:
▹ M-Mechanism
▹ I- Injuries
▹ S-Symptoms
▹ T-Treatment given
– Gather information on what happened and the mechanism of trauma. Be aware of high-risk
mechanisms including:
• Motor vehicle accident (MVA) at high-speed
• Pedestrian or bicycle hit by car
• Fall > 3 metres (or twice body height)
• MVA with ejection from vehicle or death of other passengers
– Perform a full clinical examination, take vital signs and complete the head-to-toe assessment
of any other injuries not picked up during the primary survey. Record all injuries identified.

Additional investigations (if not already done)


– X-rays as indicated based on injury: CXR and pelvic x-ray.
– Point-of-Care Ultrasound (POCUS) EFAST:
• Indication: blunt abdominal and chest trauma (penetrating trauma only if stable)
• Assessment: free abdominal fluid (blood), pericardial or pleural effusion, pneumothorax.
• Contraindication: clear indication for surgery, unstable patient, untrained clinicians.

EFAST
Considerations
Outcome

• Discuss patient stabilisation and possible surgery with team.


• Abdominal free fluid - does patient need surgery?
Positive • Pericardial effusion - does patient need pericardiocentesis?
• Pleural effusion/ pneumothorax - does patient need thoracentesis/
chest tube?

• May need to repeat in few hours (ideally within 6 hours), depending on


patient condition.
Negative
• A negative EFAST does NOT exclude internal injury. Always correlate
clinically.

Particularities of trauma in children (in comparison to adults) to consider


– Same mechanism of injury can have different consequences.
– Flexible thoracic cage compresses easily, so rib fractures and flail chest are rare but there
may be extensive intrathoracic damage from a blunt injury27.

56
Chapter 2: Emergencies

– Flexible spinal skeleton results in possible cervical spine injuries without radiographical signs 2
of fracture.
– Intracranial injuries more common (head size large in proportion to body size in younger age
groups).
– More blood loss with fracture of the long bones or pelvis.
– Initial good compensation to injuries then sudden decompensation.
– Medication and fluid calculations require the weight of the child. If recent weight unknown,
calculate an estimated weight based on age (see below) or use a colour-coded length-based
tape (e.g. Pediatapeg) that provides key drug and fluid doses by length.
Age-based weight estimation:
1 year and below: weight = (age in months/2) + 4
1 to 5 years: weight = (age in years x 2) + 8
6 to 12 years: weight = (age in years x 3) + 7

Note: neither the age-based or tape-based weight estimations can be used accurately in
children with severe acute malnutrition.

2.7.3 Specific injuries

Head injury
For head injury, see Section 2.8.

Chest injury
Tension pneumothorax
– Tracheal deviation: pneumothorax is on the side that the trachea is deviated away from.
– Reduced air entry with hyper-resonant percussion on affected side.
– Emergency management required:
• Insert large bore needle into 2nd intercostal space mid-clavicular line, or 5th intercostal
space mid-axillary line to immediately release tension. Hissing sound of air being released
will be heard.
• Follow with insertion of chest drain.
Open pneumothorax
– Usually due to penetrating chest injury which allows air to be sucked into and blown out of
the wound site.
– Cover with a rectangular dressing that is taped on only 3 sides, allowing air to be expelled
during expiration but preventing it from being sucked in during inspiration.
– Follow with insertion of chest drain.
Massive haemothorax
– Reduced chest movement, reduced air entry and dull to percussion on affected side. If
bleeding significant, child may be in shock.
– Treat haemorrhagic shock (see Section 2.5) and insert chest drain prior to surgery (save
blood, if possible, in sterile container/bag for possible autotransfusion).

g Paediatric Triage Smart Tape or alternatives are Broselow tape or PAWPER tape.

57
Chapter 2: Emergencies

Pulmonary contusion
– Significant internal bruising usually due to blunt trauma.
– Hypoxia results from capillary bleeding that fills up alveoli.
– CXR may initially be normal but can later develop into full white-out from widespread
interstitial shadowing.
– Observe carefully, treat with oxygen to maintain SpO2 > 94% and consider respiratory
support where available (see Chapter 4, Section 4.1.3).
Flail chest
– Occurs if there are multiple rib fractures and a section of the rib cage is moving in the
opposite direction to the rest of the chest.
– Less common in younger children due to their mobile chest walls.
– Manage with analgesia (see Chapter 15, Section 15.4) and respiratory support (see Chapter 4,
Section 4.1.3), if necessary and available.

Abdominal injury
– Consider if abdominal pain, bruising, signs of shock or history of a high-risk mechanism of
injury (e.g. handlebar injury to the abdomen, high speed motor vehicle accident, fall from
great height).
– Visceral injuries might present with a negative EFAST and delayed onset of peritonitis. If in
doubt, admit for serial abdominal examinations and obtain surgical consultation early.
– Examine for: abdominal distension or rigidity, tenderness or guarding on palpation, presence
of blood in urethral meatus (if present, do not catheterise).
– Investigate with: POCUS (EFAST) where available to assess for bleeding into the abdomen
(see above). Upright CXR for presence of free air under diaphragm indicating perforated
bowel.
– Treatment: decompress stomach with NGT if not contraindicated. Refer for surgical
exploration or intervention where possible.

Pelvic trauma
– Fracture of the pelvic bone causes massive internal bleeding and there may be injury to the
bladder and bowel.
– Examine: palpate for tenderness by gentle bilateral compression of the iliac crests from
lateral to medial. Assess for abnormal or asymmetric motion, crepitus, and/or pain. Check
urethral meatus for blood and perform rectal exam.
– Investigate: Pelvic x-ray to check for fracture of pelvic ring. POCUS (EFAST) where available
to look for free intraabdominal fluid (bleeding).
– Treatment: treat shock (see Section 2.2) and give analgesia (see Chapter 15, Section 15.4).
Apply pelvic stabiliser (correct level is at anterior superior iliac spines).
– Refer for surgery if open fracture.

58
Chapter 2: Emergencies

2.8 Head injury 2

Common presentation to emergency departments, of which majority are minor head injuries
but few may have intracranial injury. The patterns of head injury in children differ to those
in adults: developmental level of the child, anatomical variations in the brain/head, the
possibility of inflicted head injury, and the response of the child’s brain to trauma. Delay in
diagnosis and intervention can have significant consequences on patient outcomes, but given
the difficulties in accessing neuroimaging and risks of exposure to radiation, the approach
needs to be systematic and based on risk stratification.

2.8.1 Assessment and initial management


– Perform primary survey and manage ABCDE as necessary (see Section 2.7.1 and Section 2.1.2).
– If unconscious or vomiting recurrently, insert NGT (or OGT if concern of basal skull fracture).
Leave on free drainage, keep NBM until alert and stable.
– Once primary survey completed and any life-threatening conditions stabilised, perform
secondary survey:
• Take a thorough history:
▹ Details regarding the time and mechanism of injury.
▹ Recall of events including any loss of consciousness, seizures, behaviour and activity
since injury.
▹ Identify any co-morbidities that predispose to intracranial injury.
• Complete full clinical examination from head-to-toe including complete neurological
examination (see Chapter 7, Section 7.2).
• Palpate for bogginess or swelling of the scalp.
• Look for signs of basal skull fractures such as Battle’s sign or Panda eyes.
• Examine for haemotympanum or CSF leak from ears or nose.
– Consider an inflicted head injury when there are any of the following features:
• Inadequate history provided for a serious head injury.
• A serious head injury after a reportedly minor fall/injury.
• Significant change in history between parents/carers or over time.
• An unreasonable delay in presentation.
• Any sub-conjunctival or retinal haemorrhage.
• Any other unexplained injuries.

Risk stratification
Use risk stratification to guide management (Table 2.3). A high index of suspicion is required
for younger children due to the difficulty in clinical assessment. Children aged less than 1 year
are at particular risk and need to be assessed very carefully. There is also a greater risk of
inflicted injury in this age group. Patients in the high-risk group are more likely to have a
significant intra-cranial injury that would require neurosurgical intervention therefore referral
is indicated.

59
Chapter 2: Emergencies

Table 2.3 - Risk stratification in children with head injury

Low risk Intermediate risk* High risk

Mechanism Low-mod speed MVAa High-speed MVA


of injury Fall 0 to 3 m Fall > 3 m

Nil injury seen Laceration > 5 cm Tense fontanelle


Laceration < 5 cm (< 1 year)
Open skull fracture
Depressed skull
fracture
Any sign of basal skull
Injury
fracture:
• Haemotympanum
• “Panda eyes”
• CSF leak from nose/
ear
• Battle’s sign

Alert/normal Persistently reduced


Level of
(GCS 15 or A on AVPU) or fluctuating LOC
consciousness
(GCS < 15 or V,P,U on
(LOC)
AVPU)

Neurological Nil Any focal neurological


deficit sign

Loss of Nil or < 5 minutes > 5 minutes


consciousness

Normal or mild Severe agitation or


Behaviour
agitation drowsiness

Seizures Nil Yes (in non-epileptic)

Vomiting < 2 episodes > 2 episodes

Headache Nil or mild Persistent

Nil Bleeding disorders


Co-morbidities Intra-cranial shunt
AV malformations
* Patients with 2 or more intermediate-risk features are classified in the HIGH-RISK GROUP.
Note: The following features signify poor prognosis and referral is not recommended:
– Unresponsive pupils and GCS < 5 or U on AVPU.
– Reduced LOC with GCS < 9 or P or U on AVPU at 24 hours or more.

a MVA – motor vehicle accident

60
Chapter 2: Emergencies

Figure 2.11 - Overview of management of children with head injury 2


Primary Survey & resuscitation
Secondary Survey & stabilisation

Risk stratification

High-risk group
Low- or intermediate-risk group
Or ≥ 2 intermediate-risk factors

CT scan and neurosurgery


available?

NO YES

CT scan and
Observe for at
neurosurgical Normal CT least 6 hours
referral

Any deterioration or
development of any
high-risk sign

Abnormalities
Medical If patient
on CT scan
management remains stable,
should be
and close discharge home
managed as per
observation for with advice to
neurosurgical
at least return if any
advice if
24 hours concern
available

61
Chapter 2: Emergencies

2.8.2 Management
See also Figure 2.11, page 61 for management algorithm.

Low- and intermediate risk


– Admit for close observation for at least 6 hours.

High-risk or ≥ 2 intermediate risk


– Refer for CT scan and neurosurgical consultation, where available. Stabilise child prior to
transfer.
– If CT scan not possible, admit for close observation in a high dependency unit, where
available, and provide supportive management for minimum 24 hours.
Observation
– Evaluate and record vital signs and level of consciousness:
• HR, RR, BP and SpO2
• Temperature
• Level of consciousness (GCS or AVPU)
• Pupillary response and size
– Pain assessment
• High risk: every 30 minutes for 2 hours, then every hour if stable
• Low/intermediate risk: every hour
– Monitor BGL at least every 4 hours.
– Clinical signs of deterioration include:
• Decrease in level of consciousness.
• Development of severe or increasing headache, or persistent vomiting.
• Development of agitation or abnormal behaviour including new confusion or hallucinations.
• Any seizure activity.
• Any focal neurological sign.
• Clinical signs consistent with raised intracranial pressure or herniation:
▹ Cushing’s triad – hypertension, bradycardia and irregular respirations.
▹ Extensor posturing or hemiparesis.
▹ Pupillary signs – sluggish reaction, or unilateral/bilateral pupillary dilation.
Where possible, ensure all children admitted with head injury are seen by an experienced
senior clinician.
Supportive management
– Nurse at 30 degrees and keep head in midline.
– Temperature: aim for normothermia and avoid hyperthermia at all times.
– Repeated vomiting: administer ondansetron IV or PO: 0.15 mg/kg.
– Seizures: follow treatment algorithm for seizures (Chapter 7, Section 7.2). Consider seizure
prophylaxis by starting maintenance treatment in high-risk cases.
– Analgesia: if necessary, give paracetamol or ibuprofen. If pain level higher give stronger
analgesia, taking into account the level of consciousness of the child. See Chapter 15,
Section 15.4 for more detail on pain management.
– If IV fluids are necessary, administer IV maintenance fluids restricted to 70% of usual
maintenance volumeb given the risk of cerebral oedema (see Chapter 15, Section 15.2).

b Increased ADH secretion can cause water retention, leading to fluid overload.

62
Chapter 2: Emergencies

– Monitor BGL and treat hypoglycaemia (BGL < 3.3 mmol/L or < 60 mg/dL) with 2 mL/kg 2
of glucose (dextrose) 10% IV/IO over 2-3 minutes, or 10 mL/kg via NGT. See Chapter 9,
Section 9.3 for further detail on ongoing management of hypoglycaemia.
– Keep NBM if possible neurosurgical intervention (high risk patients under observation). Do
not insert an NGT if concern of basal skull fracture.
– Administer antibiotic treatment (cefazolin and metronidazole) for penetrating head injury.
Start immediately but do not delay referral.
– Monitor blood electrolytes, if available.
– Deep vein thrombosis (DVT) prophylaxis is not recommended in children.

2.8.3 Raised intracranial pressure


If signs of raised intracranial pressure are evident, consider treatment with hyperosmolar fluid
(staff should be trained and experienced in its administration). Use prior to referral as a bridge
before neurosurgery.
First line: hypertonic saline (preferred due to safety of administration and monitoring)

hypertonic saline (NaCl 3%) IV: 5 mL/kg over 5 to 10 minutes

Alternative: mannitol28,29

mannitol 20% IV: 5mL/kg over 20 to 30 minutes

If hyperosmolar therapy is commenced, a urinary catheter should be inserted to monitor urine


output closely and electrolytes should be monitored, if possible.

2.8.4 Discharge criteria


– Low/intermediate risk or high-risk with normal CT scan:
• After minimum 6 hours of observation, child remains asymptomatic with normal
neurological examination.
• If any symptoms persist beyond 6 hours, monitor for at least 24 hours until symptoms
resolved.
– If severe concussive symptoms, monitor for at least 48 hours.
– High-risk but no CT scan available:
• After minimum 24 hours of observation, child has been asymptomatic with normal
neurological examination for the last 12 hours.
– Ensure parents/carers are informed of the danger signs and significance of changing
symptoms, including when to seek urgent review.

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2.9 Poisoning

Poisoning or intoxication of a child may occur due to ingestion, inhalation or exposure to a


natural or chemical substance. A poisoned child may be asymptomatic or in a life-threatening
condition. Initial management is to stabilise the child and to try to identify the toxin involved,
provide supportive care, decontaminate to prevent further absorption of the toxin, and where
possible, to give an antidote or specific treatment for the identified toxin.
Common substances or situations to consider:
– Drugs: paracetamol, ibuprofen, codeine (in cough syrups), phenobarbital, morphine,
diazepam.
– In small children: accidental ingestion of a drug or toxic substance is most common, or
inappropriate administration of prescribed or over-the-counter medicines.
– In older children: intentional drug overdose or recreational drugs should be considered.
– In contexts with traditional medical practices: consider toxicity due to administration of
traditional medicines (often plant based with plant toxic effects).
– Environmental: pesticidesa, heavy metals (lead), corrosives (bleach), insecticides
(organophosphates, cholinergic agents) and carbon monoxide.
– Food-borne (mycotoxins/aflatoxinb). Incorrectly prepared foods such as Konzo disease from
insufficiently processed bitter cassava.
– Household products, toxic alcohols (methanol, ethylene glycol, ethanol).
Contact a local or national poisons centre where available. Advice is also available from the
WHO International Programme on Chemical Safety poisons centres sources30,31,32.
A global Poisons Centres Directory can be accessed at: https://www.who.int/data/gho/data/
themes/topics/indicator-groups/poison-control-and-unintentional-poisoning.

2.9.1 Diagnosis and approach to the suspected poisoned child


The child’s condition can range from stable and asymptomatic to life-threatening, depending
on the nature of the toxin(s), the severity of the poisoning and the phase of poisoning the child
is in. Diagnosis and management should be approached by the clinical condition of the child
and based on the signs and symptoms.

Try to identify the toxin


Specific history
– Type of drug/toxin given, administered or taken.
– What time?
– Amount?
– Other substances taken (other drugs, herbs, etc.)
– Underlying health problem or condition.

a Various pesticides used in agriculture and insecticides cause both intentional and unintentional poisoning.
b It is estimated that 25% of the world’s crops are affected by mould or fungal growth. Mycotoxin (especially
aflatoxin) poisoning (sometimes acute) is a real public health concern.

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Chapter 2: Emergencies

Clinical examination 2
– Full clinical examination (see Chapter 1, Section 1.3).
– Look for specific signs and symptoms that may indicate poisoning:

System Signs or symptoms

General Temperature instability, hypoglycaemia


Neurological Altered mental status or level of consciousness
Agitation, disorientation, hallucinations
Seizures
Abnormal muscle tone, presence of clonus, increased reflexes,
diminished motor response
Abnormal pupillary reactivity and ocular movements
Cardiovascular Bradycardia, tachycardia, prolonged CRT, hypo- or hypertension,
arrhythmias
Gastrointestinal Hypo- or hyperactive bowel sounds, abdominal pain, diarrhoea,
nausea, vomiting, signs of GI bleeding
Respiratory Tachypnoea, bradypnoea, breath odour, wheezes, stridor, rhonchi,
crackles
Liver Jaundice, hepatomegaly, bleeding
Renal Oliguria, haematuria, metabolic acidosis
Skin Dry/moist, flushed/pale, blisters/macules
Mouth Salivation, laryngeal oedema, oral ulcers, oral and pharyngeal pain,
mucous membranes (dry/moist)
Eyes Dilated pupils (mydriasis), constricted pupils (miosis)

Investigations
– FBC, Hb, BGL
– Electrolytes, serum bicarbonate, urea and creatinine, if available
– Urine dipstick
– ECG, if available
– Chest x-ray, if suspected inhalational exposure
– Toxicology, if available

2.9.2 Initial management and approach


Following initial resuscitation, whether the toxic agent(s) is identified or not, the key to good
management of the child is attentive supportive treatment and the prompt reduction of the
absorption of the poison.

Initial management and stabilisation


– Assess ABCDE and resuscitate as needed (see Section 2.1).
– Open and secure airway with adjuncts if necessary.
– If feasible, place in recovery position to prevent any aspiration (especially if vomiting).

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Chapter 2: Emergencies

– Administer high-flow oxygen via face mask, aiming to maintain SpO2 > 94%. Treat with
100% oxygen if suspected carbon monoxide poisoning (e.g. burns, found by heating device);
altered mental state, ‘reddish’ skin and lips.
– Get IV or IO access. If signs of circulatory impairment, treat as shock (see Section 2.2).
– Check BGL and treat hypoglycaemia. See Chapter 9, Section 9.3.
– Manage seizures (see Chapter 7, Section 7.2).
– Consider decontamination if appropriate: for potentially life-threatening ingestions or skin
exposure, refer to Section 2.9.4.

Evaluate the phase of the poisoning


Based on history obtained and clinical signs and symptoms, whether toxin known or not, try to
assess the phase of acute poisoning the child is in to guide management:
– Pre-clinical phase: after exposure but before the development of signs and symptoms.
Treatment is guided by the history and is aimed at reducing or preventing the predicted
toxicity.
– Toxic phase: the period from the onset to the peak of clinical symptoms of toxicity. The
treatment objectives are to shorten the duration and lessen the severity of toxicity.
Treatment is guided largely by clinical examination.
– Resolution phase: the period from peak toxicity to recovery.

2.9.3 Toxic agent not known: the toxidromic approach33,34


When the toxic agent(s) is not known or cannot be identified, try to identify whether specific
signs and symptoms correspond to a toxidrome (see Table 2.4). A toxidrome is a syndrome
caused by excessive levels of toxin in the body, for example, cholinergic or muscarinic toxidrome.
Recognising the toxidrome the child is presenting may help identify the possible toxic agent.
Specific treatment, where available, corresponding to the toxidrome should be given as an
adjunct to supportive treatment.

Supportive treatment
– Reassess ABCDE and the child’s clinical condition regularly and provide supportive treatment
accordingly.
– Protect airways, be particularly attentive in children with reduced consciousness or absence
of cough reflex.
– Administer oxygen if necessary, aiming to maintain SpO2 between 94% - 98%.
– Keep in recovery position and aspirate gastric contents if necessary. Keep NBM until alert.
– Close observation with vital sign monitoring. When clinically indicated and available, repeat
ECG every 6 to 12 hours.
– Start IV maintenance fluids while NBM to ensure adequate hydration. If there are signs of
impaired circulation, treat for shock (Section 2.2).
– Monitor temperature (treat fever with paracetamol if able to confirm paracetamol was not
source of poisoning or no signs suggestive of liver failure such as bleeding).
– Assess urine output. If there are signs of urinary retention, insert urethral catheter carefully.
– If aspiration of gastric contents suspected, start IV antibiotic treatment for pneumonia
(Chapter 4, Section 4.5.3).

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Chapter 2: Emergencies

Specific management 2
– Seizures: treat with benzodiazepines (see Chapter 7, Section 7.2).
– Clinical signs or suspicion of muscarinic toxidrome: administer atropine.
– Clinical signs or suspicion of cytotoxic toxidrome: administer hydroxocobalamine IV:
70 mg/kg (maximum 5 g) over 15 minutes and sodium thiosulphate IV: 400 mg/kg (1.6 mL/kg)
maximum 50 mL (25% solution) where available.
Management of gastritis or gastrointestinal haemorrhage
– Keep NBM for 24 hours from the time of suspected ingestion or the time symptoms indicating
gastritis or gastrointestinal haemorrhage developed.
– If no signs of further bleeding after 24 hours, introduce oral fluids and monitor over 24 hours.
If this is well tolerated, solid food can be reintroduced.
– Administer omeprazole IV: 0.5 mg/kg slow IV (over 5 minutes) once daily.
– Once tolerating solid food, change to omeprazole PO: 10 mg (weight < 20 kg) or 20 mg
(weight ≥ 20 kg) once daily for 10 days.
Management of hepatic toxicity
– Signs of hepatotoxicity include coagulopathy, encephalopathy, hepatomegaly, and jaundice.
– Administer IV acetylcysteine in an intensive care unit where possible.
acetylcysteine IV: 300 mg/kg in glucose (dextrose) 5% IV perfusion total over 20 hours
• Loading dose: 200 mg/kg over 4 hours
• Followed by 100 mg/kg over next 16 hours
Monitor carefully. Anaphylaxis may occur, particularly in children with a history of
asthma.

– Monitor for signs of coagulopathy (bruising, bleeding, prolonged bleeding time). Only in the
case of active bleeding, administer a single dose of vitamin K slow IV: 1 to 2 mg in infants or
5 mg in children ≥ 12 months.
– Avoid antiplatelet and hepatotoxic drugs (NSAIDS, ibuprofen, paracetamol).
– Administer IV omeprazole as a precaution and treatment of gastrointestinal haemorrhage
(see above).
– Monitor BGL regularly and treat hypoglycaemia. See Chapter 9, Section 9.3.
– If signs of hepatic encephalopathy develop, lactulose may be given:

lactulose PO: < 1 year: 2.5 mL 2 times daily; ≥ 1 year: 10 to 30 mL 3 times daily

Table 2.4 - Toxidrome by drug groups35


Common causative
Drug group Common signs
agents
Anticholinergic Delirium, tachycardia, dry flushed skin and Antihistamines,
(antimuscarinic) mucosa, dilated pupils, myoclonus, raised antipsychotics,
temperature, urinary retention, decreased antispasmodics,
bowel sounds. Seizures and dysrhythmias in atropine, cyclic anti-
severe cases. depressants, belladonna
alkaloidsc, toxic
mushrooms

c Belladona plant also known as deadly nightshade, including the Datura species.

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Chapter 2: Emergencies

Common causative
Drug group Common signs
agents
Cholinergic Muscarinic toxidrome Nicotinic toxidrome Organophosphates,
(muscarinic and DUMBELS: MTWtHFSS (days of the pesticides, nerve agents,
nicotinic receptor • Diaphoresis week in English): tobacco, liquid nicotine,
stimulation) • Urination • Mydriasis some mushrooms
• Miosis • Tachycardia
• Bronchorrhoea, • Weakness
bradycardia, • Hypertension
bronchospasm • Fasciculations
• Emesis • Seizures
• Lacrimation • Somnolence
• Salivation, Sweating
Cytotoxics Delayed abdominal pain, nausea, vomiting, Cyanogenic glycosides
altered mental status, seizures, cardiovascular (e.g. poorly processed
collapse, lactic acidosis, multisystem organ cassava)
failure.
Opioids Sedated, respiratory depression, bradycardia, Morphine, codeine,
hypotension, hypothermia, constricted pupils. fentanyl, methadone
Sedatives Reduced mental state, but mostly normal vital Barbiturates,
Hypnotics signs. Possible reduced RR and hypoglycaemia. benzodiazepines, ethanol,
amitraz (pesticide).
Sympathetic nervous Tachycardia (or bradycardia), hypertension, Amphetamines, cocaine,
system stimulants dysrhythmias, dilated pupils, delirium, delusions, decongestants, ephedrine,
paranoia, hyperreflexia, seizures, raised methamphetamines,
temperature, diaphoresis, piloerection. salbutamol

2.9.4 Decontamination

Skin decontamination in case of skin exposure (e.g. pesticides)


– Remove contaminated clothing and place in sealed plastic bag.
– Flush exposed areas with lukewarm water for minimum 20 minutes.

Eye decontamination
– Flush each eye with lukewarm water or sodium chloride 0.9% (≥ 1 L/eye) for 10-15 minutes.
– Refer to ophthalmologist, if available, for examination of the cornea.

Gastrointestinal decontamination in case of toxin ingestion


This has a limited role in most cases of intoxication, particularly when presentation is delayed
or timing of ingestion is unclear. Before initiation it is important to consider the risk/benefits
of the intervention and discuss with a senior clinician if available. Induced vomiting is
contraindicated and gastric lavage is no longer recommended. Other methods should only be
considered in a conscious patient that is not at imminent risk of seizures.
Gastric aspiration
This is rarely performed unless child has taken a very toxic substance or is intubated.
– If the child is not intubated, place the child in an upright position.
– Using a larger sized NGT (conical tip) with respect to the size of the child, suction any oral
secretions and aspirate gastric contents gently.

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Chapter 2: Emergencies

– Look for signs of the toxic substance within the gastric aspirates. 2
Caution: if possible caustic ingestion, aspiration or suctioning is contraindicated.
Absorption with activated charcoal36
The most effective way to decontaminate a child with moderate to severe poisoning is activated
charcoal, which can bind most therapeutic drugs and reduce further absorption from the
gastrointestinal tract. However, metals (including iron substances), corrosives, hydrocarbons
(gasoline, kerosene) and alcohols are poorly adsorbed by activated charcoal.
Activated charcoal:
– Can be administered up to 4 hours post ingestion.
– Is contraindicated in a child with reduced level of consciousness (unless intubated).
– Is contraindicated in gastrointestinal haemorrhage or corrosive ingestion.
Use with caution: aspiration of activated charcoal can cause significant morbidity and
even mortality. If giving via NGT, strictly confirm the tube is in the correct position first.
Give activated charcoal as soon as possible, within 4 hours of ingestion or if toxic substance is
found during stomach aspiration:

activated charcoal PO/NGT, give slowly to reduce risk of vomiting


• < 1 year: 1 g/kg, once
• 1 to 12 years: 1 to 2 g/kg or 25 to 50 g/dose (maximum 50 g), once
• > 12 years: 50 to 100 g/dose, once
Add a minimum of 240 mL of drinking water with 20 to 30 grams of charcoal and mix well
until smooth. If necessary, juice or ice-cream can be added to improve taste. 1 tablespoon
of charcoal powder = 30 grams.

2.9.5 Toxic agent known: specific treatment


Consult a local or national poisons information centre as soon as possible, where this is
available. For some drugs or agents that can lead to poisoning, specific antidotes may be
available (refer to Table 2.5, page 70).

Paracetamol overdose
– Administer activated charcoal if within 4 hours of ingestion37. Activated charcoal may be less
effective in younger children if liquid paracetamol was consumed.
– Where possible, measure serum paracetamol levels.
– Administer IV acetylcysteine (as above) as an antidote in the following cases:
• Known toxic ingestion: acute ingestion of ≥ 200 mg/kg or repeated supratherapeutic
ingestion of > 100 mg/kg/day, or
• Signs of hepatic toxicity.

Methanol
Refer to MSF Methanol Poisoning protocol.
– Metabolite (formic acid) is highly toxic and responsible for metabolic acidosis.
– Contamination of traditional beverages (intentional or unintentional).
– History: consumption of household products (e.g. windshield liquid wash) or traditionally
made alcoholic contaminated beverages.

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Chapter 2: Emergencies

– Key signs: tachypnoea (acidosis), blurred vision, abdominal pain, nausea, vomiting; can lead
to blindness, coma, death.
– If symptomatic, administer ethanol (via NGT) which will compete with methanol.

Morphine or codeine-based drugs


Refer also to MSF Perioperative Management of Surgical/Trauma Pain protocol.
– Excessive sedation is the first sign of morphine overdose, followed by respiratory depression.
– If intoxication occurs during morphine-based treatment, stop morphine treatment and
stimulate verbally and via tactile stimulation.
– Start supportive treatment with oxygen and bag-mask ventilation if necessary.
– Naloxone is a morphine antagonist and is indicated in patients who cannot be aroused and/
or have significant respiratory depression (respiratory pauses, apnoea) despite stimulation.
– In cardiorespiratory collapse, begin CPR immediately and call for help (see Section 2.1.1).

Organophosphates
Refer to MSF Exposure to Chemical Agents Manual.

Table 2.5 - Specific antidotes for common toxins


Substance/toxin Specific antidote

Benzodiazepines flumazenil IV: 10 micrograms/kg every 1 minute if required (max.


dose 200 micrograms) up to 5 times
Beta-blockers If bradycardia: atropine IV: 40 micrograms/kg (max. 3 mg per dose)
If cardiogenic shock, no response to atropine, administer glucagon
IV: 50-150 micrograms/kg (max. 10 mg per dose) in glucose
(dextrose) 5%. Then IV infusion of 50 micrograms/kg/hour.
Calcium-channel blockers calcium
insulin/glucose
Iron (> 40 mg/kg of Iron chelation if available: desferrioxamine IV: 15 mg/kg/hour until
elemental iron) serum iron < 60 micromol/L or asymptomatic
Isoniazid pyridoxine

Methanol ethanol or fomepizole and bicarbonate (see MSF Methanol


Poisoning protocol).
Narcotics naloxone IV: 5 micrograms/kg (0.25 mL/kg)d repeated every 1 to
Morphine or codeine-based 2 minutes until: RR > 20 in < 1 year; RR > 15 in 1-5 years; RR > 10
drugs in > 5 years; and child is awake. If life-threatening effects of opioid
overdose (e.g. apnoea), naloxone IV: 100 micrograms/kg (max.
2 mg).
Organophosphates atropine IV: 20 micrograms/kg every 5 to 10 minutes until skin
(insecticides) or nerve agent flushed and dry, pupils dilate, bradycardia resolved.
Certain mushrooms
(cholinergic syndrome)
Paracetamol (> 200 mg/kg acetylcysteine IV: Loading dose: 200 mg/kg over 4 hours, followed
acute ingestion, or by 100 mg/kg over next 16 hours
> 100 mg/kg/day for
> 72 hrs)

d Dilution: 1 vial of 0.4 mg naloxone + 19 mL normal saline = 20 micrograms/mL

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Chapter 2: Emergencies

2.9.6 Prevention 2
Medicines are the most common product that causes accidental poisoning in children, and
particularly so in children under 5 years of age38. This can be avoided by ensuring that medicines
are not left in a place where children can reach them. Medicines should be stored safely in a
place that can be locked or cannot be accessed by children. If available, ask for containers with
child-proof caps. Dispose of any medicines that have expired.

Traditional medicine
If there are multiple cases of suspected poisoning from the use of traditional medicines, try to
identify the products and/or practices that are potentially harmful.

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Chapter 2: Emergencies

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38. Mowry JB, Spyker DA, Brooks DE, McMillan N, Schauben JL. 2014 Annual Report of the
American Association of Poison Control Centers’ National Poison Data System (NPDS):
32nd Annual Report. Clin Toxicol. 2015;53(10):962-1147.
https://doi.org/10.3109/15563650.2015.1102927

74
Chapter 3:
Acute febrile illness
3

3.1 Approach to a child with fever................................................................................ 77


3.1.1 Identifying underlying cause............................................................................ 77
3.1.2 Investigations and management..................................................................... 79
3.1.3 Management of fever...................................................................................... 83
3.2 Severe bacterial infection or sepsis......................................................................... 85
3.2.1 Clinical features............................................................................................... 85
3.2.2 Initial management......................................................................................... 85
3.2.3 Investigations................................................................................................... 86
3.2.4 Ongoing management..................................................................................... 86
3.3 Meningitis and encephalitis.................................................................................... 88
3.3.1 Clinical features............................................................................................... 88
3.3.2 Initial management......................................................................................... 89
3.3.3 Investigations................................................................................................... 90
3.3.4 Ongoing management..................................................................................... 92
3.3.5 Steroid therapy................................................................................................ 93
3.3.6 Complications.................................................................................................. 93
3.3.7 Chemoprophylaxis and prevention.................................................................. 94
3.4 Malaria..................................................................................................................... 95
3.4.1 Clinical features............................................................................................... 95
3.4.2 Investigations................................................................................................... 96
3.4.3 Management................................................................................................... 96
3.4.4 Prognosis....................................................................................................... 102
3.4.5 Prevention...................................................................................................... 103
3.5 Tetanus................................................................................................................... 104
3.5.1 Clinical features............................................................................................. 104
3.5.2 Management................................................................................................. 105
3.5.3 Prevention...................................................................................................... 108
3.6 Enteric (typhoid and paratyphoid) fever...............................................................109
3.6.1 Clinical features............................................................................................. 109
3.6.2 Diagnosis....................................................................................................... 110
3.6.3 Management................................................................................................. 110
3.6.4 Prevention...................................................................................................... 112
3.7 Measles.................................................................................................................. 113
3.7.1 Clinical features............................................................................................. 113
3.7.2 Management................................................................................................. 114
3.7.3 Prevention...................................................................................................... 116
3.8 Orbital and peri-orbital cellulitis........................................................................... 117
3.8.1 Clinical features............................................................................................. 117
3.8.2 Management................................................................................................. 118
References Chapter 3................................................................................................... 120
Chapter 3: Acute febrile illness

3.1 Approach to a child with fever

3
Fever is a physiological response characterized by an elevation of body temperature above
normal daily variation1. It is defined as an axillary temperature of over 37.5 °Ca for all age
groups in this guideline2.
Fever is a common presentation of many paediatric conditions in all age groups. The most
common cause is infection. In children up to 3 years of age, around 80% of cases are due to
a viral infection, however, the younger the child is, the higher the probability that a fever is
due to a severe bacterial infection or sepsis1. Non-infectious causes include inflammatory,
immune-mediated, and neoplastic conditions. When the cause of a fever of less than one
week cannot be identified by history and clinical examination, it is classified as a ‘fever without
source’3.
Fever of unknown origin (FUO) is a diagnosis of exclusion and is defined in children as a
fever lasting more than one week with negative preliminary investigations (see Chapter 14,
Section 14.1).

3.1.1 Identifying underlying cause


Any fever in a child should be considered as a potential symptom of an underlying infectious
condition. If there are any signs of severe bacterial infection or sepsis, treat as such (see
Section 3.2). In the absence of signs of severity, it is important to try to find the focus of the
infection to guide treatment:
– Take a detailed medical history (including social and family history, and history of exposure),
including:
• When did the fever start and what is the pattern of the fever?
• Have any medicines been given? If yes, which one(s), how much, and how often?
• Is there fever every day or are there days with no fever?
• Is the child able to perform their normal daily activities?
• Has the child been in contact with someone who is unwell?
• Any travel history in endemic areas for specific infectious diseases (e.g. malaria)?
• Any insect bites or exposures to animals or abattoirs?
• Are there associated symptoms and signs? If so, ask about onset, duration, pattern,
severity, precipitating and alleviating factors, previous episodes. Table 3.1, page 78,
describes commonly associated signs and symptoms and their potential diagnoses. It is
not exhaustive and there may be overlap between symptoms of different pathologies, but
it may help to guide the clinician to a diagnosis.
– Perform a comprehensive clinical examination (cardiac, respiratory, abdominal, neurological,
musculoskeletal, ear, nose and throat (ENT), and skin).
– Consider necessary investigations.
– Check immunisation and nutritional status.

a The definition of fever is generally accepted as a core temperature of more than 38 °C. Axillary temperature
is not an accurate reflection of core temperature, therefore the cut-off point is lower. It is recommended
to measure temperature when the child is at rest, in a comfortable environment and not wearing excessive
clothing. For accurate readings, the thermometer should be placed over the axillary artery for 3 minutes.
Rectal temperature is not recommended for hygiene and safety purposes.

77
Chapter 3: Acute febrile illness

Table 3.1 - Potential causes of fever with associated symptoms and signs

Associated symptoms or signs Potential common causes

Irritability, altered consciousness, meningeal Meningitis, meningoencephalitis, severe


signs, seizures, focal neurologic findings, malaria
refusal to feed, bulging fontanelle

Opisthotonos, seizures Meningitis, tetanus

Lethargy/altered consciousness, poor Sepsis, severe bacterial infection


feeding, vomiting, cold hands and feet,
pain/discomfort, tachypnoea, tachycardia,
non-blanching skin rash

Unilateral eye swelling, red eyelid Orbital or peri-orbital cellulitis

Ear pain, ear discharge Otitis media

Redness and tenderness behind the ear, Mastoiditis


swelling of ear lobe that sticks out

Sore throat, cervical lymphadenopathy, Streptococcal pharyngitis, diphtheria,


difficulty swallowing, nasal voice, white or peritonsillar abscess, epiglottitis
grey tonsillar membranes, rash

Difficulty swallowing, multiple Gingivostomatitis, Coxsackie virus


oropharyngeal papular or vesicular lesions

Rhinorrhea, cough with bilateral chest Viral respiratory infections


wheezing, bilateral fine crackles

Barking cough Croup

Cough, unilateral decreased breath Pneumonia


sounds or crepitations, decreased appetite
or vomiting, abdominal pain (if basal
pneumonia), chest pain

Dental ache, unilateral facial swelling Caries, dental abscess

Chest pain, palpitations, heart murmur, Pericarditis, myocarditis, endocarditis


arrhythmia

Intense abdominal pain, vomiting, Appendicitis, peritonitis, enteric fever


diarrhoea or constipation (especially if relative bradycardia), amoebic/
bacterial liver abscess

Vomiting, diarrhoea Gastroenteritis, enteric fever

78
Chapter 3: Acute febrile illness

Associated symptoms or signs Potential common causes

Flank/back pain, dysuria, vomiting Pyelonephritis, urinary tract infections


(especially in neonates and infants)
3
Jaundice, hepatomegaly Viral hepatitis, malaria, visceral leishmaniasis

Anaemia Malaria

Skin macular rash, conjunctivitis, Measles


rhinorrhoea, Koplik’s spots

Skin rash Viral infections (non-specific, rubella,


parvovirus, haemorrhagic fevers), Strep A
(scarlet fever), varicella

Bleeding signs (epistaxis, gingival bleeding, Viral haemorrhagic fevers, leukaemia, severe
haematuria), petechiae malaria, visceral leishmaniasis, dengue

Skin redness, tenderness, and warmth Bacterial skin infections (erysipelas,


cellulitis), skin abscess

Limping, bone pain, decreased range of Osteomyelitis, leukaemia, septic arthritis


limb motion, joint pain or swelling, redness
around a joint

Joint pain, skin rash Rheumatic disease, dengue, chikungunya

Anaemia, jaundice, generalized body pain Sickle cell disease, malaria, dengue

Anaemia, hepatomegaly, splenomegaly Malaria, visceral leishmaniasis

3.1.2 Investigations and management


In a child who is febrile and presents with signs of severe bacterial infection or sepsis, see
Section 3.2. In a child who is febrile but who does not present with any signs indicative of
potential severe bacterial infection or sepsis, manage according to age group:
– < 1 monthb: treat as a neonatal sepsis (see MSF Neonatal Care Guidelines) and try to identify
a source of infection.
– 1 to 3 months: consider as high-risk for serious illness. Perform investigations based on
clinical appearance and potential focus of infection (see Figure 3.1, page 80).
– Above 3 months of age: investigate based on clinical appearance and potential focus of
infection (see Figure 3.2a page 81 and Figure 3.2b page 82).
These criteria are valid not only for the first clinical approach to the patient, but also for any
new onset of fever during the admission period. All admitted children should have vital signs
monitored and recorded as often as required using an early warning system (see MSF Manual
of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).

b Note that in this age group severe infections can also present without fever or with hypothermia.

79
80
Figure 3.1 - Management of febrile infants 1 to 3 months WITHOUT signs of severe bacterial infection or sepsis

Malaria test and Hb, Febrile infant 1 to 3 months WITHOUT


if endemic region signs of severe bacterial infection or sepsis

Admit for clinical observation Malnourished or


Positive Negative
Chapter 3: Acute febrile illness

and monitoring for 48 hours nutritionally at risk

Search for focus of infection on clinical examination:


Check for
+ Urine dipstick and urine culture if possible Start amoxicillin PO:
signs of severe
+ Blood tests (FBC, blood culture if possible, malaria RDT) 50 mg/kg 2 times daily
malaria and treat
+ Lung ultrasound or CXR if respiratory signs for 5 days
accordingly
+ Lumbar puncture if signs suggestive of meningitis
(see Section 3.4)

Positive investigations Negative investigations


Consider other
focus of infection
also, especially
if infant doesn’t Treat according If infant develops If infant remains
quickly improve to focus If persistent
signs of severe well after
with treatment* fever (> 7 days),
bacterial 48 hours and
investigate
infection or fever ≤ 7 days,
for FUO (see
sepsis, start IV discharge home
Chapter 14,
antibiotics (see with advice on
Section 14.1)
Section 3.2) when to return

*Children in malaria endemic regions often have concomittant infections


Figure 3.2a - Management of febrile children above 3 months of age WITHOUT signs of severe bacterial infection or sepsis with fever ≤ 72 hours

Malaria test and Hb, Febrile child > 3 months with fever for ≤ 72 h WITHOUT
if endemic region signs of severe bacterial infection or sepsis
If malnourished,
Search for focus of infection admit and start
Positive Negative on clinical examination amoxicillin PO:
50 mg/kg 2 times
daily for 5 days

Check for Focus identified No focus identified


signs of severe
malaria and treat
accordingly Age < 24 months Age ≥ 24 months
(see Section 3.4) Treat according to
focus and admit if
necessary Previous UTI No previous UTI

Consider other
focus of infection Urine dipstick and Urine dipstick and
also, especially culture if possible culture if possible
if child doesn’t
quickly improve If child clinically
with treatment* well, send home
Negative Positive Negative
with advice on
when to return

Admit for clinical observation and monitoring for Treat for febrile UTI (see Chapter 8,
24 hours, malaria RDT, and search again for focus Section 8.1) and admit if necessary

If negative RDT, fever not worsening If child develops signs of severe


and child clinically well, discharge bacterial infection or sepsis, start IV
home with advice on when to return antibiotics (see Section 3.2)
Chapter 3: Acute febrile illness

81
* Children in malaria endemic regions often have concomittant infections.
3
82
Figure 3.2b - Management of febrile children above 3 months of age WITHOUT signs of severe bacterial infection or sepsis with fever > 72 hours

Malaria test and Hb, Febrile child > 3 months with fever > 72 h WITHOUT
if endemic region signs of severe bacterial infection or sepsis
If malnourished,
Search for focus of infection admit and start
Positive Negative (including ears, joints, skin) amoxicillin PO:
50 mg/kg 2 times
daily for 5 days
Chapter 3: Acute febrile illness

Check for Focus identified No focus identified


signs of severe
malaria and treat
accordingly
(see Section 3.4) Treat according to Investigate:
focus and admit if + Urine dipstick and send for culture if possible
necessary + Blood tests (FBC, blood culture if possible, malaria RDT)
+ Lung ultrasound or CXR
+ Lumbar puncture if signs suggestive of meningitis
Consider other
focus of infection
also, especially
if child doesn’t
quickly improve Positive investigations Negative investigations
with treatment*

Treat according If child develops signs of If child clinically well


If persistent fever
to focus and admit severe bacterial infection and fever ≤ 7 days, send
(> 7 days), investigate
if necessary or sepsis, home with advice on
for FUO (see Chapter 14,
start IV antibiotics when to return and
Section 14.1)
(see Section 3.2) follow-up in 48 hours**

* Children in malaria endemic regions often have concomittant infections.


** If unable to return for follow-up, consider admission to hospital for observation and monitoring.
Chapter 3: Acute febrile illness

On discharge, explain to the parents/carers to seek immediate medical advice or return to


hospital if the child develops any of the following signs:
– Neck stiffness or photophobia
– Non-blanching rash
– Skin pallor or cold extremities 3
– Profuse vomiting and refusing to drink
– Oliguria for more than 12 hours
– Increased lethargy or reduced conscious level
– Inconsolable crying, agitation or pain not relieved by medication
– Breathing difficulties
– Seizures, including febrile seizures
– Persistence or recurrence of fever for more than 3 days

3.1.3 Management of fever


The aim of management is to treat the underlying cause of the fever, not the fever itselfc.
However, if the fever is causing discomfort to the child, it should be managed symptomatically.

Non-pharmacological measures
– Undress the patient.
– Do not wrap children in wet towels or cloths (it increases their discomfort and increases risk
of hypothermia).
– Encourage drinking, especially for young infants continue frequent breastfeeding.

Pharmalogical measures
Give paracetamol and/or ibuprofen as antipyretics. Prescribe for maximum of one day and
re-evaluate need:
– paracetamol PO or via nasogastric tube (NGT): 15 mg/kg (maximum dose 1 g), every 6 to
8 hours as required (maximum 60 mg/kg/day or 4 g/day).
• In the case of SAM: 10 mg/kg, every 8 hours as required.
• IV paracetamol should not be used as an antipyretic, but is reserved for analgesia in the
case of children who are strictly nil by mouth (NBM).
• Paracetamol is not recommended in hepatic disorders
– ibuprofen PO: 10 mg/kg, every 8 hours as required (maximum 30 mg/kg/day) with milk or
food (to reduce the risk of gastrointestinal irritation).
• In the case of SAM: 5 mg/kg, every 8 hours as required. Do not give in Phase I of nutrition
treatment.
• Do not give to children younger than 6 months or with severe dehydration, renal failure,
gastrointestinal bleeding, or haemorragic fevers (including dengue).

Aspirin (acetylsalicylic acid) should not be used in children as an antipyretic due to the
risk of Reye’s syndrome.
Use paracetamol and ibuprofen with caution in malnourished children.

c There is no evidence that reducing fever decreases the morbidity or mortality from febrile illness (even malaria)
or prevents febrile seizures. Nor is there evidence that fever 40 °C or higher is associated with brain damage.

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Chapter 3: Acute febrile illness

Important points to remember:


– For any fever in a malaria endemic area, malaria should be ruled out first.
– It may not be possible to find a source of infection during the first 48 hours of a febrile
illness.
– Not all fevers are sepsis.
– Teething does not cause fever.
– Response to antipyretics and length of fever do not predict the cause or severity of the
infection.
– Febrile seizures are common in young children during febrile illness. A simple febrile seizure
is not necessarily indicative of bacteraemia or meningitis (see Chapter 7, Section 7.3 for
more information on the assessment and management of febrile seizures).

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Chapter 3: Acute febrile illness

3.2 Severe bacterial infection or sepsis

3
Sepsis is a clinical syndrome that usually results from severe bacterial infection, though may also
be caused by viruses and fungi. It is an uncontrolled and toxic systemic response that includes
inflammation, immune dysfunction, impaired circulation in the capillaries and oxygen deficit.
It can lead to multiple organ failure and death within hours in the absence of treatment. Even
with prompt and adequate administration of antibiotics, sepsis can be fatal if advanced vital
organ support, such as artificial ventilation and inotropic support, is unavailable. Bacteria that
commonly cause sepsis include Neisseria meningitidis, Streptococcus pneumoniae, Escherichia
coli, Staphylococcus aureus, Salmonella and Haemophilus influenza type B. In infants less than
3 months old, Listeria monocytogenes should also be considered4. Although sepsis can also
be caused by viruses and fungi, for the purposes of this chapter treatment will be focused on
the management of severe bacterial infection (the most common cause of sepsis in projects
where MSF works).

3.2.1 Clinical features


Severe bacterial infection or sepsis is diagnosed in any child with fever or hypothermia who is
severely unwell with any of the following features:
– General appearance and behaviour: reduced activity, poor feeding, no smile, unfocused
gaze, unresponsive stare, hypotonia, decreased response to stimuli, lethargy, weak or high-
pitched cry.
– Colour: mottled appearance, ashen, blue, or pale skin color.
– Breathing: difficulty breathing (dyspnoea, tachypnoea, grunting, chest indrawing, nasal
flaring) or apnoea
– Circulation and hydration: dry mucous membranes, persistent tachycardia despite reduction
in fever, central CRT > 3 seconds, weak pulse, cool extremities, reduced skin turgor, reduced
urine output.
– Neurological: neck stiffness, bulging fontanelle, focal neurological signs, prolonged seizures.
– Other: fever for more than 5 days; presence of a non-blanching rash (i.e. petechiae or
purpura).

3.2.2 Initial management


Severe bacterial infection or sepsis is a medical emergency. If any of the above signs are
present, stabilise and administer antibiotics immediately:
– Call for help.
– Move child to the resuscitation area and assess and manage ABCDE (see Chapter 2,
Section 2.1).
– Administer oxygen, aiming for SpO2 between 94 - 98%.

85
Chapter 3: Acute febrile illness

– Get IV access and start empirical antibiotic treatment as soon as possible, depending on
availabilitya:

First choice:
ampicillin IV: 50 mg/kg every 8 hours + gentamicin IV: 7.5 mg/kg once daily
or benzylpenicillin IV: 50 000 IU/kg (30 mg/kg) every 8 hours (max. 4 MIU or 2.4 g/dose)
+ gentamicin IV: 7.5 mg/kg once daily
Second choice:
ceftriaxone IV: 80 mg/kg (max. 4 g if < 50 kg; max. 2 g if ≥ 50 kg) once daily
or cefotaxime IV: 50 mg/kg every 8 hours
or cloxacillin IV: 25 mg/kg every 6 hours + amikacin IV: 15 mg/kg once daily (if infection
with S. aureus and/or gram-negative bacteria and/or antibiotic resistant bacteria is
suspected)

If sepsis with signs of circulatory impairment or shock, treat as septic shock (see Chapter 2,
Section 2.2).

3.2.3 Investigations
– FBC (including differential WBC if possible)
– Blood glucose level (BGL)
– C-reactive protein (CRP), if available
– Malaria RDT, if endemic
– Blood culture (especially if purpuric rash is present)
– Urine dipstick, microscopy and culture, if available
– CXR or lung US if respiratory signs
– LP, if available and not contraindicated

3.2.4 Ongoing management


– After initial stabilisation and treatment (see Section 3.2.2), move the patient to an ICU area
for further management.
– Provide supportive care as needed (oxygen to maintain saturations 94 - 98%, IV maintenance
fluids).
– NBM initially and insert NGT and gradually start enteral feeding after 24 to 48 hours (see
Chapter 15, Section 15.5).
– Treat fever (see Section 3.1.3) if needed.
– Monitor and record vital signs and urine output as often as required using an early warning
system (see MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts:
Vital sign charts).
– Provide standard nursing care, especially if the patient is in a coma (including mouth care,
positioning, physiotherapy exercises).
– Reassess and adjust antibiotic treatment once the cause is identified or according to blood
culture results (where available).

a Empiric treatment with ceftriaxone/cefotaxime may be more appropriate in settings where invasive non-
typhoidal Salmonella are a major cause of bloodstream infection.

86
Chapter 3: Acute febrile illness

– Duration of antibiotic treatment should be determined by the child’s clinical condition and
response to treatment. Continue IV/IM treatment for at least 3 days and switch to oral when
the child is improving and eating and drinking. IV/IM treatment duration is likely to be longer
in younger, sicker children and in malnourished children. When clinically appropriate, switch
to amoxicillin/clavulanic acid (ratio 7:1 or 8:1) PO. Dosage expressed in amoxicillin: 3
• < 40 kg: 50 mg/kg 2 times daily
• ≥ 40 kg:
Ratio 8:1: 3000 mg daily (2 tablets of 500/62.5 mg 3 times daily)
Ratio 7:1: 2625 mg daily (1 tablet of 875/125 mg 3 times daily)
Total antibiotic treatment should last for 7 - 10 days.
– If there is no improvement with antibiotic treatment, consider viral or fungal causes of
sepsis.

87
Chapter 3: Acute febrile illness

3.3 Meningitis and encephalitis

Meningitis is inflammation of the meninges and encephalitis is inflammation of the brain


parenchyma. Both are serious diseases which need prompt treatment as they can lead to
death or permanent neurological disabilities.
Most cases of meningitis and encephalitis are caused by infections which can be bacterial,
viral, fungal, or parasitic. The list of pathogens can vary by context, age, immunisation status,
and underlying medical conditions (e.g. severe acute malnutrition, HIV infection, sickle cell
disease). Immunisation with H. influenzae type B (Hib), pneumococcal conjugate vaccines
and Meningococcal ACWY have reduced the incidence of bacterial meningitis where vaccine
coverage is high, however infection by the following pathogens still affects millions of children
worldwide:
– Bacterial: Streptococcus pneumoniae, Group B Streptococcus, Neisseria meningitidis,
HiB, Listeria monocytogenes, Escherichia coli, Staphylococcus aureus, Salmonella spp.,
Mycobacterium tuberculosis, Klebsiella (< 2 months).
– Viral: enterovirus, measles virus, herpes viruses (including Epstein-Barr virus, herpes simplex
viruses and varicella-zoster virus), mumps virus, Rubella virus, influenza virus, arboviruses,
HIV, Dengue virus, Japanese encephalitis virus, rabies virus, CMV.
– Fungal: Cryptococcus, Histoplasma, Blastomyces, Coccidioides, Aspergillus, Mucormycosis,
Candida.
– Parasitic: Plasmodium spp., Naegleria fowleri, Angiostrongylus cantonensis, Baylisascaris
procyonis, Gnathostoma spinigerum, Taenia solium, Onchocerca volvulus, Toxoplasma.
Non-infectious causes include cancers, autoimmune diseases, systemic lupus erythematosus,
drugs, head injury, brain surgery.

Epidemiology
The route of transmission varies by organism. Most bacteria that cause brain infections such
as meningococcus, pneumococcus, and Haemophilus influenzae are carried in the human
upper respiratory tract. They can be spread by respiratory droplets or throat secretions. The
incubation period is 4 days on average but can range between 2 and 10 days5. The highest
incidence of disease is registered in the African Meningitis Belt (region of sub-Saharan Africa),
with epidemics of meningococcal (Neisseria meningitidis A or C or W135) and pneumococcal
meningitis, generally occurring in the dry season (between October and April)5. Meningitis
can also propagate where people are living in close quarters (refugee camps, mass gatherings,
overcrowded households).

3.3.1 Clinical features


Clinical presentation may be variable and non-specific, but children older than 1 month most
commonly develop the following:
– Fever, nausea, vomiting, anorexia, irritability (often the first sign in young infants),
photophobia, seizures (mostly generalised), and respiratory distress
– Altered consciousness (present in most children) with lethargy, confusion, coma

88
Chapter 3: Acute febrile illness

– Meningeal signs (not always present, especially in young infants):


• Back pain
• Nuchal rigidity (absent in patients with focal neurologic deficits)
• Kernig’s signa
• Brudzinski’s signb 3
– Signs of increased intracranial pressure: headache (older children), irritability and bulging
fontanelle or widening of the cranial sutures (in infants), bradycardia, hypertension,
anisocoria
– Abnormal eye movements due to paralysis of the third, fourth or sixth cranial nerves
– Focal neurologic findings (hemiparesis, quadriparesis, facial palsy, visual field defects)
– Petechiae and purpura (can occur in fulminant meningococcal sepsis).
Clinical distinction between meningitis and encephalitis may be difficult but is important as
causative pathogens differ. The following clinical features may help to differentiate between
the two:
– Meningitis more likely: fever with absent or incomplete immunisation history, bulging
fontanelle or meningeal signs, purpuric rash.
– Encephalitis more likely: fever with altered mental status and focal neurological signs or
vesicular rash.
Initial empiric treatment often covers both.

Diagnosis
Based on history (including immunisations) and clinical examination (including neurological
assessment).

3.3.2 Initial management


Meningitis or encephalitis is a medical emergency. If suspected, stabilise and administer
antibiotics immediately:
– Call for help.
– Move child to the resuscitation area and assess and manage ABCDE (see Chapter 2, Section 2.1).
– Administer oxygen, aiming for SpO2 between 94 - 98%.
– Get IV access and start empiric antibiotic treatment as soon as possible, depending on
availability:

First choice:
ceftriaxone IV: 100 mg/kg every 24 hours (max. 4 g)
or cefotaxime IV: 50 mg/kg every 6 hours

Second choice:
ampicillin IV: 50 mg/kg every 8 hours
or amoxicillin IV: 50 mg/kg every 12 hours
or benzylpenicillin IV: 100 000 IU/kg (60 mg/kg) every 6 hours (max. 4 MIU or 2.4 mg/
dose)

a Kernig sign: child is supine, one hip and knee are flexed to 90 degrees by the examiner, the examiner then
attempts to passively extend child’s knee: positive if there is pain along spinal cord, and/or resistance to knee
extension.
b Brudzinski sign: child is supine with legs extended, the examiner grasps child’s occiput and attempts neck
flexion: positive if there is reflex flexion of child’s hips and knees with neck flexion.

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Chapter 3: Acute febrile illness

– Consider a lumbar puncture (LP, see below for more detail) if it can be done rapidly (within
30 minutes) and will not delay antibiotic administration (see Appendix 6). Ideally, the LP
should be done before antibiotic administration but if there is any contraindication or
likely delay, it may be performed 2 to 3 days later, once antibiotics have already been
initiatedc.
– Isolate the patient (where possible), ensuring that the patient can be closely monitored.

3.3.3 Investigations
– FBC (including platelets if possible)
– CRP, if available
– BGLd
– Malaria RDT, if endemic
– Blood culture (especially if purpuric rash is present)
– Perform an LP for CSF microscopy, biochemistry and culture, and GeneXpert (where
available).
• Ensure that there are no contraindications to doing an LP and that consent has been given
by the parent/carer.
• Contraindications for LP:
▹ Severe cardiopulmonary instability that potentially requires prompt resuscitation
measures (e.g. shock)
▹ Obvious signs of increased intracranial pressure (ICP), other than bulging fontanelle:
decerebrate or decorticate posturing, absent doll’s eye reflex, abnormal respiratory
pattern, unequal pupil size or dilatation of pupils
▹ Focal neurological signs
▹ Focal seizures or seizures within the last 30 minutes
▹ Bradycardia, hypertension
▹ Obvious bleeding disorder and/or low platelet count (< 80 000 platelets/microlitre)
▹ Skin infection over the site for LP

c CSF gram stain and culture will almost certainly be negative if LP is performed 2-3 days after antibiotics have
been commenced, but WBC, glucose and protein levels may remain abnormal.
d If CSF glucose is available, calculate the ratio of CSF glucose to blood glucose; in bacterial meningitis, it will be
< 0.6 (glucometer cannot be used to test CSF glucose as it is not sufficiently accurate).

90
Table 3.2 - CSF findings and interpretation

Opening Protein mg/dL


Aspect CSF glucose WBC/mm3 Other tests
pressure (Pandy test)

Normal > 2/3 of blood < 40


Normal CSF Clear <5
(10-28 cm H2O) glucose Pandy test negative

Bacterial Usually very Very low:< 40 mg/dL Typically > 1000, 100-500 Gram stain shows
Turbid, cloudy
meningitis elevated (2.2 mmol/L) mainly neutrophils Pandy test positive bacteria

Normal to slight Usually normal or 10-700, 50-250


Viral meningitis Clear Gram stain negative
elevation slightly reduced mainly lymphocytes Pandy test negative

Acid fast bacilli


Clear or Low: 10-45 mg/dL < 500, > 250
TB meningitis Elevated positive
yellowish (0.6-2.5 mmol/L) mainly lymphocytes Pandy test positive
GeneXpert

Cryptococcal Low: 10-45 mg/dL < 800,


Very elevated Clear Pandy test negative India Ink positive
meningitis* (0.6-2.5 mmol/L) mainly lymphocytes

* Mainly in severely immunocompromised patients, such as patients with AIDS.

Note: Aseptic meningitis can be due to partially treated meningitis.


If presence of red cells: the safest interpretation of a traumatic tap is to count the total number of white cells and disregard the red cell count. If there
are more white cells than the normal range for age, then the safest option is to treat. Consider subarachnoid haemorrhage when there is unexplained
or persistent RBCs in CSF.
Chapter 3: Acute febrile illness

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3
Chapter 3: Acute febrile illness

3.3.4 Ongoing management


– After initial stabilisation and treatment (see Section 3.3.2), admit for further management
into ICU.
– NBM initially.
– Administer IV maintenance fluids restricted to 70% of usual maintenance volumee (see
Chapter 15, Section 15.2).
– Insert NGT and gradually start enteral feeding as soon as possible (see Chapter 15,
Section 15.5).
– Manage seizures if present (see Chapter 7, Section 7.2).
– Treat fever (see Section 3.1.3) and/or headache (see Chapter 15, Section 15.4) if needed.
– Monitor and record vital signs and urine output as often as required using an early warning
system (see MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts:
Vital sign charts).
– Neurological examination should be performed daily and head circumference measured in
patients < 2 years old every 3 days, looking for hydrocephalus.
– Provide standard nursing care, especially if the patient is in a coma (including mouth care,
positioning, physiotherapy exercises).
– Adjust antibiotic or change to other treatment once CSF results confirm underlying pathogen.
See Table 3.2 for CSF findings and interpretation.
The length of treatment in non-epidemic situations depends on the pathogen if it is known:
– Neisseria meningitidis: 5 to 7 days
– Haemophilus influenzae: 7 to 10 days
– Streptococcus pneumoniae: 10 to 14 days
– Group B streptococcus and Listeria: 14 to 21 days
– Gram-negative bacilli: 21 days
If the pathogen is unknown, the length of treatment should be as follows:
– Children ≤ 3 months: complete 14 days of intravenous treatment after the first sterile CSF
culture, or complete 21 days intravenous treatment.
– Children > 3 months: complete 10 days intravenous treatment. If fever persists past day 10,
continue IV treatment and assess for alternative diagnosis or complications.
In children making a rapid and uncomplicated recovery (afebrile and neurological status fully
recovered in 48 hours), if no specific organism identified, consider stopping ceftriaxone IV on
day 7.

Re-examination of CSF
Consider repeating LP if:
– Poor clinical response despite 24 to 36 hours of appropriate antibiotic treatment.
– Persistent or recurrent fever
In the context of a meningitis epidemic, refer to MSF Clinical Guidelines and MSF Management
of epidemic meningococcal meningitis guidelines.

Suspected viral encephalitis


– Strong suspicion based on clinical features (see above) and/or CSF findings (see Table 3.2)
and/or not improving after 48 hours of antibiotic treatment.
– Treat as for bacterial meningitis and add acyclovir IV: 20 mg/kg every 8 hours for 21 days.

e Increased antidiuretic hormone (ADH) secretion can cause water retention, leading to fluid overload.

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– Where CSF culture is available and was taken before antibiotic treatment started, in the
case of a negative culture, consider stopping antibiotic treatment and continue only antiviral
treatment.

Cerebral malaria 3
See Section 3.4.

TB meningitis
See Chapter 4, Section 4.11.6 and MSF Tuberculosis Guidelines.

Cryptococcal meningitis
See Chapter 13, Section 13.2.

3.3.5 Steroid therapy


Treatment with dexamethasone in meningitis is not recommended for children6, due
to insufficient evidence of significant benefit in low-resource settings7, where delayed
presentation and lack of identification of causative organism are commonf. The only exception
to this is TB meningitis (see Chapter 4, Section 4.11.6 and MSF Tuberculosis Guidelines).

3.3.6 Complications
– Persistent fever after 4 to 6 days of treatment, consider:
• Nosocomial infection
• Subdural effusion or empyema
• Cerebral abscess or parameningeal foci of ongoing infection
• Inadequate treatment
– Purpura fulminans and skin necrosis if associated meningococcal septicaemia
– Hearing impairment
– Neurodevelopmental impairment
– Multi-organ involvement due to primary pathogen or secondary to septic shock
– Venous sinus thrombosis
– Persistent seizures, subsequent epilepsy
– Permanent focal neurological deficit
– Hydrocephalus
It is important to explain to the family the possibility of these complications and start to treat
them if they appear while the child is admitted (e.g. physiotherapy exercises to treat impaired
motor function and sensory integrity).

Neuroimaging
Where there is the possibility of neurosurgical intervention, consider CT scan of the head
(where available and can be read) for suspected complications including subdural empyema,
brain abscess, cerebral vascular thrombosis, or hydrocephalus.

f The use of adjuvant dexamethasone has no significant impact on overall mortality in either high- or low-
resource settings, though there is a favourable effect on mortality from meningitis due to S. pneumoniae if
given early in the course of the illness. In high-income settings only, adjuvant dexamethasone has been shown
to reduce hearing loss in meningitis due to H. influenza if given early in the course of the illness7.

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3.3.7 Chemoprophylaxis and prevention


– Close contacts of a person with meningococcal meningitis should be given a single dose of
prophylactic antibiotic treatment to reduce the risk of transmission (see Table 3.3).
– Check national guidance in the case of epidemics.
Table 3.3 - Preferred regimens for antimicrobial prophylaxis in bacterial meningitis6

Drug Route Age Dose

1 month to 4 years 30 mg/kg (max. 125 mg)

Ciprofloxacin PO 5 to 11 years 250 mg

12 to 17 years 500 mg

< 15 years 125 mg


Ceftriaxone IM
≥ 15 years 250 mg

Although systemic fluoroquinolones are not routinely used as a first-line agent in children,
it is reasonable to use a single dose of ciprofloxacin as chemoprophylaxis for meningococcal
disease. Apart from chemoprophylaxis and hygiene measures in overcrowded households, the
best prevention possible is to ensure that most children receive adequate vaccinations against
the major pathogens causing meningitis (Streptococcus pneumoniae, Neisseria meningitidis,
Hib).

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3.4 Malaria

3
Malaria is a parasitic infection caused by the protozoa Plasmodium which is transmitted to
humans via the bite of the female Anopheles mosquito. More rarely, malaria can also be
transmitted through transfusion of infected blood and transplacentally. 5 species of Plasmodium
can cause malaria in humans: P. falciparum, P. vivax, P. ovale, P. malariae and P. knowlesi.
All species may cause uncomplicated malaria, while severe malaria is almost always due to
P. falciparum.
Malaria remains one of the leading causes of morbidity and mortality in children, mostly in
sub-Saharan Africa, despite being both preventable and treatable. In 2021, there were an
estimated 247 million cases of malaria worldwide, with 617 000 estimated deaths due to
malaria. 80% of these deaths were among children under 5 years old8.

3.4.1 Clinical features


Consider malaria in any patient presenting with fever (or history of fever in the previous
48 hours) who is living in, or coming from, an endemic area. Uncomplicated malaria should be
diagnosed and treated promptly as it rapidly progresses to severe malaria in the absence of
adequate treatment. Severe malaria is almost always fatal without treatment.

Uncomplicated malaria
Defined as a person who presents with symptoms of malaria and has a positive parasitological
test, with no features of severe malaria (below). Signs of uncomplicated malaria are non-
specific with fever (or history of fever), general malaise, fatigue, headache, chills, abdominal
pain and muscle aches. Diarrhoea and vomiting, and pallor (from anaemia) are common in
children with malaria.

Severe malaria
In addition to the features of uncomplicated malaria above, patients present with one or more
of the following clinical or laboratory complications (based on WHO criteria9):
– Impaired consciousness: VPU on AVPU or < 3 on Blantyre Coma Scale (see Appendix 3 and
Appendix 13).
– Prostration: extreme weakness, unable to sit, stand or walk. Inability to feed in infants.
– Multiple seizures: > 2 episodes in 24 hours (generalised or focal onset)
– Acidosis: plasma bicarbonate level < 15 mmol/L or venous plasma lactate ≥ 5 mmol/L.
Acidosis can be suspected clinically in the presence of Kussmaula breathing.
– Hypoglycaemia: blood or plasma glucose < 2.2 mmol/L (< 40 mg/dL)b.
– Severe malarial anaemia:
• Children < 12 years old: Hb ≤ 5 g/dLc or haematocrit < 15%
• Children ≥ 12 years old: Hb < 7 g/dL or haematocrit < 20%
– Renal impairment: Urine output < 0.5 - 1 ml/kg/hr despite adequate hydration

a Kussmaul breathing is regular, rapid, deep, laboured breathing and is highly indicative of metabolic acidosis.
b This is definition of hypoglycaemia for diagnosis of severe malaria and does not correspond to the treatment
threshold, which is < 3.3 mmol/L (< 60 mg/dL).
c This definition is for the purposes of malaria severity classification according to the WHO and does not
necessarily indicate the need for blood transfusion.

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– Jaundice or evidence of haemolysis: yellow conjunctivae and/or palms, haemoglobinuria


– Pulmonary oedema
– Significant bleeding: recurrent or prolonged nose bleeds, haematemesis, melaena
– Shock: all 3 of weak/absent pulse or tachycardia, lower limb temperature gradient, and CRT
≥ 3 seconds
– Hyperparasitaemia: P. falciparum parasitaemia > 10% (this may vary according to transmission
setting)
The most common manifestations of severe malaria in children in high transmission areas are
cerebral malaria (impaired consciousness, prostration, seizures) and severe malarial anaemiad.
Hypoglycaemia is also common in children with malaria. Where endemic, malaria frequently
occurs concomitantly with other diseases e.g. meningitis, sepsis, severe pneumonia and enteric
fever: it is therefore important to keep these in mind even when a confirmed parasitological
diagnosis of malaria has been made.

3.4.2 Investigations
Parasitological diagnosis of malaria should be confirmed whenever possible using:
– Malaria rapid diagnostic test (RDT). Two different antigen tests exist, HRP2 and pan-pLDH,
which can also exist in combination:
• HRP2 tests are P. falciparum specific, but may stay positive for up to 42 days after the start
of anti-malarial treatment, therefore important to ascertain if patient has been treated
for malaria in the preceding 1-2 months and consider other causes of fevere.
• Pan-pLDH tests detect all species of plasmodium and are slightly less sensitive and specific
than HRP2, but become negative within 2-4 days after the start of treatment.
– Microscopy (thick and thin blood films)f:
• Thick blood films enable parasite detection and quantification.
• Thin blood films enable species identification, quantification and monitoring of
parasitaemia.
If testing is not available, treatment of suspected malaria (especially if severe) should not be
delayed. If malaria RDT is negative in a child with a high clinical suspicion of severe malaria,
treat as such but continue to look for other causes of fever and perform microscopy. If malaria
RDT is negative in a child without signs of severity, repeat RDT and/or microscopy in 2-6 hours
and continue to look for other causes of fever.
In addition to parasitological diagnosis, for all children with suspicion of severe malaria:
– Hb: to check for anaemia
– BGL: to check for hypoglycaemia
– Urine dipstick: to check for haemoglobinuria (indicating haemolysis)

3.4.3 Management
Uncomplicated falciparum malaria
Treatment of uncomplicated falciparum malaria is with artemisinin-based combination therapy
(ACT) given orally for 3 days, and full recovery is expected with prompt treatment. ACTs are

d A child may have several episodes of malaria in one year in high-transmission areas, which quickly leads to
severe anaemia as the Hb does not have time to recover to normal values between episodes.
e There are emerging strains of P.falciparum with genetic mutations to HRP2/3 making these tests less reliable
in affected areas e.g. Sudan.
f Accuracy of interpretation and quantification can be variable depending on the experience of laboratory staff.

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typically prescribed as fixed-dose combinations in blister packs to simplify treatment regimens


and improve treatment adherence, and to avoid monotherapy which can lead to artemisinin
resistance. The first-line ACT is chosen according to therapeutic efficacy in the area where the
patient is living. If the first line ACT is unavailable, contra-indicated or has failed despite being
correctly taken, use another ACT. In addition to ACT, in low malaria endemic areas, all children 3
over 6 months who are diagnosed with P. falciparum malaria should also receive a single dose
of primaquineg PO, 0.25 mg/kg to reduce the risk of transmission.
Treatment of uncomplicated falciparum malaria:

ACT Presentation Dosage

Co-formulated tablets of On D1, the first dose is given at 0 hour


lumefantrine (AL)

20 mg artemether/ 120 mg lumefantrine and the second dose at 8-12 hours.


Artemether/

Subsequent doses on D2 and D3 are given


2 times daily (morning and evening).
Blister child 5 to < 15 kg, 6 tab/blister —> 1 tab 2 times daily on D1, D2, D3
Blister child 15 to < 25 kg, 12 tab/blister —> 2 tabs 2 times daily on D1, D2, D3
Blister child 25 to < 35 kg, 18 tab/blister —> 3 tabs 2 times daily on D1, D2, D3
Blister child ≥ 35 kg, 24 tab/blister —> 4 tabs 2 times daily on D1, D2, D3

Co-formulated tablets
Artesunate/amodiaquine

Blister child 4.5 to < 9 kg, tab of —> 1 tab once daily on D1, D2, D3
AS 25 mg/AQ base 67.5 mg, 3 tab/blister
(AS/AQ)

Blister child 9 to < 18 kg, tab of —> 1 tab once daily on D1, D2, D3
AS 50 mg/AQ base 135 mg, 3 tab/blister
Blister child 18 to < 36 kg, tab of —> 1 tab once daily on D1, D2, D3
AS 100 mg/AQ base 270 mg, 3 tab/blister
Blister child ≥ 36 kg, tab of —> 2 tabs once daily on D1, D2, D3
AS 100 mg/AQ base 270 mg, 6 tab/blister

Co-formulated tablets
Dihydroartemisinin/piperaquine

Blister child, tab of 5 to < 8 kg —> 1 tab 20/160 mg


DHA 20 mg/PPQ 160 mg, 3 tab/blister once daily on D1, D2, D3
Blister child, tab of 8 to < 11 kg —> 1½ tab 20/160 mg once
DHA 40 mg/PPQ 320 mg, 3 tab/blister daily on D1, D2, D3
(DHA/PPQ)

Blister child, tab of 11 to < 17 kg —> 1 tab 40/320 mg once


DHA 40 mg/PPQ 320 mg, 6 tab/blister daily on D1, D2, D3
Blister adolescent, tab of 17 to < 25 kg —> 1½ tab 40/320 mg once
DHA 40 mg/PPQ 320 mg, 9 tab/blister daily on D1, D2, D3
25 to < 36 kg —> 2 tab 40/320 mg once
daily on D1, D2, D3
36 kg to < 60 kg —> 3 tab 40/320 mg
once daily on D1, D2, D3

g Caution with use of primaquine in children with G6PD deficiency as primaquine-induced haemolysis may
occur.

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Special note for young children and infants10


– Monitor administration and retention of the first dose in children as they are more likely to
refuse, regurgitate or vomit oral treatment. If anti-malarial is vomited or regurgitated within
1 hour of administration, repeat the dose.
– Consider parenteral treatment (see below) early in young children and infants who do not
tolerate oral treatment as they can quickly deteriorate. Complete treatment with a 3-day
course of oral ACT as soon as oral medication is toleratedh.
– There is limited evidence on the correct dosage of anti-malarials for children less than 5 kg.
Dosage should be calculated in mg/kg using the same target dose range as for infants > 5 kg
as follows:
• Artemether/lumefantrine (AL) – 2 (range 1.6 to 8) mg/kg/day artemether and 12 (range
10 to 48) mg/kg/day lumefantrine
• Artesunate/amodiaquine (AS/AQ) – 5 (range 2 to 10) mg/kg/day artesunate and 10 (range
7 to 15) mg/kg/day amodiaquine
• Dihydroartemisinin/piperaquine (DHA/PQ) – 4 (range 2.5 to 10) mg/kg dihydroartemisinin
and 24 (range 20 to 32) mg/kg piperaquine
Simplified dosing instructions for AS/AQ and AL in infants < 5 kg:

AS/AQ AL

Dilute one AS/AQ tablet (25 mg Dilute one AL tablet (20 mg


Dilution artesunate/67.5 mg amodiaquine) artemether/120 mg lumefantrine)
in 2 mL of clean drinking water in 10 mL of clean drinking water

Weight (kg) Dose (mL) Dose (mL)

2.0 to 2.4 0.7 mL once daily 2.2 mL two times daily

2.5 to 2.9 0.9 mL once daily 2.8 mL two times daily

3.0 to 3.4 1.0 mL once daily 3.2 mL two times daily

3.5 to 3.9 1.2 mL once daily 3.8 mL two times daily

4.0 to 4.4 1.3 mL once daily 4.2 mL two times daily

4.5 to 4.9 1.5 mL once daily 4.8 mL two times daily

Quinine
The use of quinine PO is no longer recommended in MSF, however continues to be
recommended in some national guidelines in the absence of ACT. Follow local protocols for
dosing and administration.

Non-falciparum malaria
Most malaria in children is due to falciparum, which is the predominant species in Africa.
However, transmission of non-falciparum malaria is high in certain areas of the world,
predominantly in Asia, Central and South America, the Middle East and the Horn of Africa.
Treatment of choice for uncomplicated non-falciparum malaria is with ACT (see above),

h It is not necessary to continue parenteral treatment for minimum 24 hours in this case, and there is no need
to wait 24 hours before starting oral ACT after giving parenteral antimalarials.

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however in areas where more than 5% of malaria diagnoses are due to non-falciparum malaria
and chloroquine is still effective, treatment with chloroquine (CQ) PO can be considered for
confirmed P. vivax or P. ovale mono-infection:
– Day 1: 10 mg base/kg once daily
– Day 2: 10 mg base/kg once daily 3
– Day 3: 5 mg base/kg once daily
The benefits of ACT over chloroquine include: quicker parasite clearance; promotion of
simplified protocols for all forms of uncomplicated malaria; longer half-lives of many ACTs
which provide a longer period of suppressive post-treatment prophylaxis against relapse and
reinfection; ensuring treatment of undiagnosed P. falciparum in possible mixed infectionsi.
Relapse can occur with P. vivax and P. ovale due to dormancy of parasites in the liver, therefore
treatment with primaquinej PO 0.25 to 0.5 mg/kg once daily for 14 days in children ≥ 15 kg can
be given to eliminate these parasites after initial treatment with CQ or ACT in all transmission
settings.

Severe malaria
Severe malaria is a medical emergency and all children with severe malaria should be
hospitalised:
– Assess and manage ABCDE (see Chapter 2, Section 2.2).
– Administer oxygen if SpO2 < 92% in room air or severe respiratory distress or severe anaemia
(pending transfusion).
– Obtain IV/IO access and take bloods for Hb and BGL, as well as blood culture (if available).
– Treat for hypoglycaemia if BGL < 60 mg/dL (3.3 mmol/L), see Chapter 9, Section 9.3.
– Administer parenteral anti-malarial treatment as soon as possible (see below).
– Administer antibiotic for possible sepsis or severe bacterial infection (see below).
– Treat any seizures (see Chapter 7, Section 7.2).
– Manage specific complications of severe malaria (see below):
• Severe anaemia
• Cerebral malaria

Pre-hospital anti-malarial treatment


If the child is seen at community or primary health centre level, stabilise and administer
pre-referral treatment as follows:
– Preferred: first dose of artesunate IV/IM or, if unavailable, first dose of artemether IM (see
below for dosing).
– Alternative for children < 6 years old where IV/IM artesunate is not available: one dose of
rectal artesunate, 10 mg/kg:
• Children 2 months to < 3 years (≤ 10 kg): 1 rectal capsule (100 mg)
• Children 3 to 6 years (≤ 20 kg): 2 rectal capsules (200 mg)

In-hospital anti-malarial treatment


– Artesunatek slow IV over 3-5 minutes (if not possible, slow IM injection):
• Children < 20 kg: 3 mg/kg/dose
• Children ≥ 20 kg: 2.4 mg/kg/dose

i For confirmed mixed infections (P. falciparum plus P. vivax or P. ovale), ACT is the treatment of choice, as
chloroquine is not effective against P. falciparum.
j Caution with use of primaquine in children with G6PD deficiency as primaquine-induced haemolysis may occur,
consider preventing relapse by giving 0.75 mg/kg once a week for 8 weeks under close medical supervision.
k Post-artemisinin delayed haemolysis (PADH) is a rare phenomenon which can occur 1-3 weeks after initiation
of treatment with injectable artesunate. Clinicians should be aware of this potential complication.

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Chapter 3: Acute febrile illness

– First dose on admission (H0); second dose 12 hours after admission (H12)l; third dose 24 hours
after admission (H24); and then every 24 hours. If artesunate is unavailable, artemether IM
(should be stored separately and clearly labelled to avoid accidental IV administration):
• First dose: 3.2 mg/kg on admission
• Subsequent doses: 1.6 mg/kg once daily
– The use of quinine IV is no longer recommended in MSF, however continues to be
recommended in some national guidelines if neither artesunate nor artemether are
available. Follow local protocols for dosing and administration.
– Continue parenteral treatment for a minimum of 24 hours (3 doses of artesunate; 2 doses
of artemether) before switching to oral ACT to complete a 3-day course when the child is
improving and able to swallowm.
– Oral ACT can be started at any time after the last artesunate dose, it is not necessary to wait
24 hours before starting oral ACT after giving parenteral antimalarials.
– If the child is never able to tolerate oral treatment, continue parenteral treatment for 7 days.
Rectal artesunate does not count as the first dose of antimalarial treatment in severe
malaria. Any child who received rectal artesunate prior to arrival in hospital should
receive artesunate IV/IM (or artemether IM) as soon as possible, regardless of the time of
administration of rectal artesunate, and should complete a minimum of 24 hours of IV/IM
treatment.

Sepsis or severe bacterial infection


Sepsis is common in children with severe malaria and various bacteria have been identified in
blood cultures, the most common of which is non-typhoidal Salmonella (NTS). Infection with
invasive NTS carries higher mortality when combined with malaria, and children with severe
malarial anaemia are at increased risk11,12,13,14. As such, treatment with antibiotics should
be administered to all children presenting with severe malaria, in addition to anti-malarial
treatment, until severe bacterial infection has been excluded:
– Start ceftriaxone IV: 80 mg/kg (max. 4g if < 50 kg; max. 2g if ≥ 50 kg) every 24 hours (or
100 mg/kg (max. 4g) if suspicion of meningitis, see Cerebral malaria, page 101).
– Switch to oral antibiotics when child is well, tolerating oral intake and has been afebrile for
24 hours to complete a total of 7 days of antibiotic treatment. Give amoxicillin/clavulanic
acid (ratio 7:1 or 8:1) PO. Dosage expressed in amoxicillin:
• < 40 kg: 50 mg/kg 2 times daily
• ≥ 40 kg:
Ratio 8:1: 3000 mg daily (2 tablets of 500/62.5 mg 3 times daily)
Ratio 7:1: 2625 mg daily (1 tablet of 875/125 mg 3 times daily)
– Consider stopping antibiotics early in the following cases and monitor the child for a further
24-48 hours off antibiotics before discharge:
• The child shows good clinical improvement with antimalarials, and blood/CSF cultures
(where available) are negative. If cultures have not been taken, continue oral antibiotics
as above to complete a total of 7 days of antibiotic treatment.
• The child shows rapid, significant clinical improvement within 24 hours of starting malaria
treatment making the original indication for starting antibiotics (i.e. diagnosis of severe
malaria with sepsis or severe bacterial infection) highly unlikely.

l If the timing of the second dose does not coincide with a regular medication administration round, the second
dose can be administered earlier but never later than 12 hours after the first dose.
m If the child is still on parenteral treatment on day 5, continue until 7 days rather than switching to oral ACT.

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Chapter 3: Acute febrile illness

Severe malarial anaemia


Anaemia is common in malaria, especially in young children, and can be rapidly progressive
as erythrocytes become infected and haemolyse. Severe malarial anaemia is defined as a Hb
≤ 5 g/dL or haematocrit < 15% in children under 12 years old (Hb < 7 g/dL or haematocrit
< 20% if 12 years and over). Children with severe malarial anaemia are at risk of cardiac failure 3
therefore should be touched/moved as little as possible to limit metabolic demand. If repeated
transfusions are necessary, ideally blood from the same donor should be used to minimise risk.
Indications for blood transfusion in severe malarial anaemia (excluding infants < 2 monthsn):
– Profound anaemia: Hb < 4 g/dL, or
– Complicated severe anaemia: Hb ≥ 4 and < 6 g/dL with one or more signs of decompensation:
• Increased work of breathing (see Chapter 4, Section 4.1.1)
• Altered level of consciousness (see Chapter 7, Section 7.5.1)
• Circulatory impairment/shock (see Chapter 2, Section 2.2.1)
– Complicated severe anaemia: Hb ≥ 4 and < 6 g/dL with evidence of ongoing blood loss:
• Haemoglobinuria (indicating intravascular haemolysis)15.
• Visible bleeding (external bleeding, haematemesis, melaena, haematuria)
See Chapter 10, Section 10.1 for detailed guidance on monitoring and blood transfusion
volumes.
Repeat Hb systematically at 8, 24 and 48 hours if Hb 4-6 g/dL with no signs of severity, and at any
time if anaemia suspected clinically, especially in those with evidence of ongoing haemolysis,
e.g. haemoglobinuria or high parasitaemia (> 2% in low-intensity transmission areas or > 5% in
high-intensity transmission areas).

Cerebral malaria
Cerebral malaria presents with a reduced level of consciousness (LOC) or coma, which may be
accompanied by seizures, and is a common presentation in young children. Seizures should
be managed in the same way as seizures due to any other cause (see Chapter 7, Section 7.2),
though phenobarbital should be used cautiously and only when respiratory support is available
due to increased risk of respiratory arrest in cerebral malaria. An isolated seizure with full
neurological recovery is likely to be a febrile seizure and is not indicative of cerebral malaria.
Children with cerebral malaria who have focal neurological signs or those who have ongoing
altered LOC following a seizure should be started on maintenance anticonvulsant medication
(see Chapter 7, Section 7.2).
It is impossible to distinguish cerebral malaria from meningitis in the absence of lumbar
puncture results, therefore all children with signs of cerebral malaria should be treated
concomitantly for bacterial meningitis:
– Consider an LP if it can be done rapidly (within 30 minutes) and there are no contraindications
(see Appendix 6). If not, LP can be performed after 2 - 3 days when the child has improvedo.
Antibiotics should not be delayed in order to carry out an LP.
– Start ceftriaxone IV: 100 mg/kg (max. 4 g) every 24 hours.
– Continue IV antibiotics for 10 days if LP confirms meningitis or if it is not possible to carry out
an LP.
– If LP excludes meningitis, continue antibiotics as for sepsis (see page 100).

n Young infants < 2 months of age have a significantly higher normal Hb than older infants (see Table 10.1,
page 299) therefore transfusion thresholds are higher.
o CSF gram stain and culture will almost certainly be negative if LP is performed 2-3 days after antibiotics have
been commenced, but WBC, glucose and protein levels may remain abnormal.

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Supportive care
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– Monitor BGL regularly and treat for hypoglycaemia if BGL < 60 mg/dL (3.3 mmol/L), see
Chapter 9, Section 9.3.
– Treat fever to improve comfort (see Section 3.1.3).
– Start IV maintenance fluids and/or feeds if tolerated (see Chapter 15, Section 15.2 and
Section 15.5). Restrict IV maintenance fluids to 70% of usual maintenance volume in cerebral
malaria due to the risk of cerebral oedema but be cautious with fluid restriction as children
tend to be dehydrated more than fluid overloaded.
– Monitor and document urine output (using a urinary catheter if possible):
• Aim for urine output ≥ 1 mL/kg/hour.
• Check regularly for haemoglobinuria.
• If no signs of dehydration and urine output < 1 mL/kg/hr for over 6 hours, administer trial
of furosemide IV, 1 mg/kg.
• If no response to furosemide, stop IV fluids and refer for management of renal failure.
– Monitor for signs of fluid overload.
– Provide specific care for children with impaired consciousness:
• Nurse with head elevated and in neutral position.
• Support and open the airway, clearing with suction only if necessary.
• Administer oxygen via face mask, aiming for SpO2 > 92%. Assist ventilation with bag-mask
device if not breathing.
• Regularly monitor neurological status (AVPU) and check pupillary response.
• Re-position child regularly to prevent pressure sores.
• Carry out regular mouth and eye care.

Malaria in young infants < 2 months old


Malaria can present differently in young infants compared to older children. Infants < 2 months
old should be diagnosed and managed as for congenital or neonatal malaria (see MSF Neonatal
Care Guidelines).

Discharge criteria
Consider discharge from hospital when child is:
– Clinically stable for at least 24 hours
– Tolerating oral ACTs (i.e. not vomiting)

3.4.4 Prognosis
Children with uncomplicated malaria can expect to make a full recovery with appropriate
treatment while mortality from severe malaria is approximately 10-20% even despite prompt
and adequate treatment. Left untreated, malaria is almost always fatal. Neurological sequelae
occur in approximately 15% of children following cerebral malaria and include epilepsy,
impaired cognitive function, neurodisabilities and behavioural disorders16. Children living in
endemic areas are at significant risk of re-infection with malaria, with repeated infections
carrying a higher likelihood of severe anaemia and a greater need for blood transfusion.

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3.4.5 Prevention
Prevention of malaria through the use of long-lasting insecticide-treated bed nets and indoor
residual spraying, as well as through strategies such as seasonal malaria chemoprevention
(SMC) and perennial malaria chemoprevention (PMC) (previously known as intermittent 3
preventive treatment (IPT)) in endemic areas can significantly reduce the burden of disease in
children. The new malaria vaccine is an additional tool which, if used in combination with other
interventions, has the potential to alter malaria epidemiology and reduce malaria morbidity
and mortality over the coming years.

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3.5 Tetanus

Tetanus is a vaccine-preventable disease that affects the nervous system, causing intensely
painful muscle spasms. Clinical features are due to the release of a potent neurotoxin by the
gram-positive, anaerobic bacterium Clostridium tetani which lives in soil and faeces and can
contaminate wounds, minor cuts or abrasions, and the umbilical stump (in neonates).
Tetanus remains endemic in resource-limited settings with low immunisation coverage, due
to poor hygiene practices during delivery and after birth, inadequate wound care, and lack
of availability of post-exposure prophylaxis. Incidence of tetanus increases following natural
disasters and in conflict and post-conflict contexts, due to disrupted vaccination programmes
and increased tetanus-prone injuries. Globally, tetanus disease burden is underestimated,
as tetanus surveillance systems are not well established in many endemic countries. While
the overall incidence of tetanus is decreasing, it remains responsible for at least 30 000 to
60 000 deaths each year, the majority of which are among neonates17,18,19. Tetanus case
fatality rate remains high in resource-limited settings20, where access to mechanical ventilation
is limited, therefore focus on vaccination programmes is essential to reduce morbidity and
mortality.
Tetanus-prone injuries include puncture wounds, foreign bodies, gunshot wounds, open
fractures, burns, and use of non-sterile instruments for cutting (e.g. umbilical cord), or for
intramuscular or subcutaneous injections.

3.5.1 Clinical features


Incubation period for tetanus ranges between 1 and 21 days, with shorter incubation periods
being associated with an elevated risk of death21. The further the entry point of infection is
from the central nervous system, the longer the incubation period. Tetanus is most commonly
generalised, affecting all muscle groups, but local tetanus and cephalic tetanusa can also occur.
Tetanus typically lasts for 4 to 6 weeks but may last longer.

Characteristic signs
Tetanus toxin interferes with the release of inhibitory neurotransmitters, leading to unopposed
muscle contraction. Initially, this manifests as stiffness before progressing to muscle spasms,
giving rise to the classic features of tetanus (see Figures 3.3, page 105):
– Trismus (‘lock-jaw’) and risus sardonicus (rigid smile) caused by facial spasm
– Opisthotonus
– Stiff neck
– Abdominal rigidity
– Dysphagia
Muscle spasms can be long and intensely painful and are easily triggered by external stimuli
(noise, touch, light). Patients with tetanus are awake and fully conscious.

a Local tetanus affects one extremity or body region and may be due to low toxin load. Cephalic tetanus is
localised to the head and neck, with cranial nerve involvement, and may be misdiagnosed as a stroke. Both
types usually progress to generalised tetanus.

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Figure 3.3b - Risus sardonicus


Figure 3.3a - Opisthotonusb
and abdominal rigidityb

Complications
– Pharyngeal and laryngeal spasms may lead to aspiration, airway obstruction, apnoeic
episodes and respiratory failure.
– In advanced disease, the autonomic nervous system is also affected, causing arrhythmias,
haemodynamic instability, fever, sweating, bowel and bladder dysfunction, and increased
respiratory secretions. The latter can complicate airway management as suctioning may
induce upper airway spasms.

Severity classification
The 'Ablett classification’22 categorises the severity of tetanus as follows:
– Grade I: mild trismus with little or no dysphagia, general rigidity with no spasms, mild or no
respiratory involvement
– Grade II: moderate trismus, marked dysphagia, fleeting spasms with moderate respiratory
involvement
– Grade IIIa: severe trismus, severe dysphagia, major spasms, severe respiratory involvement
– Grade IIIb: features of Grade IIIa with autonomic disturbance
Diagnosis is based on history and classic clinical findings. In mild or localised tetanus, diagnosis
can be challenging. Differential diagnosis may include poisoning (strychnine) or dystonic
reactions to drugs such as phenothiazines and metoclopramide. Always consider the possibility
of associated meningitis and when feasible, perform lumbar puncture for confirmation.

3.5.2 Management
Treatment consists of measures to prevent toxin production and uptake (wound care,
immunoglobulins, antibiotics), control of muscle spasms, and supportive care. For neonates,
see MSF Neonatal Care Guidelines.

b Photos, courtesy of Marianne Sutton, were taken and used with the consent of the respective patients/
parents/carers.

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Neutralisation of tetanus toxin


– Administer Human tetanus immunoglobulin (HTIG) IMc: 500 IU single dose as soon as
possibled, to be injected into 2 different sites.
– Do not administer HTIG in the same syringe or at the same injection site as the tetanus
vaccine (See Section 3.5.3).

Prevention of local proliferation of C. tetani


– Meticulously clean, irrigate and debride the wound (consider sedation and analgesia), and
guarantee regular wound care with clean, non-occlusive dressings.
– Administer antibiotics to eradicate C. tetanie,23,24:
• metronidazole IV: 10 mg/kg (max. 400 mg) every 8 hours for 7-10 days is the preferred
choice.
• Alternatively, benzylpenicillin (penicillin G) IV: 50 000 IU/kg (30 mg/kg) every 6 hours
(max. 4 MIU or 2.4 g per dose).

Supportive care
– Admit to an intensive care unit (where available)
– Establish a quiet environment or individual room where external stimuli are minimised
(light, noise and handling) without compromising surveillance and monitoring. Consider eye
shades and ear plugs to reduce stimuli.
– Monitor airway, breathing and circulation closely. Keep suctioning equipmentf and bag and
mask nearby in case of airway obstruction, apnoea or respiratory failure.
– Maintain adequate hydration using IV fluids (see Chapter 15, Section 15.2), as patients will
have increased fluid losses through fever and sweating and are at risk of rhabdomyolysis and
renal failure.
– Ensure adequate caloric intake via NGT (see Chapter 15, Section 15.5) as muscle spasms will
increase energy expenditure. Consider giving frequent, small feeds due to decreased gut
motility.
– Paralytic ileus may occur in severe tetanus with autonomic disturbance (see Chapter 12,
Section 12.3).
– Give adequate analgesia for muscle spasms (consider morphine), as they can be intensely
painful (see Chapter 15, Section 15.4).
– Treat fever, if present, for patient comfort (see Section 3.1.3).
– Where indicated, treat other infections (skin infection, sepsis, omphalitis) and be alert for
nosocomial infections which are frequent during prolonged hospitalisation.
– Administer tetanus vaccination, as recovery from tetanus infection does not confer immunity
(see Section 3.5.3).

Treatment of muscle spasms


Control of muscle spasms in tetanus is extremely difficult in resource-limited settings. Doses
of sedative medications must be carefully titrated to achieve spasm control without excessive
respiratory depression (see Chapter 1, Section 1.2 for normal respiratory rates in children).

c Administration of antitoxin via the intrathecal route has been of interest for several decades and although some
trials suggest benefit, there is currently insufficient evidence to recommend this route over IM administration.
d Some sources suggest higher doses of HTIG, refer to local or national guidelines where they exist.
e There is conflicting evidence on whether the use of antibiotics is truly beneficial in the treatment of tetanus,
however it is common practice to administer them and remains part of recommended treatment.
f Suction with caution, as this can provoke spasms.

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Benzodiazepines
Although benzodiazepines are generally effective in controlling rigidity and spasms, they can
cause hypotension and respiratory depression and should therefore be administered under
close surveillance:
– Use diazepam emulsion, where available, rather than diazepam solution for intravenous 3
administration in young children, as it has fewer side effectsg. Dosing recommendations are
the same for both preparations.
– Start diazepam: 0.1 to 0.3 mg/kg by slow IV injection (over 3-5 minutes) every 1 to 4 hours.
Start at the lowest dose and titrate upwards depending on severity and persistence of
spasms, ensuring that adequate breathing is maintained.
– If IV route is not available, consider rectal administration using diazepam solution. Note:
diazepam emulsion should not be used intrarectally.
– If spasms persist despite hourly diazepam at maximum dose, start continuous diazepam
infusion: 0.1 to 0.5 mg/kg/hour. Increase cautiously by 0.1 mg/kg/hour to achieve spasm
control (max. 0.8 mg/kg/hour), ensuring that adequate breathing is maintained.
– Once spasms are controlled and the patient is improving, gradually decrease diazepam
(either hourly bolus or continuous infusion) as tolerated until it can be safely discontinued.
Consider switching to diazepam PO/NGT while weaning as soon as the patient can tolerate
oral/NGT intake. Do not stop treatment abruptly as this can trigger new onset of muscle
spasms.
Benzodiazepines (especially if administered concomitantly with opioids) can cause
respiratory depressionh. Ensure increased nursing care, resuscitation equipment (bag
and mask) and suction is available for immediate use if required and that antidotes are readily
available for emergencies.
In the event of respiratory depression caused by benzodiazepines, administer:
– Flumazenil IV over 15 seconds: 10 micrograms/kg every 1 minute (max 200 micrograms/
dose) as required until adequate breathing resumes.

Magnesium sulphate
Magnesium sulphate is a calcium antagonist that acts as a muscle relaxant and vasodilator and
prevents catecholamine release. It can be helpful in controlling spasms in tetanus in addition
to benzodiazepines25,26 in Ablett Grade IIIa and IIIb tetanus, when benzodiazepines alone do
not adequately control spasmsi. It should be used with caution due to its potential toxicity.
– Ensure child is cared for in a closely monitored environment with ICU level nursing care.
– Administer magnesium sulphate IV via a syringe pump: loading dose 100 mg/kg over
30 minutes followed by continuous IV infusion at 40 mg/kg/hour. Increase infusion rate by
5 mg/kg/hour every 6 hours (max. 100 mg/kg/hour) until spasms are controlled. A syringe
pump is mandatory for administration of magnesium sulphate.
– Regularly monitor and record blood pressure, respiratory rate, heart rate and other vital signs
using an early warning system (see MSF Manual of Nursing Care Procedures, Assessment
and vital signs, Charts: Vital sign charts).
– If available, monitor serum magnesium concentration to maintain levels within the
therapeutic range (2 - 4 mmol/L).

g Diazepam solution can cause pain on injection, thrombophlebitis and contains benzyl alcohol, benzoic acid and
propylene glycol that can be toxic for young children, especially in accumulated doses.
h Minimum respiratory rates in children: < 1 year = 30 breaths/min; 1-5 years = 25 breaths/min; 6-12 years =
20 breaths/min; > 12 years = 14 breaths/min.
i Other medications, such as chlorpromazine and phenobarbital, may be used for spasm control according to
local availability and protocol.

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– If it is impossible to check serum magnesium concentration, loss of the patellar reflex


indicates that serum magnesium is at the upper end of the therapeutic range (4 mmol/L)
and magnesium sulphate infusion should be reduced27. Check the patellar reflex cautiously
in children with tetanus as doing so may provoke spasms.
– Other signs of magnesium toxicity and/or hypocalcaemia overlap with signs of autonomic
dysfunction therefore cannot reliably be used to identify magnesium toxicity.
– If there is a strong suspicion of magnesium toxicity, stop magnesium sulphate infusion and
administer calcium gluconate 10% solution: 0.5 mL/kg slow IV injection over 5-10 minutes.

Management of autonomic dysfunction


Magnesium sulphate can be useful for managing autonomic dysfunction in tetanus in addition
to spasm control, however it should not be administered for autonomic dysfunction alone.

3.5.3 Prevention
Tetanus infection does not induce natural immunity following recovery from the acute illness
and patients can get infected again. All patients with clinical tetanus should therefore receive
tetanus vaccination, either at the time of diagnosis or during convalescence as follows28:
– Patient completely vaccinated: tetanus booster required
– Patient not vaccinated, partially vaccinated (< 3 doses) or status unknown: Begin or complete
the tetanus vaccination schedulej
See MSF Clinical Guidelines for tetanus routine immunisation and post-exposure vaccination.

j Tetanus vaccination schedule: at least 2 doses administered 4 weeks apart, a third dose 6-12 months later, and
additional doses administered according to national recommendations.

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3.6 Enteric (typhoid and paratyphoid) fever

3
Enteric fever refers to both typhoid and paratyphoid fever which are bacteraemic febrile
illnesses. Typhoid fever is caused by Salmonella enterica serotype Typhi (formerly S. typhi),
while paratyphoid fever is caused by Salmonella enterica serotypes, Paratyphi A, B, or Ca.
Enteric fevers are endemic on the Indian subcontinent, Southeast Asia, Sub-Saharan Africa and
Latin America29 and mainly affect children under 15 years of age (with a peak between 5 and
9 years of age30). Millions of people are affected by enteric fever every year, with a global case
fatality rate of approximately 1%30. The risk of mortality is 4 times higher in children under
5 compared to over 5 years of age31. Enteric fevers are acquired by the ingestion of food or
water contaminated with excreta of symptomatic or asymptomatic carriers or by direct contact
(contaminated hands), and risk of infection is higher in areas with poor water and sanitation.
Climate change, urbanisation, overcrowded settings, and antibiotic resistance could potentially
increase the global burden of enteric fevers32.

3.6.1 Clinical features


The clinical features of paediatric enteric fevers are nonspecific and can overlap with other
infectious diseases in endemic areas. Symptom onset occurs between 5 and 21 days after
ingestion of contaminated food or water.
Prolonged fever is the predominant sign of paediatric enteric fever33, often being the single
manifestation, and may present as a fever of unknown origin. However, in young infants,
enteric fevers can also present with hypothermia31.
Along with fever, common symptoms include abdominal pain, malaise, and chills. If left
untreated, the disease classically progresses in 3 phases, each with distinct features:
– First week: fever and chills (corresponding to the bacteraemic phase).
– Second week: abdominal pain with either constipation (one-third of patients) or diarrhoea
(more frequent in young children). Rose-spots (salmon spots) may be seen (in 5 to 30% of
patients)b.
– Third week: hepatosplenomegaly, and serious complications in 10-15% such as bowel
perforation and bleeding, secondary bacteraemia due to enteric aerobic and anaerobic
microorganisms, peritonitis, and septic shock.
In patients who do not develop severe complications or die, symptoms progressively settle
over weeks to months.
Other occasional associated symptoms and signs which can be seen more frequently in children
than adults include31:
– General: arthralgia, myalgia
– Gastrointestinal: refusal to feed, paralytic ileus
– Respiratory: cough, bronchopneumonia
– Cardiac: myocarditis, endocarditis, pericarditis, pericardial effusion and relative bradycardia

a Note: Non-typhoidal salmonella (NTS) refers to illnesses caused by all other serotypes of Salmonella, and it is
a frequent cause of bacteraemia and anaemia in children living in areas of high malarial transmission.
b Rose spots are 1 to 5 mm, blanching, faint-colour pink macules-papules. They are typically distributed on
the chest, abdomen, and back, and they can persist for 2-3 days. They can rarely appear as haemorrhagic or
vesicular.

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– Neurological: febrile seizures, headache, Guillain-Barré syndrome, meningitis, brain abscess,


typhoid encephalopathy, acute cerebellar ataxia, sinus thrombosis, cerebritis, pseudo
tumour cerebri
– Hepatosplenic: typhoid hepatitis or “hepatitis typhosa”, acalculous cholecystitis, hepatic
and splenic abscesses
The symptoms of paratyphoid fever are the same as those of typhoid fever, although the illness
is usually shorter and less severe.

Differential diagnosis
The differential diagnosis of enteric fever is broad, with the main differential diagnoses
being malaria, bacterial gastroenteritis, amoebiasis, brucellosis, leptospirosis, leishmaniasis,
tuberculosis, and dengue fever.

3.6.2 Diagnosis
Diagnosis is made based on thorough medical history and full clinical examination. Culture
remains the gold standard for diagnosis but is rarely available in resource-limited settings,
therefore a diagnosis of presumptive enteric fever should be made if the following are present:
– Child appears toxic or severely unwell and/or
– Lives in an endemic area and has fever lasting over 1 week without other obvious cause,
and/or
– Severe abdominal pain
It is important to rule out malaria, in endemic regions, and acute abdomen e.g. appendicitis
(see Chapter 5, Section 5.4).
Possible investigations that can be performed:
– Blood culture (diagnostic)
– Stool or urine culture (may indicate chronic carriage rather than acute infection)34
– FBC: relative leucopenia (normal or slightly low white blood cell count despite bacteraemia)35.
Leucocytosis in the third week of illness should raise the suspicion of intestinal perforation
or an alternative diagnosis. Mild anaemia and thrombocytopenia are common.
– Widal-Felix agglutination reaction: not recommended due to poor specificity and sensitivity,
however this test is still used in certain endemic countries as it is cheap. It should not be
performed before the second week of illness. Two samples must be collected 10-15 days
apart to detect an increase in antibodies.

3.6.3 Management
Children with suspected severe enteric fever (systemic illness, unable to drink or eat, not
tolerating oral medications, altered consciousness, prolonged fever, organ system dysfunction)
should be admitted to hospital, and isolated if possible (see MSF Manual of Nursing Care
Procedures for IPC guidance). Uncomplicated cases can be managed as outpatients, with
advice on recognition of danger signs and when to seek medical attention.
Supportive care for severe cases includes:
– Oxygen if necessary to maintain saturations ≥ 92%
– Maintenance IV fluids if unable to eat or drink (see Chapter 15, Section 15.2)
– Treatment of fever (see Section 3.1.3)
– Treatment of pain if present (do not give analgesics systematically as may mask symptoms
of peritonitis)

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– Monitoring and recording of vital signs as often as required using an early warning system
(see MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign
charts).

Antibiotic treatment 3
Antibiotic choice is complicated by the spread of multi-resistant strains (increasing resistance
to first-line antibiotics: chloramphenicol, ampicillin and cotrimoxazole) and has led to the
frequent use of fluoroquinolones. Fluoroquinolone resistance is now also increasing and is
currently endemic in Asia, particularly South Asia and East Asia, with increasing resistance
reported in the Middle East36. Data from African settings is limited but reported rates of
fluoroquinolone and multidrug resistance are increasing, particularly in Democratic Republic
of Congo (DRC), Tanzania, Ghana, Kenya, Uganda and Nigeria36,37. Culture and antibiotic
susceptibility studies are therefore critical to guiding treatment, but they are rarely available in
resource-limited settings: empiric treatment on the assumption of fluoroquinolone resistance
is therefore prudent. If available, recent regional data on susceptibility of isolated strains can
help to guide treatment where local antibiograms are not available. It is important to note that
fever may persist for 4 to 5 days after the start of effective treatment, therefore ongoing fever
alone is not an indication to change antibiotic treatment.

Uncomplicated cases
First choice Azithromycin PO: 10 to 20 mg/kg (max. 1 g) once daily for 7 days

Alternative Cefixime PO: 10 mg/kg (max. 200 mg), 2 times daily for 10-14 days

Alternative, only Amoxicillin PO: 30 mg/kg (max. 1 g) 3 times daily to complete


where antibiotic 14 days of total treatment
sensitivity testing Co-trimoxazole PO: 20 mg SMX + 4 mg TMP/kg (max. 800 mg SMX +
confirms susceptibility 160 mg TMP), 2 times daily to complete 14 days of total treatment
Severe casesc
No suspected or
confirmed ceftriaxone Ceftriaxone IV: 50 to 100 mg/kg (max. 4 g) once daily
resistance
Suspected or
confirmed ceftriaxone
resistant or extensively Meropenem IV: 20 to 40 mg/kg (max. 2 g) every 8 hours
drug resistant (XDR)
typhoid
Oral switch in severe cases once patient improves
Azithromycin PO: 10 to 20 mg/kg (max. 1 g) once daily to complete
First choice
10-14 days of total treatment

Alternative, only Amoxicillin PO: 30 mg/kg (max. 1 g) 3 times daily to complete


where antibiotic 14 days of total treatment
sensitivity testing Co-trimoxazole PO: 20 mg SMX + 4 mg TMP/kg (max. 800 mg SMX +
confirms susceptibility 160 mg TMP), 2 times daily to complete 14 days of total treatment

c Start parenteral treatment and switch to oral route as soon as possible once the patient improves, to complete
recommended total days of treatment.

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If peritonitis is suspected, add metronidazole IV: 10 mg/kg (max. 500 mg) every 8 hours for
7-10 days, unless meropenem is usedd. If no improvement in 48 hours, or perforation is
suspected make the patient NBM, place an NGT and leave on free drainage and refer for
surgical review where possible.
In the case of enteric fever with severe systemic symptoms (shock, coma) in children older
than 3 months, add dexamethasone IV: initial dose 1 mg/kg followed by 0.25 mg/kg every
6 hours for a total of 48 hours (8 doses).
Relapse may occur, even in immunocompetent individuals. It usually occurs 2–3 weeks after
the resolution of the fever and should be treated with a second, longer course of antibiotics.

3.6.4 Prevention
WHO recommends vaccination with the typhoid conjugate vaccine in endemic regions38:
– Routine vaccination: a single dose of 0.5 ml IM at the same time as other vaccines
administered at the age of 9 months or in the second year of life.
– Catch-up vaccination (same dose) up to 15 years of age: according to national
recommendations.

d Meropenem covers anaerobes therefore no need to add metronidazole in this case.

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3.7 Measles

3
Measles is an epidemic-prone, highly contagious viral infection that mainly affects children.
It is caused by a paramyxovirus virus (Morbillivirus) and is spread by the airborne route via
large respiratory droplets. Measles is a vaccine-preventable disease and immunisation
against measles is included in all vaccination calendars worldwide. Despite this, measles was
responsible for more than 140 000 deaths in 2018, the majority of whom were children under
5 years old39. Children with malnutrition are especially vulnerable to measles and at risk of
developing severe complications, with measles mortality as high as 15%40.
Measles is a notifiable disease, and all cases should be reported to local or national public
health authorities.

3.7.1 Clinical features


Incubation period for measles is between 10 to 14 days from exposure to onset of fever.

Prodromal phase
– High fever (39-40 ⁰C)
– Classic triad of cough (usually non-productive), coryza (runny nose) and conjunctivitis (red,
watery eyes).
– Koplik’s spots: tiny bluish-white spots on an erythematous base found on the inside of the
cheeks which are pathognomonic of measles. They typically appear 1-2 days before the
onset of rash but can be hard to see and may not be observed in all patients with measles.
– Usually lasts for 2 to 4 days.

Eruptive phase
– Erythematous, blanching maculopapular rash that starts on the face and spreads in a
descending manner to the neck, trunk, abdomen and lower limbs over the course of 3 to
4 days.
– Fever subsides as the rash reaches the feet, and the rash subsequently recedes in the same
order as it appeared.
– Usually lasts for 4 to 7 days.
– Desquamation (peeling) of the skin around 1 to 2 weeks after the rash is common.
Any child presenting with fever, rash and one of cough, coryza or conjunctivitis should be
considered a clinical measles suspect.
Complications
Acute complications of measles are frequent and are the cause of the majority of deaths from
measles. The most common acute complications affecting children are:
– Respiratory: pneumonia (with or without empyema), otitis media, croup (laryngotracheo­
bronchitis)
– Gastrointestinal: diarrhoea (with or without dehydration), stomatitis
– Ocular: purulent conjunctivitis, keratitis, xerophthalmia (due to vitamin A deficiency
exacerbated by measles)
– Neurological: febrile seizures, encephalitis (rare)

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Post-infectious complications occur after initial resolution of measles but may also be fatal:
– Malnutrition: provoked or exacerbated by measles
– Immunosuppression: temporary immune depression following measles that increases the
risk of severe illness from respiratory infections and diarrhoea.
– Noma (gangrenous gingivostomatitis): a non-specific complication of measles associated
with extremely high mortality rates (see Chapter 14, Section 14.3).
– Subacute sclerosing pan-encephalitis (SSPE): a rare complication of measles, this progressive
degenerative disease occurs several years (average 7 years) after infection with measles.

Investigations
– Collect samples (usually serum, throat swab or urine sample) to send to relevant reference
laboratory (see MSF Collection, storage and transport of samples from field to reference
laboratory) for detection of IgM antibodies. Check local protocols for sample collection prior
to sampling.
– After confirmation of measles outbreak, it is not necessary to take samples from every
suspected case if they meet the clinical case definition and have had contact with known
measles cases.

3.7.2 Management
Uncomplicated measles
Most children with measles can be managed at home with advice on eye, nose and mouth
care, nutrition, fever management and recognition of signs of complications.
Antibiotics
Systematic antibiotic prophylaxis for uncomplicated cases is not recommended by WHO.
However, systematic antibiotic prophylaxisa for uncomplicated measles in children under
5 years old is recommended by MSF in most projects where they work due to the additional
risks inherent to such contexts i.e. situations where identification and/or treatment of
superimposed bacterial infections may not be possible (due to difficult access to healthcare,
limited capacity of health services) and where there is a high prevalence of vulnerable people.
Vitamin A
Give vitamin A to all acute measles cases under 5 years old, regardless of previous recent
vitamin A administration:
– Infants < 6 months: 50 000 IU once daily for 2 days
– Infants 6 to 11 months: 100 000 IU once daily for 2 days
– Children 12 to 59 months: 200 000 IU once daily for 2 days
This is usually the only systematic treatment required for children with uncomplicated measles.
A third dose should be given to children with signs of vitamin A deficiency (xeropthalmia,
corneal ulceration), 4 to 6 weeks laterb.
Conjunctivitis
Non-purulent conjunctivitis with clear, watery discharge does not require specific treatment,
simply wash the eyes 2 times daily with clean water. If purulent or cloudy discharge present,
treat for superimposed bacterial infection with tetracycline 1% eye ointment 2 times daily for
7 days.

a Antibiotic prophylaxis in measles is with amoxicillin PO for 5 days.


b If, for practical reasons, the patient is unlikely to receive their 3rd dose 4-6 weeks later, it is possible to give the
3rd dose from day 8 onwards.

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Complicated measles
Admit all children with measles who have malnutrition and those with acute symptoms that
cannot be managed at home, including:
– Moderate or severe respiratory distress
– Stridor
3
– Inability to feed (due to extensive oral lesions, vomiting, lethargy)
– Altered consciousness or seizures
– Moderate or severe dehydration
– Corneal lesions (pain, erosion, opacity, photophobia)
Infection prevention and control measures
– Isolate suspected cases to a single room with dedicated nursing staff and equipment to
reduce the risk of cross-infection.
– Ensure transmission-based precautions are taken, including correct use of personal
protective equipment (PPE).
– If multiple cases, group together with other cases in a separated area from other patients
(cohorting).
– Cases should remain isolated until 4 days after the appearance of the rash, as they are still
infectious during this time.
Supportive care
– Administer oxygen if SpO2 < 92% in room air or severe respiratory distress.
– Ensure adequate fluid and calorie intake (risk of weight loss). Give small and frequent oral
feeds if possible. Some patients need NGT feeding or IV maintenance fluids (see Chapter 15,
Section 15.2 and Section 15.5).
– Give vitamin A PO systematically, as above.
– Test for malaria in endemic areas, and treat if RDT positive.
– Treat fever, if required, for patient comfort (see Chapter 3, Section 3.1.3).
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– If conjunctivitis, wash the eyes with clean water 2 times daily.
– Administer tetracycline 1% eye ointment, as above, if purulent or cloudy eye discharge
present.
– Wash the mouth with salted water 4 times daily, if possible.
– Keep skin clean and dry and monitor for signs of infection.
– Manage pain with adequate analgesia (see Chapter 15, Section 15.4).
Treatment of specific complications
Empiric antibiotic treatment should be started early if there is a suspicion of a superimposed
bacterial infection40. Refer to the relevant chapter for management of specific complications:
– Pneumonia (see Chapter 4, Section 4.5)
– Empyema (see Chapter 4, Section 4.6)
– Croup (laryngotracheobronchitis, see Chapter 4, Section 4.2)
– Dehydration (see Chapter 5, Section 5.3)
– Seizures (see Chapter 7, Section 7.2)
– Sepsis or severe bacterial infection (see Chapter 3, Section 3.2)
– Urinary tract infection (see Chapter 8, Section 8.1)
Refer to MSF Management of a measles epidemic for:
– Outbreak investigation and surveillance methods
– Mass vaccination campaigns

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3.7.3 Prevention
– Vaccination is highly effective at preventing infection with measles and two doses confers
life-long immunity.
– Measles vaccine can be monovalent but is frequently combined with rubella and mumps in
a single MMR vaccine.
– Measles vaccine is part of routine childhood immunisation (as part of the Expanded
Programme on Immunisation) with primary dose at 9-12 months and second dose at
15-18 months.
– Catch-up vaccination (missed routine vaccination) should be done at any opportunity in
unvaccinated individuals.

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Chapter 3: Acute febrile illness

3.8 Orbital and peri-orbital cellulitis

3
Orbital cellulitis is an infection within the orbit of the eye, affecting the muscular and adipose
tissues posterior to the orbital septum (therefore called post-septal). It is a clinical emergency
requiring urgent referral for surgical management where possible. Major complications include
intracranial infection (abscess, empyema, meningitis), irreversible damage to the optic nerve,
loss of vision, or venous sinus thrombosis41.
Predisposing factors include sinusitis, otitis media, complicated periorbital cellulitis, orbital
trauma (e.g. fractured orbit) and foreign bodya.
Peri-orbital cellulitis is an infection of the eye lid and surrounding skin anterior to the orbital
septum (therefore called pre-septal)42. Predisposing factors include upper respiratory tract
infections, sinusitis, local trauma, insect bites and foreign bodyb.
Neither orbital nor peri-orbital cellulitis involve the ocular globe itself.
The most common causes of both conditions are Streptococcus pneumoniae, H. influenzae type
B (Hib), Moraxella catarrhalis, Staphylococcus aureus, Group-A beta haemolytic Streptococcus,
anaerobes (especially when odontogenic source) and Gram-negative bacilli (especially
post-trauma)43. Consider Neisseria gonorrhoea and Chlamydia trachomatis infections in
neonatal presentation (see MSF Neonatal Care guidelines). Consider Mucorales, Aspergillus,
Mycobacterium tuberculosis, in immunosuppressed children.

3.8.1 Clinical features


Diagnosis is based on history, clinical features, and full examination. Overlapping clinical
features in peri-orbital and orbital cellulitis can make differentiation difficult. See also Figure 3.4
page 119 for guidance on diagnosis and management of eye swelling and/or pain.
Both conditions typically present with:
– Unilaterally affected eye
– Eyelid erythema and oedema
– Eye/eyelid pain or tenderness (more common in orbital cellulitis)
– Fever or general malaise in more severe cases
In addition, certain features are only present in orbital cellulitis:
– Limited eye movements due to pain or severe oedema
– Inability to open the eye due to severe oedema
– Proptosis
– Globe displacement
– Visual impairment with reduced acuity, diplopia, and relative afferent pupillary defect
– Severe headache, or other features suggesting intracranial involvement
Assessment of both acuity and eye movements are essential. If the patient is not able to open
the eye due to significant oedema, manage the condition as orbital cellulitis.

a Educational video available on: https://www.youtube.com/watch?v=lMXFDSTgK7U


b Educational video available on: https://www.youtube.com/watch?v=Z-Jf4Kw7owY

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Chapter 3: Acute febrile illness

Differential diagnosis
– Allergic reaction (bilateral findings and/or painless oedema in a non-febrile child)
– Insect bite (unilateral macular spot on the eyelid)
– Conjunctivitis (mild oedema, eye secretions)

3.8.2 Management
If the patient presents with symptoms or signs of potential severe bacterial infection or sepsis,
treat as such (see Section 3.2).

Orbital cellulitis
– This is a medical emergency and requires urgent treatment.
– Admit and start IV antibiotic treatment as soon as possible:
ceftriaxone IV: 100 mg/kg loading dose on D1, then 50 mg/kg every 12 hours (daily max.
4 g if < 50 kg; max. 2 g if ≥ 50 kg)
+
cloxacillin IV: < 40 kg: 25 to 50 mg/kg every 6 hours (max. 8 g daily)
≥ 40 kg: 2 g every 6 hours

– Refer for surgical intervention urgently (where possible) for all cases of severe orbital
cellulitis or if there is suspected intracranial involvement.
– If signs of clinical improvement (reduction in swelling, erythema) after at least 5 days of
IV antibiotics, switch to amoxicillin/clavulanic acid (ratio 7:1 or 8:1) PO to complete 10 to
14 days of treatment (until erythema resolves). Dosage expressed in amoxicillin:
• < 40 kg: 50 mg/kg 2 times daily
• ≥ 40 kg:
Ratio 8:1: 3000 mg daily (2 tablets of 500/62.5 mg 3 times daily)
Ratio 7:1: 2625 mg daily (1 tablet of 875/125 mg 3 times daily)
– Where surgery is not available and there is no clinical improvement after 48 hours of
treatment, suspect an orbital abscess and seek ophthalmological expert advice.
In case of pain or fever, give paracetamol (see Section 3.1.3).

Peri-orbital cellulitis
Mild: treat with oral amoxicillin/clavulanic acid (ratio 7:1 or 8:1) PO for 7 to 10 days. Dosage
expressed in amoxicillin:
– < 40 kg: 50 mg/kg 3 times daily
– ≥ 40 kg:
• Ratio 8:1: 3000 mg daily (2 tablets of 500/62.5 mg 3 times daily)
• Ratio 7:1: 2625 mg daily (1 tablet of 875/125 mg 3 times daily)
Monitor as outpatient and explain to parent/carer signs of increasing severity and when to
seek immediate medical consultation.
Moderate: moderate swelling, difficult (but possible) to open the eye, systemically unwell
(fever, malaise). Treat with ceftriaxone IV: 50 mg/kg (max. 4 g if < 50 kg; max. 2 g if ≥ 50 kg)
once daily. Switch to oral treatment as above when clinically improving (after at least 48 hours
of IV treatment) to complete 7-10 days total treatment.
Severe: < 3 months age, significant swelling, unable to do adequate eye exam, no Hib vaccine.
Treat as per orbital cellulitis (above).

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Chapter 3: Acute febrile illness

Figure 3.4 - Algorithm for management of eye swelling/pain 3


(adapted from Royal Children’s Hospital Melbourne, Clinical Practice Guidelines41)

Unilateral oedema, erythema or pain


of the periorbital region NO Consider alternative diagnosis e.g.
AND
allergy, insect bite, conjunctivitis
History of fever
or upper respiratory tract infection?

YES

Signs of severe infection, YES


Treat as sepsis
systemic signs

NO

Limited or painful eye movement,


OR proptosis YES
Treat as orbital cellulitis
OR decreased visual acuity
OR severe headache

NO

Inadequate eye examination


OR significant oedema YES
Treat as severe periorbital cellulitis
OR age < 3 months
OR inadequate Hib immunisation

NO

Moderate oedema, YES Treat as moderate


difficult (but possible) to open eye,
peri-orbital cellulitis
fever, malaise

NO

Minimal oedema, YES


adequate eye movements, Treat as mild peri-orbital cellulitis
systemically well

119
Chapter 3: Acute febrile illness

References Chapter 3

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in Children: Assessment and Initial Management in Children Younger Than 5 Years. Royal
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4. Overview | Fever in under 5s: Assessment and Initial Management | Guidance | NICE.
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5. Meningitis. World Health Organisation. Accessed November 20, 2023.
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6. Kimberlin DW, Barnett ED, Lynfield R, Sawyer MH, eds. Red Book (2021): Report of the
Committee on Infectious Diseases. 32nd ed. American Academy of Pediatrics; 2021.
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7. Brouwer MC, McIntyre P, Prasad K, Van De Beek D. Corticosteroids for acute bacterial
meningitis. Cochrane Acute Respiratory Infections Group, ed. Cochrane Database Syst Rev.
2015;2018(11).
https://doi.org/10.1002/14651858.CD004405.pub5
8. Fact sheet about malaria. Accessed November 20, 2023.
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9. World Health Organization. Guidelines for the Treatment of Malaria. 3rd ed. World Health
Organization; 2015. Accessed November 20, 2023.
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10. WHO Guidelines for Malaria. World Health Organization; 2023. Accessed November 20, 2023.
https://www.who.int/publications-detail/guidelines-for-malaria
11. Nyirenda TS, Mandala WL, Gordon MA, Mastroeni P. Immunological bases of increased
susceptibility to invasive nontyphoidal Salmonella infection in children with malaria and
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12. Takem EN, Roca A, Cunnington A. The association between malaria and non-typhoid
Salmonella bacteraemia in children in sub-Saharan Africa: a literature review. Malar J.
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13. Mooney JP, Galloway LJ, Riley EM. Malaria, anemia, and invasive bacterial disease: A
neutrophil problem? J Leukoc Biol. 2019;105(4):645-655.
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14. Church J, Maitland K. Invasive bacterial co-infection in African children with Plasmodium
falciparum malaria: a systematic review. BMC Med. 2014;12(1):31.
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15. Maitland K, Olupot-Olupot P, Kiguli S, et al. Transfusion Volume for Children with Severe
Anemia in Africa. N Engl J Med. 2019;381(5):420-431.
https://doi.org/10.1056/NEJMoa1900100
16. Christensen SS, Eslick GD. Cerebral malaria as a risk factor for the development of epilepsy
and other long-term neurological conditions: a meta-analysis. Trans R Soc Trop Med Hyg.
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2015;109(4):233-238.
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17. Tetanus. World Health Organisation. Accessed November 20, 2023.
https://www.who.int/news-room/fact-sheets/detail/tetanus
18. Yen LM, Thwaites CL. Tetanus. The Lancet. 2019;393(10181):1657-1668.
https://doi.org/10.1016/S0140-6736(18)33131-3
19. Kyu HH, Mumford JE, Stanaway JD, et al. Mortality from tetanus between 1990 and 2015:
findings from the global burden of disease study 2015. BMC Public Health. 2017;17(1):179.
https://doi.org/10.1186/s12889-017-4111-4
20. Thwaites L. Tetanus. UpToDate. Published June 2022.
https://www.uptodate.com/contents/tetanus
21. Pinkbook: Tetanus | CDC. Published October 19, 2022. Accessed November 20, 2023.
https://www.cdc.gov/vaccines/pubs/pinkbook/tetanus.html
22. Cook TM, Protheroe RT, Handel JM. Tetanus: a review of the literature. Br J Anaesth.
2001;87(3):477-487.
https://doi.org/10.1093/bja/87.3.477
23. Rodrigo C, Fernando D, Rajapakse S. Pharmacological management of tetanus: an evidence-
based review. Crit Care. 2014;18(2):217.
https://doi.org/10.1186/cc13797
24. Tetanus. One Health Trust. Accessed November 20, 2023.
https://africaguidelines.onehealthtrust.org/treatment/neonatal-and-pediatric/tetanus/
25. Shanbag P, Mauskar A, Masavkar S. Intravenous magnesium sulphate infusion as first-line
therapy in the control of spasms and muscular rigidity in childhood tetanus. Paediatr Int
Child Health. 2019;39(3):201-207.
https://doi.org/10.1080/20469047.2018.1542884
26. Thwaites C, Yen L, Loan H, et al. Magnesium sulphate for treatment of severe tetanus: a
randomised controlled trial. The Lancet. 2006;368(9545):1436-1443.
https://doi.org/10.1016/S0140-6736(06)69444-0
27. Ceneviva GD, Thomas NJ, Kees-Folts D. Magnesium sulfate for control of muscle rigidity
and spasms and avoidance of mechanical ventilation in pediatric tetanus: Pediatr Crit Care
Med. 2003;4(4):480-484.
https://doi.org/10.1097/01.PCC.0000090015.03962.8B
28. World Health Organization. Current recommendations for treatment of tetanus during
humanitarian emergencies : WHO technical note. Published online 2010. Accessed
November 20, 2023.
https://iris.who.int/handle/10665/70219
29. Crump JA, Mintz ED. Global Trends in Typhoid and Paratyphoid Fever. Clin Infect Dis.
2010;50(2):241-246.
https://doi.org/10.1086/649541

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30. Stanaway JD, Reiner RC, Blacker BF, et al. The global burden of typhoid and paratyphoid
fevers: a systematic analysis for the Global Burden of Disease Study 2017. Lancet Infect Dis.
2019;19(4):369-381.
https://doi.org/10.1016/S1473-3099(18)30685-6
31. Britto C, Pollard AJ, Voysey M, Blohmke CJ. An Appraisal of the Clinical Features of
Pediatric Enteric Fever: Systematic Review and Meta-analysis of the Age-Stratified Disease
Occurrence. Clin Infect Dis. 2017;64(11):1604-1611.
https://doi.org/10.1093/cid/cix229
32. Typhoid. World Health Organisation. Accessed November 20, 2023.
https://www.who.int/health-topics/typhoid
33. Azmatullah A, Qamar FN, Thaver D, Zaidi AK, Bhutta ZA. Systematic review of the global
epidemiology, clinical and laboratory profile of enteric fever. J Glob Health. 2015;5(2):020407.
https://doi.org/10.7189/jogh.05.020407
34. Basnyat B, Qamar FN, Rupali P, Ahmed T, Parry CM. Enteric fever. BMJ. Published online
February 26, 2021:n437.
https://doi.org/10.1136/bmj.n437
35. Kumar S, Rizvi M, Berry N. Rising prevalence of enteric fever due to multidrug-resistant
Salmonella: an epidemiological study. J Med Microbiol. 2008;57(10):1247-1250.
https://doi.org/10.1099/jmm.0.2008/001719-0
36. Wain J, Hendriksen RS, Mikoleit ML, Keddy KH, Ochiai RL. Typhoid fever. The Lancet.
2015;385(9973):1136-1145.
https://doi.org/10.1016/S0140-6736(13)62708-7
37. Browne AJ, Kashef Hamadani BH, Kumaran EAP, et al. Drug-resistant enteric fever worldwide,
1990 to 2018: a systematic review and meta-analysis. BMC Med. 2020;18(1):1.
https://doi.org/10.1186/s12916-019-1443-1
38. Burki T. Typhoid conjugate vaccine gets WHO prequalification. Lancet Infect Dis.
2018;18(3):258.
https://doi.org/10.1016/S1473-3099(18)30087-2
39. Measles. World Health Organisation. Accessed November 20, 2023.
https://www.who.int/news-room/fact-sheets/detail/measles
40. World Health Organization. Guide for Clinical Case Management and Infection Prevention
and Control during a Measles Outbreak. World Health Organization; 2020. Accessed
November 20, 2023.
https://iris.who.int/handle/10665/331599
41. Clinical Practice Guidelines : Periorbital and orbital cellulitis. The Royal Children’s Hospital
Melbourne. Accessed November 20, 2023.
https://www.rch.org.au/clinicalguide/guideline_index/Periorbital_and_orbital_cellulitis/
42. Wald ER. Periorbital and Orbital Infections. Pediatr Rev. 2004;25(9):312-320.
https://doi.org/10.1542/pir.25-9-312
43. Sanford Guide | Antimicrobial Stewardship. Accessed November 20, 2023.
https://www.sanfordguide.com/

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Chapter 4:
Respiratory conditions
4

4.1 Approach to a child with a respiratory complaint................................................125


4.1.1 Respiratory symptoms and signs...................................................................125
4.1.2 Management................................................................................................. 129
4.1.3 Respiratory support....................................................................................... 129
4.2 Croup (laryngotracheitis and laryngotracheobronchitis)................................................. 132
4.2.1 Clinical features............................................................................................. 132
4.2.2 Management................................................................................................. 132
4.3 Epiglottitis.............................................................................................................. 136
4.3.1 Clinical features............................................................................................. 136
4.3.2 Management................................................................................................. 136
4.3.3 Prevention...................................................................................................... 138
4.4 Bacterial tracheitis................................................................................................. 139
4.4.1 Clinical features............................................................................................. 139
4.4.2 Management................................................................................................. 139
4.5 Pneumonia............................................................................................................. 141
4.5.1 Clinical features............................................................................................. 141
4.5.2 Investigations................................................................................................. 142
4.5.3 Management................................................................................................. 143
4.6 Empyema............................................................................................................... 146
4.6.1 Clinical features............................................................................................. 146
4.6.2 Management................................................................................................. 147
4.7 Bronchiolitis........................................................................................................... 148
4.7.1 Clinical features............................................................................................. 148
4.7.2 Management................................................................................................. 148
4.8 Diphtheria.............................................................................................................. 151
4.8.1 Clinical features............................................................................................. 151
4.8.2 Management................................................................................................. 152
4.8.3 Prevention...................................................................................................... 153
4.9 Pertussis (whooping cough).................................................................................. 154
4.9.1 Clinical features............................................................................................. 154
4.9.2 Management................................................................................................. 154
4.9.3 Post-exposure prophylaxis............................................................................. 156
4.9.4 Prevention...................................................................................................... 156
4.10 Asthma................................................................................................................. 157
4.10.1 Acute exacerbation of asthma..................................................................... 157
4.10.2 General management of asthma.................................................................161
4.10.3 Asthma education and action plan..............................................................164
4.11 Tuberculosis......................................................................................................... 166
4.11.1 Stages of infection....................................................................................... 166
4.11.2 Clinical features........................................................................................... 166
4.11.3 Diagnostic approach.................................................................................... 168
4.11.4 Investigations............................................................................................... 169
4.11.5 Paediatric diagnostic algorithms.................................................................170
4.11.6 Management............................................................................................... 173
4.11.7 Prevention and screening............................................................................. 175
4.12 Mastoiditis........................................................................................................... 177
4.12.1 Clinical features........................................................................................... 177
4.12.2 Management............................................................................................... 177
References Chapter 4................................................................................................... 179
Chapter 4: Respiratory conditions

4.1 Approach to a child with a respiratory complaint

Children of all age groups frequently present with respiratory symptoms, however, the most
common causes vary significantly between age groups and in the presence of underlying
conditions. Acute respiratory infection is the most common cause, with pneumonia accounting 4
for over 800,000 deaths in under 5-year-olds worldwide every year1. Additionally, annually
over 1 million children become symptomatic with tuberculosis2. Malnutrition, poor hygiene
and sanitation, and indoor and outdoor air pollution are all factors that may exacerbate
respiratory conditions in children.
Children presenting with a respiratory emergency, including acute respiratory distress,
obstructed upper airway, acute exacerbation of asthma, and hypoxia, need urgent assessment
and prompt management as critical deterioration can be rapid.
This chapter will cover the most common respiratory conditions that require hospital-level
care. For simple respiratory and ear, nose and throat (ENT) conditions that can be managed in
an out-patient department (OPD) setting and/or at home, refer to MSF Clinical Guidelines. For
OPD follow-up for longer term management of asthma, see Section 4.10.2.

4.1.1 Respiratory symptoms and signs


Diagnosis is often based on clinical history, descriptive factors of symptoms and signs, and
clinical examination.

History
– Take a comprehensive history of the presenting symptoms or signs, including onset, duration,
pattern, severity, precipitating and alleviating factors, associated features, previous episodes,
etc.
– Use direct questioning to gather descriptive factors relevant to the symptom:

Symptom Descriptive factors

Dyspnoea On exertion/at rest.


(difficult or laboured Ability to speak in full sentences.
breathing) and/or Impact on feeding (especially in infants).
tachypnoea (fast
breathing)

Cough Dry or productive; sputum volume, colour, consistency.


Sporadic or in bouts; barking or ‘whooping’
Exacerbating factors; worse/better at what time of day.
Duration.

Wheeze Triggering factors; worse/better at what time of day.

Sore throat Impact on swallowing, drinking. Change to voice or cry. Bad breath.

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Chapter 4: Respiratory conditions

Symptom Descriptive factors

Ear pain or hearing Rubbing ears (infants), discharge from ear


loss

Haemoptysis Duration, volume, colour.


(blood in sputum)

Chest pain Sharp/stabbing, dull/ache, site, radiation.

Systemic symptoms Fever; rigors; night sweats; loss of appetite; headache; vomiting
and diarrhoea; weight loss

ENT symptoms Nasal congestion/discharge, sneezing, vertigo, tinnitus, facial pain


and swelling

– Ask about past medical history including asthma, chronic respiratory or cardiac conditions,
surgical history and other medical co-morbidities as well as vaccination history (particularly
diphtheria, pertussis, measles, Haemophilus influenzae type B, pneumococcus vaccines).
– Family history: ask if there are any household members diagnosed with TB (or been in
contact with someone with TB); any smokers; parental HIV status; known cystic fibrosis.
– Social history: living conditions (draughts, damp, overcrowding, sanitation), indoor/outdoor
air pollution (check if cooking fire within living quarters), smoking.

Examination
Perform a full clinical examination (Chapter 1) and specific respiratory examination:
– General: overall appearance, position, activity level, ability to speak or cry, any obvious
acute respiratory distress or cyanosis, and vital signs.
– Expose the child’s chest and, where possible, position them at a 45-degree angle (semi-
sitting position).
– Observation: look for deformities, asymmetry, scars or signs of trauma; and rate, rhythm
and depth of breathing.
– Palpation: tracheal position, bilateral chest expansion, bone tenderness. Palpate for any
enlarged lymph nodes (adenopathy) in the retro-auricular, submandibular, supraclavicular,
and axillary areas.
– Percussion: across chest including supraclavicular, infraclavicular, bilateral chest wall (upper,
middle and lower), axillary regions for dullness or hyper-resonance.
– Auscultation: listen throughout both lung fields for presence or absence of breath sounds
and any additional sounds.
– Conduct a brief full-body examination paying attention to face, neck, hands and legs.
– Test for sinus tenderness by tapping the upper molars or the frontal or maxillary sinuses
with one finger.
– Use an otoscope to examine the tympanic membranes and the throat.

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Chapter 4: Respiratory conditions

– Check for signs indicative of underlying respiratory cause or condition:

Sign Likely cause

On observation

Central cyanosis: blue discolouration seen Low levels of oxygen in central arterial
on the tongue and lips. blood
Peripheral cyanosis: blue discolouration Low levels of oxygen in peripheral arterial 4
seen in nail beds of hands and/or feet. blood
Signs of respiratory distress: Pathologies of lung tissue or airways
• Grunting: a low, short repetitive noise on e.g. pneumonia (Section 4.5), asthma
expiration (Section 4.10), bronchiolitis (Section 4.7),
• Nasal flaring: nostrils widen on inspiration empyema (Section 4.6)
• Intercostal retraction: muscles between or
ribs pull inwards during inspiration. Cardiac pathologies (Chapter 6)
• Subcostal retraction (chest wall
retractions): inferior thoracic wall
depresses on inspiration as the superior
abdomen expands.
• ‘Head bobbing’ due to use of accessory
muscles: use of muscles in neck/
abdomen to assist inspiration.
Barking cough Croup (Section 4.2)
Stridor: abnormal, high pitched sound on Upper airway obstruction e.g. croup,
inspiration. epiglottitis (Section 4.3)
Barrel shaped chest: a rounded or bulging Chronic respiratory disease e.g. asthma
chest. (Section 4.10), cystic fibrosis, tuberculosis
(Section 4.11)
Clubbing: thickening of the tissue at the Tuberculosis (Section 4.11), chronic
base of the fingernails. respiratory disease

On palpation

Tracheal deviation Tension pneumothorax


Enlarged lymph nodes of neck, Indicate inflammatory process in region e.g.
supraclavicular, axillary. infection or malignancy.

On percussion

Dull percussion Increased tissue density e.g. empyema,


pleural effusion, pneumonia, haemothorax
Hyper-resonant percussion Reduced tissue density e.g. pneumothorax

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Chapter 4: Respiratory conditions

Sign Likely cause

On auscultation

Absence of breath sounds Pleural effusion, pneumonia (Section 4.5),


pneumothorax, haemothorax
Bronchial breathing: harsh breath sounds Pneumonia
with a gap between inspiratory and
expiratory sounds.
Crepitations: crackling or rattling sounds. Pneumonia, bronchiolitis, pulmonary
oedema
Pleural rub: squeaking or grating sound Empyema (Section 4.6), pleural effusion
Wheeze: continuous coarse whistling sound Asthma, bronchiolitis
most commonly heard on expiration

Evaluate severity of respiratory distress (if present) using clinical signs. The Clinical Respiratory
Score, (see Table 4.1 and Appendix 7) is a simple scoring system that can be used to guide
the assessment of respiratory distress and response to treatment. Based on the total score
obtained, the child can be classified as having mild, moderate or severe respiratory distress.

Table 4.1 - Clinical Respiratory Score (CRS) (adapted for the purposes of these guidelines from:
see references3,4)
Assess Score 0 Score 1 Score 2

Respiratory rate Age < 2 months: < 50 Age < 2 months: 50-60 Age < 2 months: > 60
(breaths/minute) Age 2-11 months: < 40 Age 2-11 months: 40-50 Age 2-11 months: > 50
Age 1-5 years: < 30 Age 1-5 years: 30-40 Age 1-5 years: > 40
Age > 5 years: < 20 Age > 5 years: 20-30 Age > 5 years: > 30

Auscultation Good air movement, Depressed air Diminished or absent


expiratory scattered movement inspiratory breath sounds, severe
wheezing or loose and expiratory wheezes wheezing or rales/
rales/crackles or rales/crackles crackles or marked
prolonged expiration

Use of accessory Mild to no use of Moderate intercostal Severe intercostal and


muscles accessory muscles, retractions, mild to subcostal retractions,
mild to no retractions moderate use of nasal flaring
or nasal flaring on accessory muscles,
inspiration nasal flaring

Mental status Normal to mildly Irritable, agitated, Lethargic


irritable restless

Room air SpO2 > 95% 90-95% < 90%

Colour Normal Pale to normal Cyanotic, dusky

Based on the total score obtained, 3 categories of respiratory distress are possible:
Mild (≤ 3), Moderate (4-7), Severe (8-12)

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Chapter 4: Respiratory conditions

Investigations
Peak flow assessment, chest X-ray or sputum samples can help to confirm or guide diagnosis.
Where relevant, these are described in further detail in disease-specific texts throughout the
chapter.
Consider cardio-pulmonary Point-of-Care Ultrasound (POCUS):
– Requires dedicated intensive training and should not be performed by untrained or
inexperienced clinicians.
– Indications: dyspnoea, hypoxia 4
– Perform 12-zone lung ultrasound (LUS) to evaluate for signs of consolidation, pleural
effusion/ empyema, pulmonary oedema, and to rule out pneumothorax.
– Can also be used for ultrasound-guided procedures (thoracocentesis) with appropriate
training only. Include 5-view cardiac exam if applicable.

4.1.2 Management
Refer to disease or syndrome specific management in respective sub-chapters.

Emergency management of an acutely unwell child with respiratory symptoms


Treat in emergency department or area with resuscitation equipment.
– Assess and manage ABCDE (Chapter 2, Section 2.2)
– Aim to keep child in a position that alleviates respiratory distress, e.g. sitting with support at
45 degrees, or in the case of infants, sitting on a parent/carer’s lap.
– Administer oxygen via face mask, aiming for SpO2 between 94 - 98%.
– Conduct a rapid examination to assess for upper airway obstruction, severity of respiratory
distress/hypoxia, or tracheal deviation to manage any life-threatening emergency
immediately.
– If signs of epiglottitis (septic, sitting upright, drooling), do not examine throat or do any
procedures that may agitate child. Call anaesthetist if available for possible upper airway
intervention.
– For signs of upper airway obstruction, refer to:
• Choking (see Chapter 2, Section 2.3)
• Croup (Section 4.2)
• Epiglottitis (Section 4.3)
• Bacterial tracheitis (Section 4.4)
• Diphtheria (Section 4.8)
– Signs of tension pneumothorax, refer to Chapter 2, Section 2.7.
– Depending on severity of respiratory distress and/or hypoxia, provide necessary respiratory
support.

4.1.3 Respiratory support


See also MSF Manual of Nursing Care Procedures, Chapter 7: Respiratory Care, for
comprehensive nursing guidance for respiratory support.

Oxygen therapy
Essential treatment for hypoxia and is indicated when oxygen saturation (SpO2) is < 92% in
stable patients, aiming to maintain SpO2 ≥ 92%. A higher threshold is used in emergency
management of critically unwell children and for specific conditions where there is impaired
delivery of oxygen to body tissues, such as in severe anaemia, severe sepsis, sickle cell disease

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and severe heart failure5, where the aim is to maintain SpO2 ≥ 94%. Oxygen can be delivered
via a simple oxygen mask, a non-rebreathing mask, or via nasal cannulae (see Chapter 15,
Section 15.1 for more information on when to use each oxygen delivery method). Always use
the minimum flow of oxygen possible to achieve desired oxygen saturations according to the
device used. Weaning should be considered in children who are stable or clinically improving
when SpO2 is consistently ≥ 92%, if continuously monitored, or ≥ 92% on at least two separate
consecutive readings taken several hours apart. Oxygen should be prescribed, with target SpO2
indicated to allow for nurse-led weaning and adjustment of flow rates to meet the desired
target. See also MSF Manual of Nursing Care Procedures, Procedure: Oxygen therapy.
Humidification
No humidification is needed for standard oxygen flow rates. Humidification is only needed if
the patient receives high flow rates for more than 2 hours. High flow rates are > 2 L/min for
1 month to < 2 years old, > 4 L/min for 2 to 12 years old, and > 6L/min for over 12 years old.
Standard flow rates via nasal cannula by age

Age Standard oxygen nasal cannula flow rate

1 month to < 2 years 1 to 2 L/min

2 to 12 years 2 to 4 L/min

Over 12 years 4 to 6 L/min

High-flow nasal cannula (HFNC)a


Effective, safe, non-invasive method to provide acute respiratory support in moderate to
severe respiratory distress when oxygen therapy alone is insufficient6. HFNC systems consist
of a flow generator, an air-oxygen blender, a humidifier and wide-bore nasal cannula. Flow
and oxygen requirements can be titrated independently to meet the patient’s needs, and flow
rates of 8 - 20L/min in infants, up to 30 - 50 L/min in children 12-18 years can be achieved7.
The heated, humidified gas is well tolerated as it avoids drying of nasal mucosa. High flow
rates wash out pharyngeal dead space and improve functional residual capacity (FRC) while
humidification helps to remove secretions, leading to reduced work of breathing8. Follow local
protocols for further guidance on implementation where HFNC is available.

Non-invasive ventilation: continuous positive airway pressure (CPAP)b


CPAP enables delivery of a continuous level of positive airway pressure which helps to splint
airways open and prevent collapse of alveoli. In addition to continuous flow of oxygen, this
improves diffusion of oxygen into the blood, which reduces the work of breathing and thus
provides comfort to the child.
CPAP is indicated in severe respiratory distress, when HFNC (where available) has failed. It can
only be used in spontaneously breathing patients, since it delivers a continuous low pressure
and does not initiate breaths. CPAP should be reserved for children with reversible respiratory
conditions, and is unlikely to be beneficial in children whose respiratory distress is secondary
to a non-respiratory cause (e.g. cardiac condition, shock).

a HFNC is not yet widely available in MSF projects. It should be noted that standard oxygen concentrators alone
cannot be used to administer safe and effective HFNC.
b Note: ‘Home-made’, improvised or locally-adapted bubble CPAP devices should not be used in MSF projects.
Only validated CPAP machines that have been designed for this purpose should be used.

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Administer CPAP only where intensive medical care is available with appropriately trained
staff, medical devices, and a validated local user protocol. The use of CPAP with certain patient
groups or where intensive medical care is limited carries a risk and may be harmful9. Ensure all
safety precautions are implemented as per local protocol.

Invasive ventilation: intubation


Requires specialised facilities and staff and is considered outside the scope of these guidelines.
It is, therefore, not included as a management option in disease-specific text. 4
General management tips for common respiratory complaints
– Saline nose drops and/or a bulb syringe can be used to clear accumulated nasal secretions
(see MSF Manual of Nursing Care Procedures, Procedure: Naso-Oropharyngeal suctioning).
– Ensure child gets adequate daily fluid intake and maintains a good hydration status avoiding
over or dehydration.
– Vitamin C, cough or cold medications, are not effective at reducing either the symptoms or
the duration of respiratory disease.
– Antihistamines are only recommended if there is an allergic component to the symptoms or
in the history.
– Antibiotics should only be used if a bacterial infection is suspected.
– Steroids should be used with caution and reserved for conditions where clear benefit has
been demonstrated, e.g. asthma, croup.
– Many respiratory diseases are infections. In such cases, depending on the aetiology,
appropriate transmission-based precautions (e.g. droplet precautions) should be adopted
by parent/carer, medical staff and other close contacts to limit risk of transmission. These
are detailed in disease-specific texts.
– All children presenting with respiratory disease should have their vaccination status checked.
If incomplete, refer the family to the local EPI (Expanded Program on Immunisation) or
vaccinate the child during admission if possible.

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4.2 Croup (laryngotracheitis and laryngotracheobronchitis)

Common respiratory infection amongst children with peak incidence between 6 months and
3 years (though may rarely occur in infants as young as 3 months old and in older children
up to 7 years of age), with a characteristic inspiratory stridor and barking cough. It is most
often caused by parainfluenza virus type 1, but also by respiratory syncytial virus (RSV) or
adenovirus; other viral infections have been known less commonly to cause croup (including
measles, influenza, coronaviruses). In most cases it is mild and self-limiting, though secondary
bacterial infection, significant upper airway obstruction or respiratory distress may occur.
Croup is also called laryngotracheitis, or laryngotracheobronchitis if accompanied by wheezing.
It is called laryngitis when hoarseness is the only symptom, as in older children. Spasmodic
croup is characterised by the sudden onset of inspiratory stridor at night, short duration
(several hours) and sudden cessation. Spasmodic croup recurs frequently and is also called
"allergic croup."

4.2.1 Clinical features


Diagnosis based on clinical history and presentation.
– Initial symptoms of common cold with nasal discharge.
– Develops fever, hoarseness, barking cough and stridor over 12 to 48 hours.
– With worsening airway obstruction, stridor may get louder and child may develop other
signs of respiratory distress. If significant airway obstruction, the ‘loud’ stridor may become
absent and paradoxically replaced by a ‘quiet’ stridor indicating severe croup.
– Indication of higher risk of severity: sudden onset or rapidly progressing symptoms
(inspiratory stridor at rest after < 12 hours of illness); previous episodes of croup.
Symptoms are exacerbated when the child gets distressed – try to keep child comfortable
while examining, e.g. sitting on parent/carer’s lap, examine oropharynx without using a tongue
depressor to avoid triggering the gag reflex.

4.2.2 Management
– Administer oxygen if SpO2 < 92% in room air or severe respiratory distress.
– Manage according to severity of croup.
– Treat fever for the child’s comfort.
– Antibiotic treatment is not routinely required as most croup cases are of viral aetiology.
Consider antibiotic treatment in clinical conditions where a secondary bacterial infection is
suspected.

Mild croup
– No stridor at rest, no signs of severe respiratory distress, drinking well, SpO2 > 94%.
– Give one dose of dexamethasone PO: 0.15 - 0.6 mg/kga (maximum dose 16 mg) or alternatively
prednisolone PO: 1 mg/kg.
– Discharge home with advice to parents/carers to ensure adequate hydration and to return
if condition deteriorates.

a 0.15 mg/kg of dexamethasone is the preferred dose for children who are easily able to return to hospital in
case of deterioration or return of symptoms. If access to healthcare is difficult, the higher dose of 0.6 mg/kg
should be used.

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– Consider admission for observation in any of the following situations:


• Infants < 6 months of age
• Dehydration present
• Live far from health facility

Moderate and severe croup


– Stridor present at rest (either intermittent or persistent), signs of severe respiratory distress,
unable to drink, hypoxia. 4
– Administer oxygen if SpO2 < 92% in room air or severe respiratory distress.
– Give dexamethasone PO: 0.6 mg/kg (maximum dose 16 mg) or alternatively prednisolone
PO: 1 mg/kg. Administer IV or IM if unable to tolerate oral treatment.
– Administer epinephrine via a nebulizer every 20 minutes as needed. Prepare the epinephrine
(0.5 mg/kg/dose, max. 5 mg), diluting with sodium chloride 0.9% if necessary to obtain a
total of 4 to 5 mL in the nebulizing chamber. If severe tachycardia (HR > 200 beats per min)
develops, stop epinephrine until it resolves.
– Admit child, preferably to an ICU. Monitor closely for need of respiratory support.
– Ensure adequate calorie and fluid intake.
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).

Differential diagnoses
Ensure other causes of stridor and/or respiratory distress are differentiated, including
epiglottitis, bacterial tracheitis, diphtheria, peritonsillar and retropharyngeal abscesses and
foreign body aspiration (see Table 4.2 and Figure 4.1a to Figure 4.1c, pages 134 and 135).
Table 4.2 - Comparative table of upper airway conditions (adapted for the purposes of these
guidelines from: see references10,11)
Croup Epiglottitis Bacterial tracheitis
Incidence Common Rare Less common
Aetiology Parainfluenza type 1 H. influenzae type B S. aureus, Moraxella
Respiratory syncytial catarrhalis,
virus (RSV) M. pneumoniae,
Adenovirus S. pyogenes,
S. pneumoniae
Age 6 months - 3 years 1-7 years 6 months - 14 years
Onset of stridor Progressive Very rapid Rapid
Fever Low grade/variable High High
Cough Common Less common Common
Dysphagia No Yes Rare
Drooling No Yes Rare
Voice Hoarse Muffled, dull Normal to very
hoarse

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Croup Epiglottitis Bacterial tracheitis


Preferred position Variable Tripod Variable

X-ray findingsb Steeple sign; Pre-stenotic dilatation Oedematous tracheal


Hypopharyngeal and distinctive walls with narrowing
c
dilatation with ‘thumb sign’
subglottic narrowing
Response to Very good No response No/partial response
nebulised
epinephrine
Response to Very good Unclear No/minimal response
corticosteroids
Response to No response Very good Very good
antibiotics

Figures 4.1 - Neck x-ray features of conditions causing stridor a) normal b) croup c) epiglottitis
4.1a - Normal lateral neck x-ray, childd

4.1b - Croup
e
AP neck x-ray, child : Lateral neck x-ray, childf:

Characteristic tapering of the upper Demonstrates distension of the


trachea (steeple sign) suspicious of croup hypopharynx consistent with croup

b X-rays are not usually indicated in croup or bacterial tracheitis, however findings may support diagnosis when
unclear. See also Figure 4.1a to Figure 4.1c.
c Oedematous and enlarged epiglottis which is seen on lateral soft-tissue radiograph of the neck and has the
shape of a thumb.
d Case courtesy of Ian Bickle (image reversed from original), Radiopaedia.org, rID: 80232.
https://radiopaedia.org/cases/80232
e Case courtesy of Michael Sargent, Radiopaedia.org, rID: 6086. https://radiopaedia.org/cases/6086
f Case courtesy of Frank Gaillard (image reversed from original), Radiopaedia.org, rID: 6258.
https://radiopaedia.org/cases/6258

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4.1c - Epiglottitis
Lateral neck x-ray, adultg:

Classic ‘thumbprint sign’ in adult characterised by thickening of the epiglottis,


reflecting oedema and inflammation (compare to normal thin epiglottis in Figure 4.1a).

Lateral neck x-ray, childh:

Thickened epiglottis in child (compare to normal thin epiglottis in Figure 4.1a).


Image duplicated on right with mark-up to demonstrate ‘thumbprint’.

g Case courtesy of Andrew Ho, Radiopaedia.org, rID: 22906. https://radiopaedia.org/cases/22906


h Case courtesy of Jonathan Muldermans, Radiopaedia.org, rID: 54890. https://radiopaedia.org/cases/54890

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4.3 Epiglottitis

Inflammation of the epiglottis and supraglottic tissue which can rapidly progress to upper
airway obstruction and become life-threatening.
This is an upper airway medical emergency. Call for a senior clinician or an anaesthetist
where available.

Aetiology
– Bacterial infection12: Haemophilus influenzae type B (Hib) most common (unless Hib vaccine
coverage is high), S. aureus including MRSA are increasingly the most common cause where
Hib vaccination coverage is high, other H. influenzae strains, and streptococci.
– Less commonly viral (influenza A13) or fungal infection.
– Non-infectious causes: injury due to burns/inhalation of smoke or toxic substances, or
ingestion of a foreign body or toxic substance.
Epiglottitis caused by infection occurs mostly in younger children between 1 and 7 years of
age, though again, Hib vaccine coverage may shift this to older age groups.

4.3.1 Clinical features


– Sudden onset high fever, very sore throat, drooling and difficulty swallowing. Symptoms
progress very rapidly (in less than 12 to 24 hours), and child can develop severe breathing
difficulties14.
– Child adopts typical ‘tripod’ position: sitting up and leaning forward on outstretched arms
for support.
– Visible distress: mouth open, appearing anxious, and ‘looks toxic or septic’15.
– Stridor and “hot potato voice” (muffled voice or aphonia) may be present (but, as opposed
to croup, hoarse voice and cough are usually absent).
– Signs of critical condition: weak grunting or crying, drowsiness, difficult to arouse,
unconjugate or anxious gaze, pallor or cyanosis, general hypotonia.
See also Table 4.2 and Figures 4.1 for differentiation between other causes of stridor.
Allow the child to sit in a comfortable position or on the parent/carer’s lap. Do NOT lie the child
down (may precipitate airway obstruction and respiratory arrest). Avoid any examination that
will upset the child, including examination of the mouth and throat.

4.3.2 Management
Airway management
Securing the airway is a life-saving intervention in epiglottitis with airway obstruction but
carries significant risk. Senior medical staff (anaesthesia and intensive care) with extensive

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experience in paediatric airway management should be consulted early. In the absence of the
required skills and/or equipment, refer the patient to a facility with such capacity as soon as
possible.
Initial basic airway management
– Manage patient in an intensive care or resuscitation area where staff have capacity to carry
out emergency resuscitation, if necessary.
– Ensure close observation and monitor and record vital signs as often as required using an
early warning system (see MSF Manual of Nursing Care Procedures, Assessment and vital 4
signs, Charts: Vital sign charts).
– Keep the child calm with minimal disturbance.
– Do not lie the child down, keep in a seated position.
– Administer oxygen, if possible, without distressing the child (see Chapter 15, Section 15.1).
– Get IV access and start IV maintenance fluids (see Chapter 15, Section 15.2), and administer
antibiotic treatment (see below). Avoid agitating the child with multiple attempts at IV
access.
– Consider a trial of nebulised epinephrine (see Section 4.2.2 for dosing). Stop immediately if
any deterioration or if the nebulisation upsets and aggravates the childa. Consider croup as
differential diagnosis if significant response to epinephrine nebuliser.
– If the child stops breathing, administer bag and mask ventilation with high-flow oxygen until
airway is secured.
Advanced airway management
– In the case of imminent airway obstruction, endotracheal intubation should be attempted
only under the following conditions:
• By senior medical staff with extensive experience in paediatric airway management.
• In an operating theatre under general anaesthesia.
• In the presence of a surgeon capable of performing an emergency surgical airway should
intubation attempts fail.
– Patients recovering from epiglottitis may be extubated when repeated direct laryngoscopy
at 24- to 48-hour intervals indicates reduced size and inflammation of the epiglottis.

Antibiotic treatment
– Administer IV ceftriaxone and IV clindamycin, or alternatively high-dose IV amoxicillin/
clavulanic acid for 5 days.
– Avoid IM route (may agitate the child and precipitate a respiratory arrest), consider only if
unable to obtain prompt IV access.
– Switch to PO amoxicillin/clavulanic acid treatment to complete a total of 7 to 10 days
treatment, when child tolerating oral intake, has reduced fever and respiratory distress, and
SpO2 stable.

50 mg/kg (max. 4 g if < 50 kg; max. 2 g if ≥ 50 kg) every


ceftriaxone IV
24 hours

clindamycin IV 10 mg/kg every 8 hours (max. 2700 mg/day or 900 mg/dose)

a Evidence of efficacy is very limited, however in contexts where advanced airway interventions are limited,
a nebuliser can be attempted, assessing carefully for any positive effect and any signs of worsening airway
obstruction. Nebulised epinephrine may cause a rebound deterioration of airway obstruction so should be
trialled with caution and very close monitoring.

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Chapter 4: Respiratory conditions

amoxicillin/clavulanic • < 3 months: 50 mg/kg every 12 hours


acid • ≥ 3 months and < 40 kg: 50 mg/kg every 8 hours (max. 6 g
IV
(dosage expressed in daily)
amoxicillin) • ≥ 40 kg: 2 g every 8 hours

amoxicillin/clavulanic • < 40 kg: 50 mg/kg 2 times daily


acid • ≥ 40 kg:
ratio 7:1 or 8:1 PO Ratio 8:1: 3000 mg daily (2 tabs of 500/62.5 mg 3 times
(dosage expressed in daily)
amoxicillin) Ratio 7:1: 2625 mg daily (1 tab of 875/125 mg 3 times daily)

4.3.3 Prevention
H. influenzae type B (Hib) vaccine should be administered according to the national immunisation
programme (commonly at 2, 4 and 6 months, plus booster at 12 to 15 months). The Hib vaccine
does not cover all strains that may cause epiglottitis, but it is 90 to 95% effective14.

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4.4 Bacterial tracheitis

Secondary bacterial infection of the trachea resulting in mucopurulent exudates that may
cause obstruction of the upper airway and become life-threatening11. It is uncommon, but
may occur as a secondary infection following an acute viral respiratory illness. Consider as a 4
differential in young children presenting with upper airway obstruction or viral croup that is
not improving.
Commonly isolated bacterial pathogens include: S. aureus (including MRSA)16, S. pneumoniae,
group A Streptococcus, and Haemophilus influenzae strains17,18,19. Viral pathogens isolated
that may have been the primary infection include parainfluenza, influenza A and B, measles,
RSV20.
Occurs primarily between 6 months and 14 years of age, most commonly between 3 and
8 years11.

4.4.1 Clinical features


– Critically unwell, high fever and signs of upper respiratory obstruction (stridor, hoarseness,
cough, tachypnoea)11.
– Usually presenting with a history of several days of a viral respiratory infection (e.g. croup)
with acute deterioration. (To differentiate with epiglottitis which is acute onset with no
gradual history, and child prefers to lie down in bacterial tracheitis).
– Systemic features including weak grunting or crying, drowsiness/impaired level of
consciousness/difficulty to arouse, anxious gaze, pallor or cyanosis, general hypotonia.
– In severe cases there is a risk of complete airway obstruction, especially in very young
children, sepsis and toxic shock syndrome, pulmonary oedema, and acute respiratory
distress syndrome21.

Investigations
Concurrent pneumonia or chest x-ray (CXR) abnormalities are found in at least 50% of case
series22. Consider a chest and lateral neck x-ray where it may be useful.
CXR: recommended once child is stable enough to exclude concurrent pneumonia.
Lateral neck x-ray: oedematous tracheal walls with subglottic narrowing, with or without
intraluminal membranes11.

4.4.2 Management
– Assess and manage for ABCDE as needed. Secure airway if necessary.
• If severe airway obstruction or impending respiratory failure, consider intubation if
advanced ICU and airway management available (see Section 4.3.2).
– Administer oxygen if SpO2 < 92% in room air or severe respiratory distress.
– Administer bag and mask ventilation if necessary.

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– If stridor present, administer a trial of nebulised epinephrinea (see Section 4.2.2 for dose).
– If wheezing, administer a trial of nebulised salbutamol (see Section 4.10.1 for dose).
– Stop immediately if any deterioration or if the nebulisation upsets and aggravates the child.
Consider croup as differential diagnosis if significant response to epinephrine nebuliser.
– Get IV access and start IV maintenance fluids to ensure adequate hydration. Avoid agitating
the child with multiple attempts at IV access.
– Administer combined antibiotic treatment with IV ceftriaxone and clindamycin23. Avoid IM
route (may agitate the child and precipitate a respiratory arrest), consider only if unable to
obtain prompt IV access.
– Treat high fever with antipyretics for the comfort of the child.
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– Continue IV antibiotic treatment for at least 5 days. If the clinical condition has improved
(low or no fever, less respiratory distress, improved SpO2) and child tolerating oral intake,
switch to oral antibiotic treatment with amoxicillin/clavulanic acid PO (ratio 7:1 or 8:1) to
complete 10 days of treatment24.

50 mg/kg (max. 4 g if < 50 kg; max. 2 g if ≥ 50 kg) every


ceftriaxone IV
24 hours

clindamycin IV 10 mg/kg every 8 hours (max. 2700 mg/day or 900 mg/dose)

amoxicillin/clavulanic • < 40 kg: 50 mg/kg 2 times daily


acid • ≥ 40 kg:
ratio 7:1 or 8:1 PO Ratio 8:1: 3000 mg daily (2 tabs of 500/62.5 mg 3 times
(dosage expressed in daily)
amoxicillin) Ratio 7:1: 2625 mg daily (1 tab of 875/125 mg 3 times daily)

a Evidence of efficacy is very limited, however in contexts where advanced airway interventions are limited,
a nebuliser can be attempted, assessing carefully for any positive effect and any signs of worsening airway
obstruction. Nebulised epinephrine may cause a rebound worsening of airway obstruction so should be
trialled with caution and very close monitoring.

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Chapter 4: Respiratory conditions

4.5 Pneumonia

Pneumonia is an acute infection of the lower respiratory airways, resulting in inflammation,


fluid or pus in the alveoli and alveolar walls. This causes cough, fever, and difficulty in breathing.
Globally, pneumonia remains one of the main causes of mortality amongst children under 4
5 years of age, accounting for 14% of worldwide under-5 mortality in 201925.

Aetiology
Pneumonia in children is most commonly community acquired. Infectious organisms can be
viral, bacterial, fungal or parasitic. Common pathogens vary widely by context, region, age, and
underlying clinical conditions (e.g. severe acute malnutrition (SAM), HIV infection, sickle cell
anaemia). Immunisation with H. influenzae type B (Hib) and pneumococcal conjugate vaccines
have reduced pneumonia where vaccine coverage is high, however the following infections
still impact millions of children worldwide:
– Bacterial: Hib, Streptococcus pneumoniae, Salmonella spp., Klebsiella pneumonia,
Staphylococcus aureus, Streptococcus pyogenes, Mycobacterium tuberculosis
– Viral: Respiratory syncytial virus (RSV), Influenza A and B, adenoviruses, parainfluenza,
measles, coronaviruses, human metapneumovirus
– Atypical bacteria: Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella
pneumophila (common in older children)
– Opportunistic fungal: Pneumocystis jirovecii (in HIV infected), Aspergillus spp
– Aspiration pneumonia caused by oral anaerobic flora
Non-infectious causes include foreign body inhalation, acid or other toxic fluid aspiration, or
exposure to chemical toxins.
Diagnosis is based on history, clinical features and examination, and where available, a chest
x-ray and/or lung ultrasound may be supportive. Assess the severity of pneumonia and
respiratory signs using the CRS (see Table 4.1 and Appendix 7) to promptly provide respiratory
support if needed and administer antibiotic treatment.

4.5.1 Clinical features


– Cough: can vary from very mild to deep/chesty and may be productive of green or yellow
coloured sputum, or even rarely be blood-stained.
– Difficulty in breathing: may present as tachypnoea, dyspnoea, cyanosis/hypoxia, respiratory
distress.
– Fever: is often high (≥ 39 °C), but may be low-grade or absent.
– Infants and younger children often present also with difficulty in feeding, restlessness or
irritability, vomiting and diarrhoea.
– Older children may complain of chest pain on deep breathing or coughing (pleuritic chest
pain) and occasionally abdominal pain.
– Children with SAM or underlying immunocompromise (HIV infection) are at high risk of
developing pneumonia but may not elicit a cough or fever.
– For persistent cough and fever for > 2 weeks duration, check for any other signs of TB, any
contact history with TB, and exclude TB with careful clinical assessment and follow-up.

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Atypical pneumonia (due to Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella


pneumophila) has a slightly different presentation, with symptoms often being insidious in
onset and non-specific. It is common in school-age and older children and should be considered
in special populations, such as children with sickle cell disease, where it can lead to acute chest
syndrome (see Chapter 10, Section 10.2).
Typical symptoms include:
– Low grade fever
– Fatigue
– Malaise and myalgia
– Headache
– Non-productive cough: typically slow onset and gradually worsening, can last for several
weeks or even months

Examination
Perform a full clinical assessment and examination, including:
– Adequacy of oxygenation (vital signs, SpO2, cyanosis, neurological state/level of
consciousness).
– Level of respiratory distress (see Table 4.1), effort/exhaustion, need for respiratory support.
– Percussion: dullness appears on the affected side.
– Auscultation: decreased breath sounds, bronchial breath sounds, inspiratory crackles
(crepitations) may appear over the affected lobe or lung.
Signs of severe pneumonia include:
– Central cyanosis or oxygen saturations (SpO2 < 90% in room air)
– Severe respiratory distress (see Table 4.1)
– Altered level of consciousness
– Inability to drink or breast feed
– Vomiting everything (all foods and liquids)
– Appears severely ill, toxic or septic
Examine and/or investigate for any underlying causes including tuberculosis (see Section 4.11),
malnutrition, malaria (see Chapter 3, Section 3.4). In children with recurrent pneumonia or
poor response to treatment, check for HIV infection.

Complications
If the child has bacterial pneumonia (such as staphylococcal pneumonia), it can lead to
empyema (see Section 4.6). Dehydration can also be a complication of severe pneumonia if
the child becomes too lethargic to drink.

4.5.2 Investigations
– FBC, Hb, blood glucose level (BGL)
– CRP, if available
– Chest X-ray (CXR), or lung ultrasound:
• There is significant overlap in radiographic findings between different aetiologies of
pneumonia (e.g. viral vs bacterial pneumonia), and findings are often non-specific.
• A lobar pneumonia (homogeneous consolidation of an entire lobe of lung) is most
commonly bacterial (see Figure 4.2).

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Chapter 4: Respiratory conditions

• Consider follow-up CXR (or lung ultrasound) if there is no improvement with antibiotics,
clinical deterioration, or suspicion of complications (such as empyema).
• Note that immunocompromised children may have normal chest radiographs despite
having severe pneumonia.
– Consider sickle cell disease screening in high prevalence contexts.
– Malaria RDT in endemic areas
– TB screening: microscopy and culture, or GeneXpert, if available (see Section 4.11 for further
investigations if TB suspected)
– HIV testing: see note above 4
– Blood culture (if severe pneumonia or signs of systemic illness)
Figure 4.2 - CXR features of lobar pneumonia
Frontal CXR, childa:

Dense homogeneous consolidation in the right upper lobe with air bronchograms,
highly suggestive of bacterial pneumonia.

4.5.3 Management
Indications to admit for hospitalisation:
– Less than 6 months of age
– Clinically severe pneumonia
– Severe acute malnutrition
– Concerns regarding the ability of the parents/carers to treat or if the parents/carers cannot
bring the child back for a follow-up examination

Severe pneumonia
– Assess and manage ABCDE (see Chapter 2, Section 2.2) and admit for close observation,
ideally to an ICU, if available.
– Administer oxygen via face mask, aiming for SpO2 between 94 - 98%.
– If necessary, increase level of respiratory support (see Section 4.1.2).
– Administer antibiotics (see following page).
– Treat fever and pain to improve comfort (see Chapter 15, Section 15.4).
– Administer anti-malarial treatment if malaria test positive.
– Monitor and record vital signs and BGL as often as required using an early warning system
(see MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign
charts).

a Case courtesy of Ian Bickle, Radiopaedia.org, rID: 74630. https://radiopaedia.org/cases/74630

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Antibiotic treatment
– Administer ampicillin (or amoxicillin) IV (or IM) 50 mg/kg every 8 hours + gentamicin IV (or
IM) 7.5 mg/kg every 24 hours.
– For children over 5 years old or if suspicion of atypical pneumonia in any age group, add
azithromycin PO 10 mg/kg once daily for 5 days.
– Continue IV antibiotic treatment for 48 hours and re-assess clinical condition:
• Child clinically improvedb and tolerating oral intake: replace IV with PO amoxicillin/clavulanic
acid (ratio 7:1 or 8:1) to complete 7 days treatment. Dosage expressed in amoxicillin:
▹ < 40 kg: 50 mg/kg 2 times daily
▹ ≥ 40 kg:
Ratio 8:1: 3000 mg daily (2 tablets of 500/62.5 mg 3 times daily)
Ratio 7:1: 2625 mg daily (1 tablet of 875/125 mg 3 times daily)
• If child not clinically improved after 48 hours, change to cefotaxime IV 50 mg/kg every
8 hours or ceftriaxone IV (or IM) 80 mg/kg (max. 4 g if < 50 kg; max. 2 g if ≥ 50 kg) every
24 hours. Consider treating for empyema (see Section 4.6) in children with measles
complicated by pneumonia who do not improve quickly with antibiotics.
• If condition deteriorates, or if MRSA suspected, add clindamycin IV 10 mg/kg every
8 hours. If atypical pneumonia suspected add azithromycin PO 10 mg/kg once daily for
5 days. Switch to oral antibiotic (as above) when child has improved and is tolerating oral
intake. If IV clindamycin administered, oral switch to clindamycin PO, 10 mg/kg 3 times
daily.
Suspected aspiration pneumonia:
– Administer ceftriaxone IV (dose as above) + metronidazole IV 10 mg/kg every 8 hours for
72 hours.
– Alternatively, administer clindamycin IV 10 mg/kg every 8 hours as an alternative to
metronidazole, or amoxicillin/clavulanic acid IV:
• 1 to 3 months of age: 30 mg/kg every 12 hours
• > 3 months of age: 30 mg/kg every 8 hours
– If clinical improvement and tolerating oral intake, replace IV with PO amoxicillin/clavulanic
acid (dose as above) to complete 7 days treatment.

HIV exposed or infected:


– Add trimethoprim-sulfamethoxazole IV/PO to cover for Pneumocystis jirovecii (see also
Chapter 13).

Fluid and nutritional intake support


– Ensure adequate fluid intake (monitor oral intake)
• If unable to drink sufficiently or showing signs of dehydration, support with oral or
nasogastric feeds (see Chapter 15, Section 15.5).
• If enteral feeding is not tolerated or the clinical condition is unstable, cautiously start IV
maintenance fluids (see Chapter 15, Section 15.2), ensuring careful monitoring of fluid
balance. Fluid restriction should be considered for severe casesc.
• In the case of severe respiratory distress, nil-by-mouth for first 24 hours to avoid risk of
aspiration and start IV maintenance fluids as outlined above. Begin to give frequent small
feeds after 24 hours, as tolerated. Show parent/carer how to support child upright at
30 degrees after feeds.

b Improvement is indicated by the following: improved respiratory distress, diminished fever, improvement in
SpO2 level or less oxygen is required to maintain saturation, improved ability to drink and or eat and improved
activity.
c Increased ADH secretion in respiratory conditions can cause water retention, leading to fluid overload.

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Discharge criteria
Consider discharge from hospital when child is:
– Clinically improving, with no fever for at least 24 hours
– Able to tolerate oral intake
– Maintaining oxygen saturations ≥ 92% in room air
– Tolerating oral antibiotics
– Going home to an environment where completion of treatment can be assured
4
Pneumonia with no signs of severity
Children older than 6 months:
– Give oral amoxicillin 30 mg/kg 3 times daily.
– Treat for fever if the child is uncomfortable.
– Follow-up after 48 to 72 hours and assess clinical condition:
• Improvement: complete amoxicillin PO for a total of 5 days.
• No improvement: complete amoxicillin PO for a total of 5 days and add azithromycin PO:
10 mg/kg once daily for 5 days.
• Clinically worse: admit for further investigations and management.

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4.6 Empyema

Empyema is a collection of pus in the space between the lung and the inner surface of the chest
wall (pleural space). It is a complication of a bacterial pneumonia, most often staphylococcal
pneumonia and can often occur as a complication of measles. In children presenting with
empyema, evaluate with history and examination if there are any indications of underlying
tuberculosis (TB) as a differential diagnosis.

4.6.1 Clinical features


– Persistent fever and/or cough, chest pain, dyspnoea and oxygen requirement.
– May prefer to lie on the affected side to reduce pain.
– Consider if no improvement after 48 to 72 hours of treatment for community-acquired
pneumonia, or if a child diagnosed with pneumonia has additional signs such as:
• Shallow respirations to minimise pain.
• Decreased air movement heard on auscultation.
• Dullness to percussion.
• Increased resonance of voice sounds (due to enhanced transmission).
• Rarely severe respiratory distress, sepsis and shock.
• Possibly a pleural rub on the side of the fluid collection.

Investigations
– CXR and/or lung ultrasound, if available, to visualise fluid (see Figure 4.3). Check for any
radiological signs of TB.
– Pleural aspiration (ultrasound-guided ideally): check fluid appearance (colour, blood-stained,
straw-coloured, translucency, etc) and perform Gram stain and culture, if available.
– Tuberculosis screening: microscopy and culture or GeneXpert where available.
– Malaria RDT (in endemic areas).
– Check Hb
– CRP, where available
– Blood culture
Figure 4.3 - CXR features of a loculated pleural effusion (empyema)
Supine AP CXR, adulta:

Lenticular shaped loculated pleural collection forming an obtuse angle with the chest wall
(marked-up on right-hand image), characteristic of empyema.

a Case courtesy of Ian Bickle, Radiopaedia.org, rID: 48160. https://radiopaedia.org/cases/48160

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4.6.2 Management
– Admit, preferably to an ICU facility, for treatment and stabilisation.
– Treat any fever to improve the patient’s comfort and give analgesia if pain (such as chest
pain) is present (see Chapter 15, Section 15.4).
– Administer oxygen if SpO2 < 92% in room air or severe respiratory distress.
– If the child is in severe respiratory distress, nil-by-mouth is recommended.
– Administer antibiotic treatment.
– Ensure adequate fluid and calorie intake and monitor BGL over the first 24 to 48 hours, as 4
there is a risk of dehydration and hypoglycaemia.
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).

Antibiotic treatment
– Administer ceftriaxone IV 80 mg/kg (max. 4g if < 50 kg; max. 2g if ≥ 50 kg) every 24 hours (or
cefotaxime IV 50 mg/kg every 8 hours) and cloxacillin IV 25 mg/kg every 6 hours.
– Alternatively, administer amoxicillin/clavulanic acid IV (dosage expressed in amoxicillin):
• 1 to 3 months of age: 30 mg/kg every 12 hours
• > 3 months of age: 30 mg/kg every 8 hours
– Continue for at least 7 days of parenteral (IV) treatment and until afebrile for 3 days.
– Then switch to oral antibiotic treatment (if able to take oral medication):
amoxicillin/clavulanic acid (ratio 7:1 or 8:1) PO to complete a minimum of 14 days of
treatmentb.
Dosage expressed in amoxicillin:
• < 40 kg: 50 mg/kg 2 times daily
• ≥ 40 kg:
Ratio 8:1: 3000 mg daily (2 tablets of 500/62.5 mg 3 times daily)
Ratio 7:1: 2625 mg daily (1 tablet of 875/125 mg 3 times daily)
– If confirmed MRSA or no improvement after 48 hours: replace cloxacillin with clindamycin IV
10 mg/kg every 8 hours.
– If slow improvement despite antibiotics, consider tuberculosis (see Section 4.11 and MSF
Tuberculosis Guidelines).

Surgical drainage
Small empyemasc do not require surgical drainage. However, for large empyemasd or empyema
that does not respond to antibiotics, the definitive treatment is removal of pus through the
placement of a chest tube (thoracostomy)26:
– If clinician familiar with the procedure and anaesthesia/surgery is available, proceed to
insert a chest drain under anaesthesia in the operating room.
– If surgery/anaesthesia is not available but a clinician trained to perform the procedure is, insert
a chest drain under sedation. Refer to MSF Standards for Paediatric Procedural Sedation.
– If there is no possibility to insert a chest drain due to lack of trained staff, consider referral.
– As a last option, if no trained staff are available and referral is not an option, perform
repeated pleural punctures for pus drainage.
– Upright chest x-ray (if available and the child is stable) is recommended after placement
of a chest drain or after pleural puncture to confirm position of the drain and exclude a
pneumothorax.

b Extend total duration of antibiotic treatment to 3 weeks for large empyemas.


c Less than 10 mm on lateral decubitus x-ray or opacifying less than ¼ of the hemithorax.
d Opacifying more than ½ of the hemithorax.

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4.7 Bronchiolitis

Acute inflammation and oedema of the smaller airways (bronchioles) of the lower respiratory
tract that occurs commonly in young children up to 2 years of age. The majority of cases are
caused by an infection with the respiratory syncytial virus (RSV), though other viral infections
may also trigger it (e.g. rhinovirus, parainfluenza, adenovirus, coronavirus)27,28. Though
bronchiolitis is a self-limiting illness which is usually uncomplicated in previously healthy
children RSV-associated lower respiratory tract infections are one of the most common reasons
for hospital admission and a significant cause of mortality amongst children29. Infants at risk
of severe bronchiolitis or complications include those with a history of being preterm or low
birth weight, < 3 months of age, and those with underlying respiratory, cardiac or neurological
conditions30.

4.7.1 Clinical features


– Fever, cough, respiratory distress (tachypnoea, wheezing, crepitations), associated with
reduced appetite and irritability.
– Often starts with nasal discharge or congestion for a couple days prior to peak of symptoms
above around day 3.
– Severe signs include lethargy, increasing respiratory distress (worsening tachypnoea, use
of accessory muscles, chest indrawing/retractions), unable to feed, frequent or prolonged
apnoea, and hypoxia.
– Uncommonly, the child may develop respiratory exhaustion and a silent chest which requires
emergency intervention.
– Most cases resolve in 7 to 10 days, though the cough may persist for several weeks.
– Diagnosis is usually clinical.

Investigations
Chest x-ray: not routinely recommended; consider if there is clinical deterioration, if there is
a suspected superimposed bacterial infection or pneumonia, or if other differential diagnosis
suspected.
Lung ultrasound: consider if available and trained staff present.

4.7.2 Management
There is no specific treatment for the viral infection triggering bronchiolitis, however some
children may need hospital admission for supportive management.
Children with clinical signs of severe illness should be admitted:
– Inability to feed (feeding less than 50% of usual volume) or dehydration
– Apnoea
– Moderate to severe respiratory distress (see Table 4.1)
– Oxygen saturations persistently below 92% (at rest, when feeding or when sleeping)
– Lethargy
– Central cyanosis31.

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Consider admission if feasible for all children at risk of severe disease: chronic lung
disease, prematurity (particularly < 32 weeks), congenital heart disease, < 3 months of age,
neuromuscular disorders.

Respiratory support
– Position the child around 10 to 30 degrees upright to support breathing.
– Administer oxygen if SpO2 < 92% in room air or severe respiratory distress.
– More advanced respiratory support, such as HFNC or CPAP, may be required if there is no
improvement with oxygen via nasal prongs (see Section 4.1.3). 4
– Continuous or near-continuous monitoring (RR, HR, SpO2) where feasible and if nursing
ratios allow, especially in very young infants or those with severe respiratory distress.
– Saline nasal drops and gentle nasal suctioning, especially pre-feeds (see MSF Manual of
Nursing Care Procedures, Procedure: Nasopharyngeal and Oropharyngeal Suctioning).
– Bronchodilators are not routinely recommended in the treatment of bronchiolitis, as
infant airways are not usually responsive to this treatment. However, in severe respiratory
distress, a trial of inhaled bronchodilators (salbutamol or epinephrine, see Section 4.10.1
and Section 4.2.2, respectively, for dosing) can be administered and continued if there is
clear evidence of improvement.
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).

Fluid and nutritional intake support


– Ensure adequate fluid intake (monitor oral intake)
• If unable to drink sufficiently or showing signs of dehydration, support with oral or
nasogastric feeds (see Chapter 15, Section 15.5).
• If enteral feeding is not tolerated, cautiously start IV maintenance fluids, ensuring careful
monitoring of fluid balance. Fluid restriction should be considered for severe casesa.
• In the case of severe respiratory distress, nil-by-mouth for first 24 hours to avoid risk of
aspiration and start IV maintenance fluids as outlined above. Begin to give frequent small
feeds after 24 hours, as tolerated. Show parent/carer how to support child upright at 30
degrees after feeds.

Suspected secondary bacterial infection or co-infection


– Routine antibiotic treatment is not recommended.
– Examine for secondary bacterial infection, co-infection or pneumonia if:
• Appears septic and/or very high fevers.
• New onset of fever and clinical deterioration after 2 days of hospitalisation.
• New onset of fever or increased work of breathing after re-starting oral feeds.
• Radiographic indications or changes (on CXR).
– Start antibiotic treatment for pneumonia (Section 4.5)
– Monitor RR and SpO2 carefully and be alert to signs of exhaustion.

Infection prevention and control measures


– Ensure transmission-based precautions are taken, including correct use of personal
protective equipment (PPE).
– Admit to a separated area or with physical distance from other admitted children with
dedicated nursing staff and equipment to reduce the risk of cross-infection.
– If multiple cases, group together with other cases in a separated area from other patients
(cohorting).

a Increased ADH secretion in respiratory conditions can cause water retention, leading to fluid overload.

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Discharge criteria
Consider discharge from hospital when the child is30,32:
– Maintaining oxygen saturations persistently ≥ 92% without supplemental oxygen (for at
least 4 hours), including during sleep.
– Tolerating feeds.
– Clinically stable with no signs of moderate or severe respiratory distress.

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4.8 Diphtheria

Diphtheria is a bacterial infection due to Corynebacterium diphtheriae, spread from person to


person through inhalation of infected respiratory droplets of symptomatic or asymptomatic
individuals, or direct contact with contaminated objects or diphtheria skin lesions33,34. The 4
incubation period is 1 to 5 days (maximum 10 days) during which C. diphtheriae multiplies in
the upper respiratory tract and secretes a toxin that causes local and systemic inflammation
and complications. Mortality may result from upper airway obstruction or systemic damage
from the toxin, including damage to the myocardium and neurological system.
Diphtheria is a notifiable disease, and all cases should be reported to local or national public
health authorities.
Diphtheria is a vaccine-preventable disease and vaccination is part of routine childhood
immunisation programmes (EPI).

4.8.1 Clinical features


Respiratory and upper airway signs include:
– Pharyngitis, rhinopharyngitis, tonsillitis or laryngitis with tough, greyish, firmly adherent
pseudo-membranes of the pharynx, nasopharynx, tonsils, or larynx.
– Dysphagia and cervical adenitis, at times progressing to massive swelling of the neck.
– Airway obstruction and possible suffocation when the infection extends to the nasal
passages, larynx, trachea and bronchi.
Systemic signs resulting from the toxin:
– Low-grade fever
– Cardiac dysfunction (tachycardia, arrhythmias), severe myocarditis with heart failure and
possibly cardiogenic shock 3 to 7 days or 2 to 3 weeks after onset of the disease.
– Neuropathies in 2 to 8 weeks after the onset of disease leading to nasal voice and difficulty
with swallowing (paralysis of the soft palate), vision (ocular motor paralysis), breathing
(paralysis of respiratory muscles) and ambulation (limb paralysis).
– Oliguria, anuria and acute renal failure.
Differential diagnoses include epiglottitis (Section 4.3), bacterial tracheitis (Section 4.4), and
acute pharyngitis (see MSF Clinical Guidelines).

Investigations
– Collect swab samples before starting antibiotic treatment (see MSF Collection, storage and
transport of samples from field to reference laboratory):
• Swab affected areas: throat (tonsils, pharyngeal mucosa, soft palate, exudate, ulcer, etc.)
and nasopharynx, for culture (and sensitivity) to isolate C. diphtheriae.
– PCR test (detection of diphtheria toxin gene) if available.

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4.8.2 Management
Infection prevention and control measures
– Ensure transmission-based precautions are taken, including correct use of personal
protective equipment (PPE).
– Admit to a separated area or with physical distance from other admitted children with
dedicated nursing staff and equipment to reduce the risk of cross-infection.
– If multiple cases, group together with other cases in a separated area from other patients
(cohorting).
– Cases can remain infectious up to 8 weeks after initial infection. Antibiotic treatment can
reduce infectiousness to 6 days.

Diphtheria antitoxin (DAT)


– Administer diphtheria antitoxin (DAT) (derived from horse serum) as soon as possible:
• Ensure close monitoring and immediate availability of resuscitation equipment as there is
a risk of an anaphylactic reaction to DAT, especially in children with asthma.
• Administer with the Besredka method: inject 0.1 mL SC and wait 15 minutes. If there is no
allergic reaction (no erythema at the injection site or a flat erythema of less than 0.5 cm
in diameter), inject a further 0.25 mL SC. If there is no reaction after 15 minutes, inject the
rest of the product IM or IV depending on the volume to be administered.
• Dosing is according to severity and extent:

Clinical signs Dose in units Administration route

Laryngitis or pharyngitis
20 to 40 000
or duration < 48 hours
IM or IV infusion in 250 mL
Rhinopharyngitis 40 to 60 000 of sodium chloride 0.9% in 2
to 4 hours for doses of more
Severe disease (respiratory than 20 000 units.
distress, shock), cervical 80 to 100 000
oedema or duration ≥ 48 hours

Antibiotic treatment
– Start as soon as possible without waiting for bacteriological confirmation.
– Give for 14 days or according to length of treatment recommended by the national protocol:
First-line:
azithromycin PO 10 to 12 mg/kg once daily (max. 500 mg daily)
Alternatively:
erythromycin PO
< 40 kg: 10 to 15 mg/kg (max. 500 mg) 4 times daily
≥ 40 kg: 500 mg 4 times daily
or
phenoxymethylpenicillin (penicillin V) PO:
< 40 kg: 10 to 15 mg/kg (max. 500 mg) 4 times daily
≥ 40 kg: 500 mg 4 times daily

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– Administer via IV or IM if the child is unable to take oral treatment. Switch to oral antibiotic
treatment as soon as possible. Complete a total of 14 days of treatment.
benzylpenicillin (penicillin G) IM or slow IV
25 000 IU/kg (15 mg/kg) every 6 hours (max. 4 MIU or 2.4 g per day)
Alternatively:
procaine benzylpenicillin IM
< 25 kg: 50 000 IU/kg (50 mg/kg) once daily (max. 1.2 MIU or 1.2 g daily)
≥ 25 kg: 1.2 MIU (1.2 g) once daily
4
Never administer procaine benzylpenicillin by IV injection or infusion.
If penicillin-allergy:
erythromycin IV infusion (60 minutes)
12.5 mg/kg every 6 hours (max. 2 g daily)

– Evaluate and manage respiratory distress or any airway obstruction. In case of stridor and/or
respiratory distress and/or bull neck, administer dexamethasone IV, 0.6 mg/kg loading dose
followed by 0.1 mg/kg every 6 hours (max. 10 mg per dose). Intubation or tracheotomy may
be necessary with severe upper airway obstruction (see local protocols).
– Update vaccination status before hospital discharge. If the patient has been administered
DAT and can receive adequate home-based follow-up after hospital discharge, wait 3 weeks
after administration of DAT before vaccination.
Refer to MSF Clinical Guidelines, Diphtheria for:
– Management of close contacts and antibiotic prophylaxis
– Outbreak surveillance methods

4.8.3 Prevention
– Vaccination prevents severe disease though it does not prevent transmission.
– Clinical disease does not confer immunity, therefore vaccination should be part of case
management.
– Diphtheria vaccine is part of routine childhood immunisation (EPI):
• 3 doses of conjugate vaccine containing the higher potency (D) formulation of diphtheria
toxoid as soon as possible as of 6 weeks of age and at 4 week intervals.
• D booster: between 12 and 23 months, then between 4 and 7 years.
• Booster with a vaccine containing a reduced dose (d) of diphtheria toxoid: between 9 and
15 years35.
– Catch-up vaccination (missed routine vaccination):
• 1 to 6 years: 3 doses of D conjugate vaccine at least 4 weeks apart.
• 7 years and above: 3 doses of d conjugate; 4 weeks between dose 1 and 2, then at least
6 months between dose 2 and 3. Administer 2 subsequent booster doses containing d at
least 4 weeks apart.

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4.9 Pertussis (whooping cough)

A highly contagious, acute respiratory illness caused by the bacterium Bordetella pertussis, with
a high mortality in infants. The incubation period for B. pertussis is usually 9 to 10 days and it
is transmitted via airborne droplets36. The risk of transmission is greatest during the catarrhal
phase and patients with pertussis are considered infectious until they have completed 5 days
of appropriate antibiotic treatment or 21 days if not treated.
Pertussis is a vaccine-preventable disease and immunisation against pertussis is included in all
vaccination calendars worldwide.
Pertussis is a notifiable disease, and all cases should be reported to local or national public
health authorities.

4.9.1 Clinical features


The classic presentation of pertussis includes paroxysms of coughing, an inspiratory whoop
and post-tussive vomiting. The illness evolves in 3 stages:
– Catarrhal stage (1 to 2 weeks): Symptoms similar to the common cold (runny nose, cough). In
contrast to the common cold, the cough in pertussis gradually worsens instead of improving.
– Paroxysmal stage (1 to 6 weeks):
• Typical presentation: increase severity of cough, occurring in characteristic bouts
(paroxysms), followed by a laboured inspiration causing a distinctive sound (whoop),
or vomiting. Fever is absent or moderate, and clinical examination is normal between
coughing bouts; however, the patient becomes more and more fatigued.
• Atypical presentations:
▹ Infants < 6 months: paroxysms are poorly tolerated, with apnoea, cyanosis; coughing
bouts and whoop may be absent.
▹ Older children: prolonged cough, often without other symptoms.
• Complications:
▹ Major: in infants, secondary bacterial pneumonia (new-onset fever is an indicator);
apnoea (frequent cause of death in infants); severe weight loss and dehydration
secondary to feeding difficulties; rarely, seizures, encephalopathy; sudden death.
▹ Minor: subconjunctival haemorrhage, petechiae, hernias, rectal prolapse.
– Convalescent stage: symptoms gradually resolve over weeks or months.

4.9.2 Management
Admit children who37:
– Are 3 months or younger.
– Have signs of severe illness (severe respiratory distress, apnoea, cyanosis, pneumonia,
seizures/impaired consciousness).
– Are unable to feed.

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Infection prevention and control measures


– Ensure transmission-based precautions are taken, including correct use of personal
protective equipment (PPE).
– Admit to a separated area or with physical distance from other admitted children with
dedicated nursing staff and equipment to reduce the risk of cross-infection.
– If multiple cases, group together with other cases in a separated area from other patients
(cohorting).
– Contact with young children and women in late pregnancy should be avoided until at least 4
5 days of antibiotics completed.
For children who do not need admission: explain to parents/carers the signs that should lead
to re-consultation (fever, deterioration in general condition, apnoea, cyanosis, inadequate oral
intake or dehydration).

Antibiotic treatment
Indications include:
– Infants < 6 months
– Within 3 weeks of onset of cough
– Consider antibiotic treatment if child requires admission:

azithromycin PO:
< 6 months: 10 mg/kg once daily for 5 days
≥ 6 months: 10 mg/kg (max. 500 mg) single dose on day 1, then 5 mg/kg (max. 250 mg)
once daily from day 2 to day 5
Alternative:
co-trimoxazole PO: 20 mg/kg SMX + 4 mg/kg of TMP 2 times daily for 14 days
or
erythromycin PO: 15 mg/kg 3 times a day for 7 to 14 daysa

Supportive care
– Place the child in a semi-reclining position.
– Administer respiratory support via bag and mask ventilation in case of apnoea that does not
quickly resolve with external stimulation.
– Administer oxygen if SpO2 < 92% in room air, in severe respiratory distress or if recurrent
apnoeasb.
– Do not perform any deep suction (as it increases the risk of paroxysmal cough). If secretions
are present, gently wipe the mouth and the nose with gauze.
– Ensure adequate fluids and calorie intake (risk of weight loss). Give small and frequent oral
feeds if possible. Some patients need nasogastric feeding or IV maintenance fluids (see
Chapter 15, Section 15.2 and Section 15.5).
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– Record weight, and strictly monitor urine output and oral intake.
– Do not administer salbutamol, corticosteroids or antitussives.

a 7 days of treatment with erythromycin is sufficient in the majority of cases though there is a small risk of
relapse compared to 14 days of treatment.
b Use of oxygen via nasal prongs may provide enough stimulation to prevent apnoea, however oxygen itself is
not an adequate treatment for apnoea.

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Discharge criteria
Most infants will continue to have coughing spells after discharge. Minimum criteria for
discharge include the following:
– No apnoea or oxygen supplementation needed in last 48 hours.
– Coughing episodes tolerated without becoming hypoxic and/or bradycardic.
– Ability to feed enough to gain weight.
– Family can care for child at home and are comfortable with the child's condition.
Consider food supplements for several weeks after discharge, especially if weight loss occurs
during hospital stay.

4.9.3 Post-exposure prophylaxis


Antibiotic prophylaxis (same as antibiotic treatment) is recommended, regardless of vaccination
status, for all household and close contacts of confirmed cases, and for exposed individuals in
high-risk groups who are at risk of developing severe or complicated disease. Prophylaxis is
most effective if given within 21 days of the onset of cough in the confirmed case.
High-risk groups include38:
– Infants less than 1 year old, particularly those less than 4 months old.
– Pregnant womenc, particularly in the 3rd trimester39.
– People with pre-existing medical conditions that may be exacerbated by pertussis infection,
e.g. immunocompromise, chronic lung disease, moderate to severe asthma, cystic fibrosis.
– People who have contact with any of the high-risk individuals described above.

4.9.4 Prevention
Routine vaccination with polyvalent vaccines containing pertussis antigens (e.g. DTP, or DTP +
Hep B, or DTP + Hib + Hep B) from the age of 6 weeks or according to national protocol.
Neither vaccination nor natural disease confers lasting immunity. Booster doses are necessary
to reinforce immunity and reduce the risk of developing disease and transmitting it to young
children.

c Macrolides should be used with caution in pregnancy and avoided in the first trimester of pregnancy due to
increased risk of congenital malformations.

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4.10 Asthma

Consider asthma in a child that presents with cough, wheeze and shortness of breath or difficulty
breathing. Asthma is a chronic disorder that can have an acute and severe presentation, or
present with a longer history of recurring or persisting mild symptoms. Children or parents/ 4
carers may have noticed that the symptoms are present or worse at night or during exercise.
Although asthma-like symptoms with cough and wheezing present frequently in younger
children in association with a viral respiratory illness, the diagnosis of asthma is generally
considered in children over 5 years of age.
Asthma is a chronic inflammatory process of the airways in which smooth muscle constriction,
mucous plugs and/or wall thickening causes narrowing of the airways, thereby restricting the
flow of air in the lungs. Treatment is with bronchodilators (to re-open the airways) and steroids
(for their anti-inflammatory effects) to reverse the symptoms. Longer term management and
prevention of acute attacks should be supported with patient and family education.
Asthma often coexists with atopy and allergies40.

4.10.1 Acute exacerbation of asthma


Assess the severity of an acute exacerbation based on clinical features (see Table 4.3). Mild
exacerbations may be managed in an outpatient or home setting, but moderate to severe
asthma should be managed in an emergency care setting. All patients presenting with severe
or life-threatening asthma should be admitted to hospital, while those with mild or moderate
exacerbations may be managed as outpatients if they show a good response to treatment (see
below for details).
Table 4.3 - Acute asthma exacerbation severity assessment41,42

Severe or
Mild Moderate
life-threatening

Shortness of breath While walking At rest At rest


Infant: difficulty Infant: unable to
feeding feed

Oxygen saturation > 94% 90 to 94% < 90%


in air

Ability to verbalise Talking in sentences/ Talking in short Only using single


(age-appropriate) Long strong cry sentences/ words/Weak cry
Shortened cry Unable to speak/cry

Wheeze Mild, at end of Loud, throughout Loud, throughout


expiration expiration inspiration and
expiration, or absent
(silent chest)

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Severe or
Mild Moderate
life-threatening

Respiratory rate Mild increase Moderate increase Severe increase

Heart rate Normal range for Mild to moderate Tachycardia (or


age tachycardia for age bradycardia) for age

Mental state Normal Normal Agitated, drowsy or


confused

Accessory muscle None Mild to moderate Moderate to


use maximal (or
exhaustion)

Cyanosis None None Any cyanosis of


concern

Immediate management of severe or life-threatening exacerbation


– Stabilise in the Emergency Room (ER) before transferring the patient.
– Keep child seated at around 45 degrees upright (if necessary, keep child sitting on parent/
carer’s lap) to achieve most comfortable position to help breathing.
– Administer nebulised salbutamol combined with ipratropium bromide over 20 minutes and
repeat to administer 3 doses in total (start a new dose every 20 minutes):

salbutamol nebuliser solution (5 mg = 2.5 mL)


≤ 5 years: 2.5 mg (1.25 mL)
> 5 years: 5 mg (2.5 mL)
ipratropium bromide nebuliser solution (0.25 mg/mL = 1 vial)
≤ 5 years: 0.25 mg (1 mL)
> 5 years: 0.5 mg (2 mL)

– Administer oxygen via nasal cannula at the same time as the nebulisera, aiming for SpO2
between 94 - 98%.
– After 3 combined nebulisers, continue with nebulised salbutamol alone every 20 minutes
(i.e. continuously), assessing for improvement between each dose without stopping the
continuous nebuliser.
– If a nebuliser is not available, administer inhaled bronchodilators via a spacer, ensuring
that every puff is inhaled separately and effectively. Repeat combined inhalers every 10 to
20 minutes up to 3 times in total, then continue with salbutamol inhaler alone:

salbutamol metered dose inhaler (MDI):


≤ 10 kg: 4 to 8 puffs
> 10 kg: 10 puffs
ipratropium bromide metered dose inhaler (MDI), if available:
4 puffs

a Unless nebuliser driven by oxygen, in which case supplementary administration of oxygen via nasal cannula is
not necessary.

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– Start IV maintenance fluids (and consider adding potassium, see Chapter 15, Section 15.2.3).
– Start corticosteroidsb as soon as possible43,44:

prednisolone PO: 2 mg/kg (max. 60 mg) once daily


Alternative, if prednisolone unavailable:
dexamethasone PO: 0.6 mg/kg once daily (max. 16 mg)

If unable to take oral medication:


dexamethasone IV/IM*: 0.6 mg/kg once daily (max. 16 mg) 4
Switch to oral prednisolone as soon as possible.
* hydrocortisone IV: 4 mg/kg every 6 hours may be used as an alternative if dexamethasone
IM/IV unavailable.

– After stabilisation, or in case of need of magnesium sulphate, transfer the child to ICU
immediately.
– If no improvement or deterioration despite nebulisers and corticosteroid, administer
magnesium sulphate IV: 40 mg/kg (max. 2 g) diluted in sodium chloride 0.9% over 20 minutes
using a syringe pump:
• Continuous monitoring (or every 10 minutes) including BP must be available and feasible
(risk of hypotension).
• Assess neurological status every 10 minutes for at least first hour.
• In case of hypotension, add a bolus of Ringer lactate IV: 10 mL/kg over 20 minutes.
– If no improvement after 20 minutes of magnesium sulphate, administer epinephrine IM/SC:
0.01 mg/kg (see MSF Vasopressor Therapy - Adrenaline protocol). Repeat after 20 minutes
if needed.
– When the child starts to improve, stop continuous nebuliser and start weaning down
the salbutamol (follow weaning steps described below in management of moderate
exacerbation) and oxygen while monitoring SpO2. Duration of prednisolone at discharge is
to complete 5 days total as for management of moderate exacerbation.
– Monitor and record vital signs at least every 30 minutes using an early warning system
(see MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign
charts).
– If the child deteriorates again within 1 hour of stopping continuous salbutamol, restart
continuous salbutamol every 20 minutes for 1 hour and then reassess.

Moderate exacerbation
– Administer combined nebulised or inhaled bronchodilators using the same dosing as for
severe exacerbation, and repeat every 20 minutes until clinical improvement, up to 3 doses
in total.
– Administer oxygen via nasal cannula, aiming for SpO2 between 94 - 98%.
– Give prednisolone PO: 1 to 2 mg/kg (max. 40 mg). Alternatively, dexamethasone PO: 0.3 to
0.6 mg/kg (max. 16 mg).
– Reassess clinical condition and severity after each combined bronchodilator dose.
Inhaled bronchodilators are preferred for moderate exacerbations if correct, effective
delivery using a spacer can be guaranteed. If inhaler delivery technique is in doubt,
nebulisers should be administered.

b Oral corticosteroids are preferred to IM/IV where oral route is possible. Only administer parenteral
corticosteroids if the child is vomiting, or respiratory distress is too severe to allow safe administration of oral
medication.

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Response to bronchodilator treatment


Marked clinical improvement (diminished or absent wheezing, significant reduction in the use
of accessory muscles, increased air entry) within the first hour of bronchodilator treatment:
– Stop bronchodilators and wean off oxygen, stopping if SpO2 ≥ 92% in room air.
– If sustained improvement for at least one hour after completing the last bronchodilator
treatment, reassess hourly. If the child shows sustained improvement without the need for
bronchodilator treatment for up to 4 hours after initial treatment, discharge home with an
Asthma Action Plan (see Appendix 8) and oral corticosteroid (as above) to complete 5 days
(or 2 days if dexamethasone used).
Good improvement after completion of second or third combined bronchodilator dose, but
with persisting symptoms:
– Wean off oxygen, stopping if SpO2 ≥ 92% in room air.
– Wean down salbutamol under observation, reassessing hourly:
• Administer 4 to 6 puffs of salbutamol inhaler via spacer 2-hourly, twice.
• If child remains stable, continue with 4 to 6 puffs of salbutamol inhaler 3-hourly, twice.
• If child remains stable, continue with 4 to 6 puffs of salbutamol inhaler 4-hourly (goal
frequency), twice.
– If no improvement or child worsens at any stage, keep the same space between doses, i.e. if
child is on 2-hourly salbutamol, continue on 2-hourly until there is improvement, and then
wean to 3-hourly intervals.
– When child remains stable on 4-hourly salbutamol, can be discharged home with an Asthma
Action Plan (see Appendix 8) and oral corticosteroid (as above) to complete 5 days ((or
2 days if dexamethasone used).
Slight improvement, symptoms still moderate after completion of third combined
bronchodilator dose:
– Administer salbutamol nebuliser or inhaler alone (doses as above) every 30 to 60 minutes,
depending on response after each dose. Reassess after each treatment.
– Continue oxygen if SpO2 < 92% in room air but aim to wean down to stop oxygen when SpO2
≥ 92%.
– Good improvement: start weaning salbutamol following above management.
– No improvement or deteriorating despite salbutamol every 30 to 60 minutes for 3 hours,
treat as for severe exacerbation and transfer to ICU for IV magnesium sulphate and IV fluids.

Mild exacerbation
– Administer salbutamol inhaler 4 to 6 puffs via spacer and reassess.
– Repeat same dose of salbutamol inhaler every 20 minutes if child remains symptomatic, up
to 3 doses total and reassess:
• No improvement and/or child requires oxygen, treat as for moderate exacerbation.
• Improvement: aim to administer salbutamol inhaler at 4-hourly intervals and observe for
any symptoms between treatments. If needed, administer salbutamol inhaler earlier and
note the interval spacing.
– When child has remained stable with minimal or no wheeze 4 hours after the last salbutamol
inhaler treatment, review for discharge home.
– On discharge, provide an Asthma Action Plan (see Appendix 8) and oral prednisolone 1 to
2 mg/kg (max 40 mg) to complete 3 days, or oral dexamethasone 0.3 to 0.6 mg/kg (max
16 mg) to complete 2 days.
Note: At any suitable moment, complete history, perform full clinical examination and relevant
diagnostics to identify potential underlying trigger, e.g. infection, and treat accordingly.

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Discharge home
Clinical criteria:
– Stable in room air and minimal respiratory distress on 4-hourly salbutamol (ideally at least
2 doses at 4-hourly interval).
Medication:
– Oral corticosteroids to complete 3 or 5 days according to severity.
– Salbutamol inhaler (4 to 6 puffs):
• Home on 4-hourly during waking hours and as needed or up to 4-hourly during sleeping 4
hours for first 48 to 72 hours.
• Wean down salbutamol inhaler as tolerated, aiming to stop between days 5 and 7 after
discharge.
• Ensure spacer given together with inhaler and that child/family know how to use it
correctly (see Appendix 9 and Appendix 10).
– Assess need for controller medication and provide if necessary.
Follow-up:
– Organise outpatient follow-up (see Section 4.10.3).
– Provide basic asthma education (recognition of exacerbation, management, when to seek
medical consultation).
– Provide an Asthma Action Plan (see Appendix 8).

4.10.2 General management of asthma


Children may present with history, signs and symptoms indicating asthma or require follow-up
management after an episode of acute exacerbation of asthma.
– Typical symptoms include:
• Dry cough (often prominent at night and early morning)
• Wheezing on expiration
• Shortness of breath or difficulty breathing
– Symptoms may not be present all the time but may be recurring.
– Symptoms may present or get worse at night or during exercise, or other triggers may have
been noticed by the child or parents/carers.
– Atopic disorders or a personal or family history of atopy (eczema, allergic rhinitis/
conjunctivitis) or a family history of asthma increases probability of asthma (though their
absence does not exclude asthma).
On examination, respiratory signs indicating asthma include:
– Decreased air entry or wheezing either on auscultation or without auscultation when severe
– Prolonged expiratory phase on auscultation
– Increased anterior-posterior diameter of the chest due to air trapping
Note that between exacerbations, respiratory examination may be completely normal and
signs and symptoms absent.

Diagnosis of asthma
– Presence of typical symptoms and history characteristic of asthma, after excluding other
diagnoses.
– Response to inhaled bronchodilators e.g. salbutamol inhaler or nebuliser.
– It is recommended to determine a diagnosis of asthma only in children 5 years of age and
above.

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– In children under 5 years, viral upper respiratory tract infections can cause similar symptoms
to asthma (recurrent wheezing, cough) without the child necessarily having asthma. Consider
a diagnosis of asthma and whenever possible refer for further evaluation in children < 5 years
with recurrent wheezing if45:
• Cough or wheezing during sleep or associated with environmental irritants.
• Symptoms exacerbated by exercise, laughing, or without a concomitant upper respiratory
infection.
• History of allergy.
• Response after 2 to 3 months of controller treatment (suggested trial of beclomethasone
0.05 mg/puff, 1 puff 2 times daily, and refer for further management if good response seen).
Differential diagnoses to consider or exclude:
– Bronchiolitis (if < 2 years; usually not responsive to salbutamol)
– Bacterial tracheitis (more inspiratory stridor than expiratory wheezing)
– Foreign body aspiration (often unilateral or focal wheezing, history or CXR diagnosis)
– Cardiac disease and congestive heart failure
– Pulmonary oedema
– TB
– Congenital anomalies (CCAM, bronchomalacia, tracheomalacia)
– Gastro-oesophageal reflux (infants)
– Lymphocytic Interstitial Pneumonia in HIV positive children

Investigations
– CXR, if available: non-specific findings include hyperinflation of the lungs, bronchial wall
thickening, and patchy atelectasis; CXR can also be normal.
– Lung ultrasound (if available and trained clinicians present) to exclude other differential
diagnoses (e.g. pneumonia, pulmonary oedema).

Management
– Assess symptom frequency and start treatment with salbutamol inhaler, with or without a
low-dose inhaled corticosteroid (ICS) such as beclomethasone, according to frequency (see
Table 4.4).
– Ensure spacer given together with inhaler and that child/family know how to use it correctly
(see Appendix 9 and Appendix 10).
– Check and eliminate trigger factors if possible.
– Evaluate after 4 to 8 weeks to assess asthma control and response.
– Adjust therapy according to clinical evaluation plus a stepwise treatment approach.
Table 4.4 - Assessment and initial treatment of asthma45
Asthma symptoms
Infrequent Frequent Troublesome Severe
≥ 2 days/month Most days,
Symptoms < 2 days/month Most days
but not daily throughout the day
Night-time
- - ≥ 1/week ≥ 1/week
awakenings

Initial Step 1 Step 2 Step 3 Step 3 or 4


treatment Follow-up and assess in 4 to 8 weeks. Adjust treatment according to asthma control
step and response.

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Asthma medications (see Table 4.5)


– Short-acting beta 2-agonist (SABA): salbutamol inhaler
– Long-acting beta 2-agonist (LABA): salmeterol inhaler (should be used in combination with
ICS)
– Montelukast can be used as an alternative to a LABA.
– Inhaled corticosteroid (ICS): beclomethasone
– Combination LABA-ICS may also be available.

Table 4.5 - Asthma maintenance treatment drug table for children > 5 years old 4
Asthma medication Dosing and indication
Salbutamol Metered dose inhaler (0.10 mg/puff)
Short-acting beta 2-agonist Rapid relief of asthma symptoms and bronchoconstriction:
(SABA) bronchodilator • Onset of action: within minutes
• Duration of action: ± 4 hours
• 4 puffs as needed; maximum 4 times daily
Prophylaxis of exercise-induced bronchoconstriction:
2 puffs, 5 to 20 minutes before exercise.
Salmeterol Metered dose inhaler (0.025 mg/puff)
Long-acting beta 2-agonist • 5 to 11 years: 2 puffs 2 times daily
(LABA) bronchodilator • 12 years and older: 2 puffs 2 times daily, up to maximum
4 puffs 2 times daily if severe
Must always be used with an ICS (risk if used alone)46
Beclomethasone dipropionate Metered dose inhaler (0.05 mg or 0.10 mg/puff)
Inhaled corticosteroid (ICS) • Low-dose ICS:
0.05 mg/puff, 1 to 2 puffs 2 times daily
0.10 mg/puff, 1 puff 2 times daily
• Medium-dose ICS:
0.05 mg/puff, 2 to 4 puffs 2 times daily
0.10 mg/puff, 1 to 2 puffs 2 times daily
ICS is the most effective long-term control therapy but
may have long-term adverse effects at high doses. Patients
should be maintained on the lowest possible dose of ICS.
Reduce dose slowly, 25 to 50% at a time.
Montelukast Oral tablet (as alternative to LABA if poor response to
Leukotriene receptor LABA)
antagonist (LTRA) • 5 years: 4 mg once daily in the evening
• 6 to 12 years: 5 mg once daily in the evening
• > 12 years: 10 mg once daily in the evening
Budesonide/Formoterol Budesonide 80 micrograms/Formoterol 4.5 micrograms/
Combination ICS-LABA puff, for use in children over 5 years.
• Low dose:
1 puff = 80 micrograms budesonide/4.5 micrograms
formoterol, 2 times daily
• Medium dose:
2 puffs = 160 micrograms budesonide/9 micrograms
formoterol, 2 times daily

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Stepwise treatment approach45


– Start treatment at the step most appropriate to the child’s condition, and then maintain
control by stepping treatment up or down if necessary.
– For children aged 5 to 12 years, refer to Figure 4.4. For children over 12 years, refer to the
adolescent and adult stepwise treatment table in the MSF Clinical Guidelines.
Figure 4.4 - Stepwise treatment approach for children 5 to 12 years

* Alternative treatment in Step 1 is to give low-dose ICS whenever salbutamol is given45,47.

– Assess understanding and acceptance of use of inhalers and provide counselling and
information where there are misconceptions or concerns.
– Check inhaler and spacer technique – all inhaler treatments in children should be administered
via a spacer (see Appendix 9 and Appendix 10).
– Do not step-up if the child is unwell or breathless during the visit - treat as an acute
exacerbation.
– Step-up asthma treatment if there are persistent symptoms (e.g. persistent cough), between
every 4 to 8 weeks.
– Step-up if asthma is poorly controlled i.e. using a reliever inhaler > 3 times per week, waking
at night with symptoms more than once a week.
– If asthma still not well controlled with Step 4 treatment, seek or refer for specialist advice.
– Step-down if well controlled for 3 months. Decision on which drug to stop first and at what
rate depends on the severity of asthma, treatment side effects, time on current dose,
beneficial effects achieved, and patient preference.
– Inhaled corticosteroids are the most effective long-term control therapyc. When able to
step down, reduce dose gradually 25 to 50% at a time until lowest dose of inhaled steroids
reached with child stable.

4.10.3 Asthma education and action plan


At each visit review the following:
1. Self-monitoring: Ensure the child and/or the parents/carers are able to recognise symptoms
of deteriorating control. Agree on treatment goals. Include an Asthma Action Plan.

c Note that antihistamines, antitussives, mucolytics, oral salbutamol/salbutamol syrup are not recommended
for asthma treatment.

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2. Medication: Explain how and when to take prescribed medication.


• Long-term “preventer” medications reduce inflammation and should be taken daily. They
do not provide quick relief but prevent/reduce exacerbations that interfere with daily life
or require hospitalisation.
• “Reliever” medications relax airway muscles and provide fast symptom relief. If used more
than three times per week, may need to start/increase long-term preventer medication.
• Check inhaler technique.
3. Adherence: Explain the importance of continuing to take their inhalers and medication
as prescribed and continue to use their “preventer” medications even when symptoms 4
improve, are mild, or infrequent.
4. Avoid/reduce exposure to triggers that worsen asthma. Cooking on open fires indoors
should also be avoided or adequate ventilation for the smoke to leave the building should
be set up. For children with severe asthma, recommend possible environmental measures
to eliminate triggers where possible.
5. Involve family and other healthcare providers (pharmacist, nurse etc), provide
encouragement.
6. Explain the importance of attending follow-up appointments.
7. Encourage exercise on a regular basis.
Manage comorbidities: eczema, gastro-oesophageal reflux, obstructive sleep apnoea, rhinitis
and sinusitis, stress, or depression. Treatment of these conditions may improve asthma control.
Exercise induced bronchospasm (EIB): Encourage physical activity. EIB should not limit child’s
participation in sport. Include advice in Action Plan to take 2 puffs of salbutamol 30 minutes
before exercise. EIB is often a marker of inadequate asthma control so consider adding/
increasing dose of inhaled corticosteroid.

Asthma Action Plan


– Where available, use the national or local Asthma Action Plan, otherwise use the MSF
Asthma Action Plan (see Appendix 8).
– Complete the Asthma Action Plan so that the child and/or family are prepared in the case of
an exacerbation and able to manage their symptoms.
– Include daily actions to control asthma, how and when to adjust medications in response to
worsening asthma, when to seek medical care.
– Ensure child has a copy of their Asthma Action Plan and that it is shared with their school
and other sites outside of home where the child spends time (particularly for those with
severe asthma).

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4.11 Tuberculosis

Tuberculosis (TB) is an infectious disease caused by Mycobacterium tuberculosis. It is


transmitted person to person through tiny infectious droplets that are spread by patients with
pulmonary or largyneal TB through coughing, speaking or sneezing. TB typically attacks the
lungs, but can also affect other parts of the body, especially in children. Although TB disease
has become rare in high-income countries, it remains a major public health problem in low-
and middle-income countries where approximately 10 million new cases of TB occur each year.
Globally, WHO estimates that more than 1 million children have TB every year48 and that 60%
of cases are not diagnosed or unreported49. The risk of death from TB is high in children under
2 years or children with malnutrition or HIV infection. Almost all of deaths due to TB in children
occur in those not receiving TB treatment, the vast majority in children under 5 years50.

4.11.1 Stages of infection


Primary infection and latent TB infection
After transmission via inhaled droplet nuclei, M. tuberculosis multiplies slowly, in most cases
in the terminal alveoli of the lungs (primary focus) and in the lymph nodes of corresponding
drainage areas: this is the primary infection. Over the course of one to two months, the
primary focus is contained and encapsulated by a healthy immune response and is usually
undetectable on chest x-ray. In most cases, the pulmonary lesions gradually heal, and the
majority of patients with a primary TB infection are asymptomatic.
During primary infection, specific immunity develops and may persist without clinical signs of
TB – the patient is infected by M. tuberculosis but does not develop the disease. This is referred
to as latent tuberculosis infection (LTBI). In 5-10% of infected people, primary infection and/or
LTBI progresses to active TB.

Active TB
Before immunity is established, bacilli from the primary focus or from a nearby lymph node
can be transported and disseminated throughout the body. Secondary foci can develop in this
way, particularly in the lungs, lymph nodes, serous membranes, meninges, bones and kidneys.
As for primary infection, these foci usually resolve or are contained by an effective immune
response.
Different factors can reduce the immune response and lead to reactivation of TB and
multiplication of the bacilli in one or more of these foci. This reactivation or progression of
primary or secondary foci results in active TB51. After exposure, the risk of TB infection and
progression to active TB is high in children under 5 years old52. Progression to active TB is
rapid (within 12 months) in children under 2 years53, and HIV is a significant risk factor for
developing TB in children under 1 year54.

4.11.2 Clinical features


Pulmonary TB (PTB) is the most common presentation in both adults and children, but
children (especially those who are malnourished or HIV-infected) also commonly present with
extrapulmonary or disseminated TB due to their relative immunodeficiency. They may have
symptoms of both pulmonary and extra-pulmonary TB.

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Pulmonary TB
Signs of pulmonary TB in children include:
– Prolonged cough (more than 2 weeks), often without sputum production
– Weight loss
– Anorexia
– Fatigue
– Haemoptysis
– Shortness of breath 4
– Fever
– Night sweats
Signs and symptoms generally evolve in a chronic, insidious manner. In endemic areas, the
diagnosis of PTB should be considered in any child presenting with respiratory symptoms
lasting more than 2 weeks. Children less than 10 years old are not considered infectious unless
they have extensive lung involvement and/or cavitary PTB.

Extrapulmonary TB
Extrapulmonary TB (EPTB) occurs when there is active TB infection in areas of the body
outside of the lung parenchyma, including the lymph nodes, meninges, bones and joints,
abdomen, serous membranes and kidneys. In young children, miliary and meningeal TB are
more frequently seen, while in older children TB lymphadenitis and osteoarticular TB are more
common.
Lymph node TB
Particularly common in older children, with the following characteristics:
– Painless, non-inflammatory adenopathy
– Frequently cervical, but axillary and mediastinal also common
– Multiple (often bilateral), or single, enlarged nodes
– Chronic evolution leading to fistulation
Tuberculous pleural effusion
One of the most common forms of EPTB, it is often asymptomatic if small and frequently
occurs concurrently with PTB. Constitutional symptoms are as for PTB, and shortness of breath
and unilateral chest pain occur when the effusion is large.
TB meningitis
Most common in children under 2 years old and in HIV-infected patients. Typically has subacute,
insidious course over days or weeks. Symptoms include:
– Headaches
– Irritability
– Fever
– Vomiting
– Altered mental status
– Meningeal syndrome (stiff neck, photophobia and headache)
TB of bones and joints
TB can affect the vertebrae and intervertebral disks, causing destruction and deformation of
the spine (Pott’s disease), most commonly affecting the thoracic spine. Localised back pain
is the main symptom, and neurological complications can develop. TB may also affect the
joints (commonly the hips, knees, elbows and wrists) causing a chronic painless mono-arthritis
accompanied by joint destruction.

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Abdominal TB
Less common and difficult to diagnose. Presents as ascites resulting from peritoneal TB
infection, sometimes accompanied by an abdominal mass (often in the right lower quadrant),
pain and diarrhoea. Constitutional symptoms may be present.

Disseminated or miliary TB
Generalised massive infection caused by haematogenous diffusion of M. tuberculosis
throughout the body. It occurs most commonly in children, young adults and HIV-infected
patients. In children, the risk of meningitis is high55. Clinical picture is characterised by:
– Deterioration over days or weeks
– Simultaneous involvement of multiple organs
– Marked wasting
– Headache
– Constant high fever
– Miliary findings on CXR
– Moderate hepatosplenomegaly (occasional)

4.11.3 Diagnostic approach


Diagnosis and approach to TB in older children is similar to that for adults, see MSF Tuberculosis
guideline. This section relates only to the diagnosis of TB in children less than 10 years old,
where diagnosis is more challenging and adult-based algorithms are not applicable.
Children with TB usually have non-specific symptoms. Clinicians should therefore look for TB,
particularly in children:
– Under 2 years of age
– With HIV infection or severe acute malnutrition (SAM)
– In contact with a TB case
– Not responding to antibacterial and/or nutritional treatment.
The diagnosis of TB is often made without bacterial confirmation as:
– Children under 5 years have low bacillary load and bacteriological tests are often negative.
Bacterial load is generally higher in older children.
– Collection of respiratory and extrapulmonary (EP) specimens is challenging in young children.
Therefore, history of exposure to TB, repeated clinical assessment and investigations including
radiography if available, are key components of the diagnosis of TB in children.
To facilitate the diagnosis of PTB and enable rapid treatment in children at high risk of death from
TB, WHO has developed evidence-based diagnostic algorithms which should be used to help reach
a diagnosis in any child with a suspicion of TB (see Section 4.11.5). The diagnosis of EPTB uses the
same diagnostic approach, however there are no evidence-based algorithms currently available.
A trial of treatment with TB drugs is not recommended as a method to diagnose TB - once a
decision is made to treat TB in a child, a full course of treatment should be given.

History of exposure to TB
Establish if the child has had contact with a confirmed or presumed index case. Children are at
higher risk of TB if:
– The index case is a household or close contact
– The index case has PTB, sputum smear-positive or with cavities on chest x-ray
– The exposure to the index case occurred in the past 12 months.

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If a TB index case is identified, their resistance profile should be assessed, as children often
have the same resistance profile as the index case.
Whenever TB is diagnosed in children, it is important to detect the index case if not already
identified, as well as any other undiagnosed cases in the household or close contacts.
Ask for symptoms suggestive of TB:
– Cough for more than 2 weeks
– Fever for more than 2 weeks
– Night sweats that soak the bed or clothes 4
– Weight loss or poor/no weight gain
– Fatigue, reduced playfulness, loss of appetite
– Haemoptysis (rare in children)
– Non-painful, enlarged cervical, submandibular, or axillary lymph nodes
– Rapid breathing

Clinical examination
Carry out a thorough physical examination, looking specifically for the following suggestive
signs:
– Fever, tachypnoea, tachycardia
– Weight loss, growth curve flattening, underweight or malnourished according to weight for
height and/or mid-upper arm circumference
– Abnormal pulmonary auscultation
– Signs of respiratory distress (see Section 4.1).
– Lethargy, altered mental status (may indicate TB meningitis)
– Signs of EPTB:
• Highly suggestive: angular deformity of the spine; loss of ability to walk, cervical lymph
node with fistula formation.
• Requiring further investigation: sub-acute meningitis not responding to antibiotic
treatment; ascites; lymph node without fistula formation; non-painful enlarged joint.
HIV status should be assessed in all children with presumed or confirmed TB.

4.11.4 Investigations
The following investigations should be performed in children suspected of PTB or EPTB
whenever possible. For children at high risk of TB or death from TB and for whom investigations
are unavailable (or results are not immediately available) treatment should not be delayed:
– HIV status should be assessed in all children with presumed or confirmed TB.
– Bacteriological tests: Rapid molecular tests (RMTs) should be performed on respiratory, stool
or extrapulmonary (EP) specimens as the initial diagnostic test. As the sensitivity of Xpert
MTB/RIF Ultra is higher than that of Xpert MTB/RIF, preferably use this for the detection of
TB and rifampicin-resistance.
• Sputum samples can be difficult to collect in children who may be unable or unwilling
to spontaneously expectorate. Explanation and encouragement are important. Chest
clapping may help expectoration, but if unsuccessful, respiratory specimens can be
obtained by invasive procedures such as sputum induction or gastric aspiration (see
Appendix 11). These procedures should only be used if the specimen is collected for
rapid molecular tests, culture or genome sequencing. These procedures should not be
performed for smear microscopy.

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• Stool specimens (which may contain swallowed sputum) are an alternative to respiratory
specimens for the diagnosis of PTB in children. Respiratory specimens are more likely
to give positive results but the use of stool specimens can avoid invasive collection
procedures.
• For children at risk of drug-resistant TB (DR-TB) i.e. those with contact with a DR-TB case
or coming from a high DR-TB prevalence area, multiple specimens (respiratory, stool and
EP) should be tested with RMTs. Every effort should be made to perform culture and
phenotypic drug susceptibility test.
– Lateral flow urine lipoarabinomannan assay (LF-LAM): LF-LAM should be performed in
HIV-infected children: with signs and symptoms of TB; with advanced HIV disease who are
seriously ill or hospitalised; or with low CD4 count.
– Medical imaging:
• Chest x-ray (CXR) is particularly useful when bacteriological tests are not available or
negative. CXR is also useful to assess the severity of TB and to determine the eligibility for
the 4-month drug-susceptible regimen. Children with PTB usually have abnormalities on
CXR, however a normal CXR does not rule out TB. Children who do not have CXR as part of
their initial evaluation should have a CXR done as soon as possible if started on treatment
for TB to assist with evaluation and treatment duration.
• Ultrasound: can be useful in the diagnosis of EP-TB including lymph node TB, pleural TB,
abdominal TB and pericardial TB.
Tuberculin skin test (TST): a positive test may be one element among many to establish the
diagnosis of active TB, however it is has many limitations, especially in children who have
received the BCG vaccination where false positives are common56.
For more information on sampling and testing procedures, see MSF Tuberculosis Guidelines.

4.11.5 Paediatric diagnostic algorithms


Paediatric diagnostic algorithms are invaluable in the diagnosis of TB in children. Two evidence-
based WHO algorithms exist, one incorporating CXR findings (Figure 4.5) and one that does
not include CXR (Figure 4.6), to guide the diagnosis of PTB in symptomatic children.

Clinical follow-up
The diagnosis may not be made at the first consultation. Follow-up after one to two weeks is
often needed including reassessment of symptoms suggestive of TB, physical examination and
growth assessment (see Section 4.11.3).
Particularly suggestive of TB are:
– Persistent of worsening pneumonia despite non-TB antibiotic treatment
– No weight gain or weight loss despite nutritional support or treatment
– Persistent fever after other causes have been ruled out or treated (e.g. malaria)
– Persistent or worsening fatigue, reduced playfulness, loss of appetite.

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Chapter 4: Respiratory conditions

Figure 4.5 - Modified WHO Algorithm A: diagnosis of PTB in symptomatic children


for settings with CXR (copied from MSF Tuberculosis guidelines, Chapter 5.3.1)
Diagnosis of PTB in symptomatic children with CXR
Danger signs(a) requiring urgent YES
treatment? Stabilize and/or transfer

NO

Age < 2 years or HIV infection RETAIN TRANSFER


Exit
or SAM(b)
4
YES NO Treat most likely non-TB condition(s).
Repeat clinical history and physical
examination in 1-2 weeks.

NO
Persistant or worsening symptoms? Exit

YES

Perform Xpert MTB/RIF or Ultra on respiratory/stool specimens in all children


and LF-LAM in HIV-infected children

M. tuberculosis detected by Xpert and/or LF-LAM?


YES NO/NOT PERFORMED/RESULT NOT YET AVAILABLE

Household/close contact with a TB case in the last 12 months?

YES NO

Score clinical and radiographic features

Signs and symptoms Radiography


Cough > 2 weeks +2
Fever > 2 weeks +5 Cavities +6
Lethargy +3 Lymph node +17 Do not start
Weight loss +3 Opacities +5 TB treatment.
Haemoptysis +4 Miliary pattern +15 Repeat clinical
Night sweats +2 Effusion +8 history, physical
Lymph node +4 examination and
Tachycardia +2 scoring in
Tachypnoea –1 1-2 weeks

Sum A Sum B

YES NO
Sum A + Sum B > 10?

Start TB treatment

(a) Danger signs:


Children < 5 years: age < 2 months; unable to eat or drink; vomiting up everything; severe dehydration; severe
pallor; stridor; SpO2 < 90%; respiratory distress; seizures; profound lethargy or coma; restless, continuously
irritable; neck stiffness or bulging fontanelle; fever > 39 °C; SAM.
Children ≥ 5 years: diarrhoea with severe dehydration; severe pallor; shock (cold extremities, capillary refill
time > 3 seconds, weak and fast pulse); obstructed or absent breathing; respiratory distress; central cyanosis;
coma (or seriously altered level of consciousness); seizures; restless, continuously irritable; fever > 39 °C;
SAM.
(b) SAM: severe acute malnutition is defined as weight-for-height in Z-score less than –3 or mid-upper arm
circumference less than 115 mm.

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Chapter 4: Respiratory conditions

Figure 4.6 - Modified WHO Algorithm B: diagnosis of PTB in symptomatic children


for settings without CXR (copied from MSF Tuberculosis guidelines, Chapter 5.3.1)

Diagnosis of PTB in symptomatic children without CXR


Danger signs(a) requiring urgent YES
treatment? Stabilise and/or transfer

NO

Age < 2 years or HIV infection RETAIN TRANSFER


Exit
or SAM(b)

YES NO Treat most likely non-TB condition(s).


Repeat clinical history and physical
examination in 1-2 weeks

NO
Persistant or worsening symptoms? Exit

YES

Perform Xpert MTB/RIF or Ultra on respiratory/stool specimens in all children


and LF-LAM in HIV-infected children

M. tuberculosis detected by Xpert and/or LF-LAM?


YES NO/NOT PERFORMED/RESULT NOT YET AVAILABLE

Household/close contact with a TB case in the last 12 months?

YES NO

Score clinical features

Signs and symptoms


Cough > 2 weeks +5
Fever > 2 weeks +10
Lethargy +4 Do not start
Weight loss +5 TB treatment.
Haemoptysis +9 Repeat clinical
Night sweats +6 history, physical
Lymph node +7 examination and
Tachycardia +4 scoring in
Tachypnoea +2 1-2 weeks

Sum

YES NO
Sum > 10?

Start TB treatment(c)

(a) Danger signs:


Children < 5 years: age < 2 months; unable to eat or drink; vomiting up everything; severe dehydration; severe
pallor; stridor; SpO2 < 90%; respiratory distress; seizures; profound lethargy or coma; restless, continuously
irritable; neck stiffness or bulging fontanelle; fever > 39 °C; SAM.
Children ≥ 5 years: diarrhoea with severe dehydration; severe pallor; shock (cold extremities, capillary refill
time > 3 seconds, weak and fast pulse); obstructed or absent breathing; respiratory distress; central cyanosis;
coma (or seriously altered level of consciousness); seizures; restless, continuously irritable; fever > 39 °C;
SAM.
(b) SAM: severe acute malnutition is defined as weight-for-height in Z-score less than –3 or mid-upper arm
circumference less than 115 mm.
(c) Once a decision to treat for TB is made, every effort should be made to obtain a CXR to assess the severity of TB.

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4.11.6 Management
A combination of several anti-tuberculous drugs is needed to treat TB and prevent the emergence
of resistance. The following section outlines the initial conventional treatment regimen for
children under 10 years old with drug-susceptible TB (DS-TB). For further information on the
treatment of TB in children including individual drug profiles, alternative regimens and drug-
resistant TB (DR-TB) regimens, as well as for all treatment regimens in older children, see MSF
Tuberculosis Guidelines.
4
Fixed dose combinations and paediatric formulations
DS-TB drugs (also referred to as first-line drugs) include Isoniazid (H); Rifampicin (R);
Pyrazinamide (Z); Ethambutol (E); Rifabutin (Rfb); and Rifapentine (P). Paediatric formulations
should be used where possible, and fixed dose combinations (FDCs) of several TB drugs are
preferred due to improved adherence. The following two quality assured FDC formulations
exist for children:
– Isoniazid/Pyrazinamide/Rifampicin (HZR): H50 mg/Z150 mg/R75 mg
– Isoniazid/Rifampicin (HR): H50 mg/R75 mg
Where paediatric formulations are not available, manipulation of adult formulations is
required:
– Preferably use scored tablets.
– Ensure that tablets/capsules can be split, crushed or opened.
– If tablets must be crushed (or capsules opened) a fraction of the powder corresponding to
the required dose should be mixed with food or liquids immediately before giving the drug.
Any remaining powder should be discarded.

Treatment of drug-susceptible TB
DS-TB treatment is indicated:
– When susceptibility to rifampicin and isoniazid is confirmed by drug susceptibility testing
(DST), or
– If the probability of resistance to rifampicin and/or isoniazid is low:
• While waiting for DST results for rifampicin and/or isoniazid,
• When susceptibility to rifampicin is confirmed and susceptibility to isoniazid cannot be
tested.
The probability of resistance is considered low in the following situations:
– No previous TB treatment
– No contact with a DR-TB patient
– The patient comes from an area of low prevalence of resistance according to drug resistance
surveys.
Conventional DS-TB regimens in children vary according to the severity of disease and the
infection site (see Table 4.6, page 174). 4-month regimens should be used for non-severe TB
in children and adolescents aged between 3 months and 16 years. In eligible children, if there
is not complete resolution of symptoms after 4 months of treatment and/or there is no weight
gain, further investigation is needed. Treatment can be extended to 6 months if causes of non-
response to treatment (including DR-TB, non-adherence and non-TB disease) are ruled out or
unlikely. For dosing, see Table 4.7, page 174.

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Table 4.6 - Conventional DS-TB regimens


Duration
Regimen Eligibility
(total)
2(HRZE)/2(HR) 4 months Children > 3 months to < 16 years with52:
PTB
• Microscopy smear-negative or Xpert result ‘negative’,
‘trace’, ‘very low’ and ‘low’, or
• Clinically diagnosed with TB lesions confined to one
lobe and no cavities on CXR
EPTB non-severe i.e.
• Pleural effusion without complications (e.g. no
empyema, pneumothorax or fistula)
If bacteriological testing and/or CXR are not available:
• Signs and symptoms not requiring hospitalisationa
• Extra-thoracic lymph node TB without involvement
of other EP sites
2(HRZE)/4(HR) 6 months PTB and EPTB (except miliary TB, TB meningitis and
bone and joint TB)57
Children and adolescents < 16 years not eligible for the
4-month regimen or when the national protocol does
not include the 4-month regimen.
2(HRZE)/10(HR) 12 months Miliary TB and TB meningitis in all children and
adolescents.
2(HRZE)/7-10(HR) 9-12 months Bone and joint TB in all children and adolescents.

Ethambutol can be removed from the 4- and 6-month regimens in non-HIV infected children
living in areas where the prevalence of HIV and/or isoniazid resistance is low with:
– PTB microscopy smear-negative, or
– Extra- or intra-thoracic lymph node TB58.
For spinal TB, rest and back support bracing are indicated in addition to drug therapy.
Table 4.7 - Dosing of TB drugs

Drugb Dose

Isoniazid (H) Child < 30 kg: 10 mg/kg (7 to 15 mg/kg) once daily (max. 300 mg daily
Child ≥ 30 kg: 5 mg/kg (4 to 6 mg/kg) once daily (max. 300 mg daily)
Rifampicin (R) Child < 30 kg: 15 mg/kg (10 to 20 mg/kg) once daily (max. 600 mg daily
Child ≥ 30 kg: 10 mg/kg (8 to 12 mg/kg) once daily (max. 600 mg daily)
Pyrazinamide Child < 30 kg: 35 mg/kg (30 to 40 mg/kg) once daily (max. 2000 mg daily
(Z) Child ≥ 30 kg: 25 mg/kg (20 to 30 mg/kg) once daily (max. 2000 mg daily)
Ethambutol (E) 15 to 25 mg/kg once daily (max. 1200 mg daily)

See MSF Tuberculosis Guidelines for dosing charts according to weight, contraindications and
side effects of TB drugs.

a Symptoms requiring hospitalisation include signs of severe respiratory disease or distress, severe acute
malnutrition, fever > 39C, severe pallor, irritability or lethargy.
b Dose reduced in renal or hepatic insufficiency, see MSF Tuberculosis Guidelines for details.

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Adjunctive therapy
– Pyridoxine (vitamin B6) prophylaxis is indicated for all patients at risk of peripheral neuropathy
i.e. children with HIV, malnutrition, diabetes, chronic hepatic disease or renal impairment.
– Corticosteroid therapy is indicated for:
• TB meningitis59 and pericarditis60
• Treatment and prevention of TB-associated immune reconstitution inflammatory
syndrome (TB-IRIS), see Chapter 13, Section 13.4.3 for more detail.
4
TB meningitis:
dexamethasone IV: 0.6 mg/kg (max. 16 mg) once daily for 4 weeks, tapered off over
4 weeks
TB pericarditis:
prednisolone PO: 1.5 mg/kg (max. 60 mg) once daily for 4 weeks, tapered off over 6 weeks

For information on monitoring response to treatment and modifications to treatment, see


MSF Tuberculosis Guidelines.

4.11.7 Prevention and screening


Globally, up to 30% of TB cases are estimated to be undetected and consequently untreated61.
Screening for active TB (also referred to as ‘intensive case finding for TB’) aims to identify,
within high TB-risk groups, individuals most at risk of TB who should undergo a TB diagnostic
test. It also identifies individuals who are eligible for TB preventive treatment (TPT) once TB
disease is ruled out. Screening allows for early diagnosis and treatment, which contributes to
improved treatment outcomes and reduced TB transmission. It should only be undertaken if
diagnostic and treatment capacities are available.
Screening for active TB should be routinely offered to the following groups:
– HIV-infected patients (outpatient or inpatient)
– Household and close contactsc of a patient with TB (index case) if:
• Contact is HIV-infected
• Contact is under 5 years old
• Index case has bacteriologically confirmed PTB or a multi-resistant PTB. Can also be
considered when the index case has EPTB or clinically diagnosed PTB.
– Prisoners
– Miners and other persons with current or past exposure to silica and patients with silicosis
Screening for active TB can be considered in patients with malnutrition, chronic disease, over
60 years, previously treated with TB, pregnant women, staff of health facilities exposed to TB,
populations living in slums, homeless, general population in areas with high TB prevalence.
Screening includes evaluation of any current symptoms (current cough, fever, poor weight gain,
night sweats etc.), contact with a TB case and imaging, depending on the high-risk group the
person belongs to. For specific screening strategies, refer to the MSF Tuberculosis Guidelines.

c WHO definitions61: A household contact is a person who shared the same enclosed living space for one or
more nights or for frequent or extended periods during the day with the index patient during the 3 months
before the start of treatment; A close contact is a person who does not live in the household but who shared
an enclosed space, such as a social gathering place, workplace or facility, with a TB case for extended periods
during the day during the 3 months before the current disease episode commenced.

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Patients who screen positive i.e. have symptoms or signs of TB, should be referred for active
TB diagnosis (see Section 4.11.3, Section 4.11.4 and Section 4.11.5). Patients who screen
negative are unlikely to have active TB and should be referred for latent TB diagnosis and/or
treatment. To demonstrate LTBI, either a tuberculin skin test (TST) or an interferon gamma
release assay may be performed. These tests are not mandatory in children under 5 years
who are a household contact of a TB case, or in HIV-infected children. In such cases, treatment
for LTBI can be commenced without confirmation. Recommended and alternative treatment
regimens for LTBI are outlined in Table 4.8.
Table 4.8 - LTBI regimens in children
Recommended
Age Dosing Alternative regimens
regimens

Child isoniazid daily for isoniazid PO once daily: rifampicin PO once daily
< 2 years 6 months (6H) < 30 kg: 10 mg/kg (7 to 15 mg/kg) for 4 months (4R):
≥ 30 kg: 5 mg/kg (4 to 6 mg/kg) < 30 kg: 15 mg/kg
(max. dose 300 mg daily) ≥ 30 kg: 10 mg/kg
(max. dose 600 mg)
OR isoniazid PO once daily:
isoniazid and < 30 kg: 10 mg/kg (7 to 15 mg/kg)
rifampicin daily for ≥ 30 kg: 5 mg/kg (4 to 6 mg/kg)
3 months (3HR) (max. dose 300 mg daily)
+
rifampicin PO once daily:
< 30 kg: 15 mg/kg
≥ 30 kg: 10 mg/kg
(max. dose 600 mg daily)

Child isoniazid daily for As above rifampicin PO once daily


≥ 2 years 6 months (6H) for 4 months (4R):
and as above
adolescent OR isoniazid PO once weekly:
isoniazid and < 30 kg and ≥ 2 years: 20 to 30 mg/kg OR
rifapentine weekly ≥ 30 kg: 900 mg
for 3 months (3HP) + isoniazid and rifapentine
rifapentine PO once weekly: daily for 1 month (1HP), if
10 to 14 kg and ≥ 2 years: 300 mg ≥ 13 years:
14.1 to 25 kg and ≥ 2 years: 450 mg isoniazid PO once daily:
25.1 to 32 kg: 600 mg ≥ 13 years: 300 mg
32.1 to 49.9 kg: 750 mg +
≥ 50 kg: 900 mg max rifapentine PO once daily:
≥ 13 years: 600 mg
OR As above
isoniazid and
rifampicin daily for
3 months (3HR)

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4.12 Mastoiditis

Infection in the mastoid cavities that is usually a secondary complication of acute otitis media
(AOM). Like AOM, it is most common in children under 2 years of age. Often there is a history
of AOM or recurrent AOM, though mastoiditis can be the first presentation of AOM. If severe 4
and untreated, it may lead to life-threatening complications.
Common pathogens are S. pneumoniae, S. pyogenes, and Staphylococcus aureus (including
methicillin-resistant S. aureus).

4.12.1 Clinical features


Presents like acute otitis media with fever, irritability, ear pain, and an abnormal tympanic
membrane on otoscopy.
Typically:
– The affected ear appears like it is sticking out or protruding.
– The area behind the ear is swollen, tender, and erythematous and feels like there is a
fluctuant mass. A draining fistula may be present.
May present with complication of mastoiditis due to spread of infection into intra- or extra-
cranial spaces. Complications include:
– Meningitis
– Intracranial abscesses
– Facial nerve paralysis
– Hearing loss
– Labyrinthitis: tinnitus, hearing loss, nausea, vomiting, vertigo, dizziness, nystagmus
– Osteomyelitis

4.12.2 Management
– Admit to hospital for IV antibiotic treatment and management of any complications.
– Refer to Ear, Nose, Throat specialist where possible for advice and to determine if surgical
intervention is necessary.
– Clean the ear canal: wipe any drainage with a cotton swab or clean tissue or gauze.
– Treat fever and pain.
– First line antibiotics recommended are ceftriaxone IV: 80 mg/kg (max. 4g if < 50 kg; max. 2 g
if ≥ 50 kg) every 24 hours and clindamycin IV: 10 mg/kg every 8 hours.
• If clindamycin is not available, add cloxacillin IV: 50 mg/kg every 6 hours.
• If pseudomonas confirmed on culture, add ciprofloxacin PO: 15 mg/kg (max. 750 mg)
2 times daily.

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Chapter 4: Respiratory conditions

– Switch to oral antibiotic when there is clear improvement (no fever for at least 24 hours,
reduced pain and swelling) and continue treatment for a total of 4 weeks:

amoxicillin/clavulanic acid (ratio 7:1 or 8:1) PO


Dosage expressed in amoxicillin:
• < 40 kg: 50 mg/kg 2 times daily
• ≥ 40 kg:
Ratio 8:1: 3000 mg daily (2 tablets of 500/62.5 mg 3 times daily)
Ratio 7:1: 2625 mg daily (1 tablet of 875/125 mg 3 times daily)
+
clindamycin PO: 10 mg/kg 3 times daily

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Chapter 4: Respiratory conditions

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37. Yeh S. Pertussis infection in infants and children: Treatment and prevention. UpToDate.
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46. 2020 GINA Pocket Guide for Asthma Management and Prevention. Global Initiative for
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47. Scottish Intercollegiate Guidelines Network, British Thoracic Society. SIGN 158 | British
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50. Dodd PJ, Yuen CM, Sismanidis C, Seddon JA, Jenkins HE. The global burden of
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Chapter 5:
Gastrointestinal conditions

5
5.1 Vomiting................................................................................................................. 187
5.1.1 Assessment.................................................................................................... 187
5.1.2 Management................................................................................................. 188
5.2 Diarrhoea............................................................................................................... 189
5.2.1 Acute diarrhoea............................................................................................. 189
5.2.2 Specific considerations for children with malnutrition...................................192
5.2.3 Persistent diarrhoea....................................................................................... 192
5.3 Dehydration........................................................................................................... 194
5.3.1 Non-malnourished children........................................................................... 194
5.3.2 Children with severe acute malnutrition (SAM).............................................198
5.4 Approach to a child with acute abdominal pain...................................................202
5.4.1 Identifying underlying cause.......................................................................... 202
5.4.2 Initial management....................................................................................... 204
5.5 Intussusception...................................................................................................... 205
5.5.1 Clinical features............................................................................................. 205
5.5.2 Management................................................................................................. 206
5.6 Acute appendicitis................................................................................................. 207
5.6.1 Clinical features............................................................................................. 207
5.6.2 Management................................................................................................. 207
5.7 Bowel Obstruction................................................................................................. 209
5.7.1 Clinical features............................................................................................. 209
5.7.2 Causes of acute bowel obstruction................................................................210
5.8 Pyloric stenosis...................................................................................................... 213
5.8.1 Clinical features............................................................................................. 213
5.8.2 Management................................................................................................. 213
References Chapter 5................................................................................................... 215
Chapter 5: Gastrointestinal conditions

5.1 Vomiting

Vomiting can be caused by a multitude of underlying conditions. Acute gastroenteritis, which


is usually viral, is a common cause among younger children and may be associated with
diarrhoea and complicated by dehydration. However, vomiting may also be a sign of a serious
or life-threatening disorder such as acute bowel obstruction or raised intracranial pressure.

5.1.1 Assessment
– Evaluate the history and clinical condition carefully to identify the cause of vomiting. 5
• Consider: age of child; duration of vomiting; characteristics (projectile, episodic/waves,
continuous), associated nausea, diarrhoea, abdominal pain, headaches; colour of vomit
(bilious, yellowish, blood-stained), presence of fever.
• Relevant medical history e.g. diabetic ketoacidosis, recent head injury, possible ingestion
of toxins, poisons or traditional/herbal medicines.
– Assess for presence of any signs of concern (see Table 5.1).
Table 5.1 - Characteristics of vomiting and possible aetiology
Characteristic of vomit or vomiting Potential indication or cause
Signs of concern
Bilious (greenish-yellow) Acute bowel obstruction, see Section 5.7
Projectile Pyloric stenosis (infants < 6 weeks), see
Section 5.8
Blood-stained Oesophageal varices, oesophageal injury
(Mallory-Weiss tear due to repetitive
vomiting), gastritis or gastric ulcer.
Protracted vomiting and acute abdominal Enteric (typhoid and paratyphoid) fever, see
distension/tenderness and fever Chapter 3, Section 3.6
Rapid onset, associated with other signs Anaphylaxis (post ingestion), see Chapter 2,
of anaphylaxis (skin, respiratory, cardiac) Section 2.4
Associated headache or when waking up Raised intracranial pressure
Associated head injury Intracranial haemorrhage causing raised
ICPa
Associated with blood in stools Intussusception (infants), see Section 5.5
Associated with fever Appendicitis (see Section 5.6),
gastroenteritis (see Section 5.2), urinary
tract infection (see Chapter 8, Section 8.1),
malaria (see Chapter 3, Section 3.4), acute
pharyngitis
Vomit contains abnormal contents Ingestion of toxin, poison, traditional/herbal
medicine (see Chapter 2, Section 2.9);
severe helminth infection

a ICP = Intracranial pressure

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Chapter 5: Gastrointestinal conditions

Characteristic of vomit or vomiting Potential indication or cause


Less concerning
Short duration; associated with watery Acute gastroenteritis (see Section 5.2)
diarrhoea, nausea, loss of appetite,
abdominal cramps; other close contacts
affected
After feeds in young infants (small Gastro-oesophageal reflux (GOR)
volume)
Associated with unilateral or spasmodic Migraine (adolescents)
localised headache
Early morning Pregnancy (adolescents)

– Assess for any secondary complications:


• Dehydration
• Hypoglycaemia
• Signs of electrolyte imbalance
• Excess weight loss or malnutrition (especially if vomiting over several days/weeks)

Investigations
– Haemoglobin (Hb)
– Blood glucose level (BGL)
– Malaria test, if endemic
– Electrolytes, if available
Conduct specific investigations according to differential diagnosis based on history and clinical
presentation.

5.1.2 Management
– Treat the underlying cause (see Table 5.1, page 187).
– Urgently refer any child suspected of acute bowel obstruction, intussusception, appendicitis,
or raised intracranial pressure for surgical consideration.
– Correct any dehydration and electrolyte abnormalities.
– Antiemetics are rarely necessary unless vomiting is incessant and/or causing significant
dehydration or electrolyte imbalance. A single dose of ondansetron PO, 100 to
150 micrograms/kg (max. 8 mg) can be given if the following conditions are met:
• Acute surgical abdomen excluded (see Section 5.4)
• Failed trial of ORS
• Confident in diagnosis of acute gastroenteritis

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Chapter 5: Gastrointestinal conditions

5.2 Diarrhoea

Diarrhoea is defined as passage of 3 or more loose or watery stools in a 24-hour period. It is the
second leading cause of under-5 deaths in children worldwide and the main underlying cause
of malnutrition. Children may present critically unwell with severe dehydration or bacterial
sepsis associated with diarrhoea. Malnourished or immune-compromised children (such as
due to HIV infection) are particularly at risk of death1.
In resource-limited settings, infectious gastroenteritis is the main pathology causing diarrhoea 5
(often associated with vomiting). Less commonly, children may present with diarrhoea as an
associated symptom of another illness, such as:
– Influenza, measles, haemorrhagic fever, HIV and malaria.
– Serious bacterial infections: pneumonia, urinary tract infection, meningitis and sepsis.
– Surgical emergencies: intussusception or appendicitis.
Diarrhoea is also a common side effect of antibiotics in children, therefore it is important to
ask about current or recent antibiotic use.
In all children presenting with diarrhoea, take a comprehensive history and always include
assessment of dehydration in the clinical examination. Examine a fresh stool to determine
whether the diarrhoea is watery or bloody (containing visible blood).
Diarrhoea that has continued for ≥ 14 days is classified as persistent diarrhoea (Section 5.2.3).

5.2.1 Acute diarrhoea


– Rapid onset, frequent stools, duration usually a few hours to days.
– Common pathogens of infectious gastroenteritis vary by context and age group. Refer to
Table 5.2 for a list of common causes in children.
Table 5.2 - Causes of acute diarrhoea in children2
Acute watery diarrhoea Acute bloody diarrhoea
Viruses Rotavirus (most common < 2 years)
Enteric adenovirus (enterovirus)
Measles
Bacteria Enterotoxigenic E.coli ( ≥ 2 years) Shigella species (most common in
Campylobacter jejuni 2 to 5 years)
Vibrio cholera Enterohaemorrhagic E. coli
Yersinia enterocolitica Campylobacter spp
Aeromonas Salmonella species (typhoid fever,
non-typhoid Salmonella)
Clostridium difficile
Parasites Giardia lamblia Entamoeba histolytica
Cryptosporidium (< 2 years; HIV Schistosomiasis (in endemic areas)
infection)

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Chapter 5: Gastrointestinal conditions

Assessment
– Evaluate the history and clinical condition carefully to try to identify the cause of the acute
diarrhoea.
• Consider: frequency per day, consistency of stool (loose, watery, mucous or blood-
streaked, rice-water appearance), associated with fever, vomiting, abdominal pain.
• Relevant medical history e.g. HIV infection, recent use of antibiotics, traditional medicines.
• Epidemiological factors such as other members of household with same symptoms, or in
context of known epidemic.
– Assess for presence of dehydration and severity (refer to Section 5.3).
– Assess for any secondary complications:
• Hypoglycaemia
• Signs of electrolyte imbalance
• Excess weight loss or malnutrition

Investigations
Most children with acute diarrhoea do not need any investigations, however the following
may be helpful:
– Hb, BGL
– Malaria test, if endemic
– Stool examination, with or without culture, if symptoms not typical of acute gastroenteritis.

Management
– Take and note the baseline weight (if not already done).
– If breastfeeding, continue if child keen to drink and alert.
– Admit children with severe diarrhoeaa or signs of critical illness, even if no evidence of
dehydration, especially if malnourished.
– Assess degree of dehydration and manage according to severity (see Section 5.3).
– Prevent dehydration in children with no dehydration (see below).
– Prevent malnutrition: continue with unrestricted usual diet. See below for breastfed infants.
– Do not give anti-diarrhoeal drugs or antiemetics.
– Treat the underlying condition, if known.
– Give zinc sulfate (see page 191 for dosing).
– Antibiotic treatment:
• Not indicated in most cases of acute watery diarrhoea, with the exception of suspected
cholera in certain cases only (see Management of a cholera epidemic, MSF).
• Indicated in acute bloody diarrhoea, as Shigellosis is the most common cause.

Prevention of dehydration
Children with simple diarrhoea and no dehydration can be treated at home with measures to
prevent dehydration:
– Explain to parents/carers how to replace fluids lost in diarrhoea by giving ORS 10 mL/kg
(5 mL/kg in children with SAM) after each loose stool (see Table 5.3 and Appendix 12).
– Breastfed children: encourage frequent feeds for as long as the child wants. ORS should be
given between feeds.
– Non-breastfed children: encourage the child to take additional ORS or clean water if the
child seeks it in addition to recommended amount of ORS.

a Profuse or dehydrating stool losses, fever or illness.

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Chapter 5: Gastrointestinal conditions

Table 5.3 - Volume of ORS after each loose stool

Non-malnourished SAM
Weight mL of ORS to be given mL of ORS to be given
(10 mL/kg) (5 mL/kg)

< 5 kg 50 25

5 to < 10 kg 100 50

10 to 20 kg 200 100

> 20 kg 300 200 5


Zinc supplementation
Zinc sulfate is given in combination with ORS in order to reduce the duration and severity
of diarrhoea, as well as to prevent further recurrences in the 2 to 3 months following
treatment:

zinc sulfate PO
• < 6 months: 10 mg once daily for 10 days
• 6 months to 5 years: 20 mg once daily for 10 days
Place the half-tablet or full tablet on a teaspoon, add a bit of water to dissolve it, and give
the entire spoonful to the child.

In malnourished children who are receiving therapeutic milk or RUTF, supplementation with
zinc sulfate is unnecessary.

Antibiotic treatment
– Diarrhoea without blood:
• Most are caused by viruses unresponsive to antibiotics.
• Antibiotic treatment is indicated in the case of cholera or giardiasis:
▹ Cholera: the most important part of treatment is rehydration. In the absence of
resistance (perform antibiotic-sensitivity testing at the beginning of an outbreak),
antibiotic treatment shortens the duration of diarrhoea. See Management of a cholera
epidemic, MSF.
▹ Giardiasis: give tinidazole PO 50 mg/kg (max. 2 g) single dose or metronidazole PO
30 mg/kg once daily for 3 days.
– Diarrhoea with blood:
Treat empirically for Shigellosis (amoebiasis is much less common).
• If the child is unwell:
▹ Admit and stabilise.
▹ Administer ceftriaxone IV/IM: 50 to 100 mg/kg once daily (max. 4 g if < 50 kg; max. 2 g
if ≥ 50 kg) for 3 days.
▹ If no improvement (treatment failure defined by persistent fever, grossly bloody
stools or unchanged stool frequency by day 3 of treatment), consider antibiotic-
resistant infection or an alternative cause such as amoebiasis (see Section 5.2.3) or
C. difficile.

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Chapter 5: Gastrointestinal conditions

• If child appears well:


▹ Treatment can be given at home.
▹ Give ciprofloxacin PO 15 mg/kg (max. 750 g) 2 times daily for 3 days.
▹ If resistance or contraindication to ciprofloxacin, or if no improvement after 48 hours,
switch to ceftriaxone (as above) or give azithromycin PO, 12 mg/kg on D1 then 6 mg/
kg once daily from D2 to D5.
▹ If no improvement, consider an alternative diagnosis such as amoebiasis and add
tinidazole PO 50 mg/kg (max. 2 g daily) for 3 days or metronidazole PO 15 mg/kg 3 times
daily for 5 days.

Prevention
– Breastfeeding reduces infant morbidity and mortality from diarrhoea and the severity of
diarrhoea episodes.
– When the child is weaned, preparation and storage of food are associated with the risk of
contamination by faecal micro-organisms: discourage bottle-feeding; food must be cooked
well; milk or porridge must never be stored at room temperature.
– Access to sufficient amounts of clean water and personal hygiene (washing hands with soap
and water before food preparation and before eating, after defecation etc.) are effective
methods of reducing the spread of diarrhoea.
– In countries with a high rotavirus diarrhoea fatality rate, the WHO recommends routine
rotavirus vaccination in children between 6 weeks and 24 months of age3.

5.2.2 Specific considerations for children with malnutrition


Children with malnutrition may have additional reasons for diarrhoea that are not infective. In
malnourished children, the lining of the small intestine is atrophied, the production of gastric
acid, digestive enzymes and bile is absent or reduced, and gut bacterial overgrowth is frequent,
all of which increase the frequency of diarrhoea in children with malnutrition. Re-nutrition or
osmotic diarrhoea is also common in children receiving therapeutic feeds (see Chapter 12,
Section 12.2).
If diarrhoea persists for more than 72 hours, in the absence of another obvious explanation for
diarrhoea (e.g. otitis media, pneumonia, UTI), consider other infective causes of diarrhoea and
treat accordingly (see Section 5.2.1).

5.2.3 Persistent diarrhoea


Persistent diarrhoea is defined as at least 3 episodes of diarrhoea per day for ≥ 14 days
despite treatment. Persistent diarrhoea can lead to malnutrition, dehydration, and increases
susceptibility to other infections such as pneumonia, indirectly contributing to increased risk
of mortality in young children.
Children with acute malnutrition or who are immunocompromised, such as with HIV infection,
are more at risk of persistent diarrhoea (see Chapter 13).
Parasitic infections such as giardiasis and amoebiasis may cause persistent diarrhoea in
children. However, in younger children, repeated acute diarrhoeal episodes with insufficient
recovery between episodes may often be the cause of persistent diarrhoea.

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Chapter 5: Gastrointestinal conditions

– Giardiasis:
• More common in children < 5 years.
• Suspect G. lamblia in cases of diarrhoea (sudden in onset; initially may be watery),
malaise, nausea/vomiting, foul-smelling and fatty stools (steatorrhea), abdominal cramps
and bloating and weight loss; fever occurs occasionally.
– Amoebiasis:
• Can cause both persistent and bloody diarrhoea in children, but it is not common.

Investigations
– Examine stools for Giardia, Cryptosporidium, and Entamoeba histolytica.
5
Management
– Same admission criteria as for acute diarrhoea.
– Prevent and/or treat dehydration if present according to severity (see above and Section 5.3).
– Assess for malnutrition and refer for management of acute malnutrition if identified.
– Prevent malnutrition by encouraging good dietary intake and breastfeeding for infants.
– Give zinc sulfate (as page 191).
– Give empiric antiparasitic treatment:

albendazole PO:
12 - 23 months: 200 mg once daily for 3 daysb
≥ 24 months: 400 mg once daily for 3 days
mebendazole PO:
≥ 12 months and > 10kg: 100 mg 2 times daily for 3 days

Amoebiasis
– Antiparasitic treatment should be given when motile Entamoeba histolytica amoebae are
found in stools or if a correct shigellosis treatment has been ineffective.
– Give tinidazole PO 50 mg/kg (max. 2 g daily) for 3 days or metronidazole PO 15 mg/kg 3 times
daily for 5 days
– Refer to MSF Clinical Guidelines, Chapter 3 for further information.
Giardiasis
– Give tinidazole PO 50 mg/kg (max. 2 g) single dose or metronidazole PO 30 mg/kg once daily
for 3 days.
– Refer to MSF Clinical Guidelines, Chapter 6 for further information.

If diarrhoea lasts for more than 4 weeks (chronic diarrhoea), consider non-infectious causes.

b Albendazole is not systematically recommended to children less than 12 months, but can be given on a case-
by-case basis according to clinician assessment at the same dose as for children 12 - 23 months.

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Chapter 5: Gastrointestinal conditions

5.3 Dehydration

Dehydration results from loss of water and salt from the body in excess of replacement.
Young children are at greater risk of dehydration as they are unable to independently replace
their fluid losses or to clearly communicate their needs. Dehydration may be associated
with electrolyte disturbance and, if prolonged, can lead to reduced end-organ perfusion
and shock. The most common causes of dehydration in children are diarrhoea and vomiting,
with dehydration being the main contributor to death from diarrhoea. In addition, children
are particularly susceptible to dehydration from severe burns due to their large body surface
area relative to their weight.
Management of dehydration depends on the underlying cause and degree of dehydration.
For children with fluid loss due to burns refer to MSF Clinical Guidelines, Chapter 10 and for
diabetic ketoacidosis refer to Chapter 9, Section 9.1.

5.3.1 Non-malnourished children


Clinical features and assessment
The degree of dehydration is difficult to assess accurately, even more so in malnourished
children. Taking a focused and detailed history of the current illness is therefore paramount.
– Ask about frequency and duration of watery diarrhoea and/or vomiting; ability to drink or
feed; urine output/wet nappies; concurrent illness, fever.
– Check for dry lips or mouth, absence of tears.
– Examine for presence and degree of dehydration. Classify according to the more severe
degree of dehydration based on the presence of two or more signs in the same category
(see Table 5.4, Figure 5.1 and Figure 5.2).
– Check for any signs of circulatory impairment.
– Monitor if there are any ongoing losses e.g. profuse diarrhoea.
Table 5.4 - Classification of degree of dehydration (adapted from WHO4)

Clinical features Classification


(Two or more of
the following signs) No dehydration Some dehydration Severe dehydration
Lethargic
Mental status Normal Restless, irritability
or unconscious
Eyes Normal Sunken Sunken
Goes back very
Skin pinch < 1 second Goes back slowly
slowly (≥ 2 sec)
No thirst, Thirsty, Unable to drink
Thirst
drinks normally drinks eagerly or drinks poorly
Absent for
Urine output Normal Reduced
several hours

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Chapter 5: Gastrointestinal conditions

Figure 5.1 - Clinical features of dehydration

How to assess skin pinch


– Pinch the abdominal skin to assess skin turgor. Skin pinch goes back very slowly (≥ 2 seconds)
in severe dehydration.

Figure 5.2 - Skin pinch assessment in infants

Management
Children with no dehydration do not require admission. Most children with some dehydration
can be managed at home after an initial period of observation (4 to 6 hours) to ensure that
they are able to tolerate adequate oral rehydration therapy.
Admit:
– All children with severe dehydration.
– Children < 4 months of age and/or < 4 kg weight with some dehydration.
– Children with some dehydration if there is no possibility for short-term observation while
starting rehydration treatment.
Manage according to degree of dehydration using WHO treatment plan A, B or C4 (see
also Appendix 12). Reassess the child’s hydration and clinical condition regularly – clinical
improvement is the best indicator of treatment response.

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Chapter 5: Gastrointestinal conditions

Severe dehydration (WHO treatment plan C)


– Assess and manage ABCDE. If signs of circulatory impairment or shock are present, stabilise
and manage accordingly (Chapter 2, Section 2.2).
– Obtain IV/IO access.
– Mark liver border with pen.
– Administer IV Ringer lactate (RL) (or alternatively sodium chloride 0.9% if RL not available)
according to the following table:

First administer 30 mL/kga Then administer 70 mL/kg


Age
over: over:

< 12 months 1 hour 5 hours

≥ 12 months 30 minutes 2½ hours

– Monitor urine output.


– Check BGL and correct hypoglycaemia if present (see Chapter 9, Section 9.3).
– Check Hb and blood electrolytes (where available), and treat anaemia if present (see
Chapter 10, Section 10.1).
– Monitor and record signs of dehydration and vital signs every 15 to 30 minutes using an
early warning system (see MSF Manual of Nursing Care Procedures, Assessment and vital
signs, Charts: Vital sign charts).
– If not improving, re-evaluate the child, consider other differential diagnoses (e.g. diabetic
ketoacidosis, shock, sepsis), assess fluid losses and increase the rate of IV fluids accordingly.
– Monitor continuously for signs of fluid overload:
• Increased RR by ≥ 10 breaths/min from initial RR, or
• Increased HR by ≥ 20 beats/min from initial HR.
Plus any one of the following:
▹ New or worsening hypoxia (decrease in SpO2 by > 5%)
▹ New onset of rales and/or pulmonary oedema (fine crackles in lung fields)
▹ New galloping heart rhythm
▹ Increased liver size (liver size must have been marked with pen on arrival)
▹ New peripheral oedema and/or puffy eyelids.
Management if signs of fluid overload present:
• Stop IV fluids.
• Administer furosemide IV: 0.5 mg/kg (repeat once if necessary).
• Place child into semi-sitting position and ensure high-flow oxygen via non-rebreathing
mask.
• Monitor every 15 minutes until child has been stable for at least one hour.
– As soon as the child is awake, alert, and can tolerate a nasogastric tube (NGT) or take oral
fluids, start ORS at 5 mL/kg/hour in addition to the ongoing IV fluid resuscitation and
encourage breastfeeding (if relevant).

a Repeat this volume if radial pulse remains weak or absent

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Chapter 5: Gastrointestinal conditions

– In addition, if tolerated, give extra ORS to replace fluids lost with each loose stool according
to plan A (below).
– Assess the degree of dehydration at the end of the fluid resuscitation (3 hours for children,
6 hours for infants). Continue further rehydration according to degree of dehydration
following the appropriate treatment plan (A, B or C).
– If hypokalaemia or, where potassium monitoring not available, if child develops signs of
hypokalaemia including general fatigue, muscle cramps and weakness, abdominal distension
and polyuria, treat for moderate hypokalaemia with 7.5% potassium chloride syrup for 2 days
(see also Chapter 15, Section 15.3):

7.5% potassium chloride syrup (1 mmol of K+/mL) PO


< 45 kg: 2 mmol/kg (2 mL/kg) daily 5
≥ 45 kg: 30 mmol (30 mL) 3 times daily

Some dehydration (WHO treatment plan B)


– If breastfeeding, encourage continuation if the child is keen and alert.
– Prescribe ORS 75 mL/kg over 4 hours:

Weight (kg) <6 6 to < 10 10 to < 12 12 to < 19 19 to < 30

Total ORS (mL)


200-400 400-700 700-900 900-1400 1400-2200
over 4 hours

– Show the parent/carer how to give ORS in small, frequent quantities e.g. using a teaspoon
or syringe for infants and young children (5 ml every 5 minutes), regular sips from a cup for
older children.
– If child vomits ORS, encourage child to take smaller volumes or sips.
– In addition to rehydration with treatment plan B, give extra ORS to replace fluids lost with
each loose stool according to plan A (below).
– Reassess degree of dehydration after 4 hours and continue with appropriate treatment plan.
If dehydration has resolved, management with plan A can continue at home.

No dehydration (WHO treatment plan A)


– Encourage oral fluids e.g. frequent breastfeeds, if breastfeeding; clean water, clear soups,
rice water, if not breastfeeding.
– Give ORS 10 ml/kg after each loose stool to prevent dehydration:

Weight (kg) <5 5 to < 10 10 to 20 > 20

ORS (mL) to be given


50 100 200 300
after each loose stool

– Explain to the parent/carer how to reassess regularly for signs of dehydration and continue
treatment with ORS after loose stools at home.

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Chapter 5: Gastrointestinal conditions

5.3.2 Children with severe acute malnutrition (SAM)


Clinical features and assessment
Dehydration is difficult to assess clinically in severely malnourished children because
malnutrition may mask signs of dehydration or cause over-diagnosis of severe dehydration:
– Signs of hypovolaemia or circulatory impairment can be masked by oedema.
– Skin pinch assessment has no value if the subcutaneous tissue has completely disappeared
because the persistent and doughy character applies to this subcutaneous tissue (deep
pinch).
– Sunken eyes can be present without dehydration.
Therefore, to diagnose dehydration and assess for severity in children with SAM, the following
criteria are more reliable (see also Table 5.5):
– A detailed history of losses (frequency and duration of vomiting and/or watery diarrhoea).
– Recent weight loss (compared to weight prior to onset of vomiting or diarrhoea, can be
measured on scales or from parent/carer history).
– Clinical features that can be measured, including mental status, thirst, urine output.
Table 5.5 - Classification of degree of dehydration adapted for SAM

Clinical features Classification


(Two or more of
the following signs) No dehydration Some dehydration Severe dehydration
Lethargic
Mental status Normal Restless, irritability
or unconscious
No thirst, Thirsty, Unable to drink
Thirst
drinks normally drinks eagerly or drinks poorly
Absent for
Urine output Normal Reduced
several hours
Recent frequent
watery diarrhoea Yes Yes Yes
and/or vomiting
Recent obvious
No Yes Yes
rapid weight loss

Management
Children with SAM and no dehydration do not require admission, unless diarrhoea is severeb
or there are signs of critical illness. In this case, admit for monitoring and management with
‘Plan A SAM’. Admit children with SAM and some or severe dehydration for close monitoring,
and manage according to degree of dehydration using treatment plans specifically adapted for
SAM (see below and Figure 5.3)c. Ideally, continue therapeutic milk at scheduled feeding hours
in addition to rehydration fluids.
Oral rehydration should be used in preference to IV fluids in the management of dehydration
of any severity in children with SAM. Target weights are used to guide treatment and are

b Profuse or dehydrating stool losses, fever or illness.


c Except in the case of cholera where more aggressive fluid management is required. See Management of a
cholera epidemic, Chapter 5.8 for advice on fluid management in children with malnutritiSF on and cholera.

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Chapter 5: Gastrointestinal conditions

calculated on the basis of assumed percentages of body water lost depending on the degree of
severity of dehydration. Reassess the child’s hydration and clinical condition regularly – clinical
improvement is the best indicator of treatment response.

Severe dehydration: ‘Plan C SAM’


– Assess and manage ABCDE.
– Assess specifically for signs of circulatory impairment or shock and stabilise accordingly
(Chapter 2, Section 2.2).
– Weigh the child.
– Calculate target weight = current weight x 1.1d; or recent previously recorded weight.
– Mark liver border with pen.
– Check BGL and correct hypoglycaemia if present (see Chapter 9, Section 9.3). 5
– Check Hb and blood electrolytes (where available), and treat anaemia if present (see
Chapter 10, Section 10.1).
– Monitor urine output.
– Monitor and record signs of dehydration and vital signs every 15 to 30 minutes using an
early warning system (see MSF Manual of Nursing Care Procedures, Assessment and vital
signs, Charts: Vital sign charts).
If no signs of circulatory impairment or shock and not vomiting:
– If breastfeeding, continue if child keen and alert.
– Give ReSoMal PO/NGT: 20 mL/kg over 1 hour.
– Reassess patient after 1 hour.
– If improving, not vomiting and still no signs of circulatory impairment/shock, move to
treatment algorithm for ‘Plan B SAM’ (without modifying target weight).
– If at any point the child deteriorates and develops signs of circulatory impairment/shock,
treat with IV fluids +/- blood transfusion (see below).
– If at any point the child begins to vomit, but there are no signs of circulatory impairment,
treat with IV fluids as follows:
• Administer glucose (dextrose) 5% - Ringer lactate (G5%-RL) IV: 10 mL/kg/hour for 2 hours.
• Reassess patient after 2 hours of IV fluids. If no improvement at all or still vomiting,
continue G5%-RL IV: 10 mL/kg/hour for another 2 hours.
• When the child begins to improve and/or is not vomiting, stop IV fluids and switch to ‘Plan B
SAM’ (without modifying target weight) starting with ReSoMal PO/NGT: 20 mL/kg/hr for
2 hours.
If signs of circulatory impairment/shock:
– Administer ceftriaxone IV: 80 mg/kg (max. 4 g if < 50 kg; max. 2 g if ≥ 50 kg) single dose.
Revise necessity of further antibiotic treatment once underlying cause identified.
– Immediately administer G5%-RL IV: 10 mL/kg/hour for 2 hours.
– Reassess patient after 2 hours of IV fluids. If deterioration or no improvement at all, check
Hbe and administer a blood transfusion5 (see Chapter 2, Section 2.2.3 and Chapter 10,
Section 10.1.2), and continue G5%-RL IV: 10 mL/kg/hour for another 2 hours.
– Do not stop IV fluid rehydration, continue IV fluids as above at the same time as blood
transfusion using a separate IV line.
– If at any point the child begins to improve and is not vomiting, stop IV fluids and begin
ReSoMal PO/NGT: 20 mL/kg/hr, following ‘Plan B SAM’ (without modifying target weight).

d Assumes approximately 10% dehydration.


e Blood transfusion for shock is not strictly dependent on Hb, however if Hb is above 10 g/dL transfusion may
not be beneficial and decision to transfuse should be based on the balance of potential risks and benefits.

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Chapter 5: Gastrointestinal conditions

Some dehydration: ‘Plan B SAM’


– If breastfeeding, encourage continuation if child keen and alert.
– Weigh the child.
– Calculate target weight = current weight x 1.06f or recent previously recorded weight
– Give ReSoMal PO/NGT: 20 mL/kg/hour for 2 hours.
– In addition, if tolerated, give extra ReSoMal to replace fluids lost with each loose stool
according to ‘Plan A SAM’ (below).
– Reassess patient and reweigh after 2 hours.
– If improving, give ReSoMal PO/NGT: 10 mL/kg/hr until:
• No signs of dehydration and/or
• Target weight reached
– Start F75 at standard volumes and times in addition to ReSoMal, if tolerated.
– Reassess and reweigh every 2 hours.
– Once there are no signs of dehydration and/or target weight is reached, continue with ‘Plan
A SAM’ to prevent recurrence of dehydration.
– If after 2-4 hours there are no signs of improvement, or there is continuous diarrhoea
with inability to keep up with stool losses using oral rehydration with ReSoMal, consider
management with G5%-RL IV as for severe dehydration with circulatory impairment.

No dehydration: ‘Plan A SAM’


– Encourage oral fluids (e.g. frequent breastfeeds, if breastfeeding; clean water, if not
breastfeeding).
– Give ReSoMal PO: 5 ml/kg after each loose stool or vomit to prevent dehydration:

Weight (kg) <5 5 to < 10 10 to 20 > 20

ReSoMal (mL) to be given


25 50 100 200
after each loose stool

– If the child is ready for discharge, explain to the parent/carer how to reassess regularly for
signs of dehydration and continue treatment with ORSg after loose stools at home.

Fluid overload
– Monitor continuously for signs of fluid overload:
• Increased RR by ≥ 10 breaths/min from initial RR, or
• Increased HR by ≥ 20 beats/min from initial HR.
Plus any one of the following:
• New or worsening hypoxia (decrease in SpO2 by > 5%)
• New onset of rales and/or pulmonary oedema (fine crackles in lung fields)
• New galloping heart rhythm
• Increased liver size (liver size must have been marked with pen on arrival)
• New peripheral oedema and/or puffy eyelids.
– Management if signs of fluid overload present:
• Stop IV fluids or ReSoMal.
• Consider administration of furosemide IV: 0.5 mg/kg, especially if IV fluids given (repeat
once if necessary).
• Place child into semi-sitting position and ensure high-flow oxygen via non-rebreathing mask.
• Monitor every 15 minutes until child has been stable for at least one hour.

f Assumes approximately 6% dehydration.


g ReSoMal should only be used for short periods in hospital under medical supervision, therefore for ongoing
treatment at home ORS is used.

200
Figure 5.3 - Management of dehydration in children with SAM (excluding cholera cases)
Child with severe acute malnutrition (SAM) and dehydration

• Assess and manage ABCDE


• Assess presence and severity of dehydration:
- History of losses (vomit/diarrhoea)
- Weigh child and check if recent weight loss
- Clinical features (adapted to SAM, see Table 5.5)
• Check Hb, BGL and electrolytes (if available) and treat, if necessary

No dehydration Some dehydration Severe dehydration


‘Plan A SAM’ ‘Plan B SAM’ ‘Plan C SAM’
Target weight = weight x 1.06 Target weight = weight x 1.1
(or recent weight if known) (or recent weight if known)

Replace each loose stool or Circulatory impairment


vomit with 5 mL/kg ReSoMal ReSoMal PO/NGT: No Yes
20 mL/kg/hr for 2h
ReSoMal ReSoMal PO/NGT: Give ceftriaxone
Weight (kg)
(mLs) PLUS 5 mL/kg after 20 mL/kg over 1h** 80 mg/kg*
<5 25 each loose stool
5 to < 10 50
10 to 20 100 No improvement G5%-RL IV:
> 20 200 or deterioration 10 mL/kg/hr for 2h
Reassess and re-weigh
Improvement
and not vomiting
Improvement No improvement
and not vomiting or deterioration
No improvement,
vomiting or severe
diarrhoea
Continue ReSoMal PO/NGT: Continue G5%-RL IV:
10 mL/kg/hr 10 mL/kg/hr for another 2h
Consider management
PLUS 5 mL/kg after each loose Check Hb and administer a
stool until target weight reached with G5%-RL IV
blood transfusion***
and/or no signs of dehydration according to severe
AND start F75, if tolerated dehydration algorithm

* Revise necessity of further antibiotic treatment once underlying infection identified.


** If vomiting, give G5%-RL IV for 2h, reassess and repeat if ongoing vomiting.
Chapter 5: Gastrointestinal conditions

201
*** If Hb is above 10 g/dL transfusion may not be beneficial and decision to transfuse should be based on the balance of potential risks and benefits.
5
Chapter 5: Gastrointestinal conditions

5.4 Approach to a child with acute abdominal pain

Abdominal pain is a common presentation in children and has a wide range of medical and
surgical causes. Gastroenteritis is the most common non-surgical cause of abdominal pain
in children (see Section 5.1 and Section 5.2), but surgical causes must be ruled out early to
prevent unnecessary morbidity and mortality. This chapter will focus on the ‘acute abdomen’ –
sudden and severe abdominal pain that may indicate a surgical emergency. It is estimated that
around 30% of global disease burden could be addressed surgically, however the provision of
available, affordable, timely and safe paediatric surgical care is often scarce in resource-limited
settings6,7,8.

5.4.1 Identifying underlying cause


Emergency stabilisation and pain management is often necessary before an assessment can
take place due to significant pain (see Section 5.4.2). Once the patient is comfortable and
stable, a focused history and examination should be done.
Important points in the history include:
– Onset of symptoms
– Detailed description of the pain: onset, nature (dull/aching/sharp/colicky), intensity,
radiation, localisation (localised/diffuse/radiating)
– Associated symptoms: fever, nausea and/or vomiting (bilious/bloodstained/faecal),
anorexia, stool pattern alterations (diarrhoea/constipation), dysuria, cough, rashes
– Possible trauma (accidental or non-accidental)
– Gynaecological history in adolescent girls (onset of menstruation/sexual activity)
– Past medical/surgical history (previous abdominal surgery, recurrent blood transfusions)
Complete a comprehensive clinical examination (Chapter 1, Section 1.3). Focus on abdominal
and extra-abdominal signs that may help identify underlying cause of pain. Assess the inguinal
region and genitalia. Consider a perianal inspection or digital rectal examination, if necessary –
this should only be done once and with the consent of the child and parent/carer.
Identify the likely underlying cause and differentiate between surgical and non-surgical
causes (see Table 5.6). Common surgical causes of acute abdominal pain in children include
intussusception, malrotation and volvulus, and acute appendicitis. Ectopic pregnancy should
be considered in all sexually active adolescent girls. Many non-surgical causes can mimic an
acute abdomen, including DKA, sickle cell crisis, haemolytic uraemic syndrome (HUS) and
pneumonia. In children, mesenteric adenitisa is commonly mistaken for acute appendicitis.
If there is any doubt about the diagnosis, a surgical review should be sought early to rule out
a surgical cause before a non-surgical diagnosis is made.

a Mesenteric adenitis is a benign lymphadenopathy of the abdominal lymph nodes that commonly occurs after
a viral infection.

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Chapter 5: Gastrointestinal conditions

Table 5.6 - Common surgical causes of acute abdominal pain

Suggestive clinical features Diagnosis Origin of acute abdomen

Redcurrant jelly stool; Intussusception


intermittent colicky severe (see Section 5.5)
abdominal pain

Pain initially peri-umbilical Acute appendicitis


then localising to right (see Section 5.6)
iliac fossa, associated with
nausea/vomiting, anorexia 5
Acute colicky pain; not Bowel obstruction
passing gas per rectum; (see Section 5.7) Surgical:
abdominal distension; Refer for emergency
bilious vomiting surgical evaluation and
intervention
Fixed, firm, painful swelling Incarcerated hernia
in groin or umbilicus; (see Section 5.7.2)
vomiting

Acute, severe, focal pain; Ovarian/testicular torsion


vomiting

Abdominal rigidity; signs of Bowel perforation (due to


systemic illness/sepsis typhoid or ischaemic enteritis)
with peritonitis

Mass felt on palpation, Masses: abdominal


variable location depending tuberculosis, tumours, intra-
on underlying cause abdominal abscess

Periumbilical or subxiphoid Pancreatitis or cholecystitis


pain radiating to back; right
upper quadrant pain
Non-surgical:
Prodrome of polydipsia, Diabetic ketoacidosis Refer to specific medical
polyuria and weight loss, (see Chapter 9, Section 9.2) management in relevant
ketotic breath chapters. Some conditions
may eventually require
Other signs of vaso- Sickle cell crisis surgical intervention.
occlusive disease (see Chapter 10, Section 10.2)

Prodrome of diarrhoea, Haemolytic uraemic syndrome


often affecting other (HUS)
members of family; may
have evidence of low
platelets e.g. petechiae

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Chapter 5: Gastrointestinal conditions

Investigations
– FBC including haemoglobin (Hb)
– BGL
– Electrolytes, if available
– Urine for microscopy
– Consider pregnancy test, if applicable
– Abdominal x-ray: obtain supine and left lateral decubitus views to evaluate acute conditions.
– Consider POCUS, if equipment and trained staff available: can be helpful in detecting free
fluid in the abdomen, especially when there is sudden clinical deterioration9.
Note that while the presence of x-ray and/or US signs may confirm pathology or support a
diagnosis, their absence does not rule it out.

5.4.2 Initial management


– Assess and manage ABCDE.
– Administer oxygen, aiming for SpO2 between 94 - 98%.
– Start IV maintenance fluids. If there are signs of dehydration, treat accordingly (see
Section 5.3).
– Check BGL and correct hypoglycaemia if present (see Chapter 9, Section 9.3).
– Administer adequate analgesia: note that early analgesia, including morphine 0.05 - 0.1 mg/kg
will not affect diagnostic accuracy10.
– Give antispasmodics with caution in children due to their anticholinergic side-effects, and
limit their use to treat active spasms. Not to be given to children under 6 years old. Give
hyoscine butylbromide PO:
• Child 6 - 11 years: 10 mg, up to 3 times daily
• Child 12 years and over: 20 mg, up to 4 times daily
– Place the child nil-by-mouth (NBM) and consider insertion of NGT (conical tip) to be kept on
free drainage with regular aspiration. Record quantity and aspect (bilious, bloody) of gastric
aspirates.
– If suspected peritonitis or perforation, start antibiotic treatment to cover both aerobes and
anaerobes:
• Administer ceftriaxone IV: 80 mg/kg (max. 4 g if < 50 kg; max. 2 g if ≥ 50 kg) every 24 hours
and metronidazole IV: 10 mg/kg every 8 hours.
• Continue for 3-10 days, depending on severity and eventual diagnosis.

Refer for urgent surgical review, identify the underlying cause and treat accordingly (see
Section 5.5, Section 5.6 and Section 5.7).

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Chapter 5: Gastrointestinal conditions

5.5 Intussusception

Intussusception occurs when one segment of the intestine invaginates into a more distal
segment. In approximately 90% of cases, this occurs at the ileocaecal junction11. It is the most
common cause of bowel obstruction in infants, with a mean incidence of 74 per 100,00012.
Although mostly seen in infants and young children (typical age range is 6 to 36 months), it
can occur in older children as well, when there is a pathologic ‘lead point’ such as lymphoma,
Meckel’s diverticulum, polyps, parasites or Henoch-Schönlein purpuraa. If the obstruction is not
corrected, the vascular supply of the bowel may become compromised, resulting in intestinal 5
ischemia and possible perforation. In high-income countries, death from intussusception is
rare, generally less than 1%, but in low- and middle-income countries (LMICs), between 6 and
25% of children who reach surgical care die13.

5.5.1 Clinical features


Typical presentation:
– Sudden onset, intermittent abdominal pain. The child appears to have episodic cramps,
drawing up the knees and crying inconsolably.
– Vomiting, typically non-bilious initially and progressing to bilious
– Pallor and lethargy (episodic)
– Abdomen may be distended and diffusely tender but may also be normal, especially between
episodes.
– Sometimes an elongated ‘sausage-shaped’ mass can be palpated in the right middle or upper
part of the abdomen, or even in the left upper quadrant. With more extended duration of
symptoms the mass may be palpable on rectal examination.
– Blood (‘red-currant jelly’) or mucus per rectum is a late sign.
The classic triad of colicky abdominal pain with a palpable mass and ‘red-currant jelly’ stool
appears in < 25% of cases.
Occasionally, children present generally unwell with lethargy and pallor, but without obvious
abdominal signs or symptoms and may be mistaken for sepsis.

Investigations
– Consider POCUS, if equipment and trained staff availableb: typically, a ‘target sign’ lesion
(concentric circles resembling a doughnut) is seen in ileocolic intussusception, with one
segment of bowel telescoping into another part. The outer wall is thickened and hypoechoic
in transverse axis14.

a Henoch-Schönlein purpura (HSP) is a common systemic vasculitis in children of unknown cause, that presents
with a rash and arthritis/arthralgia, abdominal pain or nephritis.
b Although ultrasound has high diagnostic accuracy for intussusception, positive results are user-dependent and
require high levels of training.

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Chapter 5: Gastrointestinal conditions

5.5.2 Management
– Assess and manage ABCDE.
– Ensure initial stabilisation as for acute abdomen (see Section 5.4.2).
– Refer for surgical review and definitive treatment with either:
• Radiographic barium or air enema
• Surgical reduction: in LMICs reduction is typically only partially accomplished due to
progressive ischaemia of the intussuscepted bowel, which ultimately requires resection.
• Hydrostatic reduction by warm saline enema under real-time sonography guidance, if
there are no contraindications (such as perforation, or ischemia on Doppler) and if the
ultrasonographer is skilled15,16.
In LMIC, treatment with radiological reduction is less available and operative intervention is
more common (nearly 90%)12,17. Additionally, if the patient has had symptoms of abdominal
pain for more than 24 hours, the risk of perforation of the intestine on attempted reduction by
air, barium or warm saline enema increases considerably.
Ileo-ileal intussusception of the small intestine is often transient in nature and may reduce
spontaneously without intervention, especially in younger children.

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Chapter 5: Gastrointestinal conditions

5.6 Acute appendicitis

Appendicitis is one of the most common causes of acute abdomen in children worldwide.
Typical age of presentation is 5 to 15 years with less than 5% of patients being under 5 years
old. Intraluminal obstruction of the appendix (by faecal matter, lymph nodes, foreign bodies,
parasites), leads to bacterial overgrowth and infection of the appendix. The classic pain
of appendicitis is due to local peritonitis overlying the inflamed appendix. Perforation is a
common complication if left untreated.
5

5.6.1 Clinical features


Classical presentation includes:
– Peri-umbilical pain initially that migrates to the right iliac fossaa and localises there
– Pain on movement (walking, changing position) or inability to walk
– Signs of peritoneal irritation: rebound tenderness, guarding, pain on jumping/hopping,
coughing
– Anorexia
– Nausea and/or vomiting
– Fever
Inability to walk, lower abdominal pain and nausea are the most frequent symptoms in children
under 12 years old, while the presence of a fever should raise suspicion of perforation18.
In retrocaecal appendicitis, pain may be elicited on extension of the right hip (iliopsoas sign).
Similarly, when the inflamed appendix is located in the pelvis, pain may be elicited on flexion
and internal rotation of the right hip (obturator sign).
Diagnosis is usually clinical, based on classic features.

Investigations
– WBCs may be elevated
– CRP, if available
– Consider POCUS, if equipment and trained staff available: an experienced sonographer or
POCUS practitioner may identify an inflamed enlarged appendix on ultrasound, however
sensitivity is low therefore this may be used to confirm the diagnosis, but not to exclude it.

5.6.2 Management
– Assess and manage ABCDE.
– Ensure initial stabilisation as for acute abdomen (see Section 5.4.2).

a Pain may also localise to the pelvis or suprapubic region, depending on the exact position of the appendix.

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Chapter 5: Gastrointestinal conditions

– Refer for urgent surgical review:


• Appendicectomy is indicated in all cases of early, acute appendicitis within 24 hours
of diagnosis to prevent perforation. Delay of appendicectomy can lead to gangrene or
perforation, increasing the risk of intra-abdominal infection and sepsis, as well as intra-
and post-operative complications and leading to higher mortality19.
• A single prophylactic dose of antibiotics should be administered prior to surgery with
ceftriaxone IV: 80 mg/kg (max. 4 g if < 50 kg; max. 2 g if ≥ 50 kg).
• If there are signs of peritonitis or perforation prior to surgery, administer ceftriaxone, as
above, and metronidazole IV: 10 mg/kg and continue for 3 10 days, depending on severity
and eventual diagnosis. In LMIC settings, a high percentage of patients have already
perforated at first presentation.
– In insecure settings or where referral and/or transport is not possible, antibiotic treatment
for uncomplicated early cases of appendicitis may be considered.
– For cases that present more than 3-4 days after symptom onset who are not clinically
toxic or septic, consider a trial of ceftriaxone and metronidazole (as above) and interval
appendicectomy 6-8 weeks after presentation.

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Chapter 5: Gastrointestinal conditions

5.7 Bowel Obstruction

This is a paediatric surgical emergency. In sub-Saharan Africa, the overall mortality rate of
acute intestinal obstruction has been reported around 15%, with higher rates in neonates
(20-70%)20. Prognosis of acute bowel obstruction is improved by prompt diagnosis and
management, including good peri-operative care.

5.7.1 Clinical features 5


Symptoms:
– Vomiting (bilious): frequent and early vomiting indicates proximal obstruction
– Colicky abdominal pain
– Unable to pass gas or stool
– Abdominal distension: severe distension indicates distal obstruction
Signs:
– Diffusely tender abdomen, though early in the course of the obstruction, tenderness may be
minimal until progressive intestinal ischaemia sets in
– Visible peristalsis
– Bowel sounds high-pitched (early sign) then absent (late, critical sign).
Signs of development of gut ischaemia: peritonitis, septic shock (tachycardia, fever,
hypotension), abdominal guarding.
Common causes include:
– Intussusception (see Section 5.5)
– Malrotation and volvulus
– Incarcerated or strangulated hernia
– Intestinal helminthiasis (ascariasis)
– Abdominal tuberculosis (see Chapter 4, Section 4.11)
– Adhesive disease (post-operative)
– Tumours
Occasionally, foreign bodies (e.g. through pica and bezoar formationa) may cause intestinal
obstruction.

Diagnostic investigations
– Abdominal X-ray (supine and erect, or left lateral decubitus for infants and patients unable
to stand): dilated bowel loops with air-fluid levels may indicate obstruction but can also be
seen with an ileus. Assess for pneumoperitoneum in case of perforation (see Figure 5.4).
– Consider POCUS, if equipment and trained staff available: may show fluid filled (hypoechoic),
dilated (> 2.5 cm) bowel loops with abnormal peristalsis.

a Pica is an eating disorder that causes people to eat items that are not usually considered as food, such as dirt,
clay and paper. This can lead to the formation of a tightly packed mass of partially digested or undigested
foreign material, known as a bezoar.

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Chapter 5: Gastrointestinal conditions

Management
Emergency stabilisation as for acute abdomen in Section 5.4.2 and definitive treatment
depending on underlying cause.
Figure 5.4 - AXR showing pneumoperitoneum secondary to intestinal perforation
5.4a - Upright AP viewb, infantc 5.4b - Left lateral decubitus view, infantd

Free air can be seen Free air can be seen between the liver
under the diaphragm (arrows) and right lateral abdominal wall (arrows)

5.7.2 Causes of acute bowel obstruction


Intussusception
Ssee Section 5.5.

Malrotation and volvulus


Malrotation occurs due to abnormal rotation and/or fixation of the gastrointestinal (GI) tract
during embryonic development. This results in unusually positioned intestines, with the caecum/
colon fixed in the mid-upper abdomen and the entire midgut (from jejunum to mid-transverse
colon) attached to a narrow mesenteric pedicle. Most children with malrotation present in
early infancy with classic signs of bowel obstruction either due to bands of peritoneal tissue
(Ladd’s bands) compressing the duodenum externally, or due to midgut volvulus. In volvulus,
the intestine twists on the narrow vascular pedicle, resulting in midgut vascular compromise.
When sudden volvulus occurs, patients often have disproportionate pain compared to physical
examination findings, and unless corrected, bowel ischemia and necrosis ensue. A small
percentage of children are asymptomatic or diagnosed in later childhood after having chronic
episodic abdominal pain and intermittent vomiting.
Abdominal x-ray may show signs of obstruction (dilated bowel loops, air fluid levels), but is often
non-specific. In volvulus, ultrasound may demonstrate a ‘whirlpool sign’, (where the superior

b If an upright view cannot be obtained (e.g. in neonates or infants), a left lateral decubitus view is needed to
exclude pneumoperitoneum. Pneumoperitoneum cannot be excluded on a supine view.
c Case courtesy of Hidayatullah Hamidi, Radiopaedia.org, rID: 60388, https://radiopaedia.org/cases/60388.
d Image courtesy of Juno Min.

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Chapter 5: Gastrointestinal conditions

mesenteric vein and artery are wrapped around each other21) which is a highly sensitive and
specific indicator of midgut volvulus22, though diagnosis is rarely made on ultrasound. After
stabilisation, urgent surgical intervention is required to de-torse the volvulus and reposition
the caecum/colon and small intestines to prevent recurrence. Time spent in stabilisation or
transport to a surgical centre should be minimised, as ischaemia of the entire midgut can
progress to necrosis within 1-2 hours.

Incarcerated or strangulated hernia


Inguinal hernias occur when part of the bowel herniates through the internal inguinal ring.
They are more common in male, premature infants and occur more often on the right side.
Inguinal hernias appear as a bulge in the inguinal or scrotal area during any activity that
increases abdominal cavity pressure e.g. crying, straining. They are usually easily reducible, 5
allowing bowel contents to be pushed back into the abdominal cavity with minimal effort.
Inguinal hernias may become incarcerated (stuck) and eventually strangulated (reduced blood
supply leading to ischemia) requiring emergency treatment to prevent loss of bowel. Umbilical
hernias are common in children, predominantly affecting Afro-Caribbean and premature
children. The umbilical ring usually closes spontaneously by 4 years old, and strangulation or
incarceration are uncommon.
An incarcerated hernia presents as an irreducible, tender mass which is firm on examination.
It may be accompanied by signs of bowel obstruction (vomiting, abdominal distension)
if left untreated, and is intensely painful if it becomes strangulated. In the early stages of
incarceration, if there are no signs of peritonitis, obstruction or strangulation/necrosis, manual
reduction should be attempted. This may require procedural analgesia/sedation. If manual
reduction is unsuccessful or there are signs of bowel compromise or obstruction, treatment is
emergency inguinal exploration, including verification of bowel viability23.

Ascaridial intestinal obstruction


An estimated 1.5 billion people are infested globally with Ascaris lumbricoides, representing a
quarter of the world’s population24. Annually there are nearly 730,000 cases of Ascaris-related
bowel obstruction, the majority of which occur in children due to smaller luminal diameter25.
Worms may be seen in vomit or stool, and can also be visualised on plain x-ray and ultrasound.
This may be diagnosed by actually seeing worms in vomitus or stool.
The majority of cases can be treated conservatively following emergency management of
obstruction. Normal saline or hypertonic saline enemas can be used to disentangle and expulse
colonic worms if there are no features of peritonitis present. Antihelminth treatment should
be given 24 hours after symptoms have settled:

albendazole PO
12 – 23 months: 200 mg once daily for 3 dayse
≥ 24 months: 400 mg once daily for 3 days
mebendazole PO
≥ 12 months and > 10kg: 100 mg 2 times daily for 3 days

If conservative management is unsuccessful, diagnosis is uncertain or the obstruction complete,


surgical intervention may be necessary.

e Albendazole is not systematically recommended to children less than 12 months, but can be given on a case-
by-case basis according to clinician assessment at the same dose as for children 12 – 23 months.

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Chapter 5: Gastrointestinal conditions

Adhesive small bowel obstruction


Adhesive small bowel obstruction is seen as a complication of previous abdominal surgery. It
is most common within the first year after surgery but can occur at any time after abdominal
surgery. Children present with signs of bowel obstruction and a history of previous abdominal
surgery. Management may be either surgical or conservative, depending on the location and
severity of adhesions, and whether or not any complications have occurred. Stabilisation
includes making the child NBM and placing an NGT on free drainage while providing
maintenance IV fluids. Analgesics and antibiotics are typically not appropriate in the initial
management.

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Chapter 5: Gastrointestinal conditions

5.8 Pyloric stenosis

Infantile hypertrophic pyloric stenosis (IHPS) is a common surgical cause of vomiting in


infants. It occurs in 2 to 3.5 per 100 live births, though overall incidence is lower in African
and Asian populations. It is more common in preterm infants, and boys are affected 4 to
5 times more frequently than girls26. There is a genetic predisposition, with cases occurring
more often if a parent or sibling (especially twin) also had IHPS. It usually presents in the
first 2 to 12 weeks of life, with a peak incidence at 5 weeks of age. Delay in the presentation
will be seen in infants who are premature, with vomiting typically initiating at 42 weeks 5
corrected gestational age.

5.8.1 Clinical features


So-called ‘projectile’ vomiting after feeds is the hallmark of pyloric stenosis. Progressive
hypertrophy of the pyloric muscle leads to obstruction of gastric emptying and increasingly
forceful expulsion of gastric contents immediately after feeding. Vomit is non-bilious. Infants
appear voraciously hungry but fail to gain weight despite feeding well. The hypertrophied
pyloric muscle may be palpable as an ‘olive’ in the abdomen.
If untreated, IHPS leads to dehydration and hypochloraemic, hypokalaemic metabolic
alkalosis.

Investigations
– BGL
– Electrolytes, if available
– Creatinine, if available
– Consider POCUS, if equipment and trained staff available: Ultrasound has a high diagnostic
accuracy for pyloric stenosis but positive results are user dependent and require a high
level of training. A hypertrophic pyloric muscle of > 3 mm and a pyloric canal length of
≥ 15 mm are considered diagnostic27.

5.8.2 Management
– Assess and manage ABCDE.
– Check BGL and correct hypoglycaemia if present (see Chapter 9, Section 9.3).
– Start IV maintenance fluids if no signs of dehydration, with added potassium if evidence of
urine output. Correct any dehydration and/or electrolyte disturbance (see Section 5.3 and
Chapter 15, Section 15.3).
– Place the child NBM and insert NGT (conical tip) to be kept on free drainage.
– Refer for urgent surgical review and definitive treatment once fully rehydrated and electrolyte
disturbance corrected:
• Surgical pyloromyotomy is the gold standard and should be performed as soon as the
child has received adequate fluid resuscitation and abnormalities of electrolytes have
been corrected.

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Chapter 5: Gastrointestinal conditions

– Conservative treatment with atropine IV is an alternative option where surgical management


is not possible28, as follows:
• Starting dose 0.01 to 0.06 mg/kg/day, administered in 6-8 divided doses
• Increase daily dose by 0.01 mg/kg/day (maximum 0.1 mg/kg/day) until vomiting ceases
or adequate volume of milk feeds is tolerated.
• Switch to atropine PO at twice the effective IV dose, and continue for 2-4 weeks.

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Chapter 5: Gastrointestinal conditions

References Chapter 5

1. Diarrhoeal disease: WHO fact sheet. World Health Organisation. Accessed December 1,
2023.
https://www.who.int/news-room/fact-sheets/detail/diarrhoeal-disease
2. Kotloff KL, Nataro JP, Blackwelder WC, et al. Burden and aetiology of diarrhoeal disease in
infants and young children in developing countries (the Global Enteric Multicenter Study,
GEMS): a prospective, case-control study. The Lancet. 2013;382(9888):209-222.
https://doi.org/10.1016/S0140-6736(13)60844-2
3. Weekly epidemiological record/Relevé épidémiologique hebdomadaire 1st February 2013,
88th year/1er février 2013, 88e année. 2013;5(88):49-64.
5
https://www.nitag-resource.org/sites/default/files/989018b9e380f70ab07522155f36c9f8c9515d9a_1.
pdf
4. World Health Organization. Pocket Book of Hospital Care for Children: Guidelines for the
Management of Common Childhood Illnesses. 2nd ed. World Health Organization; 2013.
Accessed November 7, 2023.
https://iris.who.int/handle/10665/81170
5. Guideline: Updates on Paediatric Emergency Triage, Assessment and Treatment: Care of
Critically-Ill Children. World Health Organization; 2016. Accessed December 1, 2023.
http://www.ncbi.nlm.nih.gov/books/NBK350528/
6. Shrime MG, Bickler SW, Alkire BC, Mock C. Global burden of surgical disease: an estimation
from the provider perspective. Lancet Glob Health. 2015;3:S8-S9.
https://doi.org/10.1016/S2214-109X(14)70384-5
7. Meara JG, Leather AJM, Hagander L, et al. Global Surgery 2030: evidence and
solutions for achieving health, welfare, and economic development. The Lancet. 2015;
386(9993):569-624.
https://doi.org/10.1016/S0140-6736(15)60160-X
8. Poenaru D. The burden of pediatric surgical disease in low-resource settings: Discovering it,
measuring it, and addressing it. J Pediatr Surg. 2016;51(2):216-220.
https://doi.org/10.1016/j.jpedsurg.2015.10.065
9. Singh Y, Tissot C, Fraga MV, et al. International evidence-based guidelines on Point of Care
Ultrasound (POCUS) for critically ill neonates and children issued by the POCUS Working
Group of the European Society of Paediatric and Neonatal Intensive Care (ESPNIC). Crit
Care. 2020;24(1):65.
https://doi.org/10.1186/s13054-020-2787-9
10. Green R, Bulloch B, Kabani A, Hancock BJ, Tenenbein M. Early Analgesia for Children With
Acute Abdominal Pain. Pediatrics. 2005;116(4):978-983.
https://doi.org/10.1542/peds.2005-0273
11. Salazar JH, Nghia “Jack” Vo. Intussusception in children. UpToDate. Published July 2022.
https://www.uptodate.com/contents/intussusception-in-children
12. Jiang J, Jiang B, Parashar U, Nguyen T, Bines J, Patel MM. Childhood Intussusception:
A Literature Review. Cameron DW, ed. PLoS ONE. 2013;8(7):e68482.
https://doi.org/10.1371/journal.pone.0068482

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13. Clark AD, Hasso-Agopsowicz M, Kraus MW, et al. Update on the global epidemiology of
intussusception: a systematic review of incidence rates, age distributions and case-fatality
ratios among children aged < 5 years, before the introduction of rotavirus vaccination. Int J
Epidemiol. 2019;48(4):1316-1326.
https://doi.org/10.1093/ije/dyz028
14. Lin-Martore M, Kornblith A, Kohn M, Gottlieb M. Diagnostic Accuracy of Point-of-Care
Ultrasound for Intussusception in Children Presenting to the Emergency Department: A
Systematic Review and Meta-analysis. West J Emerg Med. 2020;21(4).
https://doi.org/10.5811/westjem.2020.4.46241
15. Flaum V, Schneider A, Gomes Ferreira C, et al. Twenty years’ experience for reduction
of ileocolic intussusceptions by saline enema under sonography control. J Pediatr Surg.
2016;51(1):179-182.
https://doi.org/10.1016/j.jpedsurg.2015.09.022
16. Talabi AO, Famurewa OC, Bamigbola KT, Sowande OA, Afolabi BI, Adejuyigbe O. Sonographic
guided hydrostatic saline enema reduction of childhood intussusception: a prospective
study. BMC Emerg Med. 2018;18(1):46.
https://doi.org/10.1186/s12873-018-0196-z
17. Steele AD, Patel M, Cunliffe NA, Bresee JS, Borgstein E, Parashar UD. Workshop on
intussusception in African countries – Meeting report. Vaccine. 2012;30:A185-A189.
https://doi.org/10.1016/j.vaccine.2011.10.004
18. Colvin JM, Bachur R, Kharbanda A. The Presentation of Appendicitis in Preadolescent
Children: Pediatr Emerg Care. 2007;23(12):849-855.
https://doi.org/10.1097/pec.0b013e31815c9d7f
19. Seyi-Olajide JO, Ezidiegwu U, Ameh EA. Burden of Complicated Intra-Abdominal
Infections in Children in Nigeria: Recent Experience and Systematic Review. Surg Infect.
2020;21(6):501-508.
https://doi.org/10.1089/sur.2020.118
20.Adamou H, Magagi IA, Habou O, Adakal O, Ganiou K, Amadou M. Acute Mechanical Intestinal
Obstruction in Children at Zinder National Hospital, Niger: Aetiologies and Prognosis. Afr J
Paediatr Surg AJPS. 2017;14(3):49-52. doi:10.4103/ajps.AJPS_96_16.
Available at: https://pubmed.ncbi.nlm.nih.gov/29557351/
21. Sivitz AB, Lyons R. Mid-Gut Volvulus Identified by Pediatric Emergency Ultrasonography.
J Emerg Med. 2013;45(5):e173-e174.
https://doi.org/10.1016/j.jemermed.2013.05.048
22. Nguyen HN, Kulkarni M, Jose J, et al. Ultrasound for the diagnosis of malrotation and
volvulus in children and adolescents: a systematic review and meta-analysis. Arch Dis Child.
2021;106(12):1171-1178.
https://doi.org/10.1136/archdischild-2020-321082
23. Koizumi M, Sata N, Kaneda Y, et al. Optimal timeline for emergency surgery in patients with
strangulated groin hernias. Hernia. 2014;18(6):845-848.
https://doi.org/10.1007/s10029-014-1219-7
24. Soil-transmitted helminth infections. Accessed December 1, 2023.
https://www.who.int/news-room/fact-sheets/detail/soil-transmitted-helminth-infections

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25. Mishra P, Agrawal A, Joshi M, Sanghvi B, Shah H, Parelkar S. Intestinal obstruction in children
due to Ascariasis: A tertiary health centre experience. Afr J Paediatr Surg. 2008;5(2):65.
doi:10.4103/0189-6725.44178.
Available at: https://journals.lww.com/ajps/fulltext/2008/05020/intestinal_obstruction_
in_children_due_to.2.aspx
26. MacMahon B. The Continuing Enigma of Pyloric Stenosis of Infancy: A Review. Epidemiology.
2006;17(2):195-201.
https://doi.org/10.1097/01.ede.0000192032.83843.c9
27. Vinycomb T, Vanhaltren K, Pacilli M, Ditchfield M, Nataraja RM. Evaluating the validity
of ultrasound in diagnosing hypertrophic pyloric stenosis: a cross‐sectional diagnostic
accuracy study. ANZ J Surg. 2021;91(11):2507-2513. 5
https://doi.org/10.1111/ans.17247
28. Wu SF, Lin HY, Huang FK, et al. Efficacy of Medical Treatment for Infantile Hypertrophic
Pyloric Stenosis: A Meta-analysis. Pediatr Neonatol. 2016;57(6):515-521.
https://doi.org/10.1016/j.pedneo.2016.02.005

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Chapter 6:
Cardiology

6.1 Introduction........................................................................................................... 221


6.2 Cardiac failure........................................................................................................ 222
6.2.1 Clinical signs and assessment........................................................................ 222
6
6.2.2 Investigations................................................................................................. 222
6.2.3 Management................................................................................................. 223
6.2.4 Follow-up....................................................................................................... 224
6.2.5 Treatment of any reversible causes...............................................................224
6.3 Acute rheumatic fever........................................................................................... 225
6.3.1 Diagnosis....................................................................................................... 225
6.3.2 Management................................................................................................. 226
6.3.3 Prevention...................................................................................................... 226
6.4 Infantile beriberi.................................................................................................... 227
References Chapter 6................................................................................................... 228
Chapter 6: Cardiology

6.1 Introduction

The diagnosis and management of cardiac conditions in children in resource-limited settings are
challenging, with lack of access to tools to confirm diagnosis, delayed presentation, and when
specialised paediatric cardiac surgery is required for definitive treatment. Where available and
feasible for the family to access, referral to a paediatric cardiologist is recommended as early
as possible. Consider early involvement of a paediatric cardiologist for consultation, even at
a distance, including remote support for imaging interpretation for diagnosis. For example,
healthcare staff trained in point of care ultrasound (POCUS) can take key images of the heart
and share these by telemedicine or other communication tools with a cardiologist who can
make the diagnosis and provide management guidance1.
In these guidelines, the focus is on guiding diagnosis and supportive management for acute 6
cardiac presentations within the means of lower-resource settings.

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6.2 Cardiac failure

Outside of contexts with access to advanced medical diagnostic capacity, the true incidence
of cardiac failure amongst children is not well documented. However, as many children do not
have access to early diagnosis, presentation is often in the late stages of cardiac failure, with a
significant burden in terms of morbidity and mortality2.
Underlying causes that lead to cardiac failure include cardiac, extra-cardiac or iatrogenic
conditions:
– Cardiac conditions: congenital heart disease (CHD), cardiomyopathies (inherited or
acquired)a, acute rheumatic fever, cardiac arrhythmias.
– Extra-cardiac conditions: sepsis, severe anaemia, thiamine deficiency, severe acute
malnutrition (particularly in young infants).
– Iatrogenic: fluid overload due to large parenteral fluid administration over a short period.

6.2.1 Clinical signs and assessment


Cardiac failure typically presents with fast breathing and respiratory distress, but can have the
following features:
Table 6.1 - Clinical features of cardiac failure in children by age group3

Common symptoms Less common symptoms


Infants and Tachypnoea Cyanosis
young children Respiratory distress Palpitations
(0-2 years) Feeding difficulty Syncope
Sweating Oedema
Pallor Ascites
Wheezing Clubbing
Older children and Fatigue Palpitations
adolescents Effort intolerance Chest pain
Dyspnoea Oedema
Orthopnea Ascites
Abdominal pain Clubbing
Nausea & vomiting

Diagnosis is based on history and clinical examination. Radiological and laboratory investigations
can support diagnosis, identify underlying cause, and/or determine prognosis.

6.2.2 Investigations
– Haemoglobin (Hb): to assess for anaemia
Where readily available and of reliable quality, the following investigations can aid diagnosis,
management and/or prognosis:
– Electrolytes, renal function and liver function tests.

a Abnormality of the ventricular myocardium resulting from overload or congenital heart disease.

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– Chest x-ray: to assess heart size, pulmonary oedema, septal linesb (or Kerley B lines) and
pleural effusions.
– Point-of-Care ultrasound (POCUS): perform 12-zone lung exam to evaluate for signs of
bilateral pulmonary oedema and/or pleural effusions. Perform 5-view cardiac exam to
evaluate for signs of acute volume overload and/or decreased cardiac function4.
– Cardiac ultrasound: to assess cardiac structure, chamber volumes/diameters, wall thickness,
ventricular systolic/diastolic function, and pulmonary pressures.
– Throat swab or streptococcal serology.

6.2.3 Management
– Assess and manage ABCDE (see Chapter 2, Section 2.1).

Supportive management
– Start oxygen therapy (or non-invasive ventilation (NIV) if needed – see Chapter 4, 6
Section 4.1.3) when SpO2 < 90% in children with acyanotic CHD or with cardiomyopathy.
Note that in cyanotic CHD, oxygen may have little effect in raising SpO2, oxygen therapy (if
required) should be guided by target saturations as indicated by the clinician.
– Start IV maintenance fluids if unable to tolerate adequate oral or nasogastric tube (NGT)
fluid intake, restricted to 70% of usual maintenance volume (see Chapter 15, Section 15.2).
Switch to PO/NGT fluids as soon as child can safely tolerate oral intake (see Chapter 15,
Section 15.5).
– Ensure nutritional support and nutrition supplementation.
– Reduction of salt is recommended for children with oedema and fluid retention.

Diuretics
– Fluid retention can be treated with diuretics.
– Give oral furosemide, gradually increasing the dose if necessary. In the case of severe oedema
and/or the child cannot tolerate oral medication, administer furosemide IV:

furosemide PO
• 1 month to 11 years: 1 mg/kg 2 times daily
Increased if necessary up to 2 mg/kg up to 4 times daily if requiredc.
• ≥ 12 years: 20 to 40 mg once daily
furosemide IV
• 1 month to 11 years: 0.5 to 1 mg/kg every 8 hours (max. 40 mg/dose)
Increased if necessary up to 2 mg/kg every 8 hours (max. 40 mg/dose)c.
• ≥ 12 years: 20 to 40 mg every 8 hours as required.

– If symptomatic despite maximum furosemide, consider adding oral spironolactone:

spironolactone PO
0.5 to 1.5 mg/kg up to 2 times daily

b Horizontal lines reaching out from peripheral edge of lung, seen in the costophrenic angle, representing
thickened interlobular septa that result from chronic congestive cardiac failure.
c For high doses of > 3 mg/kg/day, ensure potassium monitoring, if available. If potassium monitoring is not
possible, consider providing routine oral potassium supplementation (2 mmol/kg/day).

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Chapter 6: Cardiology

Angiotensin converting enzyme (ACE) inhibitor


– Recommended if ventricular systolic dysfunction confirmed by cardiac ultrasound.
– Give enalapril, starting at low doses and subsequently titrating to the target dose. Carefully
monitor blood pressure, renal function and serum potassium.

enalapril PO

Weight Initial dose Dose increase as tolerated

< 5 kg 1.25 mg once daily No increase

5 to < 10 kg 1.25 mg 2 times daily for 1 week 2.5 mg 2 times daily

10 to < 20 kg 2.5 mg 2 times daily for 1 week 5 mg 2 times daily

10 mg 2 times daily (maximum


≥ 20 kg 2.5 mg 2 times daily for 1 week
up to 20 mg 2 times daily)

Note: there is an increased risk of hyperkalaemia when introducing enalapril treatment -


discontinue or reduce dose of spironolactone and oral potassium if prescribed.

6.2.4 Follow-up
– Discharge of the child can be considered once the child is stable on oral treatment, not
requiring supplemental oxygen and able to eat and drink.
– For children discharged on cardiac medication, arrange follow-up within 3 to 6 months.
Where available, arrange follow-up with a cardiology specialist.
– Most children will require lifelong medical management of cardiac failure if corrective
surgery or cardiac transplantation is not feasible or available.
– Regular follow-up is required to assess the need for increasing or adjusting dosage of
medication as the cardiac condition progresses.
– Inform parents/carers to bring child back to hospital if there are signs of increased respiratory
distress, cyanosis, and/or oedema.

6.2.5 Treatment of any reversible causes


– Treat any underlying systemic causes, e.g. sepsis (see Chapter 3, Section 3.2), electrolytic
imbalance (particularly hypocalcemia) (Chapter 15, Section 15.3).
– Treatment of acute rheumatic fever (see Section 6.3)
– Consider thiamine deficiency in breastfed infants or children with severe acute malnutrition
(see Section 6.4)5.
Corrective treatment of CHDs is rarely available in resource-limited settings but should be
explored if possible. Without corrective surgery, many of these cases have a poor prognosis
and medical management is indicated with a focus on symptom management and palliative
care (see Chapter 15, Section 15.6).

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Chapter 6: Cardiology

6.3 Acute rheumatic fever

Acute rheumatic fever (ARF) is an acute inflammatory disorder caused by a reaction to


infectiona with group A streptococcal bacteria (GAS), resulting in inflammation of the heart,
joints, skin and/or brain. Clinical symptoms and signs usually develop 2 to 3 weeks following
GAS infection and can range from very mild to severe. Inflammation of the heart can cause
long-term damage, resulting in rheumatic heart disease (RHD).
ARF most commonly affects children aged 5 to 20 years and in low-and middle-income
countries6. Most deaths attributable to RHD usually result from the complications of RHD,
including infective endocarditis, arrhythmias, heart failure and stroke. Where regular access to
diagnosis and antibiotics for secondary prophylaxis is limited, this is more pronounced.
6
6.3.1 Diagnosis
ARF is a clinical diagnosis based on the identification of specific major and minor features of
the illness, known as the Jones criteria (see Table 6.2). A positive throat culture or serology
confirming group A streptococcal infection is helpful if available (elevated anti-streptolysin O
or other streptococcal antibody).
Table 6.2 - Jones criteria for diagnosis of acute rheumatic fever
Major manifestations Minor manifestations
• Carditisb • Fever ≥ 38 °C
• Polyarthritis • Monoarthralgia
• Aseptic monoarthritis or polyarthralgia • ESRe ≥ 30 mm/h or CRP ≥ 30 mg/L
• Sydenham choreac • Prolonged PR interval on ECG
• Erythema marginatumd
• Subcutaneous nodules
Definite initial episode of ARF:
2 major manifestations + evidence of GAS infection, or
1 major + 2 minor manifestations + evidence of GAS infection
Probable or possible ARF: likely diagnosis as above, but lacking either:
• One major or one minor manifestation
• No evidence of preceding GAS infection
Recurrent episode of ARF
As above, or
3 minor manifestations + evidence of GAS infection

a Mostly upper respiratory and skin infections due to GAS.


b Cardiac inflammation causing tachycardia, dyspnoea, and fatigue.
c A rheumatic chorea characterized by involuntary, random, irregular movements of the face, tongue, limbs,
with hypotonia. This chorea alone can be diagnostic if other causes of chorea have been excluded.
d Annular erythema occurring on trunk and proximal extremities.
e Erythrocyte Sedimentation Rate

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Chapter 6: Cardiology

6.3.2 Management
– If heart failure is present, follow management in Section 6.2.
– Eradicate GAS infection with antibiotics:

benzathine benzylpenicillin IM once (single dose)


• < 30 kg: 600 000 IU
• ≥ 30 kg: 1.2 MIU
Alternative:
phenoxymethylpenicillin (penicillin V) PO 2 times daily for 10 days
• < 30 kg: 250 mg
• ≥ 30 kg: 500 mg
(or erythromycin if penicillin allergy)

– Treat associated arthritis with NSAIDf for at least 2 to 3 weeks and then decrease the dose
progressively over 2 weeks.

aspirin PO
50 to 100 mg/kg once daily
If unable to take aspirin or cardiac signs persist, replace with a steroid:
prednisolone PO
1 to 2 mg/kg once daily

6.3.3 Prevention
– Children who have had ARF have a high risk of another episode of ARF, and with each
recurrence severity of RHD is increased causing further valvular damage.
– In children with recurrent episodes of ARF, long-term antibiotic prophylaxis with a monthly
injection of benzathine benzylpenicillin or oral penicillin 2 times daily (doses above) is
recommended up to 5 or 10 years where it is feasible (refer to national protocol where
available).

f Aspirin is recommended for use in children only in the setting of anti-platelet action and for the treatment of
arthritis associated with acute rheumatic fever. It is not recommended in children for fever or pain.

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6.4 Infantile beriberi

Acute heart failure in breastfed infants caused by maternal thiamine deficiency.

Pernicious or acute cardiac form (Classic Beriberi)7,8


– Symptoms present usually between 1 to 3 months of age in breastfed infants.
– May start with non-specific symptoms: refusal to feed, vomiting, constipation, colic, ‘piercing
cry’9.
– Progressing to oedema, cyanosis, and acute congestive cardiac failure.
– Shoshin beriberi, a fulminant form of congestive heart failure without oedema may occur in
infants with lactic acidosis10.
– Rapid deterioration to death may occur within 2 to 4 hours without treatment. 6

Aphonic form
– Less severe and usually presents later between 4 to 7 months of age.
– Starts with cough and dyspnoea. The crying becomes hoarse until there is a loss of voice.
– Untreated cases advance into acute congestive cardiac failure and respiratory distress, and
eventually death within days.

Management
– Treat promptly with injectable thiamine which can rapidly reverse clinical signs5:

thiamine IV/PO
• Loading dose < 15 years: 100 mg slow IV infusion over 30 minutes once daily for
48 hours
If IV not possible: Give PO/via NGT at the same dose.
• Maintenance dose to be started after 48 hours of IV treatment:
▹ ≤ 12 years: 25 mg PO once daily for 1 month
▹ > 12 years: 25 mg PO 2 times daily for 1 month

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Chapter 6: Cardiology

References Chapter 6

1. Muhame RM, Dragulescu A, Nadimpalli A, et al. Cardiac point of care ultrasound in resource
limited settings to manage children with congenital and acquired heart disease. Cardiol
Young. 2021;31(10):1651-1657.
https://doi.org/10.1017/S1047951121000834
2. Ahmed H, VanderPluym C. Medical management of pediatric heart failure. Cardiovasc
Diagn Ther. 2021;11(1):323-335.
https://doi.org/10.21037/cdt-20-358
3. Kantor PF, Lougheed J, Dancea A, et al. Presentation, Diagnosis, and Medical Management
of Heart Failure in Children: Canadian Cardiovascular Society Guidelines. Can J Cardiol.
2013;29(12):1535-1552.
https://doi.org/10.1016/j.cjca.2013.08.008
4. Russell FM, Ehrman RR, Cosby K, et al. Diagnosing Acute Heart Failure in Patients With
Undifferentiated Dyspnea: A Lung and Cardiac Ultrasound (LuCUS) Protocol. Stahmer SA,
ed. Acad Emerg Med. 2015;22(2):182-191.
https://doi.org/10.1111/acem.12570
5. Dinicolantonio JJ, Lavie CJ, Niazi AK, O’Keefe JH, Hu T. Effects of thiamine on cardiac function
in patients with systolic heart failure: systematic review and metaanalysis of randomized,
double-blind, placebo-controlled trials. Ochsner J. 2013;13(4):495-499.
Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3865826/
6. Ralph AP, Noonan S, Wade V, Currie BJ. The 2020 Australian guideline for prevention,
diagnosis and management of acute rheumatic fever and rheumatic heart disease. Med J
Aust. 2021;214(5):220-227.
https://doi.org/10.5694/mja2.50851
7. Hiffler L, Rakotoambinina B, Lafferty N, Martinez Garcia D. Thiamine Deficiency in Tropical
Pediatrics: New Insights into a Neglected but Vital Metabolic Challenge. Front Nutr. 2016;3.
https://doi.org/10.3389/fnut.2016.00016
8. Thiamine deficiency and its prevention and control in major emergencies. Published online
1999.
https://www.who.int/publications/i/item/WHO-NHD-99.13
9. Duggan C, Watkins JB, Walker WA, eds. Nutrition in Pediatrics: Basic Science, Clinical
Application. 4th ed. BC Decker; 2008.
https://openlibrary.org/books/OL11988152M/Nutrition_in_Pediatrics
10. Shah S, Wald E. Type B Lactic Acidosis Secondary to Thiamine Deficiency in a Child With
Malignancy. Pediatrics. 2015;135(1):e221-e224.
https://doi.org/10.1542/peds.2014-2289

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Chapter 7:
Neurological disorders

7.1 Neurological assessment....................................................................................... 231


7.2 Acute symptomatic seizures.................................................................................. 233
7.2.1 Terminology................................................................................................... 233
7.2.2 Clinical features............................................................................................. 233
7.2.3 Management................................................................................................. 234
7.2.4 Management if acute seizures resume..........................................................238 7
7.2.5 Management of post-ictal state..................................................................... 238
7.2.6 Follow-up....................................................................................................... 238
7.3 Febrile seizures...................................................................................................... 240
7.3.1 Diagnosis....................................................................................................... 240
7.3.2 Management................................................................................................. 240
7.4 Epilepsy.................................................................................................................. 241
7.4.1 Assessment and diagnosis............................................................................. 241
7.4.2 Classification of seizures................................................................................ 241
7.4.3 Management................................................................................................. 242
7.4.4 Follow-up and monitoring.............................................................................. 244
7.5 Altered level of consciousness.............................................................................. 245
7.5.1 Clinical features and assessment...................................................................245
7.5.2 Management................................................................................................. 246
References Chapter 7................................................................................................... 250
Chapter 7: Neurological disorders

7.1 Neurological assessment

For a child presenting with a possible neurological impairment or deficit, perform a more
detailed neurological examination in addition to a full clinical examination (Chapter 1,
Section 1.3).
In the case of reduced level of consciousness, seizures, any neck stiffness (nuchal rigidity),
manage as a medical emergency and refer to Chapter 2 for initial resuscitation and
management.
In young children, cooperation for a neurological examination can be challenging. In a well
child, start by observing the child play and interact with their parents/carers.
– Assess development for age: speech, behaviour, gross motor (crawling, walking), fine motor
(playing with small objects). See Appendix 1 for more detail on developmental milestones.
– If the child can walk, ask to walk around, walk heel-to-toe, stand on one leg. Note any
abnormalities.
– Observe for any abnormal movements, fasciculations, obvious weakness or asymmetry of 7
movement.
– Examine pupils and eye movements.
Carry out a complete neurological examination, by assessing tone, power and reflexes. Consider
examination of cranial nerves if relevant.

Tone
– Tone is the inherent resistance of the muscle to passive movement and is involuntary. Usually
a person’s limb can be freely moved around by an examiner, with only slight resistance.
– Muscles with low tone show no resistance to passive movement and are usually described
as hypotonic or flaccid, while muscles with increased tone show high resistance to passive
movement and are described as hypertonic or spastic.
– Infants1: In infants muscle tone and strength are assessed together. Assess position of the
infant when supine, usually arms and legs are flexed when at rest and move spontaneously.
Pull gently by the arms to a sitting position and check for head lag, usually the head will lag
initially and then come into the midline once in a seated position. Hold the infant under
the arms, the infant with normal muscle tone and strength will flex their hips to 90 degrees
(as though in a seated position). Normal truncal and shoulder girdle tone and strength will
prevent the infant from slipping through the examiner’s hands.
– Children: Assess tone by passively flexing and extending a patient’s limb and assessing the
resistance or opposed muscle contraction. Usually, resistance to extension of limbs is felt
beyond 90 degrees.

Power
– Power is the strength of the muscle when maximally contracted and is voluntary.
– Assess power by asking the patient to move their limb against resistance, starting with
gravity then an active external resistance, e.g. opposition by the examiner2. Assessing power
in young infants is difficult and often assessed along with tone (see above).

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– Power is graded as a score out of 5:


• 0/5 – no muscle movement
• 1/5 – Flicker of movement in muscle
• 2/5 – Horizontal movement (without gravity)
• 3/5 – Movement against gravity
• 4/5 – Movement against some external pressure
• 5/5 – Movement against strong external pressure (normal)

Reflexes
– Tendon reflexes are used to identify possible upper or lower motor neuron lesions.
– Assess tendon reflexes by tapping lightly on the tendon with a tendon hammer, with the
limb relaxed and the joint at a 90 degree angle.
– Common tendon reflexes that can be tested in children include the patellar reflex (knee) and
the achilles reflex (ankle). Biceps, triceps, brachioradialis (wrist) and jaw reflexes can also be
tested.
– Tendon reflexes are described as normal, absent/diminished or exaggerated/brisk.
– Primitive or developmental reflexes, e.g. Moro reflex and asymmetric tonic neck reflex, should
be assessed in young infants. These are indicators of brain maturation and abnormalities
may indicate specific conditions such as cerebral palsy2.

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7.2 Acute symptomatic seizures

In children, a seizure may occur due to epilepsy, but more commonly it is provoked or triggered
by acute conditions, such as infections (severe malaria, meningitis), metabolic disorders
(hypoglycaemia, hyponatraemia), head injury, poisoning, intracranial tumours or other space-
occupying lesions, bleeding, or stroke. For seizures associated with a fever > 38 °C in young
children, see Febrile seizures in Section 7.3.

7.2.1 Terminology
Seizure: a paroxysmal disorder presenting as intermittent, repetitive involuntary movements
of part of or the entire body, usually accompanied with loss of consciousness or awareness.
Seizures result from a temporary disturbance in brain function “due to abnormal excessive or
synchronous neuronal activity in the brain”3.
Epilepsy: at least 2 unprovoked (or reflex) seizures occurring > 24 hours apart4. Unprovoked
7
means a seizure that occurs without an acute or reversible cause.
Status epilepticus (SE): a condition in which a seizure lasts for more than 5 minutes without
self-termination, therefore requiring treatment with anti-epileptic drugs (AEDs)5. If seizures
persist beyond 30 minutes despite the use of two AEDs, patients are considered to have
refractory SE which can have long-term consequences including neuronal death, neuronal
injury, and alteration of neuronal networks6. Non-convulsive status epilepticus is when altered
conscious level is the main manifestation of a prolonged seizure without visible convulsions
(not the same as post-ictal state).
Post-ictal state: altered consciousness, drowsiness, confusion, nausea, hypertension,
hemiparesis, headache, or other disorienting symptoms immediately after a seizure. This may
last for 5 to 30 minutes. Usually the child does not remember the seizure episode.
The use of anticonvulsants, e.g. phenobarbital, during the seizure may leave the child sedated
for longer after the seizure.
Acute repetitive seizures: 3 or more seizures in 24 hours.

7.2.2 Clinical features


Symptoms and signs
– Vary according to the type of seizure (see Section 7.4.2).
– Common features include:
• Eye deviation, staring or rapid eye blinking.
• Lip smacking or biting down (clonic)
• Loss of tone (atonic)
• Stiff extended limbs (tonic)
• Rhythmic jerking of limbs or nodding of head (tonic-clonic)

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• Loss of consciousness or impaired awareness


• Appearing confused or notion of absence
• Respiratory distress or apnoeic spells
• Loss of bladder or bowel control
• Epigastric sensation, sweating
• Vocalisation, arrest of speech
– Some children may experience an aura or a ‘warning’ sign just before a seizure is about to
happen. These can be feelings (e.g. fear, impending doom, déjà vu) or changes in vision/
flashing lights, hearing or sense of smell, or hallucinations.
– Older children over 6 years usually have similar seizures to adults, while infants and young
children are more likely to have focal seizures with impairment of awareness.
– Often seizures are short and the child may present in a post-ictal state, with a clear history
of a seizure event from the parents/carers.

Investigations
– Malaria RDT
– Blood glucose level (BGL)
– Full blood count (FBC) including haemoglobin (Hb)
– Electrolytes, if available
– Blood culture if febrile and/or suspicion of sepsis
– Lumbar puncture (LP), if suspicion of meningitis: perform only when child is stable and no
longer having seizures (see Appendix 6 for details on how to perform an LP).

7.2.3 Management
Aim to quickly and simultaneously provide care that stabilises the patient, identify any
precipitating conditions, stop any ongoing seizure, and/or manage the post-ictal state.
Most seizures are self-limiting and last a few seconds or minutes, but anticonvulsant treatment
is required for ongoing seizures when:
– Seizure lasts ≥ 5 minutes (or ongoing and duration unknown).
– 2 or more seizures within 5 minutes.

If no current ongoing seizure


– Take a full history from child and/or parents/carers.
Ask about:
• Onset: time, duration, signs/clinical features.
• What the child was doing at the time of onset and what happened afterwards.
• Warning symptoms. Dizziness or visual warnings are rare in epileptic seizures.
• Loss of consciousness.
• Recent or current illness, injury or behavioural changes.
• Previous episodes and past medical history, including birth history.
• Medication taken or given, consider illicit drugs or alcohol in adolescents.
– Perform a clinical examination including cardiac and neurological examination.
– Perform investigations if not already done: malaria RDT, BGL and blood culture if febrile and/
or suspicion of sepsis.

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Chapter 7: Neurological disorders

If ongoing seizure
See also Figure 7.1 page 239.

During first 5 minutes of a seizure


Evaluate ABCDE and call for help.
Start a timer (or check time on watch/clock).
A. Open airway and clear secretions. Do not open the mouth by force if seizure is tonic-clonic.
B. Start oxygen therapy and monitor oxygen saturations (aim > 94%). Use bag and mask
ventilation if required.
C. Establish IV access and assess/treat for shock.
D. Check BGL: if < 60 mg/dL (< 3.3 mmol/L) administer 2 mL/kg glucose (dextrose) 10% IV.
Check malaria RDT and initiate anti-malarials and appropriate antibiotics if indicated.
E. Check for rashes, bruises, signs of sepsis or trauma. Prevent and manage hypothermia;
treatment of fever is not a priority.
Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
If seizures stop at any point, manage as for post-ictal state (see Section 7.2.5). 7
Seizure ongoing at 5 minutes
Administer first line anticonvulsant treatment with a benzodiazepine (ensure bag-mask
available):
– No IV/IO access: midazolam 0.3 mg/kg (buccal) or 0.15 mg/kg (IM), max. 10 mg/dose (see
MSF Manual of Nursing Care Procedures, SOP Buccal Midazolam Administration,) or rectal
(PR) diazepam 0.5 mg/kg (< 12 years: max. 10 mg/dose; ≥ 12 years: max. 20 mg/dose).
– IV/IO access: diazepam IV 0.3 mg/kg (max. 10 mg/dose).

Seizure ongoing at 10 minutes


Repeat same dose of diazepam or midazolam (same max. doses as above).

Seizure ongoing at 15 minutes


Administer second line anticonvulsantsa.
– Children < 2 years, girls > 12 years, or suspicion of liver disease:

levetiracetam 40 mg/kg (max. 3 g) slow IV infusion over 10 minutes.


If seizure persists at the end of the infusion, repeat with half dose:
levetiracetam 20 mg/kg (max. 1.5 g) over 10 minutes (max. total levetiracetam 60 mg/kg
or 4.5 g)

Alternative:
phenobarbital 20 mg/kg (max. 1 g) slow IV infusion via syringe pump over 20 minutes
If seizure persists at the end of the infusion, repeat with half dose:
phenobarbital 10 mg/kg over 20 minutes

a Programmatic considerations include cost (levetiracetam is more expensive than phenobarbital), safe
administration of phenobarbital, availability of drug, validation by MoH, and comparative ease of administration.

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Chapter 7: Neurological disorders

– Children ≥ 2 years (except girls > 12 years)b:

sodium valproate IV
20 mg/kg (max. 1.5 g) over 5 minutes.
If seizure persists at the end of the injection, repeat once at the same dose (max. total
sodium valproate 40 mg/kg or 3 g)7.

Seizure ongoing 5 minutes after end of infusion


Administer alternative anticonvulsant:
– Children < 2 years, girls > 12 years of age, or suspicion of liver disease:
• If levetiracetam was administered, administer phenobarbital IV: 20 mg/kg
• If phenobarbital was administered, administer levetiracetam IV: 40 mg/kg
– Children ≥ 2 years:
• If sodium valproate was administered, administer levetiracetam 40 mg/kg or phenobarbital
IV: 20 mg/kg
– If other anticonvulsants are not available administer phenytoin IV: 20 mg/kg over 20 to
30 minutes, where cardiac monitoring is feasible. Phenytoin can cause hypotension and
cardiac arrhythmias. Do not exceed an infusion rate of 1 mg/kg/minute and monitor and
record HR, BP and RR every 15 minutes during and after administration using an early
warning system (see MSF Manual of Nursing Care Procedures, Assessment and vital signs,
Charts: Vital sign charts).
For children with known or suspected epilepsy, refer to Section 7.4.

Caution: anticonvulsants can cause respiratory depression and apnoea. Admit immediately to
an emergency or intensive care unit for close monitoring. Basic resuscitation equipment must
be kept at the bedside including bag and mask, oxygen and suction.

Maintenance treatment when acute seizures terminate


Short-term maintenance treatment is beneficial for the following indications and respective
duration. Use the anticonvulsant that terminated the seizure.
Indications
– Use of a non-benzodiazepine anticonvulsant for a patient who does not have an acute
reversible condition (e.g. electrolyte disturbance or severe malaria with seizuresc): continue
with maintenance therapy for 48 to 72 hours if seizures under control and then reassess.
– Acute repetitive seizures (3 or more seizures in 24h): continue with maintenance therapy for
48 to 72 hours if seizures under control and then reassess.
– Persistent focal neurological signs and/or impaired level of consciousness past the expected
post-ictal period: duration of maintenance treatment will depend on evolution and medical
condition.
– Known or suspected epilepsy: continue long term (see Section 7.4).
– Known or suspected head injury if within 24 hours of injury: continue for 7 days.

b Sodium valproate is contraindicated in girls and women of child-bearing age due to increased risk of neural
tube defects and other congenital malformations. Sodium valproate is not recommended in children less than
2 years old due to an increased risk of fatal hepatotoxicity.
c Note that if the patient has an acute reversible condition but meets one of the other indications, they should
be started on maintenance treatment as recommended for that indication.

236
Table 7.1 - Maintenance treatment dosage after acute seizure
Maintenance dose
Drug Side effectsd Comments
(PO whenever possible)
1-11 months: 5 to 6 mg/kg once daily Respiratory depression Decrease dosage by 50% if severe
1-5 years: 6 to 8 mg/kg once daily Apnoea acute kidney injury
6-12 years: 4 to 6 mg/kg once daily Hypotension
phenobarbital > 12 years: 1 to 3 mg/kg once daily Lethargy
PO/IV Start 12 hours after the loading dose Hepatic dysfunction
If age unknown, start at 5 mg/kg once daily (or
divided into 2 times daily) for children estimated
< 12 years
2.5 mg/kg 2 times daily Hypotension Contraindication: cardiopathy
Start 12 hours after the loading dose Bradycardia, arrhythmia Consider only if none of the other
Hepatitis recommended medicines are available,
phenytoin
Hyperglycaemia due to its poor safety profile and the
PO/IV
Anaemia need for cardiac monitoring
Hypersensitivity reactions,
including skin rash
< 6 months: 7 mg/kg 2 times daily Irritability Decrease dosage by 50% if severe
levetiracetam 6 months-15 years: 10 mg/kg 2 times daily Nausea & vomiting acute kidney injury
PO/IV
Start 12 hours after the loading dose
PO: 5 to 7.5 mg/kg 2 times daily (max. 600 mg/dose) Hepatotoxicity Contraindication: liver disease (or
IV: 2.5 to 4 mg/kg every 6 hours (hyperammonaemia, mild suspected metabolic disease), children
sodium valproate
Start 6-8 hours after the loading dose elevation of liver enzymes) < 2 years, girls of child-bearing agee
Teratogenic

d Several anticonvulsant medications (namely carbamazepine, phenobarbital, phenytoin and levetiracetam) can cause a rare but serious syndrome known as DRESS (drug
reaction with eosinophilia and systemic symptoms). It is important to be aware of this reaction which appears several weeks after the initiation of treatment and can be fatal.
e Sodium valproate is contraindicated in girls and women of child-bearing age due to increased risk of neural tube defects and other congenital malformations. Sodium valproate

237
Chapter 7: Neurological disorders

is not recommended in children less than 2 years old due to an increased risk of fatal hepatotoxicity.
7
Chapter 7: Neurological disorders

7.2.4 Management if acute seizures resume


Adjust treatment as follows if these scenarios occur:
– Seizure recurs > 6 hours after first seizure resolved: restart management from first step in
treatment algorithm. Ensure to record the administered dose of each anticonvulsant so as
not to exceed their respective maximum dosage in a 24-hour period.
– Seizure recurs < 6 hours after last seizure: continue to next step in treatment algorithm (no
need to restart treatment from top of algorithm).
– Recovery from seizure is not clear (child remains in coma and/or unclear if status resolved),
continue to next step in treatment algorithm (no need to restart).
– Maintenance treatment not given but treatment algorithm had to re-start more than 3 times
in 48 hours due to recurrence of acute seizures, treat as unresolved focal neurological insult
and start maintenance treatment.
– Maintenance treatment started but only partially effective (seizures resume before next
maintenance dose is due; number of intermittent seizures has decreased but the seizures
do not stop), seek expert advice where possible.

7.2.5 Management of post-ictal state


– Ensure airways patent and monitor oxygen saturations.
– Administer oxygen, aiming for SpO2 > 92%.
– Check BGL and treat if hypoglycaemia.
– Repeat neurological examination (any asymmetry or focal signs). If post-ictal state continues
for more than 30 to 60 mins, full re-evaluation including pupils, considering non-convulsive
status as a possibility.
– Start treatment of underlying cause.
– Treat fever if present.
– Monitor vital signs and observe for further seizures.

Monitoring
– Place child in recovery position and ensure airways patent.
– Monitor and record vital signs (including conscious level and SpO2) every 15 minutes initially
then as often as required using an early warning system (see MSF Manual of Nursing Care
Procedures, Assessment and vital signs, Charts: Vital sign charts). Careful attention should
be given to respiratory monitoring, especially if anticonvulsants were administered.
– Cardiac monitoring (HR, rhythm, BP) every 15 minutes if phenytoin administered.

7.2.6 Follow-up
– Short seizures that respond to treatment usually do not result in any complications and
do not need follow-up. Prolonged seizures (> 1 hour) can be fatal or result in long-term
neurologic sequelae (e.g. cerebral palsy).
– Long-term anticonvulsant treatment may not always be necessary in a first unprovoked
seizure in a child8, but inform parents/carers to monitor carefully for further seizure events
and seek medical care if they occur.
– Arrange follow-up for further management if the child:
• Requires prolonged maintenance therapy (> 72 hours for some indications and > 7 days for
those with neurological injury)
• Continues to have recurrent unprovoked seizures
• Has a suspected severe acute neurological insult.

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Chapter 7: Neurological disorders

Figure 7.1 - Acute seizure treatment algorithm

239
Chapter 7: Neurological disorders

7.3 Febrile seizures

Seizure associated with a fever > 38 °C usually in children 6 months to 5 years9. The fever is
usually caused by a concurrent illness (commonly a viral infection) or recent vaccination, but
the seizure itself is not directly linked to the trigger of the fever.
Febrile seizures are common, occurring in 2 to 4% of children under 5, but usually self-limiting
with no long-term neurologic consequences. There may be a family history. Seizures may occur
before, during or after a high fever and controlling the fever has no effect on preventing a
febrile seizure occurring. Most are simple, do not last longer than 15 minutes, are generalised
and will occur only once in 24 hours. Complex febrile seizures may occur where the child can
have focal signs, prolonged seizures (> 15 minutes), or have multiple seizures within a 24-hour
period.

7.3.1 Diagnosis
– Take a full history from parents/carers about the seizure (onset, duration, signs, awareness)
and of any recent or current illness (or signs and symptoms) including presence of fever.
– Ask about any previous febrile seizures and any other medical history.
– Take a medication history including antipyretics given (dose and timing).
– Once seizure stopped, perform a complete clinical examination to identify cause of fever.

Investigations
– FBC, Hb, BGL
– Malaria RDT, if endemic
– Consider LP if child < 1 year, has meningeal signs or appears severely unwell.

7.3.2 Management
Most febrile seizures will stop spontaneously within 5 minutes.
– Manage ABCDE and administer oxygen via face mask. Place child in recovery position.
– If not breathing, start resuscitation (see Chapter 2, Section 2.1).
– Check BGL: if < 60 mg/dL (< 3.3 mmol/L) administer 2 mL/kg glucose (dextrose) 10% IV.
– Administer anticonvulsant treatment as per seizure algorithm in Figure 7.1 page 239 if:
• Seizure lasts ≥ 5 minutes (or ongoing and duration unknown).
• 2 or more seizures within 5 minutes.
– If seizures stop, treat as per post-ictal state (see Section 7.2.5).
– Treat fever and start treatment of the source of the fever.
– If no anticonvulsant treatment was needed, observe for at least 6 hours. Child can be
discharged home with paracetamol, treatment of source of fever if applicable, and
information on fever management.
– Prophylactic long-term anticonvulsants are not indicated in simple febrile seizures, even if
they are recurrent.
In the case of complex febrile seizures, provide counselling to the parents/carers to monitor
further episodes as they require evaluation for epilepsy if there is recurrence10.

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Chapter 7: Neurological disorders

7.4 Epilepsy

Chronic neurological disorder characterised by recurrent seizures that occur without an


acute or reversible cause (unprovoked). Epilepsy is diagnosed after two or more seizures that
occurred with no link to any acute medical condition. Long-term anticonvulsant treatment is
necessary to manage further recurrences of seizures. Most (70% to 80%) of cases of epilepsy
are idiopathic in nature (cause is unknown but presumed to be genetic). Cerebral damage due
to congenital infections (e.g. rubella), or previous infections (e.g. meningitis), and cerebral
tumours are additional causes.
Approximately 50 million people are living with epilepsy worldwide. Almost 80% of them are
in low- and middle-income countries. People with epilepsy have an overall risk of premature
death that is 3 times higher than the general population11.

7.4.1 Assessment and diagnosis


– Conduct a detailed history and clinical examination (refer to Chapter 1). 7
– Refer to Section 7.2.3 to ask specific questions on the seizure event.
– Assess developmental milestones for age and conditions co-existing with epilepsy, e.g.
cerebral palsy.
– Include cardiac and neurological examination, including fundi to look for signs of raised
intracranial pressure.
– Examine for potential underlying causes of provoked seizures (e.g. acute illness/infection,
head trauma, hypoglycaemia).
– Exclude other disorders such as syncope (sudden and brief loss of consciousness associated with
loss of postural tone and spontaneous recovery), breath-holding spells and psychogenic seizures.

7.4.2 Classification of seizures


Classification of a seizure type is useful to describe seizures in a patient with epilepsy with a common
terminology and to choose the optimal treatment for that type of seizure. The type of seizure is
classified by their origin in the brain (onset). The person’s awareness during the seizure and the
presence and type of muscle movement (motor activity) can help identify the onset (Table 7.2).
Table 7.2 - Clinical assessment of seizure onset
Generalised onset Focal onset
Characteristic
(throughout the brain) (localised to part of the brain)
Awareness Impaired Normal or impaired
Motor activity • Tonic-clonic: jerking • Specific motor activity in some
(muscle movements of all limbs muscles – tonic, myoclonic, atonic.
movement) • Myoclonic: brief jerks in some Typical features include: turning
muscles of the eyes, head and/or trunk;
• Atonic: loss of muscle tone vocalisation or arrest of speech
• Absence: brief impaired • Non-motor activity – sensory,
awareness without muscle emotional, behavioural changes
movement (except some • Can become bilateral tonic-clonic
eyelid flickering)

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Chapter 7: Neurological disorders

Investigations
– FBC, Hb, BGL
– Electrolytes, if available
– Malaria RDT, if endemic
– Cranial US
– Electroencephalogram (EEG), if available but not routinely needed. A normal EEG does not
rule out epilepsy but an EEG can support the classification of seizure type outlined in Table 7.2.
– Electrocardiogram (ECG), if available, for older children.

7.4.3 Management
Treatment is long-term or life-long with the goal to minimise seizure occurrence and maintain
quality of life. Support and counselling for the child and their family is required for effective
management, as strict adherence to antiepileptic drugs (AEDs) is the best way to minimise
seizure occurrence. Most seizures occur randomly and are unprovoked, but in some cases
there is a specific trigger to seizures e.g. flashing lights or loud noises. In these rare cases,
identification and avoidance of the trigger can help to control seizure occurrence. Lack of
sleep, acute illness and use of mind-altering substances can lower the seizure threshold in
children with epilepsy.
Guiding principles to starting antiepileptic drug (AED) treatment (see Table 7.3):
– Establish the diagnosis and type or classification of seizure.
– Start initially with the preferred AED according to the seizure type and age of the child (see
Table 7.3).
– If seizures continue despite an optimal dose of first-line AED, consider changing to second
choice AED.
– Combination therapy should be considered when treatment with 2 different AEDs used
separately (in monotherapy) has failed.
– If the AED needs to be changed, introduce the new AED at its starting dose and slowly
increase to its mid-range, then start to slowly decrease the dose of the first AED.
– If a patient is seizure-free for 2 years, consider stopping the AED slowly (over 3 months) with
close supervision. If seizures recur at home, ask the patient to resume the AED at the last
dose taken and seek medical attention.
Table 7.3 - Antiepileptic drug choice by seizure type
Generalised onset Focal onset

Normal/impaired
Impaired awareness
awareness
Drug choice
Motor Non-motor Motor/non-motor

Focal to bilateral
Tonic-clonic, myoclonic, atonic Absence
tonic-clonic
< 2 years old: levetiracetam
≥ 2 years old: sodium valproate ≥ 2 years old:
1st choice carbamazepine
or levetiracetam (if girl of sodium valproate
childbearing agea)

a Sodium valproate is contraindicated in girls and women of child-bearing age due to increased risk of neural
tube defects and other congenital malformations. Sodium valproate is not recommended in children less than
2 years old due to an increased risk of fatal hepatotoxicity.

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Chapter 7: Neurological disorders

Generalised onset Focal onset

Normal/impaired
Impaired awareness
awareness
Drug choice
Motor Non-motor Motor/non-motor

Focal to bilateral
Tonic-clonic, myoclonic, atonic Absence
tonic-clonic

< 2 years old: phenobarbital


sodium valproatec
2nd choice No alternativeb
≥ 2 years old: levetiracetam or levetiracetam

carbamazepine, phenytoin phenytoin


3rd choice
or phenobarbital or phenobarbital

For antiepileptic drug starting and maintenance dosing, see Table 7.412,13.
Carbamazepine: give 2 times daily, morning and evening. After starting initial dosing,
maintenance dose should be reached within 8 days.
7
Phenobarbital: ideally aim to give once daily at bedtime (reduces drowsiness as adverse effect
during the day). Daily administration for 14 to 21 days is needed for a steady phenobarbital
level in the blood. Seizures occurring during this period do not indicate treatment failure.
– Child ≤ 11 years: start with 2 times daily dosing for 2 weeks before increasing dose. Aim to
move to once daily dosing when seizures controlled.
– Child ≥ 12 years: start with once daily dosing for 2 weeks before increasing the dose.
Phenytoin: give 2 times daily, morning and evening, for children 11 years and younger. Can be
given once daily for children 12 years and older. Small increments in the dosing can lead to
significant changes in concentration, therefore increases should be by 25 to 30 mg.
Table 7.4 - Antiepileptic drug and dosages
Child 1 month to 11 years
AEDd
Initial Step-up Maintenance
Increase by 2.5 to 5 mg/kg 5 mg/kg 2-3 times daily
carbamazepine 2.5 mg/kg 2 times daily
every 3-7 days (up to max. 20 mg/kg/day)
1 to 1.5 mg/kg 2 times 2.5 to 4 mg/kg 1-2 times
phenobarbital Increase by 2 mg/kg daily
daily daily
1.5 to 2.5 mg/kg 2 times Adjusted according to 2.5 to 5 mg/kg 2 times
phenytoin
daily response daily (max. 300 mg daily)
sodium 5 to 7.5 mg/kg 1-2 times 12.5 to 15 mg/kg 2 times
Increase gradually
valproatec daily (max. 600 mg/dose) daily

b Certain AEDs can exacerbate absence seizures or are known to be ineffective therefore there is no place for
carbamazepine, phenytoin or phenobarbital in the treatment of absence epilepsy.
c Sodium valproate is contraindicated in girls and women of child-bearing age due to increased risk of neural
tube defects and other congenital malformations. Sodium valproate is not recommended in children less than
2 years old due to an increased risk of fatal hepatotoxicity.
d Several anticonvulsant medications (namely carbamazepine, phenobarbital, phenytoin and levetiracetam) can
cause a rare but serious syndrome known as DRESS (drug reaction with eosinophilia and systemic symptoms).
It is important to be aware of this reaction which appears several weeks after the initiation of treatment and
can be fatal.

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Chapter 7: Neurological disorders

Adolescent 12 years and above


AEDe
Initial Maintenance
100 to 200 mg once daily
200 to 400 mg 2-3 times daily
carbamazepine or
(max. 1.8 g/day)
50 to 100 mg 2 times daily
1 mg/kg to 3 mg/kg (max. 180 mg)
phenobarbital 1 mg/kg (max. 60 mg) once daily
once daily
150 to 200 mg 2 times daily
phenytoin 75 to 150 mg 2 times daily
(max. 600 mg/day)
sodium 300 mg 2 times daily or 600 mg once 500 to 1000 mg 2 times daily
valproatef daily (max. 2.5 g/day)

Dosage14 for oral treatment


AED Age or weight
Increase dosage based on response and tolerance
7 mg/kg once daily
1 to 5 months Increase dose every 2 weeks by 7 mg/kg/dose
Maximum: 21 mg/kg 2 times daily
10 mg/kg once daily
6 months to 17 years
levetiracetam Increase dosage every 2 weeks by 10 mg/kg/dose
(< 50 kg)
Maximum: 30 mg/kg 2 times daily
250 mg 2 times daily
12 to 17 years
Increase by 500 mg 2 times daily every 2-4 weeks
(or ≥ 50 kg)
Maximum: 1.5 g 2 times daily

7.4.4 Follow-up and monitoring


– Review one month after any change in medications.
– Review every 6 months if the patient is stable.
At each follow-up visit:
– Check seizure frequency (review seizure diary if available) since last assessment and impact,
e.g. time off school.
– Check growth and development.
– Adjust medication if seizures are not controlled i.e. if the child is still having seizures despite
adherence to prescribed medication.
– Check treatment adverse effects.
– Review adherence. Adherence can deteriorate when symptoms become mild or less
frequent.
– Address any concerns, anxiety/depression if present.

e Several anticonvulsant medications (namely carbamazepine, phenobarbital, phenytoin and levetiracetam) can
cause a rare but serious syndrome known as DRESS (drug reaction with eosinophilia and systemic symptoms).
It is important to be aware of this reaction which appears several weeks after the initiation of treatment and
can be fatal.
f Sodium valproate is contraindicated in girls and women of child-bearing age due to increased risk of neural
tube defects and other congenital malformations. Sodium valproate is not recommended in children less than
2 years old due to an increased risk of fatal hepatotoxicity.

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Chapter 7: Neurological disorders

7.5 Altered level of consciousness

An altered level of consciousness (LOC) is any deviation from being fully awake and responsive.
There are many underlying medical conditions or traumatic events that can cause a change in
the level of consciousness. It represents an acute and potentially life-threatening emergency,
requiring prompt intervention to preserve life and brain function.
In children, the most common causes include infections (meningitis, malaria), metabolic
disturbances (hypoglycaemia, diabetic ketoacidosis (DKA), electrolyte imbalance), seizures,
poisoning (toxins or medications) and head injury.

7.5.1 Clinical features and assessment


– An altered LOC may range from being fully awake but disorientated or agitateda, to completely
unresponsive. Coma refers to the most profound level of unconsciousness.
– Approach a child with an altered LOC assessing ABCDE while checking for any obvious 7
underlying cause.
– Assess the level of consciousness (D) and note the level according to a scoring scale:
• AVPU is a simple and rapid score for initial assessment (see also Appendix 3):
▹ Alert
▹ Voice: responds to vocal stimuli
▹ Pain: responds to painful stimulib
▹ Unresponsive
• Paediatric and Adult Glasgow Coma Scale (GCS). See Appendix 13.1.
• Blantyre Coma Scale (often used for cerebral malaria). See Appendix 13.2.

Consciousness score Altered consciousness Coma

AVPU V, P or U P or U

Blantyre score <5 3

GCS < 15 ≤8

Assess for the underlying cause taking a history while stabilising the child:
– Recent medical history: excess irritability, headache, fever, malaria, infection/illness, head
trauma/accidents
– Past medical history: epilepsy/seizures, diabetes, birth asphyxia, developmental delay.
– Drug history: any medication, traditional remedies, exposure to toxins

a Agitation in children is a symptom that requires a full history, examination (where possible) and diagnosis.
Medical and social history are particularly important to identify potential contributing factors which may
include a combination of medical, surgical and/or emotional factors.
b A painful stimulus can be given by applying supra-orbital pressure at the supraorbital notch or by applying
pressure to the nailbed.

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Chapter 7: Neurological disorders

7.5.2 Management
Initial emergency management
– Assess and manage ABCDE and note vital signs including temperature.
– Support and open the airway (stabilise cervical spine if trauma is suspected).
– Clear airways (suction) only if necessary.
– Administer oxygen via mask (aim for SpO2 > 92%). Assist ventilation with bag-mask device if
not breathing.
– Obtain vascular access (IV/IO) and administer IV fluids if signs of circulatory impairment or
shock present (Chapter 2, Section 2.2).
– Perform a quick evaluation of neurological status (using AVPU scale, see above) and check
pupillary response.
– Check BGL:
• BGL < 60 mg/dL (3.3 mmol/L), treat for hypoglycaemia (Chapter 9, Section 9.3).
• BGL > 200 mg/dL or known diabetes, consider diabetic ketoacidosis and manage
accordingly (Chapter 9, Section 9.1). Check urine for ketones.
– Expose the entire body and look for signs of sepsis, meningitis, trauma, etc.
Once stable, conduct a full clinical examination to identify the underlying cause and treat.

Specific management
– If V, P, or U, evaluate GCS and further neurological assessment including posture/tone,
movements, reflexes. Check for signs of meningitis or encephalitis. Recheck AVPU (or GCS)
every 30 minutes; if GCS 12 to 14, recheck every hour.
– If head trauma suspected, see Chapter 2, Section 2.8 for further management after
stabilisation.
– If seizures are present or known epilepsy, treat accordingly (Section 7.2).
– Check haemoglobin if any pallor present.
– Check RDT malaria in endemic areas and start treatment if positive (Chapter 3, Section 3.4).
– Perform a lumbar puncture if meningitis suspected (and no contraindications).
– If high fever and/or sepsis/meningitis suspected, obtain blood cultures and start antibiotic
treatment with ceftriaxone IV/IM 100 mg/kg (max. 4 g) every 24 hours. Adjust antibiotic
treatment if needed once specific cause and/or pathogen identified. (See Chapter 3,
Section 3.2 for sepsis and Section 3.3 for meningitis).
– Admit the patient to the ICU and provide supportive care (nursing care, oxygen, fluid
maintenance, monitoring).
– If poisoning suspected (pin-point pupils, excess salivation, flushing, severe agitation,
hypertension, vomiting), refer to Chapter 2, Section 2.9).

Agitation
Children who are agitated require specific and cautious assessment and management15:
– Try to calm the situation by moving to a safe, quiet space.
– Remain calm and maintain a neutral but empathetic tone.
– Use clear, simple language that is adapted to the child’s age and developmental stage.
– Be honest and explain in advance what you are doing or what is going to happen.

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Chapter 7: Neurological disorders

– Communicate at the child’s eye level.


– Keep parent/carer together with the child.
– Validate the child’s feelings and acknowledge their fear, anger or sadness. Do not minimise
their feelings, insult, or humiliate them.
– Ask child and parent/carer if there is a preferred toy/comforter, food, drink or other familiar
item that they may like to have.
– Ensure that the child is not in pain and treat if necessary.
– Try to determine if there may be an underlying medical or surgical condition that is
contributing to the agitation and treat if possible.
– Remove any sharp or dangerous objects.
– Identify any possible medications or substances that may have triggered agitation.
– Avoid physical restraint unless deemed necessary for the safety of the patient or others, as
this is traumatic for the child and carries significant risk of adverse events such as positional
asphyxia.
Special attention is required for children with developmental delay (DD) or known behavioural
disorders, where early involvement of parents/carers who know the child well is usually very
helpful. In addition to the above:
– Ensure that the child has received any usual medications for potential agitation. 7
– Elicit specific triggers for agitation (via discussion with parents/carers and through close
observation) and reduce/minimise these.
– Minimise any unpleasant and/or unfamiliar sensations such as pain, overstimulation, bright
lights, loud noises etc.
– Have a high index of suspicion for an underlying medical or surgical condition that may be
causing pain or discomfort to the child, e.g. otitis media, especially in non- or minimally
verbal children, and treat as necessary.
– Record triggers and mitigation tactics in patient file to allow transfer of information between
medical and nursing staff.
– Ask parents/carers about previous side effects from sedative or antipsychotic medicationsc.

Medications
If these methods do not help to calm the situation and there is significant agitation, with
a risk of harm to the patient or others, consider administration of sedative or antipsychotic
medicationsd. Provide age-appropriate information to the child or adolescent prior to
medication administration, taking into account the level of agitation. The goal of medication is
calming, not sedating, so that the child can be further evaluated. The choice of medication is
dependent on underlying cause.
Oral route is preferred whenever possible, and oral risperidone or diazepam are usually
sufficient to manage agitation in children. Parenteral administration should be reserved for
violent or uncooperative patients or if there is no response to oral medicatione:

c Children with developmental disabilities are particularly vulnerable to side effects from sedative and
antipsychotic medications.
d Caution with all sedative and antipsychotic medication if renal or hepatic impairment suspected.
e Administration of parenteral medication to children for behavioural disturbance involves significant and
serious risks, both medical and psychological, and should only be done under the supervision and guidance of
an experienced clinician.

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Chapter 7: Neurological disorders

Route Medication Indication Dose Side-effects

Promethazine Agitation due to ≥ 15 yrs: 25 to 50 mg Drowsiness,


psychosis, use in headache,
combination with anticholinergic e.g.
haloperidol. dry mouth, blurred
Use only if 15 years vision, restlessness
and above.

Diazepam Severe anxiety, Child > 6 mths: 1 to Respiratory


trauma, substance 2.5 mg depression,
intoxication or Adolescent: 5 to rebound agitation,
PO

withdrawal (except 10 mg (max. 20 mg/ disinhibition and/or


alcohol intoxication), day) delirium (especially
unknown cause with in young or children
moderate agitation with DD)

Risperidone Delirium, agitation in < 12 yrs: 0.25 to 0.5 mg Extra-pyramidal


children with DD or ≥ 12 yrs: 1 mg e.g. acute
known behavioural dystonia, akathisia,
disorder bradykinesia,
rigidity, tremor

Promethazine Agitation due to ≥ 15 yrs: 25 to 50 mg Drowsiness,


psychosis, use in (max. 100 mg/day) headache,
combination with anticholinergic e.g.
haloperidol. dry mouth, blurred
Use only if 15 years vision, restlessness
and above.
IM

Haloperidol Agitation due to < 12 yrs: 0.05 to Extra-pyramidal


psychosis. Use with 0.1 mg/kg/dose (max. e.g. acute
promethazine over 2.5 mg/dose and dystonia, akathisia,
15 years. 6 mg/day) bradykinesia,
≥ 12 yrs: 2.5 mg (max. rigidity, tremor. High
15 mg/day) incidence of acute
dystonia – use with
caution

Diazepam Severe anxiety, 0.05 to Respiratory


(over 3-5 minutes)

trauma, substance 0.1 mg/kg/dose (max. depression,


intoxication or 40 mg/day) rebound agitation,
Slow IV

withdrawal (except disinhibition and/or


alcohol intoxication), delirium (especially
unknown cause with in younger children
severe agitation and those with DD)

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Chapter 7: Neurological disorders

Adolescents and children may have more severe reactions to medications used for rapid
sedation, therefore they should be closely monitored after administration, with vital signs
measurement every 15 minutes for the first hour. Ensure that a clear explanation of any urgent
medication administration is given to the child or adolescent after the acute agitation has
passed and their mental state has improved.
In the event of respiratory depression caused by benzodiazepines, administer:
– Flumazenil IV over 15 seconds: 10 micrograms/kg every 1 minute (max. 200 micrograms/
dose) as required until adequate breathing resumes.

249
Chapter 7: Neurological disorders

References Chapter 7

1. Bodamer OA. Approach to the infant with hypotonia and weakness. UpToDate. Published
online August 2021.
https://www.uptodate.com/contents/approach-to-the-infant-with-hypotonia-and-
weakness
2. Kotagal S, Morse AM. Detailed neurologic assessment of infants and children. UpToDate.
Published online August 2022.
https://www.uptodate.com/contents/detailed-neurologic-assessment-of-infants-and-
children
3. Fisher RS, Boas WVE, Blume W, et al. Epileptic Seizures and Epilepsy: Definitions Proposed
by the International League Against Epilepsy (ILAE) and the International Bureau for
Epilepsy (IBE). Epilepsia. 2005;46(4):470-472.
https://doi.org/10.1111/j.0013-9580.2005.66104.x
4. Fisher RS, Acevedo C, Arzimanoglou A, et al. ILAE Official Report: A practical clinical
definition of epilepsy. Epilepsia. 2014;55(4):475-482.
https://doi.org/10.1111/epi.12550
5. Epilepsies in Children, Young People and Adults. National Institute for Health and Care
Excellence (NICE); 2022. Accessed October 9, 2023.
http://www.ncbi.nlm.nih.gov/books/NBK581165/
6. Trinka E, Cock H, Hesdorffer D, et al. A definition and classification of status epilepticus -
Report of the ILAE Task Force on Classification of Status Epilepticus. Epilepsia. 2015;
56(10):1515-1523.
https://doi.org/10.1111/epi.13121
7. Singh A, Stredny CM, Loddenkemper T. Pharmacotherapy for Pediatric Convulsive Status
Epilepticus. CNS Drugs. 2020;34(1):47-63.
https://doi.org/10.1007/s40263-019-00690-8
8. Wilmshurst JM, Gaillard WD, Vinayan KP, et al. Summary of recommendations for the
management of infantile seizures: Task F orce R eport for the ILAE Commission of Paediatrics.
Epilepsia. 2015;56(8):1185-1197.
https://doi.org/10.1111/epi.13057
9. Millichap JJ. Clinical features and evaluation of febrile seizures. UpToDate. Published online
May 2021.
https://www.uptodate.com/contents/clinical-features-and-evaluation-of-febrile-seizures
10. Patterson KP, Baram TZ, Shinnar S. Origins of Temporal Lobe Epilepsy: Febrile Seizures and
Febrile Status Epilepticus. Neurotherapeutics. 2014;11(2):242-250.
https://doi.org/10.1007/s13311-014-0263-4
11. Epilepsy. Accessed October 9, 2023.
https://www.who.int/news-room/fact-sheets/detail/epilepsy
12. World Health Organization. mhGAP Intervention Guide for Mental, Neurological and
Substance Use Disorders in Non-Specialized Health Settings: Mental Health Gap Action
Programme (mhGAP). version 2.0. World Health Organization; 2016. Accessed October 9,
2023.
https://iris.who.int/handle/10665/250239

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13. MedicinesComplete - CONTENT > BNF for Children > Drug: Phenobarbital. Accessed
October 9, 2023.
https://www.medicinescomplete.com/#/content/bnfc/_197439058?hspl=phenobarbital
14. MedicinesComplete - CONTENT > BNF for Children > Drug: Levetiracetam. Accessed
October 9, 2023.
https://www.medicinescomplete.com/#/content/bnfc/_695768521?hspl=lecetiracetam
15. Gerson R, Malas N, Feuer V, et al. Best Practices for Evaluation and Treatment of Agitated
Children and Adolescents (BETA) in the Emergency Department: Consensus Statement of the
American Association for Emergency Psychiatry. West J Emerg Med. 2019;20(2):409-418.
https://doi.org/10.5811/westjem.2019.1.41344

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Chapter 8:
Renal and genitourinary tract

8.1 Upper urinary tract infection (pyelonephritis).....................................................255


8.1.1 Clinical features............................................................................................. 255
8.1.2 Investigations................................................................................................. 256
8.1.3 Management................................................................................................. 257
8.1.4 Follow-up....................................................................................................... 258
8.2 Post-infectious glomerulonephritis....................................................................... 259
8.2.1 Clinical features............................................................................................. 259
8.2.2 Investigations................................................................................................. 259
8.2.3 Management................................................................................................. 259
8.3 Nephrotic syndrome.............................................................................................. 261
8
8.3.1 Clinical features............................................................................................. 261
8.3.2 Investigations................................................................................................. 262
8.3.3 Management................................................................................................. 262
8.3.4 Prognosis....................................................................................................... 264
8.4 Acute kidney injury................................................................................................ 265
8.4.1 Classification and causes............................................................................... 265
8.4.2 Clinical features............................................................................................. 266
8.4.3 Investigations................................................................................................. 266
8.4.4 Management................................................................................................. 267
8.4.5 Prognosis....................................................................................................... 269
8.5 Acute painful scrotum........................................................................................... 270
8.5.1 Clinical features............................................................................................. 270
8.5.2 Investigations................................................................................................. 272
8.5.3 Management................................................................................................. 272
8.6 Paraphimosis.......................................................................................................... 273
8.6.1 Clinical features............................................................................................. 273
8.6.2 Management................................................................................................. 273
References Chapter 8................................................................................................... 276
Chapter 8: Renal and genitourinary tract

8.1 Upper urinary tract infection (pyelonephritis)

Upper urinary tract infection (UTI), or pyelonephritis, is an infection of the kidney and is a
common cause of fever in infants and young children. It is more common in children with
underlying anatomical or obstructive abnormalities, therefore investigation is always required.
The most common causative pathogen is Escherichia coli, followed by other enterobacteria.
Cystitis, which is an infection of the lower urinary tract (i.e. the bladder and urethra), is more
common in uncircumcised male infants, and in females under the age of 4. It is not associated
with fever or other systemic signs and does not usually require admission, therefore is not
discussed here.

8.1.1 Clinical features


The manifestations of upper UTIs vary with age. In infants, signs and symptoms are non-specific
and include fever, vomiting, diarrhoea, poor feeding and irritability. Upper UTI in infants can be
an occult cause of sepsis and should be considered in any febrile, generally unwell child under
2 years old.
In children 2 years and over, along with fever, symptoms usually become more localised to the 8
urinary tract:
– Dysuria, frequency, or both
– Urinary incontinence in a previously toilet-trained child
– Foul-smelling urine
– Vomiting
– Lower back or loin pain, particularly on percussion of the flanks
Any child presenting with urinary signs or symptoms who is febrile should be considered
to have pyelonephritis and treated accordingly.
Signs of severe pyelonephritis include:
– Vomiting
– Lethargy
– Reduced oral intake/poor feeding
– Irritability
– Fever > 38.5 ⁰C
– Rigors

Complications
Recurrent upper UTIs can lead to scarring of the kidneys and decreased kidney function.
Usually, there is an underlying structural abnormality or dysfunctional reason for recurrent
upper UTIs.

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Chapter 8: Renal and genitourinary tract

8.1.2 Investigations
– Urine dipsticka (see Table 8.1 for interpretation of results). To avoid contamination of the
sample and false positive results, obtain urine specimens using the most sterile technique
possible1 in one of the following ways:
• ‘Clean-catch’ sample: wash hands and clean the child’s genital area with a clean, water-
soaked gauze. Ask the parent/carer to watch and wait until the child starts to urinate
and then catch the urine directly into a sterile container (see Appendix 14.1 for more
detail). Offer drinks to encourage the child to pass urine. This is the preferred method
in children who are not severely unwell, but in practice can be difficult to successfully
achieve. Contamination rates are approximately 25%.
• Urine collection bag: after cleaning (as above), affix the paediatric urine collection bag
and wait until the child passes urine (see Appendix 14.2 for more detail). Bag specimens
can be used to rule out UTI, but if positive, another method should be used to verify
results due to the possibility of false positives. Urine from a bag specimen should not be
sent for culture as contamination rates can be high depending on the quality of cleaning.
• In-out catheter: after cleaning (as above), use a urinary catheter to collect urine directly
into a sterile container by briefly inserting it and removing it as soon as urine is obtained
(see Appendix 14.3 for full procedure). This is the preferred method if non-invasive ‘clean-
catch’ is unsuccessful; contamination rates are approximately 10%.
• Suprapubic aspirate (SPA): collect urine directly from the bladder by inserting a needle
through the abdominal wall under ultrasound guidance (see Appendix 15 for full procedure).
This is the preferred method in severely unwell young children but should only be performed
by staff trained in the procedure; contamination rates are approximately 1%.
– Urine microscopy and culture, if available – identify and quantify pyuria (white blood cells
(WBC) in urine) and/or bacteriuria (bacteria in the urine).
– Blood culture if under 2 years old.
– CRP, if available.
– Urea and electrolytes, if available and signs of severe infection.
– Consider renal ultrasound (US), see below for criteria.
Table 8.1 - Interpretation of urine dipstick results (adapted from NICE2)
3 months -
Dipstick results Under 3 months 3 years and older
< 3 years
Leukocyte
esterase and Treat as UTI and send urine for microscopy and culture
nitrite positive
Leukocyte
esterase negative
Treat as UTI and send urine for microscopy and culture
and nitrite
positive
Treat as UTI only if clinical
Leukocyte symptoms strongly suggest
Treat as UTI and send urine for
esterase positive it, otherwise send urine
microscopy
and nitrite for microscopy and culture
and culture
negative to confirm before starting
treatment

a In areas where urinary schistosomiasis is endemic, consider this as a diagnosis in children with macroscopic or
microscopic haematuria detected by urine dipstick.

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Chapter 8: Renal and genitourinary tract

3 months -
Dipstick results Under 3 months 3 years and older
< 3 years
Treat as sepsis
Leukocyte
and send urine for Do not treat as UTI and do not send urine for
esterase and
microscopy and microscopy and culture
nitrite negative
culture

8.1.3 Management
Infants less than 3 months old
Admit all infants less than 3 months old with a febrile upper UTI to hospital:
– Administer ceftriaxone IV/IM: 80 mg/kg (max. 4 g if < 50 kg; max. 2 g if ≥ 50 kg) every 24 hours
(or cefotaxime IV 50 mg/kg every 8 hours).
– Alternatively, administer gentamicin IV: 7.5 mg/kg every 24 hours or amikacin 15 mg/kg every
24 hours. If the infant is very unwell, consider concomitant administration of ceftriaxone (or
cefotaxime) and gentamicin (or amikacin).
– Start IV maintenance fluids if not tolerating oral intake (see Chapter 15, Section 15.2).
– Give paracetamol as antipyretic and analgesic, as required for comfort (see Chapter 15,
Section 15.4).
– Monitor and record vital signs and urine output as often as required using an early warning
system (see MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts:
Vital sign charts).
8
– Reassess and adjust antibiotic treatment according to urine and blood culture results, if/
when available.
– Duration of parenteral antibiotic treatment should be determined by the infant’s clinical
condition and response to treatment. Continue IV/IM treatment for at least 48-72 hours and
when the infant is improving and feeding well, switch to:
• amoxicillin-clavulanic acid (co-amoxiclav) PO (ratio 7:1 or 8:1) 50 mg/kg of the amoxicillin
component, 2 times daily, or
• ciprofloxacin PO: 10 to 20 mg/kg (max. 750 mg) 2 times daily.
– Total antibiotic treatment should last for 7 days.

Infants and children 3 months and over


Most infants and children 3 months and over with a febrile upper UTI can be treated with oral
antibiotics for 7 days3:
– Give amoxicillin-clavulanic acid (co-amoxiclav) PO (ratio 7:1 or 8:1) 50 mg/kg of the
amoxicillin component, 2 times daily.
– Alternatively, give ciprofloxacin PO 15 mg/kg (max .750 mg) 2 times daily or cefixime PO
8 mg/kg once daily.
If the child is vomiting or there are any signs of severity (see above) or sepsis (see Chapter 3,
Section 3.2) they should be admitted for IV antibiotics, as for infants less than 3 months old.

Renal imaging
Where feasible, renal US is recommended in all children with confirmed upper UTI to exclude
structural abnormalities that may predispose them to the risk of recurrence. It is particularly
indicated in the following cases2,4:
– Under 2 years old with first febrile UTI
– Any age with recurrent febrile UTIs (≥ 2 episodes of febrile UTI)

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Chapter 8: Renal and genitourinary tract

– Signs of severe infection or renal sepsis (see Section 8.1.1)


– Palpable abdominal or bladder mass
– Poor urine flow
– Raised creatinine
– Infection with non-E coli organisms
– Family history of renal disease
– Failure to respond to appropriate antibiotics within 48 hours
If renal abnormalities are detected, refer for further management to a renal specialist if
possible.

8.1.4 Follow-up
Routine follow-up is not required for children with first febrile upper UTI and normal renal
US. However, children who have had an upper UTI are at risk of recurrence; families should
therefore be instructed on the signs that may indicate a repeat infection. Upper UTI is a risk
factor for renal scarring, with approximately 15% of children developing renal scarring after a
first upper UTI5. Likelihood of renal scarring is increased with recurrent upper UTI but can be
minimised with prompt treatment.

258
Chapter 8: Renal and genitourinary tract

8.2 Post-infectious glomerulonephritis

Glomerulonephritis is an autoimmune reaction in the kidneys that is initiated by an external


trigger and is characterised by inflammation and glomerular injury. It is most often of infectious
origin in children, commonly occurring after a streptococcal throat or skin infection (particularly
Group A beta-haemolytic streptococcus, though other bacteria can also be the trigger, e.g.
Staphylococcus aureus). Antibiotics do not prevent post-infectious glomerulonephritis (PIGN)
in susceptible individuals, however adequate antibiotics to treat the acute infection reduce
circulation of nephritogenic strains among close contacts6. Prompt and adequate antibiotic
treatment, therefore, plays an important role in the control of PIGN. Although PIGN is seen in
children worldwide, 97% of cases occur in low-resource settings. It typically affects children
from 5-12 years of age and is more common in boys than girls7.

8.2.1 Clinical features


Haematuria is the predominant finding in PIGN, varying from asymptomatic benign haematuria
to acute nephritic syndrome, with the classic features of:
– Haematuria (micro or macroscopic – red or dark brown urine)
– Proteinuria (usually mild but may, rarely, be heavya)
– Oedema (often facial/orbital, but can be generalised) 8
– Hypertension (varies from mild to severe)
Patients typically also complain of lethargy, weakness and loss of appetite. Renal function
is impaired to varying degrees, though is often normal. Diagnosis is made based on clinical
presentation and a history of recent skin or throat infection (though this is not always evident).

8.2.2 Investigations
– Urine dipstick (blood and protein positive)
– Urine microscopy
– Blood creatinine (at least baseline measurement) and electrolytes, if available

8.2.3 Management
PIGN is usually a self-limiting illness that requires supportive treatment only. Management
is focused on eradication of the nephritogenic strain and treatment of fluid overload, which
causes the clinical complications of PIGN:
– Give oral antibiotics if evidence of ongoing acute streptococcal infection:
• phenoxymethylpenicillin (Penicillin V) PO for 10 days
▹ < 1 year: 125 mg 2 times daily
▹ 1 to < 6 years: 250 mg 2 times daily
▹ 6 to < 12 years: 500 mg 2 times daily
▹ ≥ 12 years: 1 g 2 times daily

a Proteinuria in PIGN is typically less than that seen in nephrotic syndrome. If proteinuria is in nephrotic range
(> 3+ on dipstick), consider nephrotic syndrome as a possible alternative diagnosis.

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• or amoxicillin PO: 25 mg/kg (max. 1g) 2 times daily, for 6 days.


• or erythromycin PO for 10 days (in case of penicillin allergy):
▹ 1 to 23 months: 125 mg 4 times daily
▹ 2 to 7 years: 250 mg 4 times daily
▹ > 7 years: 250-500 mg 4 times daily
– Restrict sodium and fluid intake: exclude salt from any meals if generalised oedema is present
and restrict fluid intake to match urine output and insensible lossesb. Exercise caution with
fluid restriction in hot climates to avoid dehydration and renal failure.
– Give furosemide PO/IV 1 mg/kg 1 or 2 times daily to stimulate diuresis and reduce blood
pressure and oedema. If significant fluid overload (displaced apex beat, distended neck
veins, pulmonary oedema, severe hypertension), furosemide PO/IV 1 mg/kg can be given
up to 3 times daily. Daily weights are helpful for monitoring, where possible.
– Monitor all urine output and record blood pressure at least once daily (ideally more
frequently). Hypertension will usually respond to diuretics, but if refractory hypertension,
begin a trial of amlodipine PO 0.1 mg/kg once daily and seek specialist medical advice.
– Monitor electrolytes and serum creatinine, if available, until the child is stable.

Overall prognosis is good in the majority of cases, with rapid resolution of symptoms once
supportive care has been started although urine abnormalities may persist for several months.
Some children with PIGN are unresponsive to supportive care and have a reduction in renal
function that requires short-term dialysis. These children should be referred for ongoing
management, where possible.

b Insensible fluid loss is the amount of body fluid lost through the skin and respiratory tract that is not easily
measurable. Estimated daily insensible losses are calculated according to body weight as follows: 1-10 kg =
25 mL/kg; > 10-20 kg = 12.5 mL/kg; > 20 kg = 5 mL/kg.

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8.3 Nephrotic syndrome

Nephrotic syndrome is a clinical condition characterised by proteinuria, oedema and low


serum albumin. It results from increased permeability of the glomeruli, allowing protein
to leak into the urine. The vast majority of cases are idiopathic without associated kidney
dysfunction and the most common finding on renal biopsy is minimal change disease (MCD),
though increasingly, focal segmental glomerulosclerosis (FSGS) is being seen, especially
among black children8. Prognosis in children with MCD is very good. More rarely, nephrotic
syndrome can be secondary to nephritic syndromes (post-infectious glomerulonephritis
(PIGN), membranoproliferative glomerulonephritis, IgA nephropathy) or systemic disease
(systemic lupus erythematosus, vasculitides and sickle cell disease). Estimated incidence is
1.15-2.1/100 000 children per year, typically affecting young children (average age 3-7 years
old), and the condition is more common in boys than girls9. Although relatively rare, it is
responsible for significant morbidity in children and relapse is not uncommon.

8.3.1 Clinical features


Idiopathic nephrotic syndrome typically follows a trigger such as an upper respiratory tract
infection. Painless, pitting oedema is usually the presenting sign and progressively increases 8
from mild localised oedema, e.g. periorbital oedema on waking or ankle oedema, to massive
generalised oedema affecting the whole body with associated complications of pleural
effusions and ascites.
Diagnosis is made based on the triad of:
– Proteinuria > 3+ on dipstick
– Oedema
– Hypoalbuminaemia < 30 g/L
Patients with MCD – the majority of those with idiopathic nephrotic syndrome – are usually
between 1 and 10 years old and typically have normal renal function, no signs of hypertension
and minimal, if any, haematuria. There may be oliguria if the patient is intravascularly depleted.
A presumptive diagnosis can be made in children with oedema and heavy proteinuria (as
above), in the absence of renal impairment, hypertension and severe haematuria. Consider
alternative diagnoses in patients with a family history of kidney disease, extrarenal disease
(arthritis, rash, anaemia) or chronic disease of another organ system. Additionally, patients
with signs of fluid overload such as pulmonary oedema are unlikely to have MCD.
The differential diagnosis of generalised oedema includes kwashiorkor (most common, see
Table 8.2), vitamin B1 deficiency, heart failure, liver failure, protein losing enteropathy and
anaphylaxis10.

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Table 8.2 - Nephrotic syndrome vs kwashiorkor

Nephrotic syndrome Kwashiorkor

Oedema Oedema of the face, followed by Oedema of the hands and feet
legs followed by the face
Ascites and generalised oedema Ascites rare
common Generalised oedema depends on
severity

Urine dipstick Protein 3+ Protein negative or 1+

Skin/hair changes No Common

Mental state Normal, attentive Irritable, inattentive, apathetic

Complications
Complications of nephrotic syndrome are rare but significant. Immune deficiency occurs due
to reduced concentrations of serum immunoglobulins and complement factors and impaired
ability of the body to produce specific antibodies. This leads to increased susceptibility to
serious bacterial infections such as peritonitis, pneumonia and empyema (particularly due
to Strep. pneumoniae), which are the leading cause of death in children with nephrotic
syndrome11. Other complications include increased coagulability leading to thromboembolism;
renal insufficiency and hypovolaemia. Growth restriction may be secondary to prolonged and
repeated courses of steroids in recurrent or persistent nephrotic syndrome.

8.3.2 Investigations
– Urine dipstick:
• Perform urine dipstick test on two separately obtained urine samples.
• Protein > 3+ is diagnostic, along with hypoalbuminaemia.
• In case of haematuria (macro or microscopic ≥ 2+), consider glomerulonephritis and other
causes such as schistosomiasis, in endemic areas.
– Blood tests, if available:
• Creatinine and blood urea nitrogen (BUN)
• Serum sodium (hyponatremia is possible)
• Serum albumin concentration: less than 30 g/L is diagnostic, along with proteinuria.
• Cholesterol (hyperlipidaemia): raised in nephrotic syndrome, can help to differentiate
between nephrotic and nephritic syndrome in mixed presentations.
• FBC: increased Hb and Hct due to haemoconcentration, thrombocytosis.

8.3.3 Management
The mainstay of treatment for idiopathic nephrotic syndrome is corticosteroid therapy, with
patients being classified as having either steroid-sensitive nephrotic syndrome (SSNS) or
steroid-resistant nephrotic syndrome (SRNS). 80-90% of children have SSNS and will respond
to treatment within 4 weeks12,13. Children who do not respond to treatment (SRNS) should be
referred for specialist input, as management can be challenging. Renal biopsy is not necessary

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before starting steroids for idiopathic nephrotic syndrome, as response to steroids is more
indicative of long-term outcome than changes on biopsy. Steroids should be started on any
child who meets the diagnostic criteria for presumptive nephrotic syndrome (see above), and
has the following clinical criteria:
– Between 1 and 10 years old
– No ongoing bacterial infection (also exclude HIV, Hep B and syphilis)
– Active TB excluded or treatment already initiated.

Initial therapy for first presentation of idiopathic nephrotic syndrome


– Prednisolone PO 60 mg/m2 or 2 mg/kg14,15 (max. 80 mg/day) once daily in the morning for
minimum of 4 weeks, until resolution of proteinuria.
– Then reduce to prednisolone PO 40 mg/m2 or 1.5 mg/kg (max. 40 mg/day) once daily in the
morning on alternate days for 4 weeks then stop prednisolone.
– Steroid therapy should not be extended beyond 2-3 months for an initial presentation of
SSNS16,17.
See Appendix 16 for calculation of body surface area (BSA) in children based on weight.
Alternatively, prednisolone dosing can be estimated based on body weight as a proxy for BSA
using the following formula18:

60 mg/m2 = (weight (kg) x 2) + 8


40 mg/m2 = weight (kg) + 11
8
Treatment of relapse in SSNSa
– Prednisolone PO 60 mg/m2 or 2 mg/kg (max. 80 mg/day) once daily in the morning until
resolution of proteinuria (negative or trace on dipstick) for 3 consecutive days.
– Then reduce to prednisolone PO 40 mg/m2 or 1.5 mg/kg (max. 40 mg/day) once daily in the
morning on alternate days for at least 4 weeksb.
Management of children with frequent relapses (FR)c, steroid-dependent nephrotic syndrome
(SDNS)d, or SRNSe is complicated and requires the input of specialists to tailor treatment to
individual needs. There is some evidence that the use of daily prednisolone during episodes
of upper respiratory tract and other infections can be helpful in preventing relapse in FR and
SDNS19.

Management of oedema
– Restrict sodium and fluid intake: exclude salt from any meals if generalised oedema is present
and restrict fluid intake to match urine output and insensible lossesf. Exercise caution with
fluid restriction in hot climates to avoid dehydration and renal failure.

a Relapse is defined as the reappearance of proteinuria > 3+ for more than 3 consecutive days at any time after
successful steroid treatment.
b Lower steroid doses may provide similar rates of remission, however there is no consensus to date.
c FR is defined as > 2 relapses within 6 months of initial response, or > 4 relapses in any 12-month period.
d SDNS is defined as two consecutive relapses during corticosteroid treatment, or within 14 days of stopping
treatment.
e SRNS is defined as failure to achieve complete remission after 8 weeks of corticosteroid treatment.
f Insensible fluid loss is the amount of body fluid lost through the skin and respiratory tract that is not easily
measurable. Estimated daily insensible losses are calculated according to body weight as follows: 1-10 kg =
25 mL/kg; > 10-20 kg = 12.5 mL/kg; > 20 kg = 5 mL/kg.

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– Diuretic therapy: children with nephrotic syndrome are often intravascularly deplete, despite
their appearance, therefore diuretics should be used with extreme caution to prevent further
intravascular depletion and shock. In cases of anasarca (massive generalised oedema with
skin breakdown and ascites) without signs of intravascular volume depletion (tachycardia,
cold/clammy extremities, oliguria), cautiously give furosemide PO/IV 1 mg/kg 1 or 2 times
daily to stimulate diuresis and reduce oedema.

Management of complications
Children should be evaluated daily for the appearance of signs and symptoms of infection. For
guidance on the management of specific infections refer to the following chapters: pneumonia
(Chapter 4, Section 4.5), empyema (Chapter 4, Section 4.6), peritonitis (Chapter 5, Section 5.4),
sepsis (Chapter 3, Section 3.2) and meningitis (Chapter 3, Section 3.3).

Immunisation
Ensure routine immunisations are up to date to minimise the risk of serious bacterial infections.
In particular:
– Administer conjugate pneumococcal vaccination (see MSF Essential Drugs).
– Postpone live vaccinations (e.g. measles, polio, BCG) until prednisolone dose is below
1 mg/kg daily (or below 2 mg/kg on alternate days)19.
– Vaccinate household members with live vaccines, if possible, ensuring child is protected
from gastrointestinal, urinary and respiratory secretions of vaccinated contacts for 3-6 weeks
after vaccination, through rigorous attention to hygiene.

8.3.4 Prognosis
Overall prognosis is good for children with SSNS, with steady resolution of symptoms once
steroids have been started. However, relapse occurs in 70-90% of children at least once13
with 40-50% of children showing steroid dependency and relapsing as soon as steroids are
tapered12. Complications associated with the use of repeated, prolonged steroid therapy
include obesity, short stature, decreased bone density, cataracts, hypertension, adrenal
suppression and behavioural changes20. Children with SRNS should be referred for specialist
management as their clinical course can be complex.

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8.4 Acute kidney injury

Acute kidney injury (AKI), previously referred to as acute renal failure, is a sudden decrease
in kidney function that compromises the normal regulation of fluid, electrolytes and the
acid-base balance. This results in fluid overload, uraemia, hypertension, hyperkalaemia,
hyperphosphatemia, hypocalcaemia and metabolic acidosis. It is a relatively common
complication among hospitalised sick children and is associated with longer lengths of stay
and higher mortality.

8.4.1 Classification and causes


AKI is classified as pre-renal, renal or post-renal, indicating the origin of the kidney injury21.

Pre-renal
Pre-renal AKI results from decreased kidney perfusion, usually due to loss of circulating
volume. The most frequent cause in children is dehydration secondary to gastroenteritis, but
acute blood loss, burns and dehydration due to diabetic ketoacidosis (DKA) are also common
causes. Pre-renal AKI may also be due to profound hypotension in an acutely unwell child.
Decreased blood supply to the kidneys leads to reduced glomerular filtration rate (GFR) and 8
concentrated urine.

Renal (intrinsic)
Includes any pathology affecting the kidney itself. Causes are numerous and diverse, including:
– Acute post-infectious glomerulonephritis (PIGN), with or without nephrotic syndrome (see
Section 8.2 and Section 8.3 respectively).
– Acute tubular necrosis (ATN), e.g. after birth asphyxia or after prolonged acute pre-renal
kidney injury. Recovery from ATN is often preceded by a polyuric phase (abnormally high
urine output) and can take days to weeks.
– Nephrotoxicity due to medications (e.g. gentamicin, NSAIDs) or venom (e.g. certain herbs or
snake bites)
– Sepsis, due to a combination of haemodynamic, inflammatory and immune mechanisms
– Malaria, due to haemolysis and high parasitaemia (usually reversible with prompt and
adequate malaria treatment)
– Haemolytic Uraemic Syndrome (HUS)
– G6PD deficiency
– Sickle cell disease

Post-renal
Also known as obstructive uropathy, as it is caused by an obstruction to the outflow of urine
from the kidneys. In children, this is most commonly caused by posterior urethral valves (in
boys only) but can also be due to kidney or bladder calculi or any other obstruction including
trauma.

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Chapter 8: Renal and genitourinary tract

8.4.2 Clinical features


Reduced urine output (oliguria or anuriaa) is the most common symptom of AKI, however in
certain cases there may be normal or even high urine output (polyuriab). Other characteristic
signs and symptoms of AKI are directly related to reduced urine output:
– Oedema
– Hypertension
Additional symptoms vary according to the underlying cause of AKI, and may include:
– Haematuria (macro or microscopic)
– Fever
– Vomiting
– Abdominal pain
– Rash
– Bloody diarrhoea
– Haemorrhage
– Pallor
Certain elements of the history may help to indicate the origin of the AKI, e.g. history of recent
infection or medication ingestion.

8.4.3 Investigations
Investigations confirm the diagnosis and help to differentiate between pre-renal, renal and
post-renal causes (see Table 8.3).
– Urinalysis, including urinary protein
– Blood pressure monitoring
– Urinary sodium and osmolality, if available
– Blood tests, if available: Urea, creatininec and electrolytes, blood urea nitrogen (BUN), FBC,
coagulation, blood gases (for bicarbonate and pH) and liver function tests
– Estimated GFR (eGFR): calculated using the formula 0.41 x height (cm) / creatinine (mg/dL).
Normal eGFR is 80 – 120 mL/min/m2.
– Renal ultrasound, if available: ideally to exclude hydronephrosis, but as a minimum to see if
the bladder is full.
– ECG or cardiac monitoring, if available: to monitor T waves.
Table 8.3 - Typical findings in investigation of AKI (adapted from NHSGGC Guidelines22)

Pre-renal Renal (intrinsic) Post-renal

Urine output Oliguria Oliguria to polyuria Variable

Urinary osmolality
> 500 < 300 < 350
(milliosmoles)

Urinary sodium
< 10 > 40 > 40
(mmol/L)

a Oliguria is defined as a urine output of < 1 mL/kg/hr in infants or < 0.5 mL/kg/hr in children; anuria is defined
as no urine output or urine output of < 1 mL/kg/day.
b Polyuria is defined as a urine output of > 3 mL/kg/hr.
c Normal values of serum creatinine vary by age and gender, see local lab references for normal ranges.

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Pre-renal Renal (intrinsic) Post-renal

Increased urea Creatinine increasing by


Hyponatraemia
Lower creatinine 45-130 mmol/L/day
Urea, creatinine Hyperkalaemia
compared to renal Hyperkalaemia
and electrolytes Hyperchloraemic
and post-renal Hypocalcaemia
acidosis
Hypernatraemia Hyperphosphataemia

Granular and epithelial


cell casts, red cell casts,
Urinalysis Often normal
pyuria, haematuria,
proteinuria

Possible structural
abnormality e.g. Obstruction of urinary
Renal ultrasound Empty bladder horseshoed or tract (full bladder),
absent kidney, renal hydronephrosis
parenchymal disease.

eGFR Reduced Reduced Reduced

8.4.4 Management 8
Management of underlying cause
Treatment of the underlying cause of AKI usually restores kidney function to normal.
Pre-renal
– Correct any dehydration, hypovolaemia or acute blood loss (see Chapter 2, Section 2.2 and
Section 2.5 and Chapter 5, Section 5.3).
– Treat shock or circulatory impairment contributing to hypotension (see Chapter 2, Section 2.2).
Renal (intrinsic)
– Manage PIGN (and nephrotic syndrome if present). See Section 8.2 and Section 8.3 respectively.
– Remove any nephrotoxic medications.
– Provide supportive care (e.g. fluid management, pain control, nutritional support) for
conditions that do not have definitive treatment, to allow time for natural resolution and
recovery of kidney function (e.g. ATN, nephrotoxic kidney injury, HUS).
– Treat sepsis (see Chapter 3, Section 3.2).
– Treat malaria (see Chapter 3, Section 3.4).
Post-renal
– Relieve urinary outflow obstruction, e.g. insert urinary cathetere in boys with suspected
or confirmed posterior urethral valves. Children often become temporarily polyuric
after relieving urinary outflow obstruction – measure urine output and replace fluid and
electrolytes as needed (see Chapter 15, Section 15.2 and Section 15.3).
– Refer for definitive surgical management.

d Horseshoe kidney is when the kidneys are fused together at the lower end, creating the shape of a ‘U’ or
horseshoe.
e If urinary catheter is unavailable, a small NG tube can be used to relieve urinary outflow obstruction temporarily
for emergency relief.

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Symptomatic management
Until the underlying cause can be identified and treated, symptomatic management is required.
This can be complex and challenging.

Fluid overload
– Fluid restriction: daily fluid requirements should only be to replace losses i.e. urine, vomiting,
diarrhoea and insensible lossesf. If significant fluid overload (displaced apex beat, distended
neck veins, pulmonary oedema, severe hypertension), restrict intake to replacement of
insensible losses only.
– Administer furosemide IV 2-5 mg/kg over 1 hour. May be repeated if there is a good diuretic
response (max. 1 g per day).
– Monitor and record blood pressure and fluid balance accurately at least 2 times daily.
– Weigh patient daily.
– Do not add potassium to oral or IV fluid intake.

Hypertension
– Measure blood pressure when the child is at rest and relaxed and ensure correct sized
cuff is used to avoid over or underestimated readingsg (see MSF Manual of Nursing Care
Procedures, Procedure: Haemodynamic assessment).
– Start amlodipine PO 0.1 mg/kg once daily if blood pressure is over the 95th centile for age
(see Appendix 17). Monitor blood pressure carefully for 1-2 hours after administration.
Increase to 0.2 mg/kg once daily if necessary.
– Treat hypertension as an emergency if there are signs of hypertensive crisis (headache,
blurred vision, seizures) or if blood pressure is 20 mmHg over the 95th centile for age.
Untreated hypertensive crisis can lead to cerebral haemorrhage, blindness and death:
• Administer furosemide IV 1-2 mg/kg over 3 to 5 minutes if fluid overloaded.
• Start labetalol via continuous IV infusion at a rate of 0.5-1 mg/kg/hr. Monitor blood
pressure every 15 minutes and increase dose gradually according to response up to a
maximum of 3 mg/kg/hr. Aim for a gradual reduction in BP until BP is ≤ 95th centile for age
(see Appendix 17). Labetalol may cause bronchoconstriction therefore should be avoided
in children with asthma or chronic lung disease. If labetalol is unavailable, atenolol PO
1-2 mg/kg once daily can be given as an alternative.

Hyperkalaemia
– Repeat serum potassium urgently to verify results, ideally via venepuncture to avoid
sampling haemolysis which will result in an inaccurately high potassium.
– Avoid potassium-rich foods (e.g. bananas, oranges, raisins, tomatoes, avocados, nuts).
– Use only fresh blood for transfusion (if required).
– Treat hyperkalaemia when K+ > 6 mmol/L, especially if there are signs of hyperkalaemia on
ECG (peaked T waves, wide QRS complex, arrythmias):
• Administer nebulised salbutamol to promote potassium uptake into cells:
▹ < 5 years: 2.5 mg
▹ ≥ 5 years: 5 mg
• Administer calcium gluconate 10% IV 0.5 mL/kg (max. 10 mL) over 3 minutes to stabilise
cardiac muscle excitability.

f Insensible fluid loss is the body fluid lost through the skin and respiratory tract that is not easily measurable.
Estimated daily insensible losses are calculated according to body weight as follows: 1-10 kg = 25 mL/kg;
> 10-20 kg = 12.5 mL/kg; > 20 kg = 5 mL/kg.
g Blood pressure cuff should be 2/3 of the length of the upper arm. A blood pressure cuff that is too small will
give a falsely high blood pressure reading, while one that is too large will give a falsely low reading.

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• If central venous access in situ, and the patient can be cared for in an ICU environment
with adequate monitoring and staffing levels, administer a mixed infusion of glucose
(dextrose) 50% 2 mL/kg and short-acting insulin 0.05 IU/kg in the same syringe over
5 to 10 minutes using a syringe pump, to promote intracellular potassium shift. Close
monitoring of blood glucose level (BGL) is required before, during and after infusion
(within an hour of administration), as insulin can cause a rapid fall in BGL.

Other considerations
– Ensure medication dosages are adapted according to renal function where necessary, and
stop all nephrotoxic drugs (e.g. gentamicin, and NSAIDs).
– If the patient has metabolic acidosis, and blood gas analysis and adequate monitoring are
available, consider correction with sodium bicarbonate according to local protocol.
– Optimise caloric value in any nutritional intake as children with AKI are in a hypercatabolic
state (see Chapter 15, Section 15.5). The majority of calories should be given as carbohydrates.
– Consider referral for dialysis if no improvement despite the above measures and correction
of the underlying cause, or seek specialist support to assist with insertion of a peritoneal
dialysis catheter if transfer is not possible.

8.4.5 Prognosis
The prognosis of AKI is directly dependent on the underlying cause and its potential for
resolution, however, children who have suffered AKI from any cause are at risk of developing
irreversible chronic or even end-stage renal failure which may occur years after the original 8
insult. Annual follow-up is recommended to monitor blood pressure and check urine dipstick
for proteinuria.

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8.5 Acute painful scrotum

Acute painful scrotum may indicate a serious underlying problem and should be promptly
evaluated to exclude conditions that may impact the viability of the testis. It is a common
complaint in young and adolescent boys. Potential causes of acute painful scrotum include
testicular torsion, epididymitis, trauma, orchitis, strangulated inguinal hernia and torsion of
the testicular appendages, with the latter being the most common cause23. Other conditions
can cause referred pain to the scrotum, including urinary tract infection, urethritis, renal calculi
and intra-abdominal pathologies.

8.5.1 Clinical features


Diagnosis is clinical in most cases and a thorough description of the pain and associated
features can help to differentiate between causes24. Presence or absence of fever, trauma
and previous similar episodes can also be helpful. Scrotal oedema and erythema are common
findings in acute painful scrotum and do not help to differentiate between causes.

Scrotal examination
Inspection
Look for any obvious swellings, lesions, trauma or discharge. Identify the presence of a ‘blue
dot’ which indicates ischaemia in torsion of the testicular appendages.

Palpation
Gently palpate the testis to identify the following:
– Tenderness: palpation may reveal a specific point of tenderness suggestive of testicular
appendage torsion or epididymitis, or more generalised testicular or scrotal tenderness
seen in testicular torsion.
– Position, orientation, and size of testis.
– Texture and character of testis, e.g. firm vs normal (hard-boiled egg); fixed vs mobile.
– Swellings of testis or surrounding tissue, e.g. any associated or reactive hydrocoele.

Transillumination
Transilluminate any identified swellings to differentiate between solid and cystic or fluid-filled
swellings. Fluid-filled swellings such as hydrocoeles will glow bright red (transilluminate) when
a light is shone through them, while solid masses will appear dark.

Reflexes
Test for presence or absence of the cremasteric reflex on the affected side by stroking the
inside of the upper thigh. Elevation of the testis on the same side indicates a positive reflex.
Consider testicular torsion in the absence of cremasteric reflex.

Table 8.4 outlines the main features of the three most common causes of acute painful scrotum
in children.

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Table 8.4 - Differentiation of main causes of acute painful scrotum (adapted from UpToDate25)

Torsion of testicular
Testicular torsion Epididymitis
appendages

Onset of pain Acute, sudden Acute, sudden Subacute, gradual

Location Whole testicle initially, Localised to torsed Localised to epididymis


of pain then more widespread. appendage initially, initially, then more
May be associated with then whole testis widespread
lower abdominal or
inguinal pain

Character Constant, severe Constant, mild to Usually mild to


of pain pain. Occasionally severe pain moderate; may be relief
intermittent if testicle is of pain with elevation
torsing and detorsing of testis (Prehn sign)

Specific scrotal Testis high in scrotum Palpable hard tender Swelling localised
features and may be lying mass at superior or to epididymis;
transverse due to inferior pole of testis Inflammatory nodule
twisting of cord; testis in an otherwise soft on epididymis may be
hard on palpation; testicle; ‘Blue dot’ sign; palpable
reactive hydrocoele Reactive hydrocoele
common; cremasteric occasionally 8
reflex absent on side of
torsion

Associated Nausea, vomiting, loss None Painful urination,


symptoms of appetite urethral discharge;
Fever

Typical age Around puberty, but Pre-pubertal (peak age Post-pubertal if


can occur in neonates 7-12 years) associated STI; pre-
pubertal

Clues in the Previous self-resolving Recent increase in size Recent viral infection,
history episodes of similar pain of testes (pre-pubertal especially in pre-
(intermittent torsion); enlargement); more pubertal boys
more common in common in winter
winter

Urinalysis Normal Normal Pyuria common

Complications
Testicular torsion that is not promptly identified and treated can lead to significant ischaemia
of the affected testicle such that it is no longer viable and requires removal. Irreversible
ischaemia and necrosis can occur in as little as 6 hours from onset23, depending on the degree
of torsion, therefore testicular torsion is considered a surgical emergency.

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Chapter 8: Renal and genitourinary tract

8.5.2 Investigations
– Urinalysis and culture
– Gram stain (with or without culture) of any discharge
– Doppler ultrasound of scrotum: may show a hypoechoic testis with reduced or no perfusion
in testicular torsion.

8.5.3 Management
Management depends on the most likely cause, as outlined below.

Testicular torsion
If testicular torsion is suspected, urgent surgical referral is required for surgical detorsion and
orchidopexy (fixation of the testicle in the scrotum). If emergency surgery is not available, or
if there is likely to be a long delay in referral, manual detorsion should be attempted to try to
restore blood flow and increase the chances of maintaining viability of the testis while the
patient awaits surgery26:
– Give adequate analgesia and sedation (see Chapter 15, Section 15.4).
– Lie the patient on his back.
– Stand at the patient’s feet and rotate affected testicle away from the midline, outwards
towards the thigh (medial to lateral) at least one complete 360-degree rotation. More than
one rotation may be necessary to fully detorse the testicle, as torsion of more than 360
degrees is possible.
– Re-evaluate the patient for signs of successful detorsion such as instant relief of pain due to
rapid return of blood flow to the testis, and lower position of the testis in the scrotum.
– If there is no relief of pain or the pain worsens during the procedure, attempt to rotate the
testicle in the opposite direction (lateral to medial).
Surgical exploration is necessary even after clinically successful manual detorsion, to ensure
complete resolution and to prevent recurrence by performing a bilateral orchidopexy.

Torsion of the testicular appendages


Management is conservative with rest, analgesia, anti-inflammatory medications and scrotal
elevation. Symptoms usually resolve within 7 days.

Epididymitis
Treatment depends on likelihood of associated sexually transmitted infection and/or urinary
tract infection. If there is pyuria or positive urine culture, antibiotic treatment should be given
for urinary tract infection (see Section 8.1). Epididymitis with negative urinalysis and culture is
most likely a post-viral inflammatory process and is therefore treated conservatively with rest
and analgesia27,28,29.

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8.6 Paraphimosis

Paraphimosis refers to a retracted foreskin that cannot be returned to its normal anatomical
position over the glans of the penis. When the foreskin is left retracted for some time, it creates
a circumferential restrictive band of tissue that causes congestion and subsequent oedema of
the glans, further limiting the ability to reduce the foreskin30. It only occurs in non-circumcised
or partially circumcised males.

8.6.1 Clinical features


Predisposing factors and causes for paraphimosis include31:
– Phimosis: a partial phimosisa may predispose patients to paraphimosis when the foreskin is
retracted for cleaning, passing urine or manipulation/stimulation.
– Iatrogenic: failure to return foreskin to usual position after genitourinary procedures such as
urinary catheterisation.
– Penile trauma and sexual activity are uncommon in pre-adolescent males.
Diagnosis is usually evident based on history and clinical findings. Patients typically complain
of penile pain and swelling.
8
Examination
Clinical examination reveals:
– Significant pain on examination, particularly tenderness of the glans and retracted foreskin.
– Oedema of the glans and foreskin.
– Constricting ring of tissue immediately behind the head of the penis (ensure that there is no
foreign body causing constriction, e.g. hair, cloth, jewellery).
– Flaccid and unaffected penile shaft.
– Decreased urinary stream in infants and young males.
In later stages:
– Firm, inelastic glans with blue or black discoloration, indicating ischaemia (rare).
– Bladder distention due to complete urinary obstruction.

Complications
If left untreated, affected tissues become increasingly oedematous and ischaemia ensues,
causing local skin necrosis. In very rare cases penile necrosis, gangrene and autoamputation
may occur.

8.6.2 Management
Paraphimosis should be considered a urologic emergency, requiring urgent reduction of the
foreskin to its anatomical position to prevent further swelling and complications. Adequate
analgesia is crucial to facilitate manipulation, and parenteral analgesia may be required.

a Partial phimosis, when the preputial opening is too small to easily fit over the glans, is usually physiologic in
young boys but may also occur after infection, inflammation, or trauma. Up to 10% of uncircumcised males will
have physiologic phimosis at 3 years of age.

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Technique32,33
– Analgesia:
• Apply lidocaine 2% gel or EMLA creamb to the glans and distal penile shaft 30-60 minutes
before the procedure and cover in plastic wrap to keep the cream in place.
• Consider parenteral analgesia or procedural sedation (see MSF Standards for Paediatric
Procedural Sedation) if extreme pain limits ability to perform reduction procedures.
– Reduction of oedema:
• Encircle the glans with a gloved hand and apply even, circumferential pressure for several
minutes to reduce swelling.
• Alternatively, wrap a self-adhesive bandage around the penis approximately 3 times,
starting at the glans and continuing up the penile shaft. The first layer should be loosely
wrapped with subsequent layers becoming tighter to exert a constant, steady pressure.
The wrap should be left in place for 10-15 minutes before removal.
• Application of a swab soaked with glucose (dextrose) 50% for 1 hour may be a useful adjunct
to reduce swelling by osmosis. In the absence of glucose (dextrose) 50%, granulated sugar
can be poured onto the swollen glans and foreskin and kept in place with a glove or swab
until swelling subsides (1-2 hours)34.
• The 'iced-glove’ method can also be used to reduce swelling35, though re-evaluation every
15-20 minutes is essential to prevent cold and/or ischaemic injury. Fill a glove with ice and
close with a knot then invaginate the thumb of the glove by sliding it over the shaft of the
penis so that the ice surrounds the penis31,36.
– Manual reduction of foreskin:
• Paraphimosis reduction should be attempted only after swelling has begun to subside via
the chosen method (see above).
• Place two thumbs on glans penis and position index and long fingers immediately behind
swollen constricting ring of foreskin.
• Apply gentle consistent traction on the ring of foreskin to ease foreskin back over the
glans while exerting counterpressure on the glans with the thumbs.
• The constricting ring should come over the glans along with the foreskin.
If manual reduction fails, refer for surgical reduction without delay. If surgery is unavailable or
there is likely to be a long delay in referral, a dorsal slit procedure should be attempted:
– Ensure adequate analgesia (see above) including procedural sedation (see MSF Standards
for Paediatric Procedural Sedation) and penile block, if possible.
– Disinfect and drape the area.
– Using a scalpel, make a 1-2 cm longitudinal incision on the dorsal aspect of the penile shaft
(see Figure 8.1):
• Start the incision just above the tight ring of constricted foreskin behind the swelling and
transect the tight ring of skin (Option 1A).
• Begin the incision superficially and gradually cut deeper until the ring is released, without
removing any skin.
• There should be a palpable and visible release of the paraphimotic ring if successful, and
an associated reduction in swelling.
• If done correctly, the released ring opens up to create a diamond shaped incision
(Option 1, B) that can then be sutured horizontally (Option 1C).
• If the ring is not completely released, or there is too much swelling of the foreskin, extend
the incision to the edge of the foreskin to open it completely (Option 2A and 2B).

b EMLA cream is a mixture of lidocaine 2.5% and prilocaine 2.5%.

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– Roll the foreskin over the glans to completely reduce the paraphimosis once the ring is cut.
If necessary, manually decompress residual swelling before/during this step to help reduce
the paraphimosis.
– Suture the edges of the incision with absorbable sutures, depending on the shape and size
of the incision after reduction of the foreskin over the glans (Option 1C or Option 2C).
– Following dorsal slit procedure, consider referral for circumcision.

Figure 8.1 - Dorsal slit procedurec

Post-reduction care
Following successful reduction of paraphimosis, patients and parents/carers should be advised:
– Not to retract the foreskin for a few days.
– That only the child should retract his foreskin for cleaning and should avoid irritants.
– To ensure that the foreskin is immediately replaced over the glans after retraction.
– That circumcision is usually unnecessary unless paraphimosis is recurrent or surgery was
required to reduce the paraphimosis.

c Original illustration by Sarah Imani.

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References Chapter 8

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21. Olowu WA, Niang A, Osafo C, et al. Outcomes of acute kidney injury in children and adults
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22. Ramage I. Acute renal failure in paediatrics (management and investigation). Published
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24. Brenner JS, Aderonke O. Evaluation of non-traumatic sctoral pain or swelling in children
and adolescents. UpToDate. Published November 2021.
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swelling-in-children-and-adolescents
25. Brenner JS, Aderonke O. Causes of scrotal pain in children and adolescents. UpToDate.
Published April 2022.
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26. Ringdahl E, Teague L. Testicular torsion. Am Fam Physician. 2006;74(10):1739-1743.
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27. Santillanes G, Gausche-Hill M, Lewis RJ. Are Antibiotics Necessary for Pediatric Epididymitis?:
Pediatr Emerg Care. 2011;27(3):174-178.
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28. Gkentzis A, Lee L. The aetiology and current management of prepubertal epididymitis.
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29. Cristoforo TA. Evaluating the Necessity of Antibiotics in the Treatment of Acute Epididymitis
in Pediatric Patients: A Literature Review of Retrospective Studies and Data Analysis.
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30. Samm BJ, Dmochowski RR. Trauma injuries and conditions affecting the penis, scrotum,
and testicles. Postgrad Med. 1996;100(4):187-200.
https://doi.org/10.3810/pgm.1996.10.101
31. Tews M. Paraphimosis: Clinical manifestations, diagnosis, and treatment. UpToDate.
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32. Choe JM. Paraphimosis: current treatment options. Am Fam Physician. 2000;62(12):
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33. Pohlman GD, Phillips JM, Wilcox DT. Simple method of paraphimosis reduction revisited:
Point of technique and review of the literature. J Pediatr Urol. 2013;9(1):104-107.
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34. González Fernández M, Sousa Escandón MA, Parra Muntaner L, López Pacios JC. Azúcar:
tratamiento de elección en la parafimosis irreductible [Sugar: treatment of choice in
irreducible paraphimosis]. Actas Urol Esp. 2001;25(5):393-395.
https://doi.org/10.1016/S0210-4806(01)72638-1
35. Mackway-Jones K, Teece S. Best evidence topic reports. Ice, pins, or sugar to reduce
paraphimosis. Emerg Med J EMJ. 2004;21(1):77-78.
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36. Houghton GR. The ‘iced-glove’ method of treatment of paraphimosis. Br J Surg. 2005;
60(11):876-877.
https://doi.org/10.1002/bjs.1800601110

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Endocrinology

9.1 Diabetes mellitus (type 1)..................................................................................... 281


9.1.1 Diagnosis....................................................................................................... 281
9.1.2 Management................................................................................................. 282
9.2 Diabetic ketoacidosis............................................................................................. 283
9.2.1 Diagnosis....................................................................................................... 283
9.2.2 Management................................................................................................. 284
9.2.3 Management of complications...................................................................... 289
9.2.4 Resolution of DKA and transition to subcutaneous (SC) insulin.....................291
9.2.5 Discharge criteria and follow-up....................................................................293
9.3 Hypoglycaemia...................................................................................................... 294
9.3.1 Clinical features and assessment...................................................................294
9.3.2 Management................................................................................................. 295
References Chapter 9................................................................................................... 296 9
Chapter 9: Endocrinology

9.1 Diabetes mellitus (type 1)

Type 1 diabetes mellitus (T1DM) is caused by destruction of beta pancreatic cells that produce
insulin, leading to an absolute insulin deficiency. It most commonly presents in childhood, with
a first peak of onset between 4 and 6 years of age and a second peak between 10 and 14 years of
age. T1DM is an autoimmune disease that is thought to be triggered by various environmental
factors in people with a genetic predisposition. It is one of the most common chronic diseases
in childhood, though there is wide geographical and ethnic variation in incidence1. Prognosis
depends on availability of treatment, with significantly reduced life expectancy in children and
young adults with untreated or poorly controlled diabetes.

Clinical features
Most commonly, children present with general malaise and lethargy, and careful history elicits
the classic triad of:
– Polyuria (increased urination)
– Polydipsia (increased drinking)
– Weight loss
If symptoms go unrecognized, acidosis ensues, and the patient will present in diabetic
ketoacidosis requiring emergency treatment (see Section 9.2).

Complications
Hypoglycaemia is a common complication for children with T1DM on treatment (see 9
Section 9.3). Long-term complications from poorly controlled diabetes include neuropathy,
retinopathy, nephropathy, and cardiovascular disease.

9.1.1 Diagnosis
The diagnosis of diabetes is based on the presence of one of the following diagnostic criteria,
in patients presenting with classic signs and symptoms2:

Test Result

Fasting blood glucose ≥ 126 mg/dL (7 mmol/L)

2-hour post-load blood glucose ≥ 200 mg/dL (11.1 mmol/L)

Random blood glucose ≥ 200 mg/dL (11.1 mmol/L)

Glycosylated haemoglobin (HbA1c) ≥ 48 mmol/mol (6.5%)

Fasting blood glucose = no calorific intake for at least 8 hours; 2-h post-load blood glucose = performed 2 hours
after ingestion of 1.75 g/kg oral glucose; Random blood glucose = measurement at any time during the day;
Glycosylated haemoglobin (HbA1c) = reflects average glycaemia over the previous 10-12 weeks.

In asymptomatic patients with elevated values, repeat testing is recommended as soon as


possible in the following days to confirm the diagnosis, ideally using the same test.

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9.1.2 Management
T1DM is a chronic illness that requires lifelong treatment with insulin (see Section 9.2.4 for
more detail on insulin initiation and titration). Age-appropriate education for the child, as well
as general education for the parent/carer, is an important part of the management plan and
information should be repeated at every opportunity to ensure sufficient understanding of the
disease and how to manage complications.
Education on the following is required:
– Basic understanding of T1DM and its cause (highlighting that it is not caused by poor diet)
– Dietary intake
– Insulin administration
– Monitoring of blood glucose level (BGL) using a blood glucose monitor
– Hypoglycaemia symptoms and management
– Hyperglycaemia and ketosis detection and management
– Sick-day management
Refer children with newly diagnosed diabetes for long-term follow-up, depending on local
resources, and arrange:
– At least once-weekly follow-up for the first month.
– Home glucose monitoring. Each patient should be provided with a glucometer and enough
strips for a minimum of three BGL measurements per day until the medical visit. A notebook
should be provided to record the BGL measurements taken.
Refer to local or national guidelines, where available, for more detail on education material
and long-term follow-up.

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9.2 Diabetic ketoacidosis

Diabetic ketoacidosis (DKA) is a medical emergency defined by the combined presence of


hyperglycemia, metabolic acidosis and ketosis in a child with diabetes. DKA can be fatal if
not diagnosed rapidly and treated promptly. Fluid replacement is initially more important
than initiating insulin as early mortality is due to dehydration and shock, but the clinical and
chemical changes must be corrected gradually to prevent complications. Cerebral oedema is a
potential and severe complication associated with the management of DKA.
In DKA there is an absolute deficiency of insulin resulting in hyperglycaemia and increased
lipolysis, leading to increased ketones in the blood, glycosuria and osmotic diuresis (which
is associated with fluid loss and potential electrolyte abnormalities). The increase in ketones
leads to a metabolic acidosis with an increased anion gap.
In up to 80% of children with type 1 diabetes mellitus (T1DM), DKA is the first presentation of
the condition3. Though much less common, children with type 2 diabetes may also present
with DKA.

9.2.1 Diagnosis
Check if known T1DM. Enquire about any interruption to or inadequate insulin therapy. If not
previously diagnosed with diabetes, enquire about symptoms of T1DM, including polydipsia,
polyuria, fatigue, irritability, vomiting, abdominal pain, weight loss and family historya. 9
DKA is diagnosed when all of the following 3 criteria are present:
– BGL ≥ 200 mg/dL (≥ 11.1 mmol/L)
– Ketonuria (++ or more)
– Plus, one or more of the following clinical features:
• Kussmaul breathingb (deep, rapid, sighing)
• Fruity breath
• Decreased level of consciousness
• Signs of dehydration
• Abdominal pain and/or vomiting
• Shock
Where possible, confirm metabolic acidosis: serum bicarbonate < 15 mmol/L or blood pH < 7.3.
Consider any precipitating factors:
– Infections (e.g. pneumonia, malaria, urinary tract infections)
– Major surgical conditions (e.g. acute abdomen)

a Family history of T1DM increases the likelihood of diabetes, however many children with T1DM have no family
history of the condition.
b Kussmaul breathing is deep, laboured breathing that is usually rapid but respiratory rate may be normal. It is a
form of hyperventilation which aims to remove carbon dioxide in response to metabolic acidosis.

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9.2.2 Management
Treatment objectives are:
– Resuscitation and correction of shock
– Fluid replacement
– Insulin to reduce glucose gradually, aiming for an hourly glucose reduction of maximum
90 mg/dL/hr (5 mmol/L/hr)
– Maintenance of potassium concentration
– Identification and management of underlying condition or precipitating factors.

Resuscitation and correction of circulatory impairment or shock4


Assess and manage ABCDE:
– A: Ensure patent airways. If necessary, protect airway.
– B: Administer oxygen > 6 L/min via mask (use non-rebreathing mask if available), aiming for
SpO2 between 94-98%.
– C: IV access and take blood for BGL, FBC, electrolytes and send blood for culture.
– Measure weight and estimate the % of body weight lost in dehydration (i.e. the fluid deficit):
• If recent weight available, compare to current weight to calculate fluid deficit.
• If recent weight unavailable, standard fluid deficit in DKA is 7.5%, or 10% if considered to
be in severe DKA.
– Treat circulatory impairment according to severity and level of consciousness (using
Paediatric Glasgow Coma Scale (GCS), see Appendix 13):
• Shock: administer a fluid bolus of 10 mL/kg Ringer lactate (or sodium chloride 0.9%) IV
over 15-30 minutes then reassess after. If signs of shock persist, repeat another bolus.
• Not in shock and GCS > 7: administer 10 mL/kg Ringer lactate (or sodium chloride 0.9%) IV
over 60 minutes.
• Not in shock but GCS ≤ 7: start IV maintenance fluids (see Chapter 15, Section 15.2).
• Avoid excessive fluid boluses due to the risk of cerebral oedema.
– Insert a nasogastric tube (NGT, conical tip) if unconscious or has recurrent vomiting. Leave
on free drainage.
– Keep nil by mouth (NBM) until alert and stable.
– Measure urine output and check for urinary ketones regularly while on insulin infusion:
hourly if urinary catheter in situ, or each time the patient passes urine otherwise.
Note: Bicarbonate administration is not recommended and should not routinely be administered
as it can worsen hypokalaemia.
Monitor closely and continue treatment in an intensive care area with capacity for increased
nursing care due to frequency of monitoring required:
– Measure and record BGL every hour until stabilized and insulin infusion stopped.
– Evaluate and record vital signs and level of consciousness every hour.
– Where available, measure electrolytes, venous pH and serum bicarbonate every 2 to 4 hours.
– Monitor fluid input and output every hour:
• Record all fluids administered.
• Urinary catheterization should be avoided but may be useful in a child with impaired
consciousness. Consider alternative methods for estimating urine output (e.g. weighing
nappies, weighing soiled bedding, urination into a potty/urinal if possible).
• Normal urine output is > 1 ml/kg/hour.
Check that there has been urine output following resuscitative boluses. If no urine
output, reassess for shock/circulatory impairment and for urinary retention. Start fluid
replacement without potassium if no urine output and add potassium to fluids only once urine
output confirmed.

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Fluid replacement
Once resuscitation is complete, start IV fluid administration. Add potassium chloride (KCl) to
IV fluids only once urine output has been confirmed. Together with appropriate maintenance
fluid requirements, standard fluid infusion calculations in DKA include: a 7.5% deficit to be
replaced over 48 hours; or, if considered to be in severe DKA (and/or confirmed with pH < 7.1),
a 10% deficit replaced over 48 hours (see Table 9.1 and Table 9.2 below)4.
Two-bag method
– Prepare two bags of IV fluid solutions with different glucose concentrations but identical
electrolyte content (see Step 1 below).
• IV fluid bag #1 has no added glucose.
• IV fluid bag #2 has added glucose.
– Ringer lactate (RL) is the preferred IV fluid, if not available, use sodium chloride 0.9% (NaCl
0.9%) as alternative.
– Ensure each bag of IV fluid is labelled with date, time, amount of KCl added (only add KCl if
urine output is confirmed) and signature of the person making the fluid bag.
– Set up a two-bag system to allow each bag to be run either separately, or at the same time,
without having to manipulate the IV line (see Figure 9.1 below):
• Hang both IV fluid bags, connect each to a paediatric infusion set and prime the IV lines.
• Connect the end of each paediatric infusion set to the same IV cannula using a 3-way
stopcock.
• Turn the 3-way stopcock as required depending on whether both bags are running
simultaneously or separately.
– Adjust the rates of each bag of IV fluid to respond to changes in BGL (see Step 2 page 286).

Figure 9.1 - Two-bag method for delivery of IV fluids in DKAc


9

c Original illustration by Sarah Imani

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Steps for administration of two-bag method of IV fluids:

Step 1: Preparation of IV fluids for two-bag method


Make IV fluid bag #1:
• Add 40 mmol/L KCl (use KCl 15%, 150 mg/mL = 2 mmol/mL (10 mL ampoule))
RL (or NaCl 0.9%) Volume of KCl 15% to add Final IV fluid bag #1
1000 mL 20 mL (2 ampoules) RL + 40 mmol/L KCl (or
500 mL 10 mL (1 ampoule) NaCl 0.9% + 40 mmol/L KCl)

Make IV fluid bag #2:


1. Add glucose (dextrose) 50% (G50%) to a bag of Ringer lactate (RL) to make G10%-RL (or
G10%- NaCl 0.9%). Follow instructions below.
2. Add 40 mmol/L KCl.
1. Make G10%-RL (or G10%-NaCl 0.9%)
RL (or NaCl 0.9%) Remove Add Intermediary solution
1000 mL G10%-RL
1000 mL 200 mL G50% 200 mL
(or G10%-NaCl 0.9%)
500 mL G10%-RL
500 mL 100 mL G50% 100 mL
(or G10%-NaCl 0.9%)
2. Add potassium to make final IV fluid bag #2
G10%-RL
Volume of KCl 15% to add Final IV fluid bag #2
(or G10%-NaCl 0.9%)
1000 mL 20 mL (2 ampoules) G10%-RL + 40 mmol/L KCl
(or G10%-NaCl 0.9%
500 mL 10 mL (1 ampoule) + 40 mmol/L KCl)

Step 2: Which IV fluid bag(s) at what speed?


Refer to Table 9.1 and Table 9.2 for fluid rates corresponding to standard, half or high-speed.
• Aim for a glucose reduction of maximum 90 mg/dL/hr (5 mmol/L/hr).
• Target blood glucose is between 145-215 mg/dL (8-12 mmol/L).
Blood glucose level (mg/dL or mmol/L) Which bag(s) at what speed?
Bag #1 at standard-speed
> 270 mg/dL (> 15 mmol/L)
None of bag #2*
Bag #1 at half-speed
145 to 270 mg/dL (8-15 mmol/L)
Bag #2 at half-speed
None of bag #1
70 to < 145 mg/dL (4-8 mmol/L)
Bag #2 at standard-speed
< 70 mg/dL (< 4 mmol/L) None of bag #1
Call clinician immediately Bag #2 at high-speed**
* These patients are receiving insulin but no glucose at this stage.
** This is a large volume of fluid and should only be continued long enough to raise the glucose to > 70 mg/dL
(or > 4 mmol/L), then immediately decrease the rate to standard-speed rate. If BGL decreases too rapidly
despite adjusting the fluid rates, insulin dose needs to be decreased. See insulin therapy, page 288.

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Table 9.1 - DKA treatment IV fluid rates (weight 3 kg to 40 kg)

Note on fluid calculations:


• Together with appropriate maintenance fluids, fluid rate calculations include replacement
of deficit over 48 hours (i.e. correction of dehydration).
• Standard speed is based on the assumption of a 7.5% fluid deficit (moderate DKA).
• High speed is based on the assumption of a 10% fluid deficit (severe DKA).

Rate (mL/hr) Rate (mL/hr)


Weight Weight
Half Standard High Half Standard High

3 kg 9 17 18 22 kg 48 96 108

4 kg 11 22 24 23 kg 50 99 111

5 kg 14 28 30 24 kg 51 102 114

6 kg 17 33 37 25 kg 52 104 117

7 kg 20 39 43 26 kg 54 107 120

8 kg 22 44 49 27 kg 55 109 123

9 kg 25 50 55 28 kg 56 112 126

10 kg 28 56 61 29 kg 57 114 129
9
11 kg 30 59 65 30 kg 59 117 133

12 kg 32 63 69 31 kg 60 119 136

13 kg 33 66 73 32 kg 61 122 139

14 kg 35 70 77 33 kg 63 125 142

15 kg 37 73 81 34 kg 64 127 145

16 kg 39 77 85 35 kg 65 130 148

17 kg 40 81 89 36 kg 66 132 151

18 kg 42 84 94 37 kg 68 135 154

19 kg 44 88 98 38 kg 69 137 157

20 kg 46 91 102 39 kg 70 140 160

21 kg 47 94 105 40 kg 71 142 163

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Table 9.2 - DKA treatment IV fluid rates (weight > 40 kg)

Speed (mL/hr)
Weight
Half Standard High

41 kg 73 145 166

42 kg 74 148 170

43 kg 75 150 173

44 kg 77 153 176

45 kg 78 155 179

46 kg 79 158 182

47 kg 80 160 185

48 kg 82 163 188

49 kg 83 166 191

50 kg 84 168 194

51 kg 86 171 197

52 kg 87 173 200

53 kg 88 176 203

54 kg 89 178 207

55 kg 91 181 210

Insulin therapy
– Once shock corrected, and one hour after starting IV fluid replacement, start IV insulind. Add
50 IU of soluble insulin to 49.5 mL sodium chloride 0.9% to make a total of 50 mL. Ensure
insulin preparation is double checked by two qualified healthcare professionals.

By syringe pump:
• < 2 years, insulin IV: 0.05 IU/kg/hour (lower dose)
• ≥ 2 years, insulin IV: 0.1 IU/kg/hour (higher dose)

d Ensure insulin is double-checked by 2 staff to ensure medicine safety. Both the syringe and line should be
changed at least once every 24 hours.

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– If no syringe pump is available, administer insulin IM: 0.1 to 0.2 IU/kg every two hours,
depending on age (as above).
– Note: subcutaneous route is not recommended for DKA treatment due to varied absorption
from poor perfusion.
– Decrease insulin dose if BGL decreases too rapidly (> 90 mg/dL/hr or > 5 mmol/L/hr) despite
adjusting the fluid rates using the two-bag method.
– Stop insulin if BGL < 70 mg/dL (< 4 mmol/L) and does not improve with adjustment of IV
fluids rates and restart insulin once BGL ≥ 90 mg/dL (≥ 5 mmol/L).
– Insulin administration must be continued while ketonuria remains present, and glucose
intake should be increased as necessary to allow this.
– Consider increasing insulin for children on the lower dose of insulin if BGL does not decrease
over 4 hours:
• Increase to 0.1 IU/kg/hour if using IV syringe pump.
• Increase to 0.2 IU/kg every 2 hours if administering via IM injection.
Hypoglycaemia
Hypoglycaemia is a common and dangerous complication.
– Monitor BGL hourly while on insulin infusion and treat promptly when BGL < 60 mg/dL
(< 3.3 mmol/L), see Section 9.3 for treatment of hypoglycaemia.
– Verify insulin and IV fluids are correctly prepared and administered.

Maintenance of potassium concentration


– Check serum potassium levels at 2 hours and then every 4 hours (where available).
– If K < 3 mmol/L at any point, stop insulin infusion for 1 to 2 hours then recheck. If serum
potassium has dropped further, give potassium chloride syrup PO/NG: 1 mmol/kg as a single
dose and check potassium again in 2 hours.
– Where ECG monitoring is available, check for peaked T-wave indicating hyperkalaemia.
9

Management of underlying condition or precipitating factor


– Consider broad spectrum antibiotic treatment if a severe infection is likely (see Chapter 3,
Section 3.2.3).
– In malaria-endemic regions perform a malaria rapid test and treat for malaria if positive (see
Chapter 3, Section 3.4.3).

9.2.3 Management of complications


Cerebral oedema
– Is a rare but major complication with a mortality rate of over 20%5. Usually it is of sudden
onset, occurring between 6 to 12 hours after starting treatment.
– Clinical features include headache and vomiting, irritability, decreasing heart rate, increasing
blood pressure, abnormal or slow breathing pattern (Cushing’s Triad), pupillary changes,
decreasing GCS, age-inappropriate incontinence and abnormal neurological signs.
– Check for the presence of criteria for cerebral oedema (see Table 9.3 page 290).
– Start treatment if: 1 diagnostic, 2 major, or 1 major and 2 minor criteria are present.

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Table 9.3 - Criteria for the diagnosis of cerebral oedema6

Criteria for the diagnosis of cerebral oedema


1. Any one diagnostic criteria
2. Two major criteria
3. One major and two minor criteria

• Abnormal motor or verbal response to pain


• Decorticate or decerebrate posture
• Cranial nerve palsy, especially III, IV and VI (e.g. asymmetrical
Diagnostic criteria pupillary light response, asymmetrical corneal light reflex,
disconjugate gaze)
• Abnormal neurogenic respiratory pattern (e.g. grunting,
tachypnoea, Cheyne-Stokes respiratione, gasping respiration)

• Altered mental status, confusion, or fluctuating level of consciousness


• Sustained HR deceleration (decrease more than 20 bpm) not
Major criteria
attributable to improved intravascular volume or sleep state
• Age-inappropriate urinary incontinence

• Vomiting
• Headache
Minor criteria • Lethargy or not easily rousable
• Diastolic blood pressure > 90 mmHg
• Age < 5 years

Treatment
– Manage A and B:
• Support airways.
• Administer oxygen via mask with reservoir bag (if available).
– Assess C and check BGL: exclude hypoglycaemia or shock as a cause for change in neurological
condition.
– Insert NGT and leave on free drainage.
– Raise the head of the bed by 15 to 30 degrees (> 40 degrees can worsen raised intracranial
pressure (ICP)).
– Consider reducing IV fluids to 70% of current fluid rate.
– Consider giving hyper-osmolar solutions (if available and staff trained in its use):

hypertonic saline (3%): 3 to 5 mL/kg over 10 to 15 minutes

Alternative, mannitol IV: 0.5 to 1 g/kg over 10 to 15 minutes. Repeat after 30 minutes if
no response.

– Electrolyte monitoring is recommended if available.

e Cheyne-Stokes respiration manifests as a cycle of fast, shallow breathing that becomes deeper and slower
before leading to periodic apnoea before the cycle begins again.

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9.2.4 Resolution of DKA and transition to subcutaneous (SC) insulin


– Evaluate resolution of DKA by assessing clinical improvement, particularly with correction of
hydration, BGL control and clearance of urinary ketones.
– Once child is stable and fully alert, and has no clinical signs of acidosis:
• Start oral fluids as tolerated by the child.
• Reduce IV fluids accordingly to not exceed recommended hourly input.
– Transition to subcutaneous insulin from IV (or IM) insulin once oral fluids are well tolerated
and the child remains clinically stable.
– Calculate total daily insulin requirementf:

insulinSC: 0.3 to 0.8 IU/kg over 24 hours, in divided doses (depending on regimen
chosen, see below for details)

– Administer first SC short-acting insulin 1 to 2 hours before stopping the insulin infusion.
– Start regular SC insulin at the next mealtime and administer it pre-meal.
– Measure BGL before each meal (pre-prandial) and at night (2 am) to monitor response and
allow adjustment of insulin regime during hospital stay.
– Allow at least 48 hours to identify pattern before adjusting insulin dose unless the change is
needed to avoid an obvious risk of hypoglycaemia or significant hyperglycaemia.
– Hospitalisation is recommended for at least 1 week to ensure BGL stabilisation and to provide
diabetes education to patient and parents/carers. Introduce the idea of home glucose
monitoring in preparation for continuation on discharge. Where feasible, all patients with
diabetes should be discharged home with a blood glucose monitor and testing strips.

Recommended regimen options


If the patient has known diabetes and was already under treatment before presenting with
9
DKA, restart same SC insulin regimen as the one followed prior to this DKA event and monitor
BGL in hospital for at least 72 hours to allow any necessary modifications to be made. If this is
a new presentation of diabetes, begin SC insulin either in basal bolus regimen or 2 times daily
dosing regimen, depending on local availability of insulin (see details below).

Basal/long-acting regimen (basal bolus regimen)


– Preferred regimen, where available, as glycaemic control is best achieved using a daily basal
dose of long-acting insuling, supplemented with boluses of short-acting insulin before meals.
– Long-acting insulin should be administered at the same time every day, preferably in the
evening.
– Administer half of the calculated total daily dose as long-acting insulin once daily, and half
as short-acting insulin before meals (3 to 4 times daily):

Example for 20 kg child:


Start with 0.3 IU/kg over 24 hours = 6 IU over 24 hours
Administer 3 IU as long-acting insulin once daily and 1 IU of short-acting insulin before
each of 3 meals.

f Start at lowest dose and increase as necessary during the hospital stay to achieve optimal glycaemic control
before discharge.
g Long-acting insulins are not yet readily available in MSF projects but should be used in preference where
available.

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Twice-daily dosing regimen


– Administration of a mixture of short- and intermediate-acting insulin together, 2 times daily.
– Each dose should consist of approximately 30% short-acting and 70% intermediate-acting
insulin (see MSF Manual of Nursing Care Procedures, SOP Mixing Insulin: Short and
Intermediate-Acting).
– Premixed insulins existh and can simplify administration, however they do not allow for
individual adjustment of dose according to patient response and can be more difficult to
manage if the child does not have stable and regular access to food7.
– Administer 2/3 of the calculated total daily dose in the morning (AM) and 1/3 in the evening
(PM), before meals:

Example for 30 kg child:


Start with 0.3 IU/kg over 24 hours = 9 IU over 24 hours
Administer 6 IU as mixed 30-70 insulin in the morning and 3 IU of mixed 30-70 insulin in
the evening (before meals).

Short-acting insulin Intermediate-acting insulin

Before breakfast 2 IU 4 IU

Before evening meal 1 IU 2 IU

– Adjust insulin dosing according to morning and evening BGL measurements to achieve BGL
stabilization prior to discharge (see Table 9.4).
– Where home glucose monitoring is not possible in the twice-daily dosing regimen, consider
intermediate acting insulin only.

Table 9.4 - Titration of twice-daily subcutaneous insulin regimen


For children < 35 kg:

Pre-prandial blood glucose level (BGL)

80 to > 200 > 250 to


< 80 mg/dL > 400 mg/dL
200 mg/dL to 250 mg/dL 400 mg/dL
(< 4.5 mmol/L) (> 22 mmol/L)
(4.5-11 mmol/L) (> 11-14 mmol/L) (> 14-22 mmol/L)

Morning Reduce PM Increase PM Increase PM Increase PM


(AM) insulin dose by No changes insulin dose by insulin dose by insulin dose by
BGL 0.05 IU/kg* 0.05 IU/kg 0.1 IU/kg 0.15 IU/kg

Evening Reduce AM Increase AM Increase AM Increase AM


(PM) insulin dose by No changes insulin dose by insulin dose by insulin dose by
BGL 0.05 IU/kg* 0.05 IU/kg 0.1 IU/kg 0.15 IU/kg

* Consider reducing even more or closely follow up if hypoglycemia is symptomatic or severe.

h Premixed combinations of intermediate and short-acting insulin: INSULIN HUMAN, BIPHASIC 30-70 IU/mL,
10 mL, vial L (Lilly), DINJINSHB1VL; INSULIN HUMAN, BIPHASIC 30-70 IU/mL, 10 mL, vial N (Novo Nordisk),
DINJINSHB1VN; INSULIN HUMAN, BIPHASIC 30-70 IU/mL, 10 mL, vial S (Sanofi), DINJINSHB1VS. It is not
recommended to switch the patient from insulin type or brand.

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For children ≥ 35 kg:

Pre-prandial blood glucose level (BGL)

< 80 mg/dL 80-200 mg/dL > 200-250 mg/dL > 250 mg/dL
(< 4.5 mmol/L) (4.5-11 mmol/L) (> 11-14 mmol/L) (> 14 mmol/L)

Reduce PM Increase PM Increase PM


Morning (AM)
insulin dose No changes insulin dose insulin dose
BGL
by 4 IU by 2 IU by 4 IU

Reduce AM Increase AM Increase AM


Evening (PM)
insulin dose No changes insulin dose insulin dose
BGL
by 4 IU by 2 IU by 4 IU

9.2.5 Discharge criteria and follow-up


Patients can be discharged when they have been stabilised on subcutaneous insulin, with no
hypoglycaemia < 60 mg/dL (3.3 mmol/L) and no hyperglycaemia > 300 mg/dL (> 16.6 mmol/L)
for at least 72 hours, and the child and parent/carer have received appropriate education
about diabetes and acute management of common complications.

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9.3 Hypoglycaemia

Defined as a blood glucose concentration that is too low to maintain normal brain function.
Hypoglycaemia cannot be identified by a specific blood glucose level (BGL)8 as the threshold
triggering a neurological response occurs across a range of values. For diagnostic purposes,
the cut-off point to treat hypoglycaemia is BGL ≤ 60 mg/dL (3.3 mmol/L).
Hypoglycaemia is a medical emergency and untreated can lead to serious neurological
consequences, including irreversible disability9.
There are many conditions that can cause hypoglycaemia. Common causes include:
– Severe infection (e.g. sepsis, malaria)
– Gastroenteritis (vomiting and/or diarrhoea)
– Dehydration
– Malnutrition
– Lack of dietary intake (e.g. during acute illness)
– Iatrogenic (e.g. incorrect administration of IV fluids, quinine therapy for malaria)
– Incorrect management of a patient with known diabetes
– Intoxication (e.g. alcohol, drugs, traditional remedies)
– Congenital disorders (e.g. adrenal insufficiency, growth hormone deficiency, metabolic
disorders)

9.3.1 Clinical features and assessment


Hypoglycaemia presents with nonspecific signs and symptoms and therefore it can be difficult
to recognise. A detailed history should address the following information:
– Current medical history, including symptoms that could precipitate hypoglycaemia (e.g.
fever, vomiting and/or diarrhoea, including their frequency and duration).
– Symptoms of hypoglycaemia (see below)
– Dietary history to check features of malnutrition
– History of toxin ingestion (see Chapter 2, Section 2.9.1 for reference to list of national poisons
centres)
– Past medical history (neonatal history of hypoglycaemia, episodes suggestive of
hypoglycaemia as undiagnosed seizure disorder)
– Family history (consanguinity, unexplained infant deaths)
Perform a complete clinical examination, looking for specific symptoms and signs of
hypoglycaemia:
– Symptoms: hunger, sweating, palpitations, tremor, anxiety, paraesthesia, poor feeding,
headache, nausea
– Signs (associated with more severe hypoglycaemia): Irritability, jitteriness, lethargy, cyanosis,
pallor, tachypnoea, hypothermia, weakness, seizures, and coma. (Note that these signs are
not specific for hypoglycaemia and may be early manifestations of other disorders, including
sepsis, malaria, and respiratory distress syndrome.)
Signs indicative of underlying cause of hypoglycaemia:
– Short stature may indicate growth hormone deficiency. Poor weight gain may be caused by
hypopituitarism and primary adrenal insufficiency.
Check weight and length/height: plot on a growth chart.

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– Midline defects (e.g. a single central incisor, cleft lip or palate, umbilical hernia) and
microphallus or undescended testicles in boys may indicate hypopituitarism and/or growth
hormone deficiency.
– Hepatomegaly is common feature of some metabolic disorders.
– Hyperpigmentation suggests primary adrenal insufficiency.
Check BGL on admission of all severely sick children, or at any time during admission if there is
clinical deterioration, or lack of intake.
Where BGL is not available, treat for hypoglycaemia if clinically suspected to avoid adverse
consequences.
In malaria-endemic regions, perform a malaria rapid test.

9.3.2 Management
Treatment of hypoglycaemia varies with the degree of hypoglycaemia and the associated
symptoms.
For children with an altered level of consciousness:
– Assess and manage ABCDE (see Chapter 2, Section 2.1).
– Obtain IV or IO access.
– Administer 2 mL/kg bolus of glucose (dextrose) 10% IV/IO over 2 to 3 minutes (do not use
undiluted glucose (dextrose) 50%a). If there is a delay in obtaining IV/IO access, administer
10 mL/kg of glucose (dextrose) 10% via NGT (sit the child upright).
– After the bolus, in non-malnourished children, start IV maintenance fluids with glucose
(dextrose) 5%/Ringer lactate (G5%/RL), unless already on maintenance G5%/RL, in which
case increase maintenance to glucose (dextrose) 10%/Ringer lactate (G10%/RL).
– Repeat BGL in 30 minutes: if still hypoglycaemic repeat IV bolus of 2 mL/kg glucose (dextrose)
10% and, in non/malnourished children, increase maintenance to G10%/RL. 9
For children who are conscious, able to drink and swallow safely, give treatment orally:
– Give a sugar-containing drink or snack by mouth, such as: 1 to 2 teaspoons of table sugar
moistened with water, or 60 mL fruit juice, milk, therapeutic milk (if SAM) or breast milk, or
5 to 10 mL honey (only if > 1 year old), or 10 mL/kg of glucose (dextrose) 10% orally or via
NGT (with child in semi-sitting position), or 1 mL/kg of glucose (dextrose) 50% under the
tongue.
– Feed the child as soon as possible.
– Repeat BGL in 15 to 30 minutes: if the child is still hypoglycaemic, administer 2 mL/kg bolus
of glucose (dextrose) 10% IV and start IV maintenance fluids with G5%/RL.
If recurrent hypoglycaemia AND adrenal insufficiency is suspected, check the electrolytes if
available, and consider hydrocortisone 5 mg/kg IV (max 100 mg).

Monitoring
– Repeat BGL every 30 minutes until BGL is stable between 70 and 120 mg/dL (3.9 to
6.7 mmol/L) for two subsequent measurements.
– Thereafter, check BGL every 2 to 3 hours until it is stable for another two consecutive
measurements.

a Glucose (dextrose) 50% (G50%) solution is too viscous and irritant to be used in children. Where glucose
(dextrose) 10% (G10%) solution is not available, remove 100mL of glucose (dextrose) 5% (G5%) from a 500mL
bottle or bag, then add 50 mL of G50% to the remaining 400 mL of G5% to obtain 450 mL of G10% solution.

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References Chapter 9

1. Levitsky LL, Misra M. Epidemiology, presentation, and diagnosis of type 1 diabetes mellitus
in children and adolescents. UpToDate. Published January 2023.
https://www.uptodate.com/contents/epidemiology-presentation-and-diagnosis-of-type-
1-diabetes-mellitus-in-children-and-adolescents
2. World Health Organization. Classification of Diabetes Mellitus. World Health Organization;
2019. Accessed October 24, 2023.
https://iris.who.int/handle/10665/325182
3. Usher-Smith JA, Thompson M, Ercole A, Walter FM. Variation between countries in the
frequency of diabetic ketoacidosis at first presentation of type 1 diabetes in children: a
systematic review. Diabetologia. 2012;55(11):2878-2894.
https://doi.org/10.1007/s00125-012-2690-2
4. BSPED |BSPED DKA Guidelines. Accessed October 24, 2023.
https://www.bsped.org.uk/clinical-resources/bsped-dka-guidelines/
5. Lawrence SE, Cummings EA, Gaboury I, Daneman D. Population-based study of incidence
and risk factors for cerebral edema in pediatric diabetic ketoacidosis. J Pediatr. 2005;146(5):
688-692.
https://doi.org/10.1016/j.jpeds.2004.12.041
6. Wolfsdorf JI, Glaser N, Agus M, et al. ISPAD Clinical Practice Consensus Guidelines 2018:
Diabetic ketoacidosis and the hyperglycemic hyperosmolar state. Pediatr Diabetes.
2018;19:155-177.
https://doi.org/10.1111/pedi.12701
7. ISPAD, LFAC, IDF. Pocket Book for Management of Diabetes in Childhood and Adolescence
in Under-Resourced Countries. 2nd ed. International Diabetes Federation; 2017. Accessed
October 24, 2023.
https://www.ispad.org/page/ISPADIDFLFaC
8. Thornton PS, Stanley CA, Leon DDD, et al. Recommendations from the Pediatric Endocrine
Society for Evaluation and Management of Persistent Hypoglycemia in Neonates, Infants,
and Children. J Pediatr. 2015;167(2):238-245.
https://doi.org/10.1016/j.jpeds.2015.03.057
9. Leon-Crutchlow DDD, Lord K. Approach to hypoglycaemia in infants and children. UpToDate.
Published May 2022.
https://www.uptodate.com/contents/approach-to-hypoglycemia-in-infants-and-children

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Chapter 10:
Haematology

10.1 Anaemia............................................................................................................... 299


10.1.1 Clinical features and history......................................................................... 300
10.1.2 Management............................................................................................... 301
10.1.3 Specific considerations in children with SAM...............................................303
10.2 Sickle cell disease................................................................................................. 304
10.2.1 Clinical features........................................................................................... 304
10.2.2 Acute painful or vaso-occlusive crisis (VOC).................................................305
10.2.3 Febrile illness................................................................................................ 306
10.2.4 Acute chest syndrome (ACS)......................................................................... 307
10.2.5 Acute anaemia in SCD.................................................................................. 307
10.2.6 Splenic sequestration................................................................................... 308
10.2.7 Aplastic crisis................................................................................................ 309
10.2.8 Stroke........................................................................................................... 309
10.2.9 Priapism....................................................................................................... 310
10.2.10 Prevention of complications....................................................................... 310
References Chapter 10................................................................................................. 313
10
Chapter 10: Haematology

10.1 Anaemia

Anaemia is defined as a haemoglobin (Hb) level below the age-specific reference value (see
Table 10.1). Severe anaemia is defined as Hb < 6 g/dL for children over 2 months of agea.
Table 10.1 - Definition of anaemia1
Age Hb level defining anaemia
< 2 months < 13.5 g/dL
2 to < 6 months < 9.5 g/dL
6 to 59 months < 11 g/dL
5 to 11 years < 11.5 g/dL
12 to 14 years < 12 g/dL
< 12 g/dL (girls)
15 years and above
< 13 g/dL (boys)

Anaemia can result from a reduction in red blood cell production, blood loss, or increased
haemolysis (see Table 10.2). In tropical settings, the causes are often multiple and overlapping
e.g. malnutrition and malaria.
In infants < 1 year of age, causes can be congenital, including:
– Maternal malaria and HIV: both cause IUGR, which is associated with anaemia.
– Maternal iron deficiency during pregnancy
– Preterm delivery
– Haemoglobinopathies and G6PD deficiency 10
Table 10.2 - Causes of anaemia

Decreased red blood Increased red blood cell


Loss of red blood cells
cell production destruction (haemolysis)

Iron deficiency Acute haemorrhage Malaria


Malnutrition (trauma, GI bleeding) Bacterial and viral infections
Micronutrient deficiencies Chronic parasitic Haemoglobinopathies
(folic acid, vitamin B12, diseases (hookworm, Sickle cell disease (SCD)
vitamin A) schistosomiasis) Thalassaemia
Depressed bone marrow Certain drugs if G6PD
function deficiency (primaquine,
Chronic infections (e.g. HIV, dapsone, co-trimoxazole)
visceral leishmaniasis) Injectable artesunate
Renal failure (delayed haemolysis)b

a For definition of severe anaemia in infants less than 2 months, see MSF Neonatal Care guidelines.
b Post-artemisinin delayed haemolysis (PADH) is a rare phenomenon which can occur 1-3 weeks after initiation
of treatment with injectable artesunate. Clinicians should be aware of this potential complication.

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10.1.1 Clinical features and history


– Symptoms include lethargy, pallor, fatigue, dizziness, shortness of breath, poor feeding or
irritability in infants.
– Clinical signs include:
• Pallor of the conjunctivae, lips, mucous membranes, nail beds, palms of hands and soles
of feet
• Dyspnoea, tachycardia, cardiac murmur
– Clinical signs of decompensation due to severe anaemia are one or more of:
• Increased work of breathing (see Chapter 4, Section 4.1.1)
• Altered level of consciousness (see Chapter 7, Section 7.5.1)
• Circulatory impairment/shock (see Chapter 2, Section 2.2.1)
– Specific signs to help identify the underlying diagnosis, consider:
• Signs of malaria, including splenomegaly
• Evidence of active bleeding: bloody stools, haematemesis, melaena, haematuria, epistaxis
• Indications of intravascular haemolysis: dark coloured urine, jaundice, hepatosplenomegaly
• Suspicion of sickle cell disease: maxillary protrusion, splenomegaly, frontal and parietal
bossing
• Suspicion of thalassaemia: maxilla hyperplasia, flat nasal bridge, frontal bossing
• Signs of malnutrition or micronutrient deficiency (cheilosis, glossitis)
• Signs of sepsis or other acute infection
• Suspicion of visceral leishmaniasis (kala azar): fever, splenomegaly, lymphadenopathy and
wasting
With chronic or recurrent anaemia, children may have no or few symptoms or signs compared
to children presenting with acute anaemia with the same Hb value, due to the body’s capacity
to compensate for anaemia over time.
Take a history, examine the child and perform relevant investigations to identify the underlying
cause of anaemia. Consider specifically asking about:
– Medical history including previous episodes of anaemia, transfusions, sickle cell disease,
thalassaemia, HIV, TB, malaria, treatment for worms, etc.
– Birth history (gestational age at birth, any neonatal jaundice/anaemia).
– Recent medication, including recent artesunate injections, traditional medicines, or any
exposure to toxins.
– Diet and nutritional status.
– Menstrual history for adolescent girls.
– Family history of sickle cell disease, TB, HIV, thalassaemia, other.
– Consider asking if the child has any unusual eating habits of non-food products, e.g. dirt,
paper, uncooked rice. This condition, described as pica, may be more common in children
with learning or developmental disabilities and sickle cell disease, and is associated with
iron-deficiency anaemia.

Investigations
– Hb
– Full blood count (FBC), if available
– In malaria-endemic regions, malaria RDT or thick and thin blood films

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– If sickle cell anaemia suspected, the following tests should be done before blood transfusionc
(see also Section 10.2):
• Sickle scan (lateral flow RDT that can detect both sickle cell disease and trait)
• Emmel test if sickle scan not available (ideally confirmed by electrophoresis, where
available)
– Blood group and crossmatch (in case of need for transfusion), including mothers’ blood
group for infants less than 4 monthsd.

10.1.2 Management
Anaemia itself may not always require treatment. Management of the underlying cause or
condition resulting in anaemia may likely correct anaemia, and a blood transfusion is often not
necessary in a clinically stable child.
Indications for blood transfusion (excluding infants < 2 monthse):
– Profound anaemia: Hb < 4 g/dL, or
– Complicated severe anaemia: Hb ≥ 4 and < 6 g/dL with one or more signs of decompensation:
• Increased work of breathing (see Chapter 4, Section 4.1.1)
• Altered level of consciousness (see Chapter 7, Section 7.5.1)
• Circulatory impairment/shock (see Chapter 2, Section 2.2.1)
– Complicated severe anaemia: Hb ≥ 4 and < 6 g/dL with evidence of ongoing blood loss:
• Haemoglobinuria (indicating intravascular haemolysis)2
• Visible bleeding (external bleeding, haematemesis, melaena, haematuria)
Note that malaria, sickle cell disease (SCD) and sepsis are not considered to be independent
anaemia severity criteria in otherwise stable children, therefore are not indications for
transfusion unless accompanied by one of the complications outlined above. See relevant
chapters for specific transfusion criteria for children with circulatory impairment/shock
(Chapter 2, Section 2.2.3) and certain complications of SCD (Section 10.2), as these may differ
from the above.
Infants < 2 months of age with anaemia should be managed as for neonates, see MSF Neonatal 10
Care Guidelines.

Initial management
– Stop any major or evident bleeding or haemorrhage (see Chapter 2, Section 2.7).
– Assess and manage ABCDE; resuscitate and stabilise (refer to Chapter 2, Section 2.1).
– Check Hb and identify any clinical signs of severity.
– Take blood for group and save, or crossmatching if transfusion required (see below).
– If history of previous transfusions or any indication of SCD, take a blood sample for testing
before transfusionc.
– Administer oxygen if clinical signs of severity, aiming for saturations ≥ 94%.
– Check axillary temperature, weight/age.

c Tests for SCD can give false results if performed within 8 weeks of a blood transfusion.
d Blood should be compatible with both the infant’s and the mother’s ABO and Rh group until 4 months of age
(see MSF Neonatal Care guidelines for more detail).
e Young infants < 2 months of age have a significantly higher normal Hb than older infants (see Table 10.1
page 299) therefore transfusion thresholds are higher. In this age group, transfusion should be considered
if Hb less than 8 g/dL in term neonates (less than 7 g/dL in preterm neonates) or if Hb less than 10 g/dL with
clinical signs of intolerance to anaemia.

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Profound anaemia (Hb < 4 g/dL) or complicated severe anaemia (Hb 4 - < 6 g/dL with
signs of decompensation or ongoing blood lossf)
– Urgent blood group and crossmatch (if not already done), including mothers’ blood group
for infants less than 4 monthsg.
– Start treatment of underlying cause (e.g. malaria).
– Administer blood transfusionh, calculating volume according to the presence or absence of
fever2, as follows:
• No fever (≤ 37.5 °C) from the time of ordering blood to the time of transfusioni: administer
30 mL/kg whole blood over 4 hours or 15 mL/kg packed red blood cells (PRBC) over
3 hours.
• Fever (> 37.5 °C) at any point from the time of ordering blood to the time of transfusioni:
administer 20 mL/kg whole blood over 4 hours or 10 mL/kg PRBC over 3 hours.
– Depending on volume required, transfusion rate may exceed the usual recommendation
of maximum 5 mL/kg/hr. Use one or more adult units of whole blood or PRBC. See MSF
Manual of Nursing Care Procedures, SOP Paediatric Transfusion Set – Blood burette and SOP
Using a Syringe Pump for Small Volume Blood Transfusions for more details on paediatric
transfusion administration.
– Monitor children closely during transfusion for any transfusion reaction and for signs of
overload, especially malnourished children who are at increased risk of fluid overload.
– Recheck Hb routinely once between 8-24 hours after the transfusion is complete3, or at any
other time if ongoing signs of decompensation or blood loss once transfusion is complete.
– Depending on the Hb level and signs of decompensation and/or ongoing blood loss (as
above) repeat transfusion may be necessary. Check for signs of fluid overload before starting
another transfusion - furosemide between transfusions is not indicated unless signs of fluid
overload are present.

Uncomplicated severe anaemia (Hb 4 - < 6 g/dL with no signs of decompensation or


ongoing blood loss)
– Admit for close monitoring:
• Monitor and record vital signs as often as required using an early warning system (see
MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign
charts).
• Review specifically for features of complicated severe anaemia that are indications for
transfusion (see above) at 4, 8, 16, 24, 36 then 48 hours.
• Repeat Hb at 8, 24 and 48 hours.
– Blood grouping (including mothers’ blood group for infants less than 4 monthsh) and save
sample in the lab for later crossmatching in case transfusion is needed.
– Start treatment of underlying cause (e.g. start malaria treatment if malaria test positive.)
– If Hb remains between 4 - < 6 g/dL, continue close monitoring, as above.
– If child develops any of the severity features or Hb decreases to < 4 g/dL, administer a blood
transfusion, with volume dependent on presence or absence of fever as outlined above.
Continue close clinical monitoring, as above.

f These criteria do not apply in haemorrhagic shock, for which transfusion volumes are different (see Chapter 2,
Section 2.5).
g Blood should be compatible with both the infant’s and the mother’s ABO and Rh group until 4 months of age
(see MSF Neonatal Care guidelines for more detail).
h Always ensure bedside verification of ABO compatibility immediately before transfusion using an ABO testing
card.
i Ensure temperature is checked and recorded at the time of ordering blood and immediately prior to transfusion
as a minimum.

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– If Hb increases to > 6 g/dL, continue with treatment of underlying cause and observation.
– Once clinically stable, consider iron and folic acid supplementation (see below).
Although malaria is by far the principal cause of severe anaemia in most MSF contexts, outside
of malaria-endemic regions the main causes of severe anaemia may be diverse. For anaemia
associated with burns, trauma or surgery follow specific guidance (See Chapter 2, Section 2.7
for trauma). If the child has known sickle cell disease with complications such as acute chest
crisis, acute splenic sequestration or cerebral vascular accident, see Section 10.2.

Iron supplementation
Start empiric treatment with iron supplementation in all children with anaemia where the
underlying cause is not evidentj and continue for 3 months:
– Iron combined with folic acid is the preferred option where available. Doses are expressed
in elemental ironk:
• 1 month to < 6 years: 1.5 to 3 mg/kg two times daily
• 6 to < 12 years: 65 mg two times daily
• ≥ 12 years: 65 mg two to three times daily
– In the case of moderate or severe anaemia, start iron only once the child is clinically stable
as it can exacerbate infection during acute illness. Folic acid alone can be started in the
meantime:
• < 1 year old: 2.5 mg once daily
• ≥ 1 year old: 5 mg once daily
– In endemic regions for hookworms, treat with albendazole in children over 6 months old
prior to commencing iron:
• Weight < 10 kg: 200 mg as a single dose
• Weight ≥ 10 kg: 400 mg as a single dose
– In malaria-endemic areas, iron combined with folic acid should only be given where malaria
prevention programmes and antimalarial treatments are widely availablel.
– For children with SAM, see specific dosing in Section 10.1.3.

10
10.1.3 Specific considerations in children with SAM
Indications for blood transfusion and transfusion volumes are the same for children with or
without severe acute malnutrition (SAM), however children with SAM are more susceptible to
volume overload therefore should be very carefully monitored.
For children with SAM admitted with moderate or severe anaemia and receiving ready to use
therapeutic food (RUTF), give iron/folic acid PO at discharge from ITFCm:
– Weight > 8 kg: 1/2 tablet once daily
– Weight ≤ 8 kg: none needed as there is enough iron and folic acid in RUTF.

j Note: Iron is contraindicated in a child who has known or suspected SCD, thalassaemia, or has received multiple
transfusions within a year.
k 140 mg/5ml syrup contains approximately 45 mg/5ml of elemental iron; 200 mg tablets of ferrous fumarate or
ferrous sulfate (with or without folic acid) contain approximately 65 mg or elemental iron (+/- 400 micrograms
of folic acid).
l Iron-folate supplementation increases the risk of clinical malaria in malaria-endemic areas where neither
prevention nor antimalarial treatments are available.
m Treatment is different to children without SAM to adjust for micronutrients contained in RUTF.

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10.2 Sickle cell disease

Sickle cell disease (SCD) is a genetic disorder producing an abnormal variant of the adult
haemoglobin (Hb). The abnormal haemoglobin (HbS) results in distortion of the red blood cells
into a classic ‘sickle’ shape, in response to a variety of triggers including dehydration, hypoxia,
infection and increased temperature4. This leads to increased destruction of red blood cells
(haemolysis), an increase in blood viscosity and obstruction of capillaries (causing vaso-
occlusive events)5. In SCD, the child inherits an HbS gene from at least one parent, and another
abnormal haemoglobin variant from the other parent (such as HbC or Hb beta thalassemia).
Sickle cell anaemia (HbSS), the most common and most severe form of SCD, occurs when a
child inherits an HbS gene from each parent.
Global data is lacking, but SCD is estimated to affect around 300,000 children born per year6.
It is most prevalent in sub-Saharan Africa (affecting up to 3% of births), though also present
amongst children born of Mediterranean (including Middle East region) and Indian origin7.
The highest prevalence of sickle cell anaemia is in the malaria-endemic zones of sub-Saharan
Africa, where it contributes significantly to under-5 deaths8.
Sickle cell trait occurs when a child inherits a sickle gene from one parent and a normal gene
from the other parent; carriers are usually asymptomatic.

10.2.1 Clinical features


– Symptoms usually begin around 4 to 6 months of age. Early manifestation: dactylitis (painful
swelling of digits of hands and feet).
– Major signs: recurrent painful crises (See Section 10.2.2), chronic anaemia, splenomegaly
and frequently, growth retardation and malnutrition.
– Life-threatening complications: stroke, severe bacterial infections, acute chest syndrome.
– Take a detailed history including a family history of similar clinical signs and perform a
comprehensive clinical examination. Assess for history of, or presence of, any acute or
chronic complications (refer to Table 10.3).
Table 10.3 - Acute and chronic complications of SCD
Acute complications Chronic complications
Acute painful crisis Cardiomyopathies, myocardial infarction,
Acute bacterial infections, particularly acute arrhythmia
severe pneumonia and sepsis Chronic compensated haemolytic anaemia
Acute chest syndrome Haematuria, proteinuria leading to renal
Acute splenic sequestration failure
Aplastic crisis Chronic cholelithiasis and liver disease
Priapism Retinopathy
Acute central nervous system events e.g. Leg ulcers
cerebral vascular accident Bone infarction and necrosis
Acute hepatic ischemia and/or sequestration Sickle cell chronic lung disease
Neurocognitive deficit
Growth failure and delayed puberty

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Investigations
– Hb
– FBC and reticulocyte count, if available
– Consider blood group and crossmatch
– In malaria-endemic regions, malaria RDT
– Diagnosis of SCD:
• All testing must be done either on blood taken prior to transfusion or at least 8 weeks
after the last transfusion.
• Sickle Scan (lateral flow RDT that can detect both sickle cell disease and trait) is
recommended as first line point-of-care test. A positive Sickle Scan result is enough to
make the diagnosis, electrophoresis is not necessary to confirm the diagnosis unless
required by national guidelines.
• Emmel test can be performed as a screening test if Sickle Scan is not available. A positive
Emmel test does not confirm the diagnosis of SCD due to low sensitivity and specificity
and inability to differentiate between sickle cell trait and disease. Confirmation using Hb
electrophoresis is recommended, where available.
• Hb electrophoresis is the gold standard diagnostic tool, but is often unavailable.

10.2.2 Acute painful or vaso-occlusive crisis (VOC)


– Painful crises are the most common type of vaso-occlusive events.
– Common triggers include infection, emotional stress, exposure to cold or high altitude,
dehydration.
– Severity and duration of pain can vary from minor, lasting minutes, to severe, lasting days.
– Pain is usually of rapid onset, deep, gnawing or throbbing, and can be accompanied by
localised tenderness, erythema, warmth and swelling.
– Commonly affects: lumbosacral spine, knee, shoulder, elbow and femur.
– Dactylitis is a variant of VOC; very common in children up to 4 years of age. It can occur as
early as 6 months of age9 and as many as 45% of infants and toddlers will have dactylitis by
2 years of age. 10
– Many painful crises can be managed at home, with adequate analgesia4.

Management
– Assess and stabilise ABCDE.
– Assess pain severity and start analgesia without delay, ideally within 30 minutes of arrival4,9
(see Chapter 15, Section 15.4).
– Admit if pain is uncontrolled, or moderate to severe and requiring opioid analgesia.
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– Administer oxygen if oxygen saturation in air is ≤ 95%4,9.
– Evaluate for dehydration and ensure adequate hydration:
• Encourage drinking fluids. If the patient is not able to drink, start IV maintenance fluids
until oral intake has improved (see Chapter 15, Section 15.2). Consider NGT if IV access is
difficult or refused.
• Correct any dehydration (see Chapter 5, Section 5.3).
– If fever present (> 37.5 °C), manage as for febrile illness below.
– Blood transfusion is not routinely indicated unless there are other clinical indications for
transfusion (see Section 10.1.2).

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– Encourage deep breathing exercises (see Section 10.2.4).


– Consider osteomyelitis as an alternative diagnosis if there are local signs of pain and
inflammation persisting for > 48 to 72 hours despite treatment for VOC. Refer to Chapter 11,
Section 11.4 for management of osteomyelitis.

10.2.3 Febrile illness


While sickle cell trait is known to confer partial protection against malaria, children with SCD
are more susceptible to severe malaria and invasive bacterial infections (pneumonia, cellulitis,
meningitis, osteomyelitis, and sepsis) due to a poorly functioning spleen and weakened
immune response9. Unvaccinated or partially vaccinated children are particularly at risk for
invasive infections due to H. influenzae, S. pneumoniae, and meningococcus, and SCD increases
susceptibility to infection by Salmonella spp10. All children with SCD presenting with fever
should be carefully assessed for these complications and should be systematically treated with
antibiotics.

Management
– In addition to admission based on clinical condition, admit to hospital all children with
known SCD or suspected SCD and any of the following criteria:
• Age < 2 years
• Fever of ≥ 38.5 °C
• Presence of acute anaemia (fall of 2 g/dL below patient’s baseline Hb value, or Hb < 6 g/dL
where baseline unknown9).
• Signs of acute haemolysis, splenic sequestration or other co-existing complications.
– Assess and stabilise ABCDE.
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– Treat presumed bacterial infection according to likely cause (all patients with SCD who
present with fever should be started on antibiotics):
• Pneumonia: refer to Chapter 4, Section 4.5.
• Meningitis: refer to Chapter 3, Section 3.3.
• Acute osteomyelitis: refer to Chapter 11, Section 11.4.
• Unknown source of infection or sepsis: refer to Chapter 3, Section 3.2.
– Evaluate for dehydration and ensure adequate hydration:
• Encourage drinking fluids. If the patient is not able to drink, start IV maintenance fluids
until oral intake has improved (see Chapter 15, Section 15.2). Consider NGT if IV access is
difficult or refused.
• Correct any dehydration (see Chapter 5, Section 5.3).
– If malaria RDT positive, treat malaria in addition to bacterial infection.
– Treat pain if present.
– Monitor for the appearance of acute anaemia.
– Change to oral antibiotics once the patient shows signs of improvement (afebrile, can eat
and drink) and discharge home to complete oral treatment.
– Complete oral antibiotic treatment in hospital if:
• Less than 2 years old
• Presence of acute anaemia (fall of 2 g/dL below patient’s baseline Hb value, or Hb < 6 g/dL
where baseline unknown9.

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10.2.4 Acute chest syndrome (ACS)


Acute chest syndrome (ACS) is caused by vaso-occlusion in the pulmonary vasculature, often
triggered by infection, which causes sickling of red blood cells and ischaemia. It is a common
reason for presentation to hospital in children with SCD and is often preceded by a peripheral
VOC. ACS can vary in severity from mild to life-threatening, and patients can deteriorate rapidly
therefore require close monitoring11.
– Leading cause of death in adolescents.
– More frequent in children with asthma or previous ACS.
– Symptoms and signs include chest pain, cough, fever, wheeze, tachypnoea, respiratory
distress, hypoxia (SpO2 < 95%). Children are less likely to complain of chest pain and
breathlessness than adults11.
– Can develop suddenly or insidiously.

Management
– Assess and stabilise ABCDE.
– Admit to hospital.
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– Assess regularly for severe anaemia and bronchospasm.
– Administer oxygen via face mask, aiming for SpO2 between 94 - 98%.
– Ensure adequate hydration as for VOC. If oral intake is insufficient, start IV maintenance
fluids (see Chapter 15, Section 15.2) while monitoring for fluid overload. If signs of fluid
overload, administer one dose of furosemide IV.
– Give adequate pain relief (see Chapter 15, Section 15.4).
– Ensure deep breathing exercises focusing on the inspiration phase (alveolar distension, e.g.
with an incentive spirometer) every 1 to 2 hours while awake.
– Administer antibiotic treatment even if no fever present:

ceftriaxone IV for 7 to 10 days:


50 to 80 mg/kg (max. 4g if < 50 kg; max. 2g if ≥ 50 kg) every 24 hours
10
+ azithromycin PO 10 mg/kg once daily for 5 days.
Alternative to azithromycin: erythromycin PO 10 mg/kg 4 times daily for 10 days.

– If clinical signs of wheezing and bronchoconstriction, treat as per asthma management


guidance (Chapter 4, Section 4.10).
– Administer blood transfusion (see Section 10.1.2) if acute anaemia present (see
Section 10.2.5).
– Consider referral for exchange transfusiona in symptomatic severe ACS (defined as oxygen
saturation < 90% despite supplemental oxygen)9,12.

10.2.5 Acute anaemia in SCD


Nearly all people with SCD have chronic anaemia, with typical baseline Hb values of 6-8 g/dL for
HbSS, 10-15 g/dL for HbSC and 9-12 g/dL for HbS-beta thalassemia9. Chronic anaemia is well
tolerated and does not routinely require transfusion in an otherwise stable child. Repeated
unnecessary blood transfusions should be avoided as they increase the risk of transfusion
reactions, iron overload and alloimmunisation.

a The goal of exchange transfusion is to reduce circulating levels of HbS to relieve symptoms, rather than to treat
anaemia.

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Chronic anaemia is often complicated by acute anaemia, defined in SCD as a drop in Hb of


2 g/dL below baseline, or Hb < 6 g/dL if baseline is unknown. Acute anaemia may require
transfusion depending on the cause and severity.
– Causes: acute severe intravascular haemolysis (often secondary to malaria with fever,
haemoglobinuria (dark urine) and yellow conjunctivae), splenic sequestration, or aplastic
crisis.
– Clinical features: increasing fatigue, pallor of conjunctivae and palms, shortness of breath,
tachycardia or heart failure.

Management
– Assess and stabilise ABCDE.
– Admit to hospital.
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– Treat malaria if present.
– Assess for complications of SCD.
– In addition to standard transfusion criteria (see Section 10.1.2), administer blood transfusionb
for the following complications of SCD presenting with acute anaemia (a drop in Hb of 2 g/dL
below baseline, or Hb < 6 g/dL if baseline is unknown)9:
• Acute splenic sequestration (see Section 10.2.6)
• Symptomatic ACS (see Section 10.2.4)
• Cerebral vascular accident (stroke) (see Section 10.2.8)
– If blood transfusion required, transfuse according to guidance in Section 10.1.2.
– Monitor Hb at 24 and 48 hours. Further transfusions may be necessary if haemolysis is
ongoing.
– If blood transfusion not required but Hb 4 - < 6 g/dL, monitor closely according to advice in
Section 10.1.2.

10.2.6 Splenic sequestration


– Sudden, rapid and massive enlargement of the spleen, with trapping of a considerable
portion of the red-cell mass. Mostly in children 1 to 4 years.
– Examination: sudden enlargement of spleen, severe left upper quadrant pain. Child becomes
suddenly weak, pale, short of breath with a rapidly distending abdomen, and shock.
– Investigations, if available, show a sharp decline in Hb level (drop of at least 2 g/dL),
reticulocytosis (distinguishing it from aplastic crisis) and thrombocytopenia.

Management
– Assess and stabilise ABCDE.
– If signs of circulatory impairment or shock, see Chapter 2, Section 2.2.
– Admit to hospital.
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– Blood group and crossmatch; order blood.
– Administer blood transfusion (see Section 10.1.2 and Section 10.2.5).

b Consider referral for exchange transfusion in symptomatic severe ACS (defined as oxygen saturation < 90%
despite supplemental oxygen) and cerebral vascular accident (stroke) to reduce circulating HbS9,12.

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– Monitor the size of the spleen.


– Administer IV antibiotics if fever (see Section 10.2.3).
– After clinical improvement, monitor for relapse (Hb, size of spleen) and repeat transfusion
as necessary according to standard transfusion criteria (see Section 10.1.2).

10.2.7 Aplastic crisis


– Transient suspension of red blood cell production by the bone marrow: impalpable spleen
and absence of reticulocytes.
– Gradual onset of fatigue, shortness of breath and sometimes syncope (sudden and brief loss
of consciousness associated with loss of postural tone and spontaneous recovery). Fever is
quite common.
– Often occurs in several people in the same family at the same time, indicating a possible
infectious cause.
– Examination may reveal signs of decompensation.
– Hb is usually far below the patient’s baseline level, and the reticulocyte count is reduced or
even zero.
– Erythropoiesis usually begins 7-10 days after aplasia, with gradual recovery of Hb.

Management
– Assess and stabilise ABCDE.
– Admit to hospital.
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– Treat malaria or associated bacterial infection if present.
– Administer blood transfusion only if standard transfusion criteria present (see Section 10.1.2)
– Repeat Hb every other day. An increasing reticulocyte count and a gradual increase of the
Hb indicates improvement. Monitor patient until their baseline Hb has been reached.
10
10.2.8 Stroke
Sudden onset of weakness, impairment of language and sometimes seizures or coma and
results in adverse motor and cognitive sequelae. It is secondary to stenosis or occlusion of the
internal carotid or middle cerebral artery, but acute chest syndrome, acute aplastic crisis or
other acute anaemic events may precipitate events.

Management
– Assess and stabilise ABCDE.
– Admit to hospital.
– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– Administer blood transfusion (see Section 10.1.2) if acute anaemia present (see
Section 10.2.5).
– Consider referral for exchange transfusionc, which is the treatment of choice for ischaemic
stroke in SCD9,12.

c The goal of exchange transfusion is to reduce circulating levels of HbS to relieve symptoms, rather than to treat
anaemia.

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– Transfer the patient to a specialized facility for further management (including prophylactic
therapy to prevent recurrences with transfusion programme, hydroxyurea).
– If the patient is awaiting transfer or if transfer is not possible:
• Oxygen continuously, to maintain the SpO2 > 94%.
• Treat seizures if present.
• After transfusion administer IV maintenance fluids for hydration (see Chapter 15, Section 15.2).

10.2.9 Priapism
– Sustained, unwanted, painful erection lasting several hours.
– Usually affects teenagers and adults but may affect younger boys.
– Prompt recognition and initiation of conservative medical management may resolve the
swelling and limit the need for more aggressive and invasive intervention. Delayed diagnosis
and treatment can result in necrosis and irreversible erectile dysfunction.

Ambulatory management
Ensure children know how to manage priapism early at home to prevent severe acute priapism.
– Home measures include:
• Drinking fluids
• Application of warm compresses
• Gentle exercise, e.g. walking
• Regular urination
• Attempting ejaculation
• Pain control
– Seek hospital care if erection lasts for longer than 2 hours.
– Consult clinician if episodes of intermittent priapism occur more than two times per month.

Hospital management of severe acute priapism


– Give adequate pain relief (see Chapter 15, Section 15.4).
– Encourage oral hydration as for a VOC; IV maintenance fluids if necessary and treat
dehydration if present.
– Encourage all above ambulatory measures, if pain allows.
– For priapism lasting > 4 hours: refer for surgical management.

10.2.10 Prevention of complications


Provide information and education to child and parents/carers regarding regular follow-up,
preventive treatments, the importance of adequate nutrition, and prompt pain management
when needed. Ensure regular psychosocial assessment and the provision of support when
necessary.
Education of children and their families:

Basic knowledge

• Disease Chronic, necessarily transmitted by both parents, non-contagious.


• Treatment Routine (see below) and symptomatic (pain).
• Monitoring Size of the spleen, temperature, baseline Hb.

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Major precipitating factors of a painful crisis and how to prevent them

• Cold Wear warm clothing, avoid bathing in cold water.


• Excessive heat For example, avoid going out at midday.
• Tight clothing Wear wide comfortable clothing without elastics.
• Dehydration Drink plenty of fluids.
• Excessive effort Moderate physical activity is beneficial.
• Infections Follow routine treatments (including vaccination).

Principal complications requiring the patient to seek urgent medical advice

• Pain unresponsive to analgesia after 24 hours or severe from the start.


• Any fever (do not treat at home).
• Respiratory problems (cough, difficulty breathing, chest pain).
• Diarrhoea/vomiting and inability to drink.
• Dehydration (dark, infrequent urine).
• Anaemia (pale or yellow conjunctivae, pale palms, enlarged spleen).

Routine follow-up
– Between crises, regular OPD consultations every 1 to 3 months (until 4 years of age), then
every 3 to 6 months for 5 years of age and above:
• Assess for chronic complications (see Table 10.3).
• Ensure adherence to regular medications and that immunisations are up to date.
• Check nutritional status and psychosocial situation.
• Ensure reproductive counselling for girls of reproductive age (increased risk of VOC during
pregnancy/childbirth, higher incidence of intrauterine growth restriction, foetal and
perinatal loss and pre-eclampsia). 10
– After a crisis: as often as necessary, according to the clinical course.
– Paracetamol for home use in case of pain.

Routine preventative care


– Ensure routine immunisations are up-to-date or missed doses are completed:

• DTP, hepatitis B, polio, measles, H. influenzae type B vaccines


• Pneumococcal conjugate vaccine (PCV13 or, if not available, PCV10)
Children
• Meningococcal conjugate vaccine in endemic areas
< 5 years
• At 2 years: pneumococcal 23-valent polysaccharide vaccine, at least
8 weeks after the last PCV13 or PCV10.

• DTP or Td, hepatitis B, polio, measles, H. influenzae type B vaccines


Children
• Pneumococcal conjugate vaccine (PCV13 or, if not available, PCV10)
≥ 5 years
• Meningococcal conjugate vaccine in endemic areas

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– Prevention of pneumococcal infections:

phenoxymethylpenicillin (penicillin V) PO until age 15 (as a minimum until age 5)


• 1 month to < 1 year: 62.5 mg 2 times daily
• 1 to < 5 years: 125 mg 2 times daily
• ≥ 5 years: 250 mg 2 times daily
Alternatively:
amoxicillin PO
• 1 month to < 5 years: 125 mg 2 times daily
• 5 to < 12 years: 250 mg 2 times daily
• ≥ 12 years: 500 mg 2 times daily

– Support of red blood cell production:

folic acid PO (life-long treatment)


• < 1 year: 2.5 mg once daily
• ≥ 1 year: 5 mg once daily
Note: iron is contraindicated in patients who have received multiple transfusions. Avoid
combined preparations of iron and folic acid in children with SCD.

– Malaria prevention (for areas with moderate to high transmission):


• Malaria infection in children with SCD is one of the most common causes of VOC.
• Children with SCD have increased susceptibility to severe malariad.
• Malaria in children with SCD further increases the risk of invasive bacterial infection.
• All patients should be given a long-lasting insecticidal net (LLIN) at diagnosis.
• As first choice in areas with malaria that occurs throughout the year, mefloquine is
recommended for children under 5 years old. Prophylaxis may also be considered in
children over 5 years, though evidence of benefit in this age group is lacking:

mefloquine PO
> 6 months and > 5 kg: 5 mg base/kg (max. 250 mg) once weekly
Do not use to treat malaria.

• In areas with variations in malaria transmission, seasonal malaria chemoprophylaxis


(SMC) may be used instead. Mefloquine should not be given concomitantly with SMC.
– Consider hydroxyurea according to local protocol, if recommended in national guidelines.

d Note that conversely, sickle cell trait confers a partial protection from malaria (though children with sickle cell
trait should still be tested for malaria if they present with clinical symptoms consistent with malaria).

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References Chapter 10

1. WHO. Haemoglobin Concentrations for the Diagnosis of Anaemia and Assessment of


Severity. World Health Organization; 2011. Accessed November 15, 2023.
https://www.who.int/publications-detail-redirect/WHO-NMH-NHD-MNM-11.1
2. Maitland K, Olupot-Olupot P, Kiguli S, et al. Transfusion Volume for Children with Severe
Anemia in Africa. N Engl J Med. 2019;381(5):420-431.
https://doi.org/10.1056/NEJMoa1900100
3. Maitland K, Kiguli S, Olupot‐Olupot P, et al. Transfusion management of severe anaemia in
African children: a consensus algorithm. Br J Haematol. 2021;193(6):1247-1259.
https://doi.org/10.1111/bjh.17429
4. Overview | Sickle cell disease: managing acute painful episodes in hospital | Guidance |
NICE. Published June 27, 2012. Accessed November 15, 2023.
https://www.nice.org.uk/guidance/cg143
5. Chakravorty S, Williams TN. Sickle cell disease: a neglected chronic disease of increasing
global health importance. Arch Dis Child. 2015;100(1):48-53.
https://doi.org/10.1136/archdischild-2013-303773
6. Sickle Cell Disease. WHO | Regional Office for Africa. Published November 13, 2023.
Accessed November 15, 2023.
https://www.afro.who.int/health-topics/sickle-cell-disease
7. Grosse SD, Odame I, Atrash HK, Amendah DD, Piel FB, Williams TN. Sickle Cell Disease in
Africa. Am J Prev Med. 2011;41(6):S398-S405.
https://doi.org/10.1016/j.amepre.2011.09.013
8. Wastnedge E, Waters D, Patel S, et al. The global burden of sickle cell disease in children under
five years of age: a systematic review and meta-analysis. J Glob Health. 2018;8(2):021103.
https://doi.org/10.7189/jogh.08.021103
9. Evidence-Based Management of Sickle Cell Disease: Expert Panel Report, 2014 | NHLBI, 10
NIH. NHLBI Publications and Resources; 2014. Accessed November 15, 2023.
https://www.nhlbi.nih.gov/resources/evidence-based-management-sickle-cell-disease-
expert-panel-report-2014
10. Vichinsky E. Overview of the clinical manifestations of sickle cell disease. UpToDate.
Published May 2022.
https://www.uptodate.com/contents/overview-of-the-clinical-manifestations-of-sickle-
cell-disease
11. Howard J, Hart N, Roberts‐Harewood M, Cummins M, Awogbade M, Davis B. Guideline
on the management of acute chest syndrome in sickle cell disease. Br J Haematol.
2015;169(4):492-505.
https://doi.org/10.1111/bjh.13348
12. Davis BA, Allard S, Qureshi A, et al. Guidelines on red cell transfusion in sickle cell disease
Part II : indications for transfusion. Br J Haematol. 2017;176(2):192-209.
https://doi.org/10.1111/bjh.14383

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Chapter 11:
Bone and joint problems

11.1 Introduction......................................................................................................... 317


11.2 Approach to a child presenting with a limp........................................................318
11.2.1 Identifying underlying cause........................................................................ 318
11.2.2 Specific common causes of limp..................................................................319
11.3 Pulled elbow........................................................................................................ 321
11.4 Osteomyelitis....................................................................................................... 322
11.4.1 Clinical features........................................................................................... 322
11.4.2 Management............................................................................................... 323
11.4.3 Chronic osteomyelitis................................................................................... 324
11.5 Septic arthritis...................................................................................................... 326
11.5.1 Clinical features........................................................................................... 326
11.5.2 Management............................................................................................... 327
References Chapter 11................................................................................................. 328

11
Chapter 11: Bone and joint problems

11.1 Introduction

This chapter explores common bone and joint problems in children that typically have an
underlying pathology or cause. It does not cover immobile or painful limbs due to trauma
(e.g. fractures) which is outside the scope of these guidelines, with the exception of toddler’s
fracture, non-accidental injury (NAI) and pulled elbow which require specific management in
children.

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11.2 Approach to a child presenting with a limp

Limp is a common presentation in children and has a wide range of potential causes. Limp can
be due to pain, weakness or deformity. Transient synovitis and minor trauma are the most
common non-infectious causes of limp in children, however certain conditions are more likely
in specific age-groups (see Table 11.1). Infectious causes (osteomyelitis (see Section 11.4),
septic arthritis (see Section 11.5), tuberculosis (see Chapter 4, Section 4.12), brucellosis, Lyme
disease), bone malignancies and haematological disease should be considered in all children.
The hip and knee are the most commonly affected joints, though pain in either of these joints
may be due to pathology in the other. Limp may be also be caused by referred pain from
another origin (testicular torsion, appendicitis, psoas abscess etc.) or may be neurological
(hemiplegia, spinal injury/compression).
Table 11.1 - Age-specific non-infectious causes of limp

0-3 years 4-10 years 11-16 years

• Toddler’s fracture • Transient synovitis • Slipped upper femoral


• Developmental dysplasia • Perthes’ disease epiphysis (SUFE)
of the hip (DDH) • Acute lymphocytic • Primary bone tumours
• Neuroblastoma leukaemia (ALL) e.g. osteosarcoma,
Ewing’s sarcoma
• Osgood-Schlatter disease

11.2.1 Identifying underlying cause


A careful history can help to elicit salient diagnostic clues. Important points in the history
include:
– Onset of symptoms (acute or chronic)
– Ability to weight-bear and/or walk
– Description of joint pain
– Possible trauma [accidental or non-accidental injury (NAI)]
– Preceding viral infection
– Associated symptoms: fever, general malaise, weight loss, bleeding, swelling of the joint,
rash, night sweats.
Perform a complete clinical examination, focusing on the affected joint towards the end of the
examination. Observe the position that the leg is held in at rest, and whether the child is able
to bear weight or not. Watch the child walking, looking specifically at the gait pattern.
– Antalgic gait: short time spent with weight on affected leg when walking, suggests pain.
– Trendelenburg gait: pelvic tilt to opposite side when bearing weight on affected side,
suggests unilateral hip pathology.
– Steppage gait: exaggerated lifting of the leg at the hip and knee to prevent dragging of the
toes on the ground due to foot drop, suggests neurological disease.
– Waddling gait: alternating pelvic tilt when walking with wide-based gait and swinging of legs
outwards (like a duck), suggests bilateral hip pathology or proximal muscle weakness.

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Examine the joints above and below the affected joint to exclude pathology in these joints
causing referred pain. Also ensure that an abdominal +/- genital examination are performed
in case of referred pain.

Investigations
– Full blood count (FBC)
– X-ray of affected limb/joint: useful in the diagnosis of fractures, DDH, primary bone tumours,
SUFE and Perthes’, though advanced imaging, such as CT scan or MRI, may be required to
confirm diagnosis.
– Ultrasound: used to detect joint effusions, but cannot differentiate between infection, blood
and reactive fluid. Fluid can be aspirated under ultrasound guidance. May show periosteal
reaction suggestive of osteomyelitis.

11.2.2 Specific common causes of limp


Transient synovitis (usually of the hip)
An acute synovial inflammation, usually of the hip (sometimes the knee), typically preceded
by a viral upper respiratory tract or gastrointestinal infection. It is more common in boys than
girls, and there may be a history of mild trauma. The child is systemically well with sudden
reluctance to weight-bear. Passive movement of the hip can be limited due to pain. Spontaneous
resolution within days to weeks, supported by analgesia and anti-inflammatories.

Toddler’s fracture
Spiral fracture of the tibia caused by a twisting injury with rotational force when a child trips,
stumbles or falls, common in ambulatory infants and young children. Toddler’s fractures may
occur after relatively minor trauma therefore parents/carers may not be aware of when/how
the injury took place. Localised tenderness at the tibial fracture site is often present but may
be difficult to elicit. Treatment is conservative with immobilisation to reduce discomfort.

Developmental dysplasia of the hip (DDH)


Often diagnosed soon after birth on initial newborn examination, but if not, it may present 11
with a painless limp when the child starts walking. In unilateral dysplasia, children present with
a Trendelenburg gait (see above for description), leg shortening, asymmetrical skin creases
in the thigh and limited hip abduction on the affected side. Bilateral DDH, presents with a
waddling gait and symmetrical limited hip abduction.

Perthes’ disease
Avascular necrosis of part or all of the femoral head. Typically seen in children aged 4 to
9 years, and three times more common in boys than in girls. Usually mild symptoms with
insidious onset of a painless limp or activity-related leg pain (may be referred to thigh or knee).
Internal rotation and abduction of the hip on examination are mild to moderately limited. The
younger the child and the less femoral head involved, the better the prognosis. Treatment in
the majority of cases is reduced mobilisation and activity, however more severe cases may
require bedrest with traction. If unrecognised and untreated, severe osteoarthritis may occur
later in life.

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Slipped upper femoral epiphysis (SUFE)


This is a misnomer as it actually is the metaphysis of the femur that slips anteriorly off the
epiphysis (head of the femur) at the site of growth plate. It is common in rapidly growing
prepubertal, and typically overweight children, and is more common in boys than in girls. It
may present acutely after a fall or minor injury, but chronic slip with insidious pain is more
common. Can present with groin, hip or knee pain, difficulty weight-bearing and restriction of
internal rotation (or abduction) of the hip. Bilateral involvement occurs in 25%-40%. Children
require immediate non-weight bearing and urgent referral to an orthopaedic surgeon for
operative stabilisation.

Osgood Schlatter’s apophysitis


A common cause of knee pain in growing adolescents caused by inflammation of the tibial
tuberosity apophysis where the patellar tendon attaches to the tibia. Rapid growth in
adolescence combined with repetitive movements cause irritation and/or stress injury at this
site. It is typically unilateral but may be bilateral, with intermittent pain after activities like
running and jumping. Apophysitis is self-limiting and most children will improve with activity
modification and analgesia. Symptoms should disappear completely when the growth plates
fuse.

Malignancy (e.g. leukaemia, neuroblastoma, bone tumours)


The child may be systemically well and present only with a limp, but usually ‘red flags’ (fever,
localised bone pain/tenderness, pain at night, pallor, easy bruising, lymphadenopathy,
hepatosplenomegaly, lethargy, weight loss, night sweats) are present, suggesting a more
sinister diagnosis. Depending on available imaging and expertise, an attempt should be made
to estimate the extent of the disease, to help to decide on potential management options
locally or nationally, and to give the child and their parent/carer an indication of prognosis.

Non-accidental injury
Usually suspected by the pattern of injury (e.g. bruising in unusual places or in an infant who
is not yet mobile), delay in seeking medical attention, changeable or implausible history, or
a mechanism of injury inconsistent with examination findings. There may be prior history of
injuries or neglect. Cases should be handled with care, and with early involvement of the
psychosocial team, if available. Follow local child protection pathways if concerns are raised
and consider safeguarding procedures for other children at home, who may still be in a
vulnerable environment.

Tuberculous arthritis
Tuberculosis (TB) can cause arthritis in the spine, hips and knees through hematogenous
spread of bacilli from other TB foci. Tuberculous arthritis is usually ‘cold’, i.e. the skin over
the painful, swollen joint is the same temperature as the rest of the skin, and not warm as in
other infective conditions. The history is usually less acute than septic arthritis and there may
be systemic symptoms of TB such as fever, night sweats and weight loss. Diagnosis is made
clinically or by analysis of exudate removed during joint aspiration, if possible (acid and alcohol
fast bacilli (AAFB) and GeneXpert). Treatment for TB should be started as soon as possible (see
Chapter 4, Section 4.11).

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11.3 Pulled elbow

A pulled elbow is a common minor injury in young children. It occurs when a child’s arm is
pulled, twisted or stretched abruptly, causing the radius to partially slip out of the annular
ligament at the elbow (subluxation). It commonly occurs in young children being pulled back
from a potentially dangerous situation by a parent/carer or older sibling. Subluxation of the
radial head causes restricted movement and pain on elbow flexion, pronation and supination.
The child typically keeps the arm immobile, in a slightly flexed and pronated position. Pain is
only elicited on movement.
There are two main techniques to reduce a pulled elbow. The first is hyper-pronation, in which
pressure is applied over the radial head, whilst hyperpronating the arm. The second technique
is supination-flexion, in which again pressure is applied over the radial head, whilst the arm is
supinating and then flexed at the elbow. There is low quality evidence that the hyperpronation
technique has a better success rate at first attempt reduction that the supination technique1.
If history is not typical of a pulled elbow, but there is potential for another diagnosis such as a
fracture, the manoeuvre should not be attempted. Ultrasound can help to detect signs of an
effusion/raised fatpad, suggesting a fracture rather than a pulled elbow.

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11.4 Osteomyelitis

Osteomyelitis is an infection of the bone that is usually bacterial in origin. In children, acute
infection most commonly occurs by haematogenous spread (bacteraemia), but can also be
due to direct trauma to the bone (e.g. open fractures, war wounds), or from an infected site
near the bone (e.g. mouth, skin ulcer). Typically, infection affects the metaphysis of the long
bones, especially the femur and tibia, but any bone may be affected and pelvic osteomyelitis,
though rare, is seen in children. Though multiple sites can be affected, infection tends to be
limited to one site. Incidence is higher in children under 5 and is twice as common in boys2.
In haematogenous spread, Staphylococcus aureus is the most likely cause, but other common
pathogens include Kingella kingae, Group A and B streptococci, Streptococcus pneumonia,
E. coli and Haemophilus influenza B (if not immunised). Methicillin-resistant Staphylococcus
aureus (MRSA) is not infrequent. In children with sickle cell disease (SCD), infection by
Salmonella spp is most common followed by other gram-negative organisms.
The following factors increase the risk of developing osteomyelitis:
– Medical: malnutrition, sickle cell disease, HIV, tuberculosis, Buruli ulcer, cellulitis, dental
infections, post-malaria infection.
– Surgical/trauma: open fractures, penetrating or puncture wounds (including bites), surgical
procedures with insertion of pins or screws.

11.4.1 Clinical features


Initial symptoms of acute osteomyelitis may be non-specific and subtle and only become more
localised once infection is established in the bone:
– Localised bone pain (point tenderness) and pain on movement.
– Reluctance to move affected limb or weight-bear, limping.
– Fever, irritability, decreased appetite, malaise may also be present.
– Swelling, warmth and soft tissue redness around the site of pain (late sign).
– If the child complains of abdominal, hip, groin or thigh pain, consider osteomyelitis of the
pelvis. During examination, pain is elicited on passive movement of the hip (simultaneously
flex, abduct and externally rotate the hip) (see Figure 11.1)
Figure 11.1 - Examination for pelvic osteomyelitis

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Investigations
– FBC
– Inflammatory markers: Erythrocyte Sedimentation Rate (ESR), C-reactive protein (CRP)a, if
available
– Blood culture, if available, or any other material for culture (e.g. deep tissue, bone collected
during debridement).
– X-ray (AP and lateral view): localised, deep, soft tissue swelling appears on day 2 to 3, though
initially may be normal. Late signs include osteopenia, lytic lesions and periosteal reaction
which are evident from 10 to 21 days3. Osseous sequestrum (intraosseous abscess): sign of
chronic osteomyelitis.
– Ultrasound: may help identify joint effusion and differentiate from septic arthritis.
– Screen for SCD and consider potential TB contacts.

11.4.2 Management
Immobilisation of the affected extremity may relieve pain and prevent fractures, but
prolonged antibiotic treatment is the mainstay of management for acute osteomyelitis from
haematogenous spread:
– If the patient is stable, obtain blood cultures and any other culture material before starting
antibiotics, but avoid any delay in giving antibiotics.
– Administer empiric antibiotic treatment to cover the most likely pathogens (as outlined in
Section 11.4)4. Second choice antibiotics are used instead of, rather than in addition to, first
choice antibiotics if first choice is unavailable, if there is a high clinical suspicion of infection
with a gram-negative organism (e.g. in sickle cell disease), or if there is non-response to first-
line treatment:
• First choice: cloxacillin IV: 25 mg/kg every 6 hours (for S. aureus)
• Second choice:
▹ amoxicillin/clavulanic acid (co-amoxiclav) IV: 30 mg/kg of the amoxicillin component,
every 8 hours (or 50 mg/kg of the amoxicillin component, every 12 hours) OR
▹ cefazolin IV: 25 mg/kg every 12 hours OR
▹ ceftriaxone IV: 80 mg/kg (max. 4 g if < 50 kg; max. 2 g if ≥ 50 kg) every 24 hours (for
Salmonella spp. or Enterobacterales) OR
▹ cefotaxime IV: 50 mg/kg every 8 hours (for Salmonella spp. or Enterobacterales) OR
▹ clindamycin IV: 10 mg/kg every 8 hours (for community-acquired methicillin resistant 11
S. aureus (CA-MRSA)b.
– Doses of antibiotics for acute osteomyelitis are generally higher than for other conditions.
– Antibiotic treatment should be tailored as culture results become available, due to the large
number of potential pathogens, including antibiotic resistant ones e.g. MRSA.
The duration of parenteral antibiotic treatment is variable and depends largely on clinical
evolution5. There is growing evidence that shorter courses of parenteral antibiotics (< 7 days)
have similar outcomes to prolonged courses if acute osteomyelitis is detected and treated
early, avoiding the need for long-term IV access and hospitalisation6,7,8. Antibiotics should
be administered parenterally until symptoms and signs decrease (usually around 3-5 days),
before switching to oral antibiotics to complete 3 weeks of total treatment in uncomplicated
osteomyelitis. Ongoing fever and raised CRP (where available) are indications to continue
parenteral treatment for longer9.

a The combination of raised CRP and ESR is the most sensitive indication of osteomyelitis.
b In contexts where prevalence of clindamycin resistance to CA-MRSA is known to be high, consider vancomycin
as an alternative.

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– Patients with sickle cell disease: ensure antibiotics cover Salmonella spp (ceftriaxone or
cefotaxime are the preferred options), which is the most likely pathogen.
– Immunocompromised patients: prolong oral treatment to give a minimum of 6 weeks of
total treatment.
– Patients presenting with, or suspected of having, subperiosteal abscess or other purulent
collection: in addition to antibiotics, surgical debridement is required to remove the infected
tissue.
– All patients with osteomyelitis resulting from an inadequately treated open fracture should
be referred for surgical debridement.
Switch to oral antibiotic treatment when all of the following are met:
– At least 3 days of parenteral treatment completed
– Clinical improvement
– Afebrile for at least 72 hours
– Able to take oral medication without a problem in the hospital
– Parent/carer able to reliably give medication to the child.
If response to treatment is not as expected, re-evaluate the child and adjust antibiotic
treatment. Always consider and exclude tuberculosis (see Chapter 4, Section 4.11).

11.4.3 Chronic osteomyelitis


Chronic infection of the bone, usually defined as lasting longer than 4 weeks. It is characterised
by the presence of bone necrosis, also called sequestrum formation (see Figure 11.2). It may
occur secondary to untreated acute osteomyelitis or as a relapse many weeks or months
after osteomyelitis that was thought to have been successfully treated10. Chronic drainage
and fistula formation can also occur, as can abscess formation. While chronic osteomyelitis
is becoming rarer due to advances in antibiotic regimens, it is still seen quite commonly in
resource-limited settings and is a significant cause of disability.

Figure 11.2 - Sequestrum formation, frontal right thigh, childc

Sequestrum seen in the distal femoral diaphysis (arrow)

c Case courtesy of Hidayatullah Hamidi, Radiopaedia.org, rID: 63366. https://radiopaedia.org/cases/63366

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Investigations
– FBC
– Inflammatory markers: ESR and CRP, if available
– Blood culture, if available
– X-ray (AP and lateral view): sequestrum formation (intraosseous abscess, seen as representing
fragments of devitalized bone).

Management
– Mainstay of treatment is surgical removal (debridement) of the sequestrum and the dead
tissue around it, as the necrotic tissue serves as a source of infection, as well as any associated
abscess.
– Surgery may be relatively straightforward if the sequestrum is localized and not affecting the
growth plates or joints, however it can be very complex when associated with pathological
fracture, bone loss, growth disruption, joint involvement and severe soft tissue damage11.
Therefore, the patient should be referred to an experienced surgical team.
– Antibiotics should be administered (as for acute osteomyelitis, above) in addition to surgical
debridement as it is difficult to ensure that there is no residual infection unless deep tissue
samples can be taken and sent for microbiology, which is rarely possible in resource-limited
settings. Complex cases may require prolonged antibiotic treatment for several months as
well as extensive wound management.
– Recurrent or TB osteomyelitis also requires surgery; these cases should be discussed with
experienced clinicians.

Follow-up
– Monitor symptoms: fever and pain with movement should improve within 7 days (usually as
soon as 3 to 4 days).
– Start physical therapy, if available.
– If possible, follow-up at 2 weeks and 3 months after discharge.

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11.5 Septic arthritis

Septic arthritis is a serious joint infection that can lead to devastating complications, with
potential joint destruction in a period of days if left untreated. It has a higher incidence in
children less than 4 years old. The knee and hip are the most commonly affected joints,
especially in younger children, but septic arthritis can affect any synovial joint12.
Like osteomyelitis, microorganisms (bacteria, fungi, viruses) can enter the joint space by
haematogenous spread, direct inoculation or extension of a contiguous focus of infection. Most
cases of septic arthritis are caused by bacteria and usually result from haematogenous spread
of Staphylococcus aureus from an open wound or mucosal lesion. The bacterial pathogens
responsible are the same as for osteomyelitis (see Section 11.4).

11.5.1 Clinical features


Young children typically present with irritability, anorexia, cellulitis, or fever. The manifestations
of joint involvement include reduced movement of the limb concerned, limp and aversion
to passive movement. Children frequently adopt specific positions to reduce pain (antalgic
positions), typically with the joint flexed to give laxity to the joint capsule.
Older children usually present with joint swelling, sensitivity and reduced movement of the
affected joint, though the joint signs can be subtle, and they may also present with systemic
symptoms such as fever and decreased appetite.
Differential diagnosis includes transient synovitis, osteomyelitis, trauma and tumours.

Examination
Examine all joints including the overlying skin, not only those visibly affected. Carry out passive
movements slowly and carefully as septic arthritis causes extreme pain in the affected joint
during passive movement. Identify any joint swelling or warmth, reduced joint movement or
antalgic position.

Investigations
– FBC
– Inflammatory markers: ESR and CRP, if available
– Blood culture, if available
– X-ray: look for joint space widening, joint effusion, soft tissue swelling or subluxation or
dislocation of joint.
– Ultrasound, if available: useful to determine if fluid is present in the joint and in guiding
needle aspiration of the joint.
– Arthrocentesis: aspiration of synovial fluid under anaesthesia and strict asepsis (in the
operating room if possible). WBC > 50,000/mm3 in synovial fluid confirms septic arthritis
and synovial fluid should be sent for culture. If pus is aspirated and trained personnel are
present, a formal drainage can be done.

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11.5.2 Management
Septic arthritis is an orthopaedic emergency and requires prompt treatment:
– Administer empiric antibiotics IV as for osteomyelitis (see Section 11.4.2).
– Refer for surgical intervention to irrigate and drain the joint. If surgical referral is not an
option, it may be possible to successfully treat septic arthritis with antibiotics alone13, with
or without serial aspiration. This should be discussed with a senior clinician.
– Immobilise the joint for 24-48 hours to provide pain relief and decrease local irritation.
– Carefully mobilise the joint after 48 hours and start physical therapy, if available, to prevent
the development of fibrous adhesions.
– Antibiotic treatment should be tailored as culture results become available.
– Continue parenteral antibiotics until there are signs of clinical improvement (usually more
than 7 days, unless uncomplicated), before switching to oral antibiotics to complete 3 weeks
of total treatment. CRP, where available, is a useful indicator of response to treatment.
– Ensure adequate pain management, including regular pain assessment and administration
of analgesia, as required (see Chapter 15, Section 15.4).
Switch to oral antibiotic treatment when all of the following are met:
– At least 5-7 days of parenteral treatment completed
– Clinical improvement
– Afebrile for at least 72 hours
– Able to take oral medication without a problem in the hospital
– Parent/carer able to reliably give medication to the child.
If response to treatment is not as expected, re-evaluate the child and adjust antibiotic
treatment. Always consider and exclude tuberculous arthritis (see Section 11.2.2).

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352-360.
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7. Zaoutis T, Localio AR, Leckerman K, Saddlemire S, Bertoch D, Keren R. Prolonged Intravenous
Therapy Versus Early Transition to Oral Antimicrobial Therapy for Acute Osteomyelitis in
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https://doi.org/10.1542/peds.2008-0596
8. Le Saux N, Howard A, Barrowman NJ, Gaboury I, Sampson M, Moher D. Shorter courses of
parenteral antibiotic therapy do not appear to influence response rates for children with
acute hematogenous osteomyelitis: a systematic review. BMC Infect Dis. 2002;2(1):16.
https://doi.org/10.1186/1471-2334-2-16
9. Dartnell J, Ramachandran M, Katchburian M. Haematogenous acute and subacute
paediatric osteomyelitis: A systematic review of the literature. J Bone Joint Surg Br.
2012;94-B(5): 584-595.
https://doi.org/10.1302/0301-620X.94B5.28523
10. Woods CR, Bradley JS, Chatterjee A, et al. Clinical Practice Guideline by the Pediatric
Infectious Diseases Society and the Infectious Diseases Society of America: 2021 Guideline
on Diagnosis and Management of Acute Hematogenous Osteomyelitis in Pediatrics.
J Pediatr Infect Dis Soc. 2021;10(8):801-844.
https://doi.org/10.1093/jpids/piab027
11. Jones HW, Beckles VLL, Akinola B, Stevenson AJ, Harrison WJ. Chronic haematogenous
osteomyelitis in children: AN UNSOLVED PROBLEM. J Bone Joint Surg Br. 2011;93-B(8):
1005-1010.
https://doi.org/10.1302/0301-620X.93B8.25951

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Chapter 11: Bone and joint problems

12. Wall C, Donnan L. Septic arthritis in children. Aust Fam Physician. 2015;44(4):213-215.
13. Gigante A, Coppa V, Marinelli M, Giampaolini N, Falcioni D, Specchia N. Acute osteomyelitis
and septic arthritis in children: a systematic review of systematic reviews. Eur Rev Med
Pharmacol Sci. 2019;23(2 Suppl):145-158.
https://doi.org/10.26355/eurrev_201904_17484

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Chapter 12:
Medical complications specific to children
with severe acute malnutrition (SAM)

12.1 Introduction......................................................................................................... 333


12.2 Re-nutrition (osmotic) diarrhoea........................................................................ 334
12.2.1 Clinical features and assessment.................................................................334
12.2.2 Management............................................................................................... 334
12.3 Refeeding syndrome............................................................................................ 336
12.3.1 Clinical features and assessment.................................................................336
12.3.2 Management............................................................................................... 337
12.3.3 Prognosis..................................................................................................... 337
12.4 Paralytic ileus (acute abdominal distension)......................................................338
12.4.1 Clinical features and assessment.................................................................338
12.4.2 Management............................................................................................... 338
12.4.3 Monitoring................................................................................................... 339
12.5 Persistent oedema............................................................................................... 340
12.5.1 Clinical features and assessment.................................................................340
12.5.2 Management............................................................................................... 340
12.6 Kwashiorkor skin lesions..................................................................................... 342
12.6.1 Management............................................................................................... 342
12.6.2 Antibiotics for infected lesions.....................................................................344
References Chapter 12................................................................................................. 345

12
Chapter 12: Medical complications specific to children with severe acute malnutrition (SAM)

12.1 Introduction

This chapter covers the management of medical conditions specific to children with severe
acute malnutrition (SAM). These include re-nutrition (osmotic) diarrhoea, refeeding syndromea,
paralytic ileus, persistent oedema, and kwashiorkor skin lesions. More details on each of these
conditions can be found in this chapter. Details of routine and nutritional management of
children 1-59 months of age with SAM can be found in the MSF ITFC Nutritional Care Protocol
2021, Children 1-59 months: Inpatient. In older malnourished children, refer to local protocols
for routine nutritional management.
Children with acute malnutrition are also more prone to certain clinical conditions that
occur in all children, whether malnourished or not. In many cases, management will be the
same for both malnourished and non-malnourished children. For specific considerations on
their management, refer to the appropriate chapter in these guidelines or other relevant
guidelines: circulatory impairment and shock (see Chapter 2, Section 2.2), sepsis (see
Chapter 3, Section 3.2), hypoglycaemia (see Chapter 9, Section 9.3), hypothermia (see
Chapter 2, Section 2.6), dehydration (see Chapter 5, Section 5.3), fluid overload (see Chapter 5,
Section 5.3.2), diarrhoea (see Chapter 5, Section 5.2), severe anaemia (see Chapter 10,
Section 10.1), pain management (see Chapter 15, Section 15.4), candidiasis (see MSF Clinical
Guidelines, Chapter 3), thiamine deficiency (see Chapter 6, Section 6.4), and ophthalmic
complications (conjunctivitis, xeropthalmia) (see MSF Clinical Guidelines, Chapter 5).

12

a Rarely, refeeding syndrome can occur in children who do not meet the anthropometric criteria for malnutrition
but have endured a period of prolonged starvation.

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Chapter 12: Medical complications specific to children with severe acute malnutrition (SAM)

12.2 Re-nutrition (osmotic) diarrhoea

Diarrhoea is a frequent presentation in acutely malnourished children, and causes are many
(see also Chapter 5, Section 5.2). Re-nutrition or osmotic diarrhoea is specific to children
with malnutrition and is common in children with SAM receiving therapeutic foods. It may be
caused by premature transition to higher osmolarity milk or to food (i.e. when starting initial
treatment with F-75, or when transitioning from F-75 to F-100 or RUTFa), or by a temporary
lactose intolerance secondary to malnutrition or infective pathogens.

12.2.1 Clinical features and assessment


Re-nutrition diarrhoea presents as loose white stools which occur soon after feeding with
therapeutic milk, often within 15-30 minutes of a feed. It usually disappears within 72 hours of
starting nutritional treatment.

12.2.2 Management
Management is based on modification of the therapeutic feeding regime to slowly allow
the child’s body to adapt to the solute load and composition of therapeutic milk. Treatment
differs depending on whether diarrhoea starts in Phase 1 or Transition phase of nutritional
treatment.

Phase 1
– Carefully monitor feeding and ensure that milk is given slowly and not rushed.
– In order of preference from least to most complex, the following solutions can be tried:
• Fraction feeds: divide the volume of feed into two or four equal parts and give in small
portions every 15 to 30 minutes to finish the feed over one hour. Carefully monitor feeding
and ensure that the feed is not rushed or forced.
• Increase feed frequency: if no improvement with fractioning feeds, divide the 24-hour
feed volume to give feeds every 1-2 hours rather than the usual 3-hourly feeds, allowing
smaller volumes to be given each time.
• Continuous feeding: if no improvement with increasing feed frequency, consider giving
feeds continuously via orogastric or nasogastric tube (OGT/NGT) using gravity or a pump
(see MSF Manual of Nursing Care Procedures, SOP – Enteral Nutrition Administration
Methods).
• Dilute feeds: if no improvement with fractioning feeds, increasing feed frequency or giving
continuous feeding, dilute F-75 by adding 30 mL of extra water to 100 mL of F-75 milk to
reduce osmolarity. Continue for a few feeds only (until improvement of diarrhoea) before
changing back to F-75, as nutritional content of diluted F-75 is inadequate for extended
use.
– If re-nutrition diarrhoea persists despite all of the above measures, screen the child for TB
and HIV (even if already done). Consider the possibility of lactose intolerance, though this is
very rare.

a RUTF = Ready to Use Therapeutic Food

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Transition phase
– If diarrhoea occurs after receiving RUTF or F-100, immediately after starting transition,
transition phase has probably been started too early. Return to phase 1 with F-75 for 24 to
48 hours.
– If there are irregular and/or inconsistent bouts of loose stool after being in transition phase
for a day or so, increase the length of stay in transition phase until resolution of the problem
(likely to improve spontaneously). If no resolution, return to phase 1 with F-75 for 24 to
48 hours.

If diarrhoea persists for more than 72 hours, in the absence of another obvious explanation for
diarrhoea (e.g. otitis media, pneumonia, UTI), consider other infective causes of diarrhoea and
treat accordingly (see Chapter 5, Section 5.2.1).

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Chapter 12: Medical complications specific to children with severe acute malnutrition (SAM)

12.3 Refeeding syndrome

Refeeding syndrome is a complex syndrome occurring upon re-introduction of feeding after


a prolonged period of starvation. It involves potentially fatal shifts in fluids and electrolytes
due to hormonal and metabolic changes and usually occurs within the first week of nutritional
treatment. The hallmark of refeeding syndrome is hypophosphataemia, though many
other electrolyte imbalances can also occur, including abnormalities in sodium, potassium
and magnesium1. Thiamine deficiency and changes in glucose, fat and protein metabolism
complicate the condition further2. Management of refeeding syndrome is challenging,
especially in resource-limited settings where electrolyte monitoring is often not possible.
Refeeding syndrome should not be confused with re-nutrition or osmotic diarrhoea which is
common in severely malnourished children starting therapeutic feeds and is not a major cause
for concern (see Section 12.2).

12.3.1 Clinical features and assessment


Children with refeeding syndrome appear unwell with a deterioration in their general condition.
Presentation is variable and non-specific, including:
– Signs of circulatory impairment or shock:
• Lower limb temperature gradient
• Weak radial pulse or severe tachycardia
• Capillary refill time of 3 seconds or more
– Signs of fluid overload:
• Increased respiratory rate and/or heart rate
• Hypoxia
• Fine crackles in lung fields (pulmonary oedema)
• Galloping heart rhythm
• Enlarged liver
• Peripheral oedema and/or puffy eyes (may overlap with kwashiorkor signs)
– Hyper- or hypoglycaemia
– Paralytic ileus with abdominal distention
– Hypo- or hyperthermia
– Altered consciousness
Always consider differential diagnoses including sepsis, decompensated anaemia, severe
dehydration or fluid overload from other causes (e.g. IV fluid administration). Where
diagnostic tests are available and treatment for electrolyte imbalance is possible, check for
hypophosphatemia, hypokalaemia, hypomagnesemia, sodium and water retention, and
thiamine deficiency.

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12.3.2 Management
– Transfer to ICU where available (or in-patient area with increased monitoring and nursing
care, depending on project capacity).
– Return to (or continue with) phase 1 treatment for SAM with F-75 therapeutic milk.
– Under the guidance of an experienced clinician, consider (see also Section 12.2.2):
• Reducing feed volumes and/or
• Fractioning feeds and/or
• Reducing the speed of feed administration.
– Where feasible and able to monitor electrolytes, correct electrolyte imbalances (see
Chapter 15, Section 15.3).
– If critically unwell, start empiric broad-spectrum IV antibiotic treatment: ceftriaxone IV/IM
80 mg/kg (max. 4 g if < 50 kg; max 2 g if ≥ 50 kg) every 24 hours.
– In cases of severe paralytic ileus, see Section 12.4.
– Assess fluid status closely.
– Administer thiamine as follows:

Loading dose:
• < 15 years: 100 mg slow IV infusion over 30 minutes once daily for 48 hours
If IV not possible: give PO/via NGT at the same dose.
Maintenance dose: to be started after 48 hours of IV treatment
• ≤ 12 years: 25 mg PO once daily for 1 month
• > 12 years: 25 mg PO 2 times daily for 1 month

12.3.3 Prognosis
Refeeding syndrome is associated with high mortality, ranging from 30-71% even in high-
resource settings3,4. Prevention, through strict adherence to feeding protocols, and early
detection of refeeding syndrome are critical to reducing morbidity and mortality from the
condition.

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Chapter 12: Medical complications specific to children with severe acute malnutrition (SAM)

12.4 Paralytic ileus (acute abdominal distension)

Paralytic ileus (sometimes called pseudo-obstruction) is a condition in which peristalsis


is temporarily impaired, leading to intolerance of oral intake. Signs and symptoms mimic
obstruction, though in this case the obstruction is functional rather than mechanical. It is
relatively common in children with SAM and diarrhoea and is associated with complications
such as infection and shock, with increased mortality5. Causes include electrolyte imbalance
(e.g. hypomagnesaemia, hypokalaemia), infection, refeeding syndrome, reduced blood supply
to the bowel (mesenteric ischaemia), and certain medications (e.g. opioids, anti-diarrhoeal
agents, anticholinergics).
Surgical conditions such as volvulus and intussusception present with similar clinical signs and
should be included in the differential diagnosis. These conditions should be excluded with a
surgical review before a diagnosis of paralytic ileus is made.

12.4.1 Clinical features and assessment


Children usually present with abdominal distension and appear unwell with:
– Absent or much diminished bowel sounds
– Vomiting (but can be absent) or bilious vomiting (sign of severity)
– Traces of blood in stools (sometimes), or few or no stools
– Reduced flatus (passing gas per rectum)
– Reluctance/refusal to feed
While the predominant sign of paralytic ileus is abdominal distension, it should be noted
that malnourished children commonly have a certain degree of abdominal distension, either
secondary to gastroenteritis or due to the same mechanisms that cause refeeding syndrome.
These cases often resolve gradually with nutritional treatment and do not require treatment
for paralytic ileus.

12.4.2 Management
– Assess and manage ABCDE.
– Make the child nil-by-mouth (NBM), insert NGT and leave on free drainage (attach to catheter
bag or other waterproof bag).
– Take a full history and carry out thorough clinical examination of abdomen.
– Get surgical review, where possible.
– Measure abdominal circumference at start of treatment and every 4 hours until resolution
of condition.
– Start glucose (dextrose) 5%-Ringer lactate (G5%-RL) IV at maintenance rate (see Chapter 15,
Section 15.2):
• Add 5 mL of potassium chloride 15% (2 mmol/mL) to a 500 mL bag (see also Chapter 15,
Section 15.2).
• Continue for 6 hours with careful monitoring (see below).

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– If paralytic ileus associated with refeeding syndrome, administer thiamine as follows:

Loading dose:
• < 15 years: 100 mg slow IV infusion over 30 minutes once daily for 48 hours
If IV not possible: give PO/via NGT at the same dose.
Maintenance dose: to be started after 48 hours of IV treatment
• ≤ 12 years: 25 mg PO once daily for 1 month
• > 12 years: 25 mg PO 2 times daily for 1 month

– Administer antibiotic treatment: ceftriaxone IV (IM): 80mg/kg (max. 4 g if < 50 kg; max 2 g if
≥ 50 kg) every 24 hours and metronidazole IV 10 mg/kg every 8 hours.
– In regions with a high helminth burden, consider giving antihelminth treatment:

albendazole PO
• 12 – 23 months: 200 mg once daily for 3 daysa
• ≥ 24 months: 400 mg once daily for 3 days
mebendazole PO
• ≥ 12 months and > 10kg: 100 mg 2 times daily for 3 days

12.4.3 Monitoring
– Monitor and record vital signs at least every hour using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– Look for signs of improvement in intestinal function:
• Decreasing abdominal circumference (measurement)
• Visible peristalsis
• Stool/flatus output
• Return of bowel sounds on auscultation
– Monitor blood glucose level (BGL) every 4 hours and correct hypoglycaemia if needed.
Review after 6 hours of management:
– Improvement (signs of intestinal motility present after 6 hours):
• Give 5 mL/kg of F-75 therapeutic milk as a trial.
• After one hour, gently aspirate the gastric residual, measure the volume and discard:
▹ If the volume aspirated is the same as, or more than the volume introduced, stop F-75
trial and wait another 6 hours before attempting to re-feed. 12
▹ If the volume aspirated is less than the volume introduced, re-administer 5 mL/kg
of F-75, and gradually increase the amount of F-75 at each 3-hourly feed until the
child reaches their full feed volume (for F-75 feed volume calculations, see MSF ITFC
Nutritional Care Protocol 2021, Children 1-59 months: Inpatient, and Appendix 18.
▹ Discontinue IV maintenance fluids when the child reaches 50% of their full feed volume.
– No improvement (no sign of intestinal motility after 6 hours):
• Continue IV fluids at same rate and measure BGL every 4 hours.
• If no improvement after another 6 to 8 hours, refer for surgical input where available.

a Albendazole is not systematically recommended to children less than 12 months but can be given on a case-
by-case basis according to clinician assessment.

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12.5 Persistent oedema

Oedema associated with malnutrition (including refeeding syndrome) usually reduces and
improves within approximately 4 days of starting therapeutic nutritional treatment. If oedema
persists beyond 4 days, investigation is required to rule out other underlying medical causes.

12.5.1 Clinical features and assessment


Before considering other underlying medical causes, it is important to ensure that therapeutic
feeds have been correctly given:
– Check that the parent/carer is not giving food other than the therapeutic feeds that have
been prescribed for the child.
– Assess if the therapeutic feeds are being prepared, given and taken correctly.
– Check if hydration fluids such as ReSoMal are properly prescribed and given and not just
freely available on the ward.
After verification that therapeutic feeds have been prescribed and given correctly, consider
other possible contributory medical conditions, including:
– Severe anaemia (see Chapter 10, Section 10.1)
– Congestive heart failure (consider beri-beri) (see Chapter 6, Section 6.2 and Section 6.4)
– Renal dysfunction (nephrotic syndrome, glomerulonephritis) (see Chapter 8, Section 8.2 and
Section 8.3)
– Cirrhosis
– Obstruction of lymphatic or venous drainage of the lower limbs
– Hypothyroidism (oedema (myxoedema) can occur at pretibial level and may be associated
with peri-orbital swelling)
– Oedema of iatrogenic origin (e.g. traditional treatments or counterfeit drugs)
– Cushing's syndrome

Investigations
– Hb to check for anaemia
– HIV and TB screening, if not already done
– Urine dipstick, to exclude renal causes of oedema

12.5.2 Management
– If non-adherent to prescribed therapeutic feeding regime, reinforce the importance of giving
the prescribed volume of milk at the designated times.
– Treat any identified underlying causes.
– Reassess dehydration status and management. Check for any new signs of fluid overload
and manage accordingly (see Chapter 5, Section 5.3.2).
– Make sure only therapeutic food is given to the child and that no traditional treatments are
used.

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Chapter 12: Medical complications specific to children with severe acute malnutrition (SAM)

If potential underlying medical causes have been ruled out or treated, consider the following
modifications to the nutritional management:
– Continue Phase 1 with F-75 therapeutic milk for at least one more week.
– For children newly diagnosed with HIV and/or TB where treatment has just been started,
switch to Transition phase, as improvement in oedema may not be seen until after 2 weeks.
Monitor closely in Transition phase for signs of intolerance or worsening of the clinical
condition, including oedema.

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Chapter 12: Medical complications specific to children with severe acute malnutrition (SAM)

12.6 Kwashiorkor skin lesions

Skin lesions are a common feature of kwashiorkor and the underlying cause is not fully
understood. Different types of lesions can develop and may at times be present simultaneously.
The lesions are characterized by hypo- or hyper-pigmentation, desquamation that flakes or
peels, and in extreme cases ulceration that may spread to any area of the body.
Epidermal ulceration gives way to exudative open skin lesions, resembling burns. This can lead
to loss of fluid and heat, with an associated risk of hypothermia.
Lesions can easily become infected. As acutely malnourished patients do not exhibit a standard
inflammatory reaction, typical signs of infection such as pus formation and fever are often
absent. Superinfection is thus more difficult to detect, and specific measures must be taken to
prevent and to treat it.

Figure 12.1 - Kwashiorkor skin lesionsa

12.6.1 Management
Management should follow a systematic and holistic approach to wound care. This means
the whole patient should be assessed and not just the lesion(s). Assessment should be
methodological and with special attention to pain management – this is especially relevant
for children with kwashiorkor. The following is a summary of important steps in management
of kwashiorkor skin lesions. For full details on management, including detailed advice on
dressings, see MSF OCB Wound Care Protocol and Kwashiorkor Wounds protocols.

a Images reprinted with permission from Kirrily de Polnay, 2016.

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Chapter 12: Medical complications specific to children with severe acute malnutrition (SAM)

General measures and prevention of complications


Organization and hygiene
– Ensure good general hygiene and infection prevention and control measures (hand hygiene,
gowns, cleaning and disinfection of reusable medical equipment).
– If possible, group kwashiorkor patients in one area to facilitate better care and improve
nursing supervision.
– Keep flies and insects away from wounds (care for patients on their beds, use mosquito
nets).
– Change bedsheets regularly (if possible, daily) and any time they are soiled/moistened.
– Ensure good toileting habits and the use of nappies/diapers or potties to keep wounds free
from urine and faeces.
– Carry out personal hygiene and wound care at the warmest time of the day to prevent
hypothermia. Personal hygiene for the patient should be performed carefully using damp
cloths to wash around the lesions. Avoid baths.
– Ensure dressing changes and wound care take place away from the patient’s bedside.
Patient care
– Cut patient’s nails to prevent scratching and minimize nails as a source of infection.
– In children with extensive perineal lesions, keep the area clean and dry and ensure that
all stool is removed after each bowel movement. If the area does not improve with these
measures, consider temporary urinary catheter placement.
– Moisturise the whole bodyb:
• Use vaseline or equivalent (not zinc oxide).
• Apply on all healthy skin, three times daily.
Pressure ulcers
Severely malnourished children, especially those who are critically unwell, may have difficulty
moving. This, together with fragile skin and a lack of underlying tissue protection, leads to an
increased risk of developing pressure ulcers (bedsores). Ulcers often affect the heels, sacrum
(lower back), ischium (hips) and occiput (back of head), however, all boney projections should
be considered at risk, including the trochanters (top of thigh bone). In addition to general
hygiene and patient care measures:
– Always use side positioning (ventral or dorsal) with a maximum 30° angle (not 90°).
– Use adapted items for appropriate patient positioning such as special foam mattresses, gel
cushions and positioning cushionsc.
– Reposition patients regularly and use an appropriate mobilization chart, such as MSF Manual
of Nursing Care Procedures, Repositioning and Turning Chart to plan and monitor changes
of position. 12
– Check skin each time the patient is repositioned.
– Take care when removing dressings and use bandages instead of adhesives for fixation.
– Be aware of the risk of pressure ulcers related to therapeutic and diagnostic devices (such as
OGT/NGTs, oxygen nasal prongs). If indicated, use protective padding under devices to avoid
friction (hydrocolloid dressing or adhesive tape elastic foamd).
– Secure medical devices (e.g. pulse oximetry probe, oxygen nasal prongs, IV cannulae) with
steristrips or similar rather than adhesive tape and change position of devices regularly
where appropriate.

b All kwashiorkor patients, including those without skin lesions or wounds, should have daily skin hydration. This
can be done by a parent/carer after appropriate instruction.
c See following items in MSF catalogue: EHOEMATTF1-, EHOECUSG001, EPHYCUSGLU+
d See following items in MSF catalogue: SDREEAHC3S-, SDRETAPA1F25

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Chapter 12: Medical complications specific to children with severe acute malnutrition (SAM)

Pain management
Kwashiorkor skin lesions are extremely painful and distressing for the child and their family.
Regular analgesia may be required for children with extensive, open skin lesions and a pain
assessment should be done routinely every day, as well as prior to wound care procedures
(see Chapter 15, Section 15.4). Consider dressing changes in theatre under anaesthesia for
extensive lesions.

12.6.2 Antibiotics for infected lesions


Superimposed infection is common in kwashiorkor skin lesions and requires treatment with
antibiotics:
– First line:
amoxicillin/clavulanic acid (ratio 7:1 or 8:1) PO for 7 days
Dosage expressed in amoxicillin:
• < 40 kg: 50 mg/kg 2 times daily
• ≥ 40 kg:
Ratio 8:1: 3000 mg daily (2 tablets of 500/62.5 mg 3 times daily)
Ratio 7:1: 2625 mg daily (1 tablet of 875/125 mg 3 times daily)
– Second line (if no clinical improvement after 48-72 hourse):
clindamycin PO 10 mg/kg, 3 times daily for 10 days

Malnourished children often heal more slowly than non-malnourished children, therefore it
is important to monitor lesions carefully and frequently to look for evidence of improvement
after starting antibiotics. Lack of immediate improvement does not always indicate treatment
failure.

e Clinical improvement includes decreased wound pain, redness and heat and reduction/absence of pus.

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References Chapter 12

1. Mehanna HM, Moledina J, Travis J. Refeeding syndrome: what it is, and how to prevent and
treat it. BMJ. 2008;336(7659):1495-1498.
https://doi.org/10.1136/bmj.a301
2. Persaud-Sharma D, Saha S, Trippensee AW. Refeeding Syndrome. In: StatPearls. StatPearls
Publishing; 2023. Accessed October 30, 2023.
http://www.ncbi.nlm.nih.gov/books/NBK564513/
3. Friedli N, Baumann J, Hummel R, et al. Refeeding syndrome is associated with increased
mortality in malnourished medical inpatients: Secondary analysis of a randomized trial.
Medicine (Baltimore). 2020;99(1):e18506.
https://doi.org/10.1097/MD.0000000000018506
4. Vignaud M, Constantin JM, Ruivard M, et al. Refeeding syndrome influences outcome
of anorexia nervosa patients in intensive care unit: an observational study. Crit Care.
2010;14(5):R172.
https://doi.org/10.1186/cc9274
5. Chisti MJ, Shahid AS, Shahunja KM, et al. Ileus in children presenting with diarrhea and severe
acute malnutrition: A chart review. Vinetz JM, ed. PLoS Negl Trop Dis. 2017;11(5):e0005603.
https://doi.org/10.1371/journal.pntd.0005603

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Chapter 13:
HIV Infection

13.1 Introduction......................................................................................................... 349


13.2 Key recommendations......................................................................................... 350
13.3 Diagnosis.............................................................................................................. 351
13.4 Management........................................................................................................ 352
13.4.1 Initial management..................................................................................... 352
13.4.2 Start antiretroviral treatment...................................................................... 357
13.4.3 HIV and tuberculosis co-infection................................................................358
13.4.4 Co-trimoxazole prophylaxis.......................................................................... 358
13.5 Prevention of Mother to Child Transmission (PMTCT)................................................... 360
13.6 Prior to discharge................................................................................................. 361
References Chapter 13................................................................................................. 362

13
Chapter 13: HIV Infection

13.1 Introduction

In 2021, 1.68 million children under 15 years of age were living with HIV worldwide (of whom
88% in sub-Saharan Africa), but only 52% were receiving anti-retroviral treatment (ART)1.
Without any intervention, it is estimated that up to 52% of children who are vertically infected
with HIV will die before the age of 2 years old2. Thus, early infant diagnosis (EID) and ART
are crucial to improving the survival of HIV-infected children. Access to EID has improved
significantly in recent years, but still only around 30% of infants with vertically acquired HIV
infection are diagnosed and treated within the recommended timeframe3.

Natural history
The vast majority of children with HIV are infected during pregnancy, childbirth or breastfeeding.
The very young age at which they are infected and an inability to mount a sufficient immune
response, results in a persistently high viral load with devastating clinical consequences.
Vertically acquired HIV infection advances rapidly in young children, with direct damage to the
immune system from the virus itself, as well as the secondary effects of recurrent and severe
acute infections, underlying chronic infection, susceptibility to malnutrition, and poor growth
and development.
This chapter covers the basic management of a sick HIV-exposed or infected child requiring
inpatient care. For comprehensive guidance on the management of children living with HIV
refer to national guidelines (where available), other MSF guides (e.g. MSF HIV/TB Clinical
Guide for Primary Care, Paediatric HIV handbook) and/or WHO resources3.

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Chapter 13: HIV Infection

13.2 Key recommendations

The 2021 WHO “Consolidated guidelines on HIV prevention, testing, treatment, service delivery
and monitoring: recommendations for a public health approach” includes the following3:
– In high HIV burden settingsa, all children admitted for inpatient care should routinely be
tested for HIV unless HIV status is already known.
– In low HIV burden settings, all children admitted for inpatient care should routinely be tested
for HIV if:
• Biological parent known to have (or suspected to have died of) HIV infection or an
undiagnosed long-term illness
• Presence of malnutrition
• Recurrent infection, fever of unknown origin, poor response to treatment
• Diagnosis of tuberculosis
– All HIV-infected children and adolescents should be commenced on ART (regardless of WHO
clinical stage and CD4 cell count) on the day of diagnosis or within 7 days thereof, except
in the case of cryptococcal meningitis, when ART should be delayed for 4 weeks after the
induction phase of treatment.
– In children diagnosed with tuberculosis, ART should be started as soon as possible within
2 weeks of starting TB treatment, except in the case of TB meningitis (delay ART for 4 weeks).

a High-burden HIV settings are those where HIV prevalence in the adult population ≥ 1%.

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Chapter 13: HIV Infection

13.3 Diagnosis

Consider an underlying HIV infection in any sick child who presents with malnutrition,
recurrent or severe infections, tuberculosis, persistent fever or who does not improve despite
appropriate treatment for their presumed diagnosis.
Diagnosis of HIV infection can be confirmed in all children 18 months of age and over (or
3 months after cessation of breastfeeding, whichever comes later) with a simple rapid
diagnostic test (RDT) for HIV antibodies. Refer to WHO or national diagnostic algorithms where
available. For infants and children younger than 18 months of age, or those who are breastfed
beyond 18 months, DNA PCR, ideally as point-of-care nucleic acid testing (NAT), is required to
make a diagnosis of HIV. Refer to Table 13.1 below and national guidelines for more detail on
testing and diagnosis of HIV in children under 18 months of age.
Pre-test information should be provided to the parents/carers and/or child (depending on age)
prior to testing.

Table 13.1 - Diagnosis of HIV in infants and children 18 months and younger

Assess exposure
Timing of DNA PCR/NAT
(if HIV status of mother unknown)

If maternal HIV 4-6 weeks of life


RDT positive or at the earliest opportunity thereafter
➔ DNA PCR/NAT
required If DNA PCR/NAT positive
Ideally, test mother ➔ consider child to be infected and start
If maternal HIV treatment. Repeat DNA PCR/NAT to confirm
RDT negative diagnosisa.
➔ no further
testing required If DNA PCR/NAT negative
➔ ensure regular clinical monitoring and repeat
DNA PCR/NAT systematically at 9 months of
age.

If mother not available, perform DNA If DNA PCR/NAT negative at 9 months


PCR/NATb on child ➔ ensure regular clinical monitoring and
perform HIV RDT systematically at 18 months
of age or 3 months after the cessation of
breastfeeding, whichever is later. 13

a If repeat NAT negative, perform a third NAT to determine final diagnosis. Continue treatment until results of
third NAT are available – if negative, treatment can be stopped.
b If DNA PCR/NAT is unavailable or it is not possible to test all babies with unknown exposure using DNA PCR/NAT,
HIV RDT can be used instead as a screening tool for exposure to HIV. However, HIV RDT only reliably identifies
exposure in infants < 4 months; in infants and children 4-18 months, a positive HIV RDT establishes exposure
but a negative HIV RDT does not fully rule out exposure, therefore DNA PCR/NAT testing may still be required.

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Chapter 13: HIV Infection

13.4 Management

The following section outlines the management of infants and children with confirmed HIV
infection.

13.4.1 Initial management


– Assess and manage ABCDE; stabilize as needed (Chapter 2, Section 2.1).
– Assess nutritional status if not already done.
– Breastfed infants should continue breastfeedinga.
– Assess, screen for and manage other concomitant infections or conditions:
• Common childhood illnesses present more frequently and more severely.
• Treatment is the same as for non-HIV infected children (refer to respective sections in
these guidelines or MSF Clinical Guidelines) for the following conditions:

Paediatric Guidelines Clinical Guidelines

• Pneumonia (see Chapter 4, Section 4.5) • Varicella zoster


• Sepsis (see Chapter 3, Section 3.2) • Herpes zoster
• Malaria (see Chapter 3, Section 3.4) • Oral/oesophageal herpes
• Meningitis and meningoencephalitis • Oral/oesophageal candidiasis
(see Chapter 3, Section 3.3) • Skin infections (fungal, bacterial,
• Diarrhoea (see Chapter 5, Section 5.2), scabies, pruritic papular eruptions)
including persistent diarrhoea • Molluscum contagiosum; warts (HPV)
• Mastoiditis (see Chapter 4, Section 4.12)
• Tuberculosis (see Section 13.4.3 and
Chapter 4, Section 4.11)

• HIV-infected children are at risk of developing opportunistic infections, such as


pneumocystis pneumonia (PCP) and cryptococcal meningitis, as well as other conditions
specific to HIV infection, e.g. lymphoid interstitial pneumonitis (LIP). These are briefly
covered in Table 13.2. Children over 10 with advanced HIV disease should be routinely
screened for cryptococcal meningitis.
• Cancers associated with HIV-infection are not in the scope of this guide; refer to other
sources.

a Breastfeeding is not contraindicated in babies born to HIV positive mothers. To mitigate the risk of transmission
of HIV through breastmilk, maternal viral load should be suppressed through ART. If it is not possible to
suppress maternal viral load, consideration should be given to continuation of infant prophylaxis beyond the
6- or 12- week period, in accordance with national guidance.

352
Table 13.2 - Opportunistic infections and conditions in children living with HIV

Condition Causes Clinical features Management

Pneumocystis Pneumocystis Common in children under 1 year Administer oxygen via facemask, aiming for SpO2 between 94 - 98%.
pneumonia (PCP) jirovecii Respiratory distress and hypoxaemia Supportive care with fluids and feeds if needed (see Chapter 15,
Acute or sub-acute onset Section 15.2 and Section 15.5 respectively).
Fever can be high, but often afebrile High-dose co-trimoxazole PO (or IV) for 21 days:
Non-productive cough 50 mg/kg SMX + 10 mg/kg TMP, 2 times daily
Feeding difficulties in infants or 25 mg/kg SMX + 5 mg/kg TMP, 4 times daily
Chest usually clear on auscultation +
For severe cases:
CXR: Diffuse interstitial infiltration,
prednisolone PO: 1 mg/kg 2 times daily for 5 days, then 1 mg/kg once
hyperinflation, pneumothorax or normal
daily for 5 days, then 0.5 mg/kg once daily for 5 days.
(20%). Effusion very uncommon with PCP.
Continue co-trimoxazole prophylaxis (see Table 13.4) after treatment
completion

Lymphoid Lympho- Slow onset: cough, dyspnoea, hypoxaemia Improvement with ART.
Interstitial proliferative (SpO2 < 92%).
Symptomatic management if needed:
Pneumonitis (LIP) infiltrate Often enlarged lymph nodes, spleen and
• Inhaled bronchodilators for wheeze (see Chapter 4, Section 4.10.1).
chronic parotitis.
Children > 3 years • Steroids may be useful. If no response observed after 1 month,
May find wheeze, clubbing, signs of right
discontinue by weaning gradually over 2 months.
heart failure.
CXR: Bilateral reticulonodular infiltrate.
Similar appearance to miliary TB, but
more irregular distribution and clinically
distinct: child with LIP may look well, child
with TB is usually more ill with fever and
weight loss.

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Chapter 13: HIV Infection

13
354
Condition Causes Clinical features Management

Mycobacterium Mycobacterium Weight loss, fatigue, unremitting fever, Combined treatment of at least 2 drugs:
avium complex avium complex chronic diarrhoea, wasting, abdominal azithromycin 10 mg/kg once daily (clarithromycin may be used as an
(MAC) pain alternative)
Enlarged lymph nodes, hepatomegaly, +
anaemia, unresolving pulmonary infiltrate ethambutol 15 to 25 mg/kg once daily
Chapter 13: HIV Infection

Investigations: Treatment should be continued for at least 12 months after sputum


Hb, FBC (anaemia, neutropaenia, culture conversion to negative.
thrombocytopaenia)
Delay starting ART for 2 weeks if not yet on ART.
Where available, raised ALP, LDH,
transaminases.
AFB and culture from sterile site (blood,
bone marrow, lymph node) if possible
Consider in suspected TB (especially EPTB)
not responding to TB treatment with
supportive lab findings.

Cryptococcal Cryptococcus Older children (> 12 years old) Delay initiation of ART for 4-6 weeks after starting antifungal
meningitis neoformans, treatment.
Fever, headache, lethargy, irritability,
especially with
abnormal cry, poor feeding, vomiting, Single high dose amphotericin B IV: 10 mg/kg
low CD4
neck stiffness, convulsions, bulging +
fontanelle 14 days of treatment with:
flucytosine PO: 25 mg/kg four times daily
Serum CrAg positive
+
CSF findings: fluconazole PO: 12 mg/kg once daily (max. 800 mg/day)
Opening pressure – very elevated
then consolidation regimen: fluconazole PO alone
CSF aspect – clear
6 – 12 mg/kg once daily (max. 800 mg/day) for 8 weeks
Specific tests - Indian ink +; crypto Ag +
WBC - < 800, mainly lymphocytes Maintenance regimen: fluconazole PO: 6 mg/kg once daily until CD4
Protein (mg/dL) – 20-500, Pandy neg > 200 cells/mm3 and viral load (VL) suppression on ART.
Glucose (mg/dL) – low < 45
Repeated therapeutic lumbar puncture should be done if raised
intracranial pressure (headache, vomiting, visual disturbance) to keep
pressure < 20 mm H2O. Remove 1 mL/kg, max. 25 mL per puncture.
Condition Causes Clinical features Management

HIV This is a diagnosis of exclusion. Early initiation of ART reduces viral damage to the brain.
encephalopathy ART may improve some established clinical features.
At least one of the following, progressing
Develops during over two months in the absence of
first 2 years of life another illness:
• Loss or failure to attain developmental
milestones, loss of intellectual capacity
• Microcephaly: head circumference
< 5th percentile for age, or stagnation
and failure of head circumference to
grow
• Motor deficits: symmetrical spastic
paresis, increased reflexes (pyramidal
tract motor deficit), gait disturbance
or ataxia. Facial motor signs such as
abnormal eye movements

Focal neurological Stroke due to Stroke: sudden onset, no signs of raised Stroke: supportive treatment (see Chapter 15)
deficits HIV associated intracranial pressure (ICP)
CNS tumour: supportive treatment (see Chapter 15) and management
vasculitis or
CNS tumour: sudden or progressive of raised ICP (see Chapter 2, Section 2.8.3).
coagulopathy
onset with signs of raised ICP (severe
Toxoplasmosis
CNS tumour headache, vomiting) and no improvement
pyrimethamine + sulfadiazine + folic acid for 6 weeks
after at least 10 days of treatment for
Cerebral or high dose co-trimoxazole for 6 weeks (see above dosing for PCP)
toxoplasmosis.
toxoplasmosis Treatment response is expected within 10 days. Secondary
Toxoplasmosis: rare in children; may occur prophylaxis is needed after treatment (see Table 13.4).
Tuberculosis
in severely immune suppressed children In settings where neuroimaging is not available, consider empiric
(tuberculoma,
not on CTX. May or may not have signs of treatment trial of high dose co-trimoxazole for all HIV-infected children
vasculitis)
raised ICP. who present with a focal deficit, with or without raised ICP.

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Chapter 13: HIV Infection

13
356
Condition Causes Clinical features Management

Persistent Pathogens More than 3 stools per day – bloody or Rehydration as required depending on assessment (see Chapter 5,
diarrhoea specific to watery Section 5.3).
(> 14 days) advanced HIV:
Dehydration – assess severity: recent Chronic diarrhoea has a high associated mortality in HIV patients.
Chapter 13: HIV Infection

or
Bacteria weight loss, reduced conscious level, Urgent ART is needed.
Chronic diarrhoea
MAC (see above) sunken eyes, reduced skin tone, thirst.
(> 28 days) If no pathogen identified, antibiotic trial for 7 days:
Protozoa Malnutrition and wasting High dose co-trimoxazole PO (see above dosing for PCP)
Cryptosporidium, +
Stool analysis on three separate samples
Isospora metronidazole PO: 15 mg/kg 3 times daily
If available: WBC and CD4
MAC (see above)
If Isospora belli confirmed by stool analysis:
co-trimoxazole PO: 50 mg/kg SMX + 10 mg/kg TMP, 2 times daily for
10 days, followed by 25 mg/kg SMX + 5 mg/kg TMP, 2 times daily for
3 weeks.
Chapter 13: HIV Infection

13.4.2 Start antiretroviral treatment


For children with confirmed HIV infection, initiate combination ART as soon as possible based
on national guidelines or according to the following WHO recommendations3:

Age/weight Preferred 1st line ARTb Alternative

Children > 3 kg – 29.9 kg ABC + 3TC + DTG ABC + 3TC + LPV/r

Adolescents ≥ 30 kg TDF + 3TC + DTG TDF + 3TC + EFV 400 mg

– Wherever possible, use pre-qualified paediatric fixed dose combinations (FDCs).


– If ABC/3TC fixed dose combination (FDC) is not available as the preferred backbone, AZT/3TC
FDC is an alternative.
– Dosing of paediatric ART is outlined in Table 13.3 below.
– In adolescents weighing 30 kg or more, give TDF 300mg/3TC 300 mg/DTG 50 mg FDC, once
daily.
– For more detailed information, refer to MSF HIV/TB clinical guide for primary care and the
WHO Paediatric ARV dosing dashboardc.

Table 13.3 - Simplified dosing of child-friendly FDCs in children 4 weeks and older (excluding
adolescents ≥ 30 kg)3
ABC/3TC Dolutegravir
(2 times daily) (once daily)
Weight
60/30 mg 120/60 mg 600/300 mg 10 mg 50 mg
dispersible tab dispersible tab tab dispersible tab tab
1 tab, morning ½ tab, morning
3 to < 6 kg – ½ tab –
and evening and evening
1½ tabs, morning ½ tab morning,
6 to < 10 kg – 1½ tabs –
and evening 1 tab evening
2 tabs, morning 1 tab, morning
10 to < 14 kg – 2 tabs –
and evening and evening
2½ tabs, morning 1 tab morning,
14 to < 20 kg – 2½ tabs –
and evening 1½ tabs evening
3 tabs, morning 1½ tabs, morning
20 to < 25 kg – 3 tabs 1 tab
and evening and evening
½ tab, morning
25 to < 35 kg – – – 1 tab
and evening
13
In children < 18 months of age with known HIV exposure who are admitted critically unwell or
with a presumptive infection (particularly an opportunistic infection), start ART while waiting
for the DNA PCR/NAT results. Ensure follow-up of DNA PCR/NAT results and final confirmation
of diagnosis of HIV in all children starting presumptive treatment (see Section 13.3).

b Abacavir (ABC), lamivudine (3TC), dolutegravir (DTG), tenofovir (TDF), lopinavir/ritonavir (LPV/r), efavirenz
(EFV), zidovudine (AZT)
c https://paedsarvdosing.org/?sfvrsn=c32f09d7_10

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Chapter 13: HIV Infection

Side effects
ART medications have a number of side effects which should be monitored at each follow-up.
Almost all ARVs can cause mild constitutional symptoms such as headache, nausea and
fatigue. In addition, specific potential side effects include renal impairment (TDF), anaemia
(AZT), neutropenia (AZT), hepatic impairment (NVP; LPV/r; EFV; DTG; TB-HIV co-treatment),
hypersensitivity reactions (ABC; NVP; EFV), CNS disturbance (EFV), and mitochondrial toxicity
(3TC; AZT; ABC; TDF).

13.4.3 HIV and tuberculosis co-infection


HIV-tuberculosis (TB) co-infection is common in newly presenting sick children with HIV. Both
HIV-exposed and infected children are at high risk of active TB and should be screened for TB:
– Take a full history including family history of TB and any potential household contacts with
TB.
– Conduct a comprehensive examination. Note that extrapulmonary TB is more common in
children therefore full clinical examination of all systems is necessary.
– Ensure relevant investigations are performed e.g. GeneXpert, TB LAM (see Chapter 4,
Section 4.11). Note that tuberculin skin test (TST) may be negative in HIV co-infection.
If TB disease is suspected: start TB treatment as soon as possible while waiting for TB investigation
and results. Refer to Chapter 4, Section 4.11. In the case of suspected TB meningitis in an HIV-
infected child, consider adding corticosteroid therapy.

Immune Reconstitution Inflammatory Syndrome (IRIS)


IRIS is a paradoxical reaction that can occur in patients with an underlying opportunistic
infection and whose immunity is rapidly improving on ART. To avoid IRIS in children with
suspected TB who are not yet on ART, delay ART initiation and start TB treatment immediately.
Initiate ART as soon as TB drugs are tolerated within 2 weeks of starting TB treatment, unless
TB meningitis is suspected. In this case, delay ART by at least 4 weeks (and initiate within
8 weeks) after starting TB treatment3.
If active TB excluded, start TB preventive treatment. Refer to Chapter 4, Section 4.11 and MSF
Tuberculosis Guidelines for details.

13.4.4 Co-trimoxazole prophylaxis


Give co-trimoxazole PO once daily to all children from 4 to 6 weeks of age who are confirmed
as HIV-exposed or infectedd:
– 50 mg/kg SMX (max. 800 mg) + 10 mg/kg TMP (max. 160 mg) once daily (see Table 13.4).

d Prophylaxis against pneumonia (especially PCP), cerebral toxoplasmosis, certain types of diarrhoea, malaria,
severe bacterial infections (strep pneumoniae, haemophilus influenzae, salmonella, legionella, nocardia,
methicillin sensitive staphylococcus aureus and many gram-negative bacilli).

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Chapter 13: HIV Infection

Table 13.4 - Simplified dosing of once daily co-trimoxazole prophylaxis in children

200/40 mg
100/20 mg 400/80 mg 800/160 mg
Weight per 5 mL oral
dispersible tab scored tab scored tab
suspension

3 to < 6 kg 2.5 mL 1 tab – –

6 to < 10 kg 5 mL 2 tabs ½ tab –

10 to < 14 kg 5 mL 2 tabs ½ tab –

14 to < 20 kg 10 mL 4 tabs 1 tab ½ tab

20 to < 25 kg – 4 tabs 1 tab ½ tab

25 to < 35 kg – – 2 tabs 1 tab

13

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Chapter 13: HIV Infection

13.5 Prevention of Mother to Child Transmission (PMTCT)

Refer to MSF Prevention of mother-to-child transmission of HIV Guidelines for full details on
PMTCT.
– All HIV-exposed infants should receive ART:
• Infants who are at high riska of acquiring HIV should receive AZT and NVP prophylaxis
once daily until 6 weeks of age, regardless of whether they are breastfed or formula fed.
• In high-risk breastfed infants, AZT and NVP prophylaxis (or NVP alone) should be continued
for an additional 6 weeks (total of 12 weeks of infant prophylaxis).
• For low-risk breastfed infants (i.e. whose mothers are receiving ART and have a suppressed
VL at least 4 weeks prior to delivery), give only NVP once daily for 6 weeks.
• For infants receiving replacement feeding whose mothers are receiving ART, give NVP
once daily (or AZT 2 times daily) for 4-6 weeks.
See also Appendix 19 for more detail, including dosing of ARV prophylaxis in PMTCT.

a A high-risk infant is defined as an infant whose mother was first identified as HIV-infected at delivery or in the
postpartum period, infected during pregnancy or breastfeeding, received less than 4 weeks of ART prior to
delivery, or did not achieve viral suppression by the time of delivery.

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Chapter 13: HIV Infection

13.6 Prior to discharge

– Ensure referral to HIV and/or maternal-child health services has been established.
– Continuity of ART and close follow-up and monitoring is vital for children growing up with
HIV.

13

361
Chapter 13: HIV Infection

References Chapter 13

1. Paediatric care and treatment. UNICEF DATA. Accessed October 30, 2023.
https://data.unicef.org/topic/hivaids/paediatric-treatment-and-care/
2. Newell ML, Coovadia H, Cortina-Borja M, Rollins N, Gaillard P, Dabis F. Mortality of infected
and uninfected infants born to HIV-infected mothers in Africa: a pooled analysis. The Lancet.
2004;364(9441):1236-1243.
https://doi.org/10.1016/S0140-6736(04)17140-7
3. Consolidated Guidelines on HIV Prevention, Testing, Treatment, Service Delivery and
Monitoring: Recommendations for a Public Health Approach. World Health Organization;
2021.
https://www.who.int/publications/i/item/9789240031593

362
Chapter 14:
Fever of unknown origin (FUO) and
neglected tropical diseases (NTDs)

14.1 Fever of unknown origin (FUO)........................................................................... 365


14.1.1 Causes.......................................................................................................... 365
14.1.2 Clinical features........................................................................................... 365
14.1.3 Investigations............................................................................................... 366
14.1.4 Management............................................................................................... 366
14.2 Leishmaniasis....................................................................................................... 372
14.2.1 Visceral leishmaniasis (kala-azar)................................................................372
14.2.2 Cutaneous leishmaniasis.............................................................................. 374
14.2.3 Post-kala-azar dermal leishmaniasis (PKDL)................................................377
14.3 Noma (cancrum oris)........................................................................................... 378
14.3.1 Clinical features........................................................................................... 378
14.3.2 Management............................................................................................... 379
14.3.3 Prognosis..................................................................................................... 382
14.3.4 Prevention.................................................................................................... 382
References Chapter 14................................................................................................. 383

14
Chapter 14: Fever of unknown origin (FUO) and neglected tropical diseases (NTDs)

14.1 Fever of unknown origin (FUO)

There is no widely agreed definition of fever of unknown origin (FUO), also known as persistent
fever, in children1. FUO is a diagnosis of exclusion, therefore the clinical definition of FUO in
children for the purposes of these guidelines is: fever at least once per day for more than
7 days, with no confirmed diagnosis after initial comprehensive assessment that includes a
detailed history, thorough clinical examination, and appropriate laboratory investigations.
Given the lack of a consensus definition, the incidence of FUO in children is uncertain.

14.1.1 Causes
Causes of FUO in children are numerous. Infectious diseases (viral, bacterial, parasitic or fungal)
are the most commonly identifiable causes, followed by rheumatologic diseases (most commonly
juvenile idiopathic arthritis (JIA) and systemic lupus erythematosus) and neoplastic disorders2.
The remainder are caused by various conditions including Kawasaki disease, inflammatory bowel
disease, immunodeficiencies, factitious fever, and drugs (see Appendix 20 for a comprehensive list
of causes). For infectious causes, consider the epidemiology of the area as well as clinical features
to guide the differential diagnosis. As potential causes of FUO are many, a systematic approach to
the patient is required. Exclude the most common causes of FUO (TB, HIV, undiagnosed malaria,
enteric fever, pneumonia) before investigating for other conditions.

14.1.2 Clinical features


Before starting a detailed diagnostic workup, it is essential to demonstrate the presence of
fever in a controlled setting. Therefore, patients with suspected FUO should be admitted for
regular monitoring and recording of fever and other vital signs. The medical team should
repeat the history and clinical examination on multiple occasions to identify clues that may
have been omitted or overlooked previously.
Specific points to be reviewed in the history include:
– Symptoms: potential undiagnosed underlying medical condition
– Growth: particularly decreased growth velocity
– Immunisations: up-to-date or missing immunisations
– Living conditions: urban/rural/nomadic
– Occupation/school
– Epidemiology of the area: malaria, TB, HIV, leishmaniasis
– Season: rainy or dry season
– Recent travel or displacement
– Diet: goat’s milk, unpasteurized products, raw meat, pica
– Exposure/Contact: animals, lakes/rivers, sand/soil, mosquitoes/ticks/bites/cats, tuberculosis,
sexual, blood products, piercing/tattoos.
Full head-to-toe clinical examination should be performed, including vital signs (especially HR 14
and temperature association) and anthropometric assessment (to rule out malnutrition or short
stature). If not done on admission, the patient with FUO should be evaluated while febrile. This is
necessary to assess how unwell the patient appears and to record any accompanying symptoms
(e.g. the rash of JIA is characteristically evanescent and may be present only during fever).

365
Chapter 14: Fever of unknown origin (FUO) and neglected tropical diseases (NTDs)

14.1.3 Investigations
Initial baseline investigations for all children with FUO:
– Full blood count (FBC), including Hb
– Blood glucose level (BGL)
– Malaria RDT and blood film
– Urine dipstick and culture, if available
– Blood culture, if available
– HIV testing
– Mantoux testing, if available
– Liver and renal function tests, if available
– Radiology:
• CXR (to check the lungs but also the hila and mediastinum)
• If CXR is not available, ultrasound of chest can be performed, although ultrasound is
limited in evaluation for TB in children. Paediatric TB is commonly characterized by hilar
and/or mediastinal lymph nodes, which are difficult to visualize on ultrasound.
• Abdominal ultrasound
Further investigations to be considered depending on clinical suspicion, evolution and
availability (see Figure 14.1):
– Recombinant kinesin antigen (rK39) testa (for visceral leishmaniasis)
– Leishmania DAT (direct agglutination test)
– TB screening: microscopy and culture, or GeneXpert where available (see Chapter 4,
Section 4.11 for further investigations if TB suspected).
– Urinary microscopy for schistosomiasis
– Stool microscopy and culture
– LP for CSF examination: biochemistry, Gram stain and culture, GeneXpert
– RDT for HIV, HBV, HCV
– Card Agglutination Test for Trypanosomiasis (CATT)
– Rose Bengal test for brucellosis
– Rickettsia IgM
– Cardiac ultrasound

14.1.4 Management
After exclusion of the most common causes of FUO, management is guided by the principal
symptoms and signs, and the organ systems affected (see Figure 14.1). Ensure close clinical
monitoring and revise diagnosis daily based on new or evolving clinical signs and symptoms.
If, after careful and detailed assessment (thorough history of symptoms, exposure, family and
past medical history; head to toe clinical examination; baseline and targeted investigations),
no source or obvious cause is identified, use empiric treatment to cover several common
pathogens while continuing to investigate:
– If hospitalised due to severity of symptoms:
• ceftriaxone IV: 50 - 80 mg/kg (max. 4 g if < 50 kg; max. 2 g if ≥ 50 kg) every 24 hours
+
• doxycycline PO: 2 - 2.2 mg/kg (max. 100 mg) 2 times daily (or azithromycin PO: 10 mg
once daily in children < 8 years)
– If treated as outpatient: doxycycline PO (or azithromycin PO in children < 8 years)

a Useful antigen in ELISA assays with high sensitivity and specificity in immunocompetent patients in the Indian
subcontinent. The sensitivity is lower and more variable in East Africa and Brazil, although specificity remains
high. This antigen rapid test requires minimal equipment and is easy to use.

366
Figure 14.1 - Algorithm for the management of a child with FUO

Child with FUO


(fever > 7 days)

Take a detailed history and perform a thorough clinical examination


to identify clues to potential focus of infection

Admit to hospital and perform baseline investigations: FBC, Hb, BGL, malaria
RDT and blood film, urine dipstick, HIV test and, if available:
Urine culture, Blood culture, liver and renal function tests, TB screening,
baseline radiology (CXR/lung US and abdominal US)

Does the child have signs YES Treat as per sepsis protocol
of severe infection? (see Chapter 3, Section 3.2)

NO

Daily monitoring (vital signs incl. temperature), minimum 2 times daily


Repeat FBC at 48 hours
Revise and record differential diagnosis every 24 hours depending on
evolution of clinical signs and symptoms according to table below

Main sign/
Potential cause Clues in history or examination Investigations (if available) Management
symptom
Hepatomegaly Visceral Leishmaniasis Known endemic area; sandfly bite; Leishmaniasis rapid test (rK39) or See Section 14.2
and/or serology (DAT); pancytopenia on
Splenomegaly FBC; raised CRP
Chapter 14: Fever of unknown origin (FUO) and neglected tropical diseases (NTDs)

367
14
368
Main sign/
Potential cause Clues in history or examination Investigations (if available) Management
symptom
Hepatomegaly Viral hepatitis Previous blood transfusion (B/C/D); HBV and HCV RDTs See MSF Clinical Guidelines,
and/or sexual contact (B/C/D); poor hygiene Chapter 8
Splenomegaly practices (A/E); jaundice
Schistosomiasis Swimming/bathing in infected water Urine dipstick, urine and stool See MSF Clinical Guidelines,
(rivers/lakes); fever and rash with microscopy Chapter 6
bronchospasm (Katayama fever)
Amoebic or bacterial liver Poor hygiene practices; lack of access to Abdominal US; leucocytosis on See MSF Clinical Guidelines,
abscess clean water FBC; raised CRP Chapter 3
Human African Sub-Saharan Africa only; known Card Agglutination Test for See MSF Clinical Guidelines,
Trypanosomiasis endemic area; tsetse fly bite; sleeping Trypanosomiasis (CATT) Chapter 6
pattern
Leptospirosis Exposure to domestic animals/rodents; CXR; Blood smear; raised CRP See MSF Clinical Guidelines,
recent heavy rain/flooding; tropical/ Chapter 7
subtropical; biphasic fever; ‘red eyes’
Brucellosis Exposure to livestock; drinking Rose Bengal test, blood culture See MSF Clinical Guidelines,
unpasteurised milk; rural areas Chapter 7
Borreliosis (Tick-Borne or Known endemic area; tick bite – Blood smear See MSF Clinical Guidelines,
Louse-Borne Relapsing temperate regions of Africa, rural; Chapter 7
Fever) body lice – Horn of Africa, epidemic in
Chapter 14: Fever of unknown origin (FUO) and neglected tropical diseases (NTDs)

cold season, overcrowding and poor


sanitation; biphasic fever
Respiratory Pneumonia (atypical/ Poorly maintained water pipes; CXR and/or lung US See Chapter 4, Section 4.5
fungalb) exposure to bird/bat droppings
TB Known endemic area; close contact with TB screening; HIV screening See Chapter 4, Section 4.11
suspected/known case and MSF TB Guidelines
Tumour Chronic symptoms CXR, lung US, FBC Consider referral

b Atypical/fungal lung infections include legionella and histoplasmosis. See also Appendix 20.
Main sign/
Potential cause Clues in history or examination Investigations (if available) Management
symptom
Cardiac Endocarditis Poor dentition; recent procedure Blood culture and cardiac US Follow local guidance

Myocarditis/Pericarditis Recent URTI Cardiac US, TB screening Follow local guidance


(bacterial/viral/TB)

American American continent; known endemic Blood microscopy, ECG, CXR See MSF Clinical Guidelines,
Trypanosomiasis (Chagas area (rural); triatomine bug faeces; Chapter 6
disease) severe constipation

Kawasaki disease Desquamation of hands and feet Clinical diagnosis, cardiac US Follow local guidance

Abdominal Enteric fever (typhoid Poor hygiene practices; lack of access Blood culture; abdominal US; See Chapter 3, Section 3.6
pain/diarrhoea and paratyphoid) to clean water; known endemic area; leucopenia; raised CRP
relative bradycardia; salmon rash

Amoebic or bacterial liver Poor hygiene practices; lack of access to Abdominal US; leucocytosis on See MSF Clinical Guidelines,
abscess clean water FBC; raised CRP Chapter 3

Appendiceal abscess Recent appendicitis Abdominal US Consider referral

HIV Previous blood transfusion; mother sick HIV testing See Chapter 13 and HIV
or known HIV positive guidelines

TB Known endemic area; close contact with TB screening See Chapter 4, Section 4.11
suspected/known case and MSF TB Guidelines

Genitourinary Pyelonephritis Recent UTI; congenital renal problem Urine dipstick See Chapter 8, Section 8.1

Schistosomiasis Recent swimming/bathing in infected Urine dipstick, urine and stool See MSF Clinical Guidelines,
water (rivers/lakes) microscopy Chapter 6

Genital infections Recent sexual activity/assault Genital swabs, urine dipstick See MSF Clinical Guidelines,
Chapter 9
Chapter 14: Fever of unknown origin (FUO) and neglected tropical diseases (NTDs)

369
14
370
Main sign/
Potential cause Clues in history or examination Investigations (if available) Management
symptom
Neurological Malaria Known endemic area; no bed net; rainy Malaria RDT +/- blood film See Chapter 3, Section 3.4
season

Meningitis (incl. TB) Missed immunisations; known Lumbar puncture See Chapter 3, Section 3.3,
epidemic-prone area Chapter 4, Section 4.11 and
MSF TB Guidelines

Mastoiditis/intracranial Recent otitis media Clinical diagnosis, CT head See Chapter 4, Section 4.12
abscess

Tetanus Missed immunisations; dirty wound Clinical diagnosis See Chapter 3, Section 3.5
(soil)

Leptospirosis Exposure to domestic animals/rodents CXR, Blood smear See MSF Clinical Guidelines,
Chapter 7

Human African Sub-Saharan Africa only, known endemic Card Agglutination Test for See MSF Clinical Guidelines,
Trypanosomiasis area; tsetse fly bite Trypanosomiasis (CATT) Chapter 6

HIV Previous blood transfusion; mother sick HIV testing See Chapter 13 and HIV
or known HIV positive guidelines

Dermatological/ Rickettsiosis Insect bite (ticks, rat fleas, mites); Rickettsia IgM See MSF Clinical Guidelines,
Chapter 14: Fever of unknown origin (FUO) and neglected tropical diseases (NTDs)

skin rash ‘inoculation eschar’: painless, black, Chapter 7


crusted lesion with erythemartous halo
at bite

Erysipelas/cellulitis Infected wound site Clinical diagnosis See MSF Clinical Guidelines,
Chapter 4

Kawasaki disease Desquamation of hands and feet Clinical diagnosis, cardiac US Follow local guidance
Main sign/
Potential cause Clues in history or examination Investigations (if available) Management
symptom
Musculoskeletal Osteomyelitis Missed immunisations; known SCD; FBC, blood culture, limb x-ray See Chapter 11, Section 11.4
recent IO access; puncture wound
Septic arthritis Missed immunisations; open wound FBC, blood culture, joint US See Chapter 11, Section 11.5
Brucellosis Exposure to livestock; drinking Rose Bengal test, blood culture See MSF Clinical Guidelines,
unpasteurised milk; rural areas Chapter 7
TB Known endemic area; close contact with TB screening See Chapter 4, Section 4.11
suspected/known case and MSF TB Guidelines
Rheumatic/neoplasm Chronic symptoms Blood smear Consider referral
Multiorgan Sepsis FBC, blood culture See Chapter 3, Section 3.2
(including
TB Known endemic area; close contact with TB screening See Chapter 4, Section 4.11
weight loss, skin
suspected/known case and MSF TB Guidelines
rash)
HIV Previous blood transfusion; mother sick HIV testing See Chapter 13 and HIV
or known HIV positive guidelines
Rickettsiosis Insect bite (ticks, rat fleas, mites); Rickettsia IgM See MSF Clinical Guidelines,
‘inoculation eschar’: painless, black, Chapter 7
crusted lesion with erythemartous halo
at bite
Borreliosis Known endemic area; tick bite – Blood smear See MSF Clinical Guidelines,
temperate regions of Africa, rural; Chapter 7
body lice – Horn of Africa, epidemic in
cold season, overcrowding and poor
sanitation
Leptospirosis Exposure to domestic animals/rodents CXR, Blood smear See MSF Clinical Guidelines,
Chapter 7
Rheumatic/neoplasm Chronic symptoms Blood smear Consider referral
Chapter 14: Fever of unknown origin (FUO) and neglected tropical diseases (NTDs)

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Chapter 14: Fever of unknown origin (FUO) and neglected tropical diseases (NTDs)

14.2 Leishmaniasis

A neglected tropical disease caused by protozoa of the genus Leishmania and transmitted by
the bite of an infected sandfly. There are different types of leishmaniasis:
– Visceral leishmaniasis (or kala-azar) (VL): most severe form
– Cutaneous leishmaniasis (CL)
– Muco-cutaneous leishmaniasis (MCL)
– Disseminated cutaneous leishmaniasis (DCL)

14.2.1 Visceral leishmaniasis (kala-azar)


Visceral leishmaniasis (VL) is a severe systemic infection primarily caused by Leishmania
donovani and L. infantum (synonym L. chagasi) and is potentially fatal if left untreated3. It
occurs predominantly in South and Central Asia, East and North Africa, Mediterranean area
of South Europe, and South and Central America. In endemic areas, children are at greater
risk than adults4. Presentation of the disease depends on several factors, including host
immune response, nutritional status, parasite burden and its virulence. The incubation period
is generally from 2 to 6 months (but can range from few weeks to several years)5.

Clinical features
Onset of signs and symptoms are usually insidious:
– Intermittent fever (generally lasting > 2 weeks) associated with (over a period of weeks to
months):
• Malaise
• Poor appetite
• Weight loss
• Abdominal tension, minimally tender or painless splenomegaly (with or without
hepatomegaly)
• Pallor or severe anaemia due to bone marrow suppression, splenic sequestration, and
haemolysis
– Thrombocytopenia: spontaneous bleeding from the nasal mucosa (epistaxis), gingiva, or
other sites.
Less commonly, fever may be associated with rapidly progressive signs.
Suspect VL in any child presenting with a history of prolonged fever (more than 2 weeks) with
splenomegaly and/or lymphadenopathy and/or wasting.
Complications include: hepatic dysfunction, jaundice, marked cachexia, diffuse oedema,
chronic diarrhoea and malabsorption, or rarely, disseminated intravascular coagulation6,7.
Secondary bacterial infections can develop due to immunosuppression, pneumonia being
among the most common and a frequent cause of death.
Differential diagnosis includes other causes of fever of unknown origin (see Section 14.1).

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Investigations8,9
– FBC (anaemia, neutropenia, thrombocytopenia)
– BGL
– Recombinant kinesin antigen (rK39) testa (first choice diagnostic test)
– Leishmania DAT (direct agglutination test)
– Malaria RDT (where endemic)
– Renal and liver function tests, if available.
Note: where VL is endemic, serum antibodies may be positive among children with subclinical
infection or those who have recovered after successful treatment. In addition, very young
infants may be serologically positive due to maternal antibodies if the mother had VL in
pregnancy. Serological tests should only be used, therefore, in symptomatic patients without a
history of VL treatment. VL relapse can only be diagnosed by tissue aspirate microscopy from
the spleen, bone marrow or lymph node.
Serum antibodies may be low or undetectable in severely immunocompromised children (e.g.
those with HIV). In these cases, diagnosis should be made on the basis of clinical suspicion if
parasitological confirmation through microscopy of tissue aspirates is not possible.

Management
– Admit to hospital and manage any complications (anaemia, thrombocytopenia, intercurrent
infections, e.g. malaria, pneumonia, TB, HIV, diarrhoea).
– Assess nutritional status. If malnourished, refer appropriately.
– Start VL treatment according to national guidelines where implemented/available or follow
treatment by region below.
– Ensure information and education provided from admission to parents/carers and child that
the treatment is long and must be followed regularly.
– Any cases of suspected VL should be notified.

East Africa
– For children < 2 years old OR with other severe disease (liver, renal, or cardiac diseases, HIV
co-infection, severe malnutrition, very poor general condition), administer:

liposomal amphotericin B (AmBisome™) IV infusion


3 to 5 mg/kg once daily for 6 to 10 days, up to a total dose of 30 mg/kg

– For children ≥ 2 years old without other severe disease, administer:

First-line:
• pentavalent antimonial IM or slow IV
20 mg/kg once daily for 17 days
• + paromomycin IM
15 mg (equivalent to 11 mg base)/kg once daily for 17 days
Second-line in case of relapse:
• liposomal amphotericin B (AmBisome™) IV infusion
3 to 5 mg/kg once daily for 6 to 10 days, up to a total dose of 30 mg/kg 14

a Useful antigen in ELISA assays with high sensitivity and specificity in immunocompetent patients in the Indian
subcontinent. The sensitivity is lower and more variable in East Africa and Brazil, although specificity remains
high. This antigen rapid test requires minimal equipment and is easy to use.

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– For HIV co-infected children:


• liposomal amphotericin B (AmBisome™) IV infusion
3 to 5 mg/kg once daily for 6 to 10 days up to a total dose of 30 mg/kg
• + miltefosine PO for 28 daysb
▹ Children 2 to 11 years: 2.5 mg/kg once daily
▹ Children ≥ 12 years and < 25 kg: 50 mg once daily
▹ Children ≥ 12 years and adults 25 to 50 kg: 50 mg 2 times daily
South Asia
– First-line treatment:
• liposomal amphotericin B (AmBisome™) IV infusion
10 mg/kg single dose
– Second-line treatment for relapse:
• paromomycin IM
15 mg (equivalent to 11 mg base)/kg once daily
• + miltefosine PO (as above), both for 10 days

Middle East, Central Asia, Mediterranean, Latin America


– First-line treatment:
• liposomal amphotericin B (AmBisome™) IV infusion
3 to 5 mg/kg once daily for 4 to 7 days, up to a total dose of 20 to 21 mg/kg

Liposomal amphotericin B requires strict cold chain during transportation, storage under
25 ⁰C and protection from light. It must not be diluted with saline solutions or mixed
with other electrolytes or medicines.

14.2.2 Cutaneous leishmaniasis


Causes ulcerated skin lesion(s), usually on exposed areas which can leave life-long disfiguring
scars10. Around 75% of the global estimate of 0.6 to 1 million cases per year occur in
Afghanistan, Algeria, Brazil, Iran, Iraq, Pakistan, and Syria, and children represent between
10 to 55% of cases11,12. Young age (lack of immunity), infants (immature immune system),
underlying malnutrition increases risk of CL, with higher first-line treatment failure in children
< 12 years3,13.
Leishmania major and tropica are the most common in Asia, Africa and Europe (mainly
southern, Mediterranean countries, especially Greece):
– Leishmania major: zoonotic transmission, more typical in rural and suburban contexts,
frequently appears as severely inflamed and ulcerated skin lesions (“wet ulcers”), which
heal spontaneously within 2-8 months, leaving an atrophic scar.
– Leishmania tropica: anthroponotic transmission, typically in urban contexts, appears as
painless, frequently multiple, dry ulcers or plaques. Normally develops and self-heals slower
(one year or longer), may develop into a chronic persistent and remitting lesion (Leishmania
recidivans). Untreated lesions can become secondary infected and can leave destructive and
disfiguring scars.
– Less common include Leishmania infantum (Mediterranean region) and aethiopica (Ethiopia
and Kenya).

b Allometric dosing based on weight, height and gender is recommended for more accurate dosing in children
under 30 kg to prevent underdosing. For advice on individual dosing, refer to specialist clinician.

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In the Americas, species include Leishmania mexicana and amazonesis, and with increased
risk of mucosal CL, braziliensis and guyanensis. Around 15.5% (with a range of < 5% to 47%
between countries) of cases were reported to be in children ≤ 10 years of age5.

Clinical features
– Erythematous papule appears at site of the sandfly bite, which enlarges to a nodule,
extending and deepening to form a scabbed ulcer (painless, unless there is secondary
bacterial or fungal infection).
– Single lesions are more frequent (40 to 75%) in children14 and in around 35 to 48% cases are
located on the head and neck.
– Lesions usually heal spontaneously, leaving a scar and life-long protection.
Diagnosis is usually clinical in endemic areas, and based on having at least 2 of the following
criteria for suspected CL:

✔ History of more than 1 month


✔ Not painful
✔ Not itchy
✔ On exposed body parts
✔ Started as a small papule or nodule when it was first noticed which did not itch.

Differential diagnoses include: cutaneous tuberculosis, leprosy, psoriasis, impetigo, verruca,


yaws, fungal infection, cutaneous mycoses, basal cell carcinoma.

Investigations
Microscopy:
– Identification of parasites in Giemsa-stained smears or culture.
– Take sample for the smear using fine needle aspiration (FNA) or skin scraping from the
nodule or active margin/raised edge of the ulcer or lesion. FNA is more sensitive and less
painful.

Management15
Treatment options are limited for children with most guidance based on extrapolation from
adult treatments (and data)10. Antimonial treatment can be toxic in children. Ensure all
effort is made to obtain parasitological confirmation and assess risk-benefit on a case-by-
case basis.
Safe and effective intra-lesional injection is sometimes not possible with a resisting child. In
those situations, it may be safer to treat the child with IM injections, or to leave the child
untreated.
Indications for treatment include if lesions are:
– Severe enough to justify systemic treatment
– Located on the face, active (with raised edges), and large
– Early (usually nodular), where treatment may prevent lesion enlarging. 14
– On a joint (e.g. wrist, elbow, knee, ankles)
– Causing a loss of function (e.g. on fingers, elbow, knee or toes).
– Lupoid (usually chronic)
– Persistent active (> 6 months)

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Chapter 14: Fever of unknown origin (FUO) and neglected tropical diseases (NTDs)

Pentavalent antimonial
meglumine antimoniate or sodium stibogluconate (SSG)

Local treatment Systemic treatment

Injection Intralesional (intradermal) Intramuscular

Indications 1 to 3 lesionsc Four or more lesions


Lesions < 5 cm diameter Lesions of ≥ 5 cm in diameter
Cooperative child and parent/carer Lesions near eyes, on lips, or in
oedematous extremities (hand, feet)
Painful injection site (fingers, toes)
Difficult to inject intralesionally due
to location (on ears or nose)
Uncooperative child < 5 years of age.

Dose 0.5 to 4 mL, depending on the size 20 mg/kg


of the lesion(s), infiltrated into the Administer under close medical
raised edges around and /or into the supervision.
base of the lesion/ulcer

Frequency 2 times/week (fixed days) Once daily

Duration 5 to 8 treatment sessions (up to 20 days (up to 28 days for L. tropica)


12 sessions for L. tropica)
Refer to specialist for follow-up.

In the case of treatment failure or contraindication to antimonials, oral miltefosine is an


alternative (effective for L. major and possibly L. tropica). Refer to specialist clinician for dosing.
For wound care, refer to MSF OCB Wound Care Protocol and refer to specialist.

Secondary infection
Most common pathogens are streptococci and staphylococci.
Examine all lesions carefully for secondary infection as it may not be evident. Palpate whole
lesion thoroughly as often infection is under the thick crust.
– Consider if one or more of the following signs and symptoms:
• Ulcerating, weeping or purulent discharge (may be hidden under the crust).
• Lesion is painful.
• Swelling or oedema around the lesion.
• Red from inflammation.
– Often good cleaning and light debridement is sufficient, but if necessary, start oral antibiotics.
Concomitant treatment with antimonials:
– Intralesional antimonial treatment: treat secondary bacterial infection before starting
antimonial treatment. If intralesional treatment already started, postpone further
intralesional treatment until antibiotic treatment completed.
– IM antimonial treatment: antibiotic treatment can start/continue simultaneously, combined
with daily wound care.

c If the patient has more than 3 lesions, but all lesions are less than 2 cm, intralesional treatment could still be
considered.

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Mucocutaneous leishmaniasis
Occurs in Latin America and, more rarely, in Africa (Ethiopia, Sudan).

14.2.3 Post-kala-azar dermal leishmaniasis (PKDL)


Post-kala-azar dermal leishmaniasis (PKDL) is a skin rash that appears in a proportion of
patients after a cured episode of VL, caused by an incomplete immune response to Leishmania
that allows for parasites to persist in the skin. Very few patients however relapse with VL after
PKDL, so it is generally seen as a sign of developing immunity. Only patients with severe or
disfiguring disease or with lesions remaining for > 6 months, and young children with mucosal
lesions that interfere with feeding, are treated.
Refer to MSF Clinical Guidelines, Chapter 6 for more details.

14

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14.3 Noma (cancrum oris)

Noma, also known as cancrum oris, is a necrotising gingivitis that causes rapid destruction of
the tissues of the mouth and face. It most frequently occurs in young children, with peak age
of onset between 2 to 6 years16. It affects all tissues of the face from soft tissue to bone and
is fatal in 90% of cases in the acute phase without treatment. Sequelae for survivors include
significant disfigurement and functional problems with eating and speaking due to trismus
and loss of facial tissue. Data are lacking on the exact incidence and prevalence of the disease
due to high mortality in the acute phase of the illness and the social stigma of the visible
sequelae which mean that many cases remain hidden and unaccounted for. Estimates from
1998 indicate that there are approximately 140 000 new cases of noma per year16, though this
is likely to be an underestimation. The majority of cases occur in sub-Saharan Africa.
The exact pathophysiology of noma remains unclear, but an altered oral microbiota is strongly
linked with the disease17. It thought to be due to a polymicrobial infection of anaerobic
commensal oral pathogens which become pathogenic when the immune system is weakened.
Both Fusobacterium necrophorum and Prevotella intermedia have been implicated in noma
pathogenesis, however the exact role they play has been inconsistently described17. Risk
factors for noma include malnutrition, poverty, recent measles or other immuno-suppressive
infection, proximity to livestock, weaning from breastmilk, and poor oral hygiene. It is not a
contagious disease.

14.3.1 Clinical features


Diagnosis is based on clinical features and history. Children typically present with a simple
gingivitis (bleeding, swollen and sensitive gums), that progresses rapidly over a few weeks
according to the following WHO stages16:

Stage of infection Signs and symptoms Duration Reversible

• Bleeding gums when brushing


Warning stage:
• Swollen and sensitive gums Indefinite Yes
Simple gingivitis
• Occasional bad breath

• Spontaneously bleeding gums


Stage 1:
• Painful ulceration of the gums
Acute necrotising Indefinite Yes
• Fetid breath
gingivitis
• Excessive salivation

• Rapid extension of gingival ulceration


• Facial swelling/oedema
Stage 2: • Painful cheek and mouth
1 to 2 weeks Yes
Oedema • High fever
• Difficulty eating, anorexia
• Lymphadenopathy (head and neck)

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Chapter 14: Fever of unknown origin (FUO) and neglected tropical diseases (NTDs)

Stage of infection Signs and symptoms Duration Reversible

• Extensive destruction of intraoral soft


and hard tissue
• Blackened necrotic lesion with well
demarcated perimeter
• Separation of the slough, leaving hole
Stage 3:
in the face often around cheeks or lips
Gangrenous 1 to 2 weeks No
• Rapid perforation of the cheek,
stage
exposing teeth and bone
• Progressive drying of the facial
gangrene
• Anorexia
• Apathy

• Trismus may occur depending on


location of lesions
Stage 4:
• Sequestration of teeth and exposure of 1 to 2 weeks No
Scarring stage
bones
• Beginning of scarring

• Disfigurement of the face


• Trismus
Stage 5:
• Tooth loss or displacement Permanent No
Sequelae stage
• Feeding and speech difficulties
• Salivary leak and nasal regurgitation

Stages 1 and 2 are reversible, while stages 3-5 are irreversible and lead to permanent damage
to facial tissues.

14.3.2 Management
Management depends on the stage of the disease when it is detected. Early stages can be
managed in the community but from stage 2 onwards, inpatient treatment is necessary.

Warning stage: Simple gingivitis


– Rinse mouth regularly with clean salted watera and help child to maintain good oral hygiene
daily.
– Give mouthwash with chlorhexidine 0.2%, 10 mL 3 times daily.
– Assess for malnutrition and start nutritional treatment if necessary (see MSF ATFC Nutritional
Care Protocol). If not malnourished, give health and nutrition education including high
protein diet (beans, meat, fish, eggs, milk, peas). 14

a Add half a teaspoon of table salt to a cup/glass of warm water and dissolve. Use the salted water to rinse the
mouth and then spit, it should not be swallowed.

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– Give Vitamin A supplementation :


• Infants < 6 months: 50 000 IU once daily for 2 days
• Infants 6 to 11 months: 100 000 IU once daily for 2 days
• Children 12 to 59 months: 200 000 IU once daily for 2 days
A third dose should be given to children with signs of vitamin A deficiency (xeropthalmia,
corneal ulceration), 4 to 6 weeks laterb.
– Ensure regular mouth inspection.
– Consider deworming (see Chapter 5, Section 5.2).
– Counsel and test for HIV.

Stage 1: Acute necrotising gingivitis


– Follow all management steps outlined above for Warning stage: Simple gingivitis.
– Give oral antibiotics for 14 days:

First choice:
amoxicillin PO: 100 mg/kg, 2 times daily
+ metronidazole PO: 15 mg/kg, 2 times daily
Alternative:
amoxicillin/clavulanic acid (ratio 7:1 or 8:1) PO
Dosage expressed in amoxicillin:
• < 40 kg: 50 mg/kg 2 times daily
• ≥ 40 kg:
Ratio 8:1: 3000 mg daily (2 tablets of 500/62.5 mg 3 times daily)
Ratio 7:1: 2625 mg daily (1 tablet of 875/125 mg 3 times daily)

– Give analgesia for pain (see Chapter 15, Section 15.4).


– Screen for and treat any co-morbidities such as malaria (see Chapter 3, Section 3.4), measles
(see Chapter 3, Section 3.7), diarrhoea (see Chapter 5, Section 5.2), tuberculosis (see
Chapter 4, Section 4.11), HIV (See Chapter 13).
– Treat anaemia, if present (see Chapter 10, Section 10.1).
– Arrange regular follow-up at health centre for monitoring until resolution.

Stage 2: Oedema
– Admit the child to hospital.
– Correct any dehydration (see Chapter 5, Section 5.3).
– Administer IV antibiotics without delay:
First choice:
amoxicillin-clavulanic acid (co-amoxiclav) IV: 50 mg/kg every 6 hours for 14 days
+ gentamicin slow IV: 5 mg/kg every 24 hours for 5-7 days
+ metronidazole IV: 15 mg/kg every 12 hours for 14 days
Alternative:
ampicillin IV: 100 mg/kg every 6 hours for 14 days
+ gentamicin + metronidazole as above

– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).

b If, for practical reasons, the patient is unlikely to receive their 3rd dose 4-6 weeks later, it is possible to give the
3rd dose from day 8 onwards.

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– Give mouthwash with chlorhexidine 0.2%, 10 mL 3 times daily.


– Give analgesia for pain (see Chapter 15, Section 15.4).
– Start IV maintenance fluids if unable to eat and drink (see Chapter 15, Section 15.2).
– Give Vitamin A supplementation as outlined above.
– Assess for malnutrition and start nutritional treatment if necessary (see MSF ITFC Nutritional
Care Protocol). If not malnourished, provide high-calorie, high-protein diet (see also
Chapter 15, Section 15.5).
– Screen for and treat any co-morbidities such as malaria (see Chapter 3, Section 3.4), measles
(see Chapter 3, Section 3.7), diarrhoea (see Chapter 5, Section 5.2), tuberculosis (see
Chapter 4, Section 4.11), HIV (See Chapter 13).
– Treat anaemia, if present (see Chapter 10, Section 10.1).
– Consider deworming (see Chapter 5, Section 5.2).

Stage 3: Gangrenous stage


– Stabilise the patient using an ABCDE approach (see Chapter 2, Section 2.1).
– Admit the child to hospital and start treatment without delay.
– Follow all management steps outlined above for Stage 2: Oedema.
– Carry out wound care and debridement of all gangrenous tissue, ensuring appropriate
analgesia given for all debridements and dressing changes (see MSF OCB Wound Care
Protocol).
– See additional steps in Stages 4 and 5 for management of scarring and sequelae.

Stage 4: Scarring stage


Patients presenting at this stage have survived the acute phase of the disease but still require
antibiotics in case of any residual infection. Focus at this stage is minimising sequelae:
– Administer IV antibiotics as in Stage 2: Oedema.
– Give other relevant treatment measures outlined in Stage 2: Oedema.
– Carry out wound care and debridement of all gangrenous tissue, ensuring appropriate
analgesia given for all debridements and dressing changes (see MSF OCB Wound Care
Protocol).
– Remove any loose teeth.
– Start physiotherapy/facial exercises to minimise restriction of movement due to scarring
and trismus.

Stage 5: Sequelae stage


At this stage, there is no longer any acute risk but irreversible damage to the face requiring
physical, psychological and social rehabilitation. Children may still die at this stage if they are
unable to eat and drink due to trismus, or if they are socially isolated and neglected. Treatment
at this stage:
– Give relevant treatment measures outlined in Stage 2: Oedema, excluding antibiotics.
– Start or continue physiotherapy/facial exercises, as above.
– Refer for reconstructive surgery, if available, to restore function and improve aesthetics
(referral to specialist surgical centres required).
– Assess for malnutrition and start nutritional treatment if necessary (see MSF ITFC Nutritional
Care Protocol). If not malnourished, provide high-calorie, high-protein diet (see also 14
Chapter 15, Section 15.5).
– Provide psychological support and social rehabilitation (see MSF Mental Health and
Psychosocial Support Guidelines).

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14.3.3 Prognosis
If patients survive the acute stages of the disease, they are left with life-changing sequelae
that can ostracise them from their communities. Trismus and loss of facial tissue, especially
the lips, cause difficulties with eating, drinking and speech. Survivors often have salivary leak
and open holes in their faces, leaving them socially outcast or obliged to cover their faces in
public. If surgery is available, survivors usually require multiple reconstructive surgeries and
both functional and cosmetic outcomes are variable. Trismus may recur despite surgery.

14.3.4 Prevention
Noma is a multifactorial disease that continues to exist in places with extreme poverty and
malnutrition. However, there are some prevention measures that can reduce the likelihood of
the disease, including:
– Increasing awareness of the disease in communities.
– Promotion of exclusive breastfeeding for the first 6 months of life and continuation until
2 years or older.
– Practising good oral hygiene.
– Using clean water for drinking and oral hygiene.
– Early recognition and treatment of simple gingivitis and acute necrotising gingivitis.
– Regular vitamin A supplementation in communities.
– Measles vaccination.
– Zinc supplementation for diarrhoeal disease.
– Systematic deworming in communities.
– Nutritional screening and treatment of children at risk.
– Routine oral examination of children at each medical visit.

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References Chapter 14

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7. Scalzone M, Ruggiero A, Mastrangelo S, et al. Hemophagocytic lymphohistiocytosis and
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https://doi.org/10.3855/jidc.6385
8. World Health Organization. Control of the leishmaniases: report of a meeting of the WHO
Expert Commitee on the Control of Leishmaniases, Geneva, 22-26 March 2010. World
Health Organization; 2010. Accessed November 13, 2023.
https://iris.who.int/handle/10665/44412
9. Chappuis F, Rijal S, Soto A, Menten J, Boelaert M. A meta-analysis of the diagnostic
performance of the direct agglutination test and rK39 dipstick for visceral leishmaniasis.
BMJ. 2006;333(7571):723.
https://doi.org/10.1136/bmj.38917.503056.7C
10. Uribe-Restrepo A, Cossio A, Desai MM, Dávalos D, Castro MDM. Interventions to treat
cutaneous leishmaniasis in children: A systematic review. Laouini D, ed. PLoS Negl Trop Dis.
2018;12(12):e0006986.
https://doi.org/10.1371/journal.pntd.0006986
11. Pan American Health Organization. Leishmaniasis: Epidemiological Report of the Americas
2018.
https://iris.paho.org/handle/10665.2/34856
14
12. Norouzinezhad F, Ghaffari F, Norouzinejad A, Kaveh F, Gouya MM. Cutaneous leishmaniasis
in Iran: Results from an epidemiological study in urban and rural provinces. Asian Pac J Trop
Biomed. 2016;6(7):614-619.
https://doi.org/10.1016/j.apjtb.2016.05.005

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Chapter 14: Fever of unknown origin (FUO) and neglected tropical diseases (NTDs)

13. Aksoy M, Doni N, Ozkul HU, et al. Pediatric Cutaneous Leishmaniasis in an Endemic Region
in Turkey: A Retrospective Analysis of 8786 Cases during 1998-2014. Pimenta PF, ed. PLoS
Negl Trop Dis. 2016;10(7):e0004835.
https://doi.org/10.1371/journal.pntd.0004835
14. Blanco VM, Saravia NG, Cossio A, Martinez JD. Clinical and Epidemiologic Profile of
Cutaneous Leishmaniasis in Colombian Children: Considerations for Local Treatment. Am
J Trop Med Hyg. 2013;89(2):359-364.
https://doi.org/10.4269/ajtmh.12-0784
15. Manual for Case Management of Cutaneous Leishmaniasis in the WHO Eastern
Mediterranean Region. WHO Regional Publications, Eastern Mediterranean Series; 2014.
Accessed November 13, 2023.
https://www.who.int/publications/i/item/9789290219453
16. Information Brochure for Early Detection and Management of Noma. WHO, Regional Office
for Africa; 2017. Accessed November 13, 2023.
https://iris.who.int/handle/10665/254579
17. Baratti-Mayer D, Gayet-Ageron A, Hugonnet S, et al. Risk factors for noma disease: a 6-year,
prospective, matched case-control study in Niger. Lancet Glob Health. 2013;1(2):e87-e96.
https://doi.org/10.1016/S2214-109X(13)70015-9

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Supportive care in hospital

15.1 Oxygen therapy.................................................................................................... 387


15.1.1 Modes of delivery........................................................................................ 387
15.1.2 Monitoring................................................................................................... 389
15.1.3 Weaning....................................................................................................... 390
15.2 Parenteral fluids................................................................................................... 391
15.2.1 Maintenance fluid composition...................................................................391
15.2.2 Calculating maintenance fluid rate..............................................................391
15.2.3 Potassium in maintenance fluids.................................................................393
15.2.4 Monitoring................................................................................................... 395
15.3 Electrolyte abnormalities.................................................................................... 396
15.3.1 Normal electrolyte ranges........................................................................... 396
15.3.2 Sodium disorders......................................................................................... 397
15.3.3 Potassium disorders..................................................................................... 401
15.3.4 Calcium disorders......................................................................................... 403
15.4 Pain management................................................................................................ 405
15.4.1 Assessment.................................................................................................. 405
15.4.2 Management............................................................................................... 407
15.4.3 Chronic pain................................................................................................. 411
15.4.4 Considerations for children with severe acute malnutrition (SAM).............411
15.4.5 Neuropathic pain......................................................................................... 412
15.4.6 Sedation or analgesia before a painful procedure.......................................412
15.5 Nutritional support for the critically unwell child..............................................414
15.5.1 Indications for enteral nutrition...................................................................414
15.5.2 Enteral nutrition products............................................................................ 415
15.5.3 Daily fluid requirements............................................................................... 416
15.5.4 Energy requirements in critical illness..........................................................416
15.5.5 Calculating target daily enteral feed volumes in the acute phase
of critical illness........................................................................................... 417
15.5.6 Administration of enteral feeds...................................................................418
15.5.7 Advancing enteral feeds.............................................................................. 419
15.6 Palliative care....................................................................................................... 420
15.6.1 Symptom management............................................................................... 420
15.6.2 Communication............................................................................................ 422
15.6.3 Psychosocial support.................................................................................... 423
References Chapter 15................................................................................................. 425

15
Chapter 15: Supportive care in hospital

15.1 Oxygen therapy

Oxygen is an essential treatment for hypoxia and is indicated when oxygen saturation is < 92%
in stable patients, aiming to maintain SpO2 ≥ 92%. A higher threshold is used in emergency
management of critically unwell children and for specific conditions where there is impaired
delivery of oxygen to body tissues1.
Administer oxygen in the following situations:
– During resuscitation: all children regardless of SpO2, aiming for SpO2 ≥ 94%
– Critically unwell children: if SpO2 < 94%, aiming for SpO2 94 - 98%
– Children with impaired delivery of oxygen to body tissues, e.g. severe anaemia, severe
sepsis, sickle cell disease, severe heart failure: if SpO2 < 94%, aiming for SpO2 94 - 98%
– Stable children: if SpO2 < 92%, aiming for SpO2 ≥ 92%

15.1.1 Modes of delivery


Oxygen can be delivered via nasal cannula, a simple oxygen mask or a non-rebreathing mask.
Choose most appropriate oxygen delivery system according to the child’s clinical condition,
age and flow of oxygen required. See also MSF Manual of Nursing Care Procedures, SOP -
When to use which mask? for more information on when to use each oxygen delivery method.
Note:
– Young children may become very distressed when an oxygen mask or nasal cannula are
placed on the face, such that the delivery of oxygen is inefficient, or the child’s condition
worsens. Keeping the child on the lap of the parent/carer to provide reassurance may help.
If the child is still distressed, ask the parent/carer to hold a simple mask as close to the
child’s face as possible, without attaching it with elastic.
– For resuscitation or during anaesthesia, oxygen should be delivered via bag-mask ventilation
(see Chapter 2, Section 2.1).
Always use the minimum flow of oxygen possible to achieve desired oxygen saturations
according to the device used. For patients who require maximum 2 litres/min of oxygen a flow
splitter can be used, to provide up to 5 patients with oxygen from a 10 L oxygen concentrator.
Use of a flow splitter also allows a more accurate regulation of flow rate. See MSF Manual of
Nursing Care Procedures, SOP Annex: How to set up an oxygen flow splitter. Monitor adequacy
of oxygen therapy using pulse oximetry, either intermittently or continuously, as required (see
Section 15.1.2 below).

Nasal cannula (NC)


Delivers oxygen via the nasal passageway that mixes with air breathed in by the mouth;
therefore the amount of oxygen received is diluted. With standard flow rates of 1 to 4-6 L/min,
between 24-35% oxygen is delivered. NC can be used in all age groups and may be better
tolerated than oxygen masks, especially in younger children (see Figure 15.1).
At standard flow rates (see Table 15.1), there is no need for humidification. High flow rates
administered for more than 2 hours can cause dryness and irritation of the nares which can
cause bleeding. Therefore, effective humidification is necessary if NC oxygen is delivered above 15
standard flow rates for more than 2 hours2.

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Table 15.1 - Standard, high and maximum flow rates via NC by age

Maximum flow rate


that can be safely
Age of child Standard flow rate High flow rate delivered via NC using
a standard oxygen
concentratora

1 month to < 2 years 1 to 2 L/min > 2 L/min 4 L/min

2 to 12 years 2 to 4 L/min > 4 L/min 6 L/min

> 12 years (≥ 30 kg) 4 to 6 L/min > 6 L/min 10 L/min

To apply, attach NC tubing to the child’s face with tapeb and/or secure behind the ears (see
Figure 15.2).

Figure 15.1 - Nasal cannula tubing Figure 15.2 - Attachment of NC to the face

Simple mask
Delivers oxygen via a mask covering the mouth and nose, secured with an elastic band around
the head (see Figure 15.3). Recommended for initial oxygen delivery in acute presentation
and/or when oxygen delivery via NC is insufficient. Standard flow rates of 5 to 10 L/min will
deliver between 35-60% of oxygen. There are two holes in the mask (see diagram) that allow
air to mix with oxygen delivered via the tubing and for exhaled air to escape the space in the
mask. A minimum flow rate of 5 L/min must be ensured to avoid rebreathing exhaled carbon
dioxide.

a High-flow nasal cannula (HFNC) systems allow greater flow rates to be delivered via specially designed
circuits, however these are not yet widely available in MSF fields. It should be noted that standard oxygen
concentrators alone with NC cannot be used to administer safe and effective HFNC respiratory support. See
Chapter 3, Section 3.1.3 for more detail.
b Use of a foam tape or hydrocolloid dressing can be used to protect the skin, particularly for malnourished
children or those at risk of skin breakdown.

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Figure 15.3 - Simple oxygen mask

Non-rebreathing mask with reservoir


Should be used in children who are breathing spontaneously but in severe respiratory distress,
respiratory failure or in shock (see Figure 15.4). With optimal oxygen flow rate of 10-12 L/min
and a good seal between the mask and face, actual oxygen delivered can reach 60-95%. Where
such high flow rates are not feasible, provide sufficient flow rate to ensure the reservoir bag
remains 2/3 full during inspiration (or as a minimum > 5 L/min in younger children and > 8 L/min
in adolescents).

Figure 15.4 - Non-rebreathing mask with reservoir

15.1.2 Monitoring
Children receiving oxygen therapy should be monitored closely. Where possible, apply
continuous saturation monitoring, ensuring that appropriate alarm parameters have been set
on the monitoring device. Otherwise monitor and record saturations along with vital signs as
often as required using an early warning system (see MSF Manual of Nursing Care Procedures,
Assessment and vital signs, Charts: Vital sign charts).
15

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15.1.3 Weaning
Weaning off oxygen should be considered in children who are stable or clinically improving
when:
– If continuously monitored: SpO2 is consistently ≥ 92% for at least 3 hours.
– If intermittently monitored: SpO2 ≥ 92% on at least two separate consecutive readings taken
several hours apart.
Oxygen should be prescribed, with target SpO2 indicated to allow for nurse-led weaning and
adjustment of flow rates to meet the desired target.
See also MSF Manual of Nursing Care Procedures, Procedure: Oxygen therapy.

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15.2 Parenteral fluids

Maintenance fluids should be administered to all children for whom oral intake is medically
contraindicated, including children with an altered level of consciousness who cannot eat or
drink (most often Glasgow Coma Score < 8 or PU on AVPU scale), intractable vomiting despite
nasogastric feeding, or severe respiratory distress from malaria, asthma, pneumonia or
bronchiolitis. Maintenance fluids preserve body water homeostasis by covering physiologic
daily fluid losses (sweating, urination, breathing) but are not sufficient for replacement of
excessive additional losses (e.g. profuse diarrhoea), or to rehydrate a clinically dehydrated
child (see Chapter 5, Section 5.3).

15.2.1 Maintenance fluid composition


Children are more prone to hypoglycaemia that adults and therefore require stable delivery of
a solution containing both salts and sugar. It is not appropriate to give glucose-free solutions
to children as maintenance fluids or to give alternating bags of Ringer lactate (RL) with bags
of glucose. The preferred choice of IV fluids to use as maintenance for all children (with or
without malnutrition) is a combined solution containing glucose (dextrose) 5%a (G5%) and
undiluted RL to create a G5%-RL solution. If RL is unavailable, sodium chloride 0.9% (NaCl 0.9%)
can be used as an alternative. See Table 15.2, for instructions on how to obtain G5%-RL, (or
G5%-NaCl 0.9%) using glucose (dextrose) 50% (G50%) if pre-mixed bags are unavailable.

Some children receiving maintenance fluids may require an increased glucose concentration in
maintenance fluids due to repeated hypoglycaemia (see Chapter 9, Section 9.3) and require a
glucose (dextrose) 10% (G10%)-RL (or G10%-NaCl 0.9%) solution (see Table 15.2).

Table 15.2 - Making maintenance fluids from available IV fluids

RL or NaCl 0.9% G50% to add Resulting solution


500 mL bag
50 mL 500 mL of G5%-RL or G5%-NaCl 0.9%
–> remove 50 ml = 450 mL
1000 mL bag
100 mL 1000 mL of G5%-RL or G5%-NaCl 0.9%
–> remove 100 ml = 900 mL
500 mL bag
100 mL 500 mL of G10%-RL or G10%-NaCl 0.9%
–> remove 100 mL = 400 mL
1000mL bag
200 mL 1000 mL of G10%-RL or G10%-NaCl 0.9%
–> remove 200 mL = 800 mL

15.2.2 Calculating maintenance fluid rate


Maintenance fluid requirement is calculated using the Holliday-Segar formula, either over
24 hours or as an hourly rate as follows (see also Table 15.3).
15
a Note: dextrose 5% is the same as glucose 5%.

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Daily maintenance fluid requirement:


– For the first 10 kg of bodyweight (0 to 10 kg), give 100 mL/kg/day;
– For the next 10 kg of bodyweight (11 to 20 kg) give an additional 50 mL/kg/day;
– For each kg above 20 kg, give an additional 20 mL/kg/day.
Hourly maintenance fluid rate (‘4:2:1’ rule):
– For the first 10 kg of bodyweight (0 to 10 kg), give 4 mL/kg/hour;
– For the next 10 kg of bodyweight (11 to 20 kg) give an additional 2 mL/kg/hour;
– For each kg above 20 kg, give an additional 1 mL/kg/hour.
e.g. An 8 kg child = 4 mL x 8 kg = 32 mL/hr
A 12 kg child = (4 mL x 10 kg) + (2 mL x 2 kg) = 44 mL/hr
A 25 kg child = (4 mL x 10 kg) + (2 mL x 10 kg) + (1 mL x 5 kg) = 65 mL/hr

Table 15.3 - Infusion rates by weight for maintenance fluids


Administer G5%-RL (or G5%-NaCl 0.9%)
(Rates rounded for ease of administration)
Weight Rate of infusion Weight Rate of infusion
(kg) in mL/hourb (kg) in mL/hour
3 15 22 65
4 20 23 65
5 25 24 65
6 30 25 65
7 30 26 65
8 35 27 70
9 40 28 70
10 40 29 70
11 45 30 70
12 45 31 70
13 45 32 75
14 50 33 75
15 50 34 75
16 55 35 75
17 55 36 75
18 55 37 80
19 60 38 80
20 60 39 80
21 60 40 80

b A paediatric infusion set should be used to administer maintenance fluids at rates less than 60 mL/hr. In
paediatric infusion sets, 1 mL = 60 drops therefore the rate in mL/hr is the same as the rate in drops/min. For
volumes over this rate, an adult infusion set may be used.

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Maintenance fluid rates may need to be reduced in critically unwell children with specific
pathologies that require fluid restriction, such as when there is suspicion of raised intracranial
pressure, e.g. meningitis (see Chapter 3, Section 3.3), cerebral malaria (see Chapter 3, Section 3.4),
head injury (see Chapter 2, Section 2.8); or increased ADH secretion, e.g. severe pneumonia
(see Chapter 4, Section 4.5), severe bronchiolitis (see Chapter 4, Section 4.7). In these cases, a
restriction of 70% of total calculated maintenance fluid is often advised (see Table 15.4).
Table 15.4 - Infusion rates by weight for restricted maintenance fluids (70%)
Administer G5%-RL (or G5%-NaCl 0.9%)
(Amounts rounded for ease of administration)
Weight Rate of infusion Weight Rate of infusion
(kg) in mL/hourc (kg) in mL/hour
3 10 22 45
4 15 23 45
5 15 24 45
6 20 25 45
7 20 26 45
8 25 27 45
9 25 28 50
10 30 29 50
11 30 30 50
12 30 31 50
13 35 32 50
14 35 33 50
15 35 34 50
16 35 35 55
17 40 36 55
18 40 37 55
19 40 38 55
20 40 39 55
21 40 40 55

15.2.3 Potassium in maintenance fluids


Hypokalaemia can cause respiratory depression and cardiac rhythm abnormalities, therefore
potassium is usually added to maintenance fluids in children who are not taking anything orally
if maintenance fluids will continue beyond 24 hours, as well as systematically for children
in diabetic ketoacidosis (DKA). However, the decision to add potassium chloride (KCl) to

c A paediatric infusion set should be used to administer maintenance fluids at rates less than 60 mL/hr. In
paediatric infusion sets, 1 mL = 60 drops therefore the rate in mL/hr is the same as the rate in drops/min. For
15
volumes over this rate, an adult infusion set may be used.

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intravenous fluids in MSF settings should not be taken lightly. Potassium is a potentially lethal
medication and can cause cardiac arrest in children if administered in excess of requirements.
Great care is required when adding potassium to IV fluids, as miscalculation of the required
amount can lead to massive differences in potassium dose. Even at therapeutic doses,
potassium is irritant to veins (causing burns and thrombophlebitis) if administered too quickly
or through small veins. KCl should never be injected directly into the vein.
Where feasible, KCl should be added to maintenance fluids according to instructions in
Table 15.5 and the MSF Paediatric Injectables Handbook. Make sure the child is urinating to
ensure that there is no renal failure before adding KCl to fluids and always ensure that the
potassium additions are checked by two senior members of nursing/medical staff. Carefully
label IV fluids bags containing potassium with the date, time and the amount of KCl added, as
well as the signatures of those preparing the medication (see Figure 15.5).
The potassium requirement for children is 2–3 mmol/kg/day. The addition of 2–3 mmol KCl to
100 mL of IV fluids (20–30 mmol KCl per litre) allows an appropriate amount of potassium to
be delivered when giving standard rate maintenance fluids. In diabetic ketoacidosis, potassium
requirements are higher, and should be 40 mmol KCl per litre (see Chapter 9, Section 9.2).
One 10-mL ampoule of KCl 15% contains 20 mmol = 2 mmol/mL. Always double check
that the ampoules contain 10 mL of KCl 15%, as content and manufacturer may vary.

Table 15.5 - Addition of KCl to maintenance fluids

G5%-RL or G10%-RL Volume of KCl 15% to add Resulting solution

1000 mL (1 litre) 10 mL (1 ampoule) G5%-RL + 20 mmol/L KCl


or
500 mL 5 mL (½ ampoule) G10%-RL + 20 mmol/L KCl

In diabetic ketoacidosis only, increased KCl administered (40 mmol/L):

1000 mL (1 litre) 20 mL (2 ampoules) G5%-RL + 40 mmol/L KCl


or
500 mL 10 mL (1 ampoule) G10%-RL + 40 mmol/L KCl

Figure 15.5 - Example of bag label for maintenance fluids with added KCl

Child’s name:________________________

Volume of original bag: _______ mL


Volume removed: _______ mL
G50% volume added: _______ mL
KCl 15% volume added: _______ mL

Date/time bag prepared: _________________


Prepared by (signature):__________________
Checked by (signature): __________________

Rate of infusion: __________mL/hr


Start date/time: _______________

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15.2.4 Monitoring
Regardless of the maintenance fluid administered, a child on intravenous fluids must be
carefully monitored and have a record of fluid balance kept, aiming for a neutral fluid balance
(see MSF Nursing Care Manual of Procedures, Fluid balance chart: User Guide). Ensure that
the volume of any additional fluids administered with medication or as IV flushes is included
in the fluid balance calculation, as this may be quite significant.
In addition, children on IV fluids should be monitored for fluid overload. Signs of fluid overload
are:
– Increased RR by ≥ 10 breaths/minute from initial RR, or
– Increased HR pulse rate by ≥ 20 beats/min from initial HR
PLUS any one of the following:
– New or worsening hypoxia = decrease in SpO2 by > 5%
– New onset of rales and/or pulmonary oedema (fine crackles in lung fields)
– New galloping heart rhythm
– Increased liver size (liver must have been marked with pen prior to fluid administration)
– New peripheral oedema and/or puffy eyelids.
Management if signs of fluid overload present:
– Stop all fluids.
– Administer furosemide IV: 0.5 mg/kg (repeat once if necessary).
– Place child into semi-sitting position and ensure high-flow oxygen via non-rebreathing mask.
– Monitor every 15 minutes until child has been stable for at least one hour.
IV maintenance fluids should be administered for as short a time as possible to minimise
the risk of electrolyte abnormalities (see Section 15.3). In addition, early feeding improves
outcomes in critically unwell children, therefore aim to start enteral feeding and wean down
IV fluids as soon as possible (see Section 15.5).

15

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Chapter 15: Supportive care in hospital

15.3 Electrolyte abnormalities

Hospitalised children, especially those who are critically unwell and/or receiving IV fluids are
at risk of electrolyte abnormalities. Children with malnutrition have an even higher likelihood
of developing electrolyte abnormalities during inpatient treatment, particularly associated
with refeeding syndrome (see Chapter 12, Section 12.3). Electrolyte abnormalities are most
commonly seen in children with gastrointestinal symptoms, especially persistent vomiting
and/or diarrhoea; renal disease, such as acute kidney injury (AKI); and endocrine disturbance,
such as diabetic ketoacidosis (DKA).
Abnormalities of sodium, potassium and calcium are the most common treatable electrolyte
imbalances and manifest with specific symptoms, though these may go undetected until life-
threatening signs and symptoms develop.

15.3.1 Normal electrolyte ranges


Table 15.6 - Normal biochemistry values for children according to age

Component Normal range

Sodium (Na) 135-145 mmol/L

Potassium (K) 3.5-4.9 mmol/L

Calcium, ionised (iCa)


1-12 months 1.24-1.49 mmol/L 5.0-6.0 mg/dL
> 12 months 1.20-1.30 mmol/L 4.65-5.25 mg/dL

Calcium, total serum (Ca)


1-12 months 2.00-2.67 mmol/L 8.0-10.7 mg/L
> 12 months 2.12-2.62 mmol/L 8.5-10.5 mg/L

Chloride (Cl) 95-105 mmol/L

Creatininea 27-62 μmol/L 0.3-0.7 mg/dL

Glucose 3.3-7.0 mmol/L 60-126 mg/dL

Bicarbonate (HCO3-) 19-28 mmol/L

Notes
– For Na, K, Cl, HCO3, and glucose, mmol/L equal to mEq/L.
– iCa = ionized calcium is physiologically active (or free) calcium and makes up 40 to 45% of
total serum calcium.

a Normal values of serum creatinine vary by age and gender, see local lab references for more specific ranges.

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15.3.2 Sodium disorders


Hyponatraemia
Hyponatraemia is one of the most common electrolyte abnormalities in children and is
typically defined as a serum sodium below 135 mmol/L. In children, it often occurs secondary
to gastroenteritis with prolonged vomiting and/or diarrhoea and rehydration with free water;
inappropriate ADH release; nephrotic syndrome; heart failure; or renal failure. It may also
occur as a side effect of diuretic use, and as a complication of certain medical conditions
such as adrenal insufficiency, cystic fibrosis (CF), hyperglycaemia and primary renal disorders.
Management depends on the fluid status of the child therefore it is important to try to
determine the most likely cause of hyponatraemia (see Table 15.7 for more detail).

Table 15.7 - Causes of hyponatremia based on fluid status

Hypovolaemia Euvolaemia Hypervolaemia


(fluid loss/dehydration) (stable fluid balance) (fluid overload)

• Gastrointestinal losses • Increased ADH secretion • Iatrogenic (excess IV fluid


(vomiting, diarrhoea) and (secondary to medical administration)
rehydration with free conditions such as severe • Nephrotic syndrome
water pneumonia, bronchiolitis, • Heart failure
• Skin losses (CF, burns) head injury, CNS infection) • Renal failure
• Hyperglycaemia • Administration of
(diabetes) hypotonic fluids by mouth
• Renal losses (diuretics, (diluted formula milk,
primary tubular disorders) excessive water)
• Adrenal insufficiency • Psychogenic polydipsia
(hypoaldosteronism) • Medications
(antiepileptics)

Clinical features
Children are usually asymptomatic if serum sodium is > 125 mmol/L. Below this level, symptoms
include the following:
– Nausea
– Malaise
– Headache
– Lethargy
– Seizures may occur below 120 mmol/L (severe hyponatraemia) and lead to irreversible
neurological damage
– In extreme cases, brain herniation may occur leading to respiratory and cardiac arrest and,
ultimately, death.

Investigations
– Blood urea and electrolytes (UE) to confirm sodium level
– Blood glucose level (BGL)
– Blood gas, if available
– Serum and urine osmolality, if available
15

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Management
Treatment of hyponatraemia depends on severity of symptoms and fluid status, with emergency
treatment required if the child has reduced conscious level or seizures. Correction should be
done slowly to prevent osmotic demyelination syndromeb.
– Mild to moderate hyponatraemia:
• Serum sodium 120 - 134 mmol/L and asymptomatic
• Monitor and record vital signs as often as required using an early warning system (see
MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign
charts).
• Treatment depends on fluid status (adapted from RCH Melbourne Clinical Practice
guidelines3):

Sodium
Fluid status Treatment Monitoring
level

Treatment for
130 - 134 dehydration with oral
mmol/L rehydration solution (see
Chapter 5, Section 5.3)
Hypovolaemia/
Measure serum sodium
dehydration
Administer maintenance levels 12 hourly
< 130 fluids with G5%-NaCl (or 4-6 hourly
mmol/L 0.9% at full rate (see if Na < 125 mmol/L)
Section 15.2) Ensure correction rate no
more than 8 mmol/L
Restrict total fluid in 24 hours
intake to 50-70% Monitor for CNS
maintenance volume, symptoms (new or
Hypervolaemia 120 - 134 ideally in enteral intake ongoing)
or euvolaemiac mmol/L rather than IV fluids.
If IV fluids required,
ensure G5%-NaCl 0.9% is
administered.

– Severe hyponatraemia - asymptomatic or mildly symptomatic but without seizures or altered


conscious level:
• Serum sodium < 120 mmol/L; or < 125 mmol/L and symptomatic.
• Monitor and record vital signs as often as required using an early warning system (see
MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign
charts).
• If completely asymptomatic, give oral hypertonic saline:

NaCl 3% PO:
3 - 5 mmol/kg/day (or 6 – 10 mL/kg/day) in 4 to 6 divided doses
NB. NaCl 3% contains 30 g/L of sodium which is equivalent to 0.5 mmol/mL

b Osmotic demyelination syndrome is diffuse demyelination of the brain that can be irreversible, leading to
profound permanent neurological symptoms such as dysarthria, confusion and coma.
c Euvolaemia = a normal circulatory or blood fluid volume in the body.

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• If mildly symptomatic but without seizures or altered conscious level, calculate volume
of NaCl 0.9% required to correct sodium deficit and replace over 48 hours, ensuring
correction rate of no more than 8 mmol/L in 24 hours:

Volume of NaCl 0.9% (mL) required = 3.9 x weight (kg) x (Target Na – Real Na)
NB. If (Target Na – Real Na) is greater than 16 mmol, correction should be done over a
longer period to ensure that correction rate does not exceed 8 mmol/24 hours

• Repeat serum sodium levels every 4-6 hours until ≥ 125 mmol/L, then monitor 12 hourly
until normal.
• Treat likely underlying cause in addition to correction with hypertonic saline (e.g. correct
any dehydration (see Chapter 5, Section 5.3), restrict fluids if hypervolaemic).
– Severe hyponatraemia with seizures or altered conscious level:
• Medical emergency requiring urgent treatment.
• Treat any seizures (see Chapter 7, Section 7.2).
• Administer NaCl 3% IV: 3-5 mL/kg over 15-30 minutes using a syringe pump and, ideally, via
a central line (see MSF Paediatric Injectables Handbook for more detailed administration
guidance). Can be repeated if ongoing seizures or Na < 125 mmol/L.
• Repeat serum sodium level, aiming to correct serum sodium by no more than 2 mmol/L
per hour in the first 3-4 hours.
• Once seizures stop, calculate volume of NaCl 0.9% required to correct sodium deficit and
replace over 48 hours, ensuring correction rate of no more than 12 mmol/L in 24 hours
including the hypertonic saline bolus(es). Consider giving oral NaCl 3% as an alternative
(as above) if asymptomatic following NaCl 3% IV bolus(es).
• Repeat serum sodium levels every 4-6 hours until ≥ 125 mmol/L, then monitor 12 hourly
until normal.
• Treat the underlying cause, e.g. dehydration (see Chapter 5, Section 5.3), hypervolaemia.

Hypernatraemia
Raised serum sodium is due either to a water deficit or sodium excess. It is seen commonly in
children who are dehydrated due to gastroenteritis and burns. See Table 15.8 for a full list of
potential causes. It is typically classified as mild, moderate or severe and treatment depends
on severity.
Table 15.8 - Causes of hypernatraemia

Water deficit
Sodium excess
(fluid loss/dehydration)

• Gastrointestinal losses (vomiting, • Ingestion of excessive sodium


diarrhoea) (inappropriately concentrated formula
• Skin losses (CF, burns) milk, salt poisoning, high osmolality
• Hyperglycaemia (diabetes) rehydration solutions)
• Renal losses (diuretics, primary tubular • Iatrogenic (hypertonic saline, sodium
disorders) bicarbonate)
• Diabetes insipidus (due to ADH • Hyperaldosteronism (nephrotic
insufficiency or insensitivity) syndrome, steroids)
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Clinical features
– Lethargy
– Weakness
– Altered level of consciousness
– Irritability
– Seizures
– Muscle cramps
– Depressed deep tendon reflexes
– Respiratory failure

Investigations
– Blood UE to confirm sodium level
– BGL

Management
Treat dehydration or hypovolaemic shock, if present, before correcting hypernatraemia (see
Chapter 2, Section 2.2). Ensure that sodium levels are repeated after any IV fluids have been
administered to accurately guide specific treatment. Aim to reduce sodium levels no faster
than 10 mmol/L in 24 hours to reduce the risk of cerebral oedema.
– Mild hypernatraemia:
• Serum sodium 146 - 149 mmol/L
• Manage the underlying cause and repeat serum sodium in 4-6 hours
– Moderate hypernatraemia:
• Serum sodium 150 - 169 mmol/L
• Monitor and record vital signs as often as required using an early warning system (see
MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign
charts).
• Calculate free water deficit (FWD) based on an estimated requirement of 4 mL/kg of fluid
to reduce serum sodium by 1 mmol/L:

FWD = 4 mL x weight (kg) x (Real Na – Desired Na)

• Add calculated FWD to the volume of fluids to be replaced according to dehydration


status (see Chapter 5, Section 5.3). Replace half of the total volume over 24 hours with
G5%-NaCl 0.9% and half over the next 24 hours.
• Repeat serum sodium levels every 12 hours until within normal range.
• Monitor for fluid overload and keep a strict fluid balance.
– Severe hypernatraemia:
• Serum sodium ≥ 170 mmol/L
• Manage as for moderate hypernatremia, calculating free water deficit (FWD) based on
an estimated requirement of 3 mL/kg of fluid to reduce serum sodium by 1 mmol/L as
follows:

FWD = 3 mL x weight (kg) x (Real Na – Desired Na)

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15.3.3 Potassium disorders


Hypokalaemia
Low serum potassium is the most common electrolyte abnormality in children and may be
due to gastrointestinal losses through vomiting and diarrhoea, renal losses, decreased intake
(anorexia), diabetic ketoacidosis, certain medications (e.g. diuretics, insulin, salbutamol) or
may be iatrogenic in children receiving prolonged IV fluids that are not supplemented with
potassium. It is defined as potassium < 4.1 mmol/L in infants (1 month to 1 year) or < 3.4 mmol/L
in children over 1 year old.

Clinical features
– Ascending muscle weakness or paralysis
– Abdominal distension
– Anorexia
– Nausea and vomiting
– Constipation (secondary to paralytic ileus)
– Cardiac arrhythmias

Investigations
– Blood UE to confirm potassium level
– BGL
– Blood gas, if available
– Electrocardiogram (ECG)

Management
Treatment of hypokalaemia depends on the severity.
– Mild, asymptomatic hypokalaemia:
• Potassium 3 - 3.4 mmol/L
• Usually doesn’t require specific treatment
• Correct underlying cause and recheck potassium level in 2-3 hours.
– Moderate hypokalaemia:
• Potassium 2.5 - 2.9 mmol/L
• Treat with potassium orally for 2 days:

7.5% potassium chloride syrup (1 mmol of K+/mL) PO:


• < 45 kg: 2 mmol/kg (2 mL/kg) once daily
• ≥ 45 kg: 30 mmol (30 mL) 3 times daily

• Repeat potassium level 2 hours after oral administration and at the end of treatment.
– Severe hypokalaemia:
• Potassium < 2.5 mmol/L or patients with symptomatic hypokalaemia
• Monitor and record vital signs as often as required using an early warning system (see
MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign
charts).

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• Treat urgently with either oral or IV potassium:

First choice - for stable patients who are able to take oral medication
7.5% potassium chloride syrup (1 mmol K+/mL) PO for 2 days:
• < 45 kg: 2 mmol/kg (2 mL/kg) once daily
• ≥ 45 kg: 30 mmol (30 mL) 3 times daily
Second choice - for patients unable to take oral medication
15% potassium chloride solution (2 mmol K+/mL) IV:
0.2 mmol/kg/hr (max. 10 mmol/hr) for 3 hours
Each mmol of potassium is diluted in 25 mL of NaCl 0.9%
Infusion may be repeated if severe symptoms persist or if serum potassium remains
< 3 mmol/L.

• Repeat potassium level 1 hour after the end of the infusion or two hours after oral
administration.

Hyperkalaemia
Hyperkalaemia is relatively common in hospitalised children and is defined as a serum
potassium above 5.5 mmol/L. It occurs in children with renal failure, in diabetic ketoacidosis
in extensive trauma and may be iatrogenic in children receiving IV fluids supplemented with
potassium.

Clinical features and complications


– Neurological signs: paraesthesia, muscle weakness
– Hypotension
– Cardiac arrhythmias (ventricular tachycardia and fibrillation)
– If severe:
• Respiratory failure
• Cardiac arrest
• Death

Investigations
– Blood UE to confirm potassium level
– BGL
– Blood gas, if available
– Electrocardiogram (ECG)

Management
Treatment of hyperkalaemia depends on the severity:
– Repeat serum potassium urgently to verify results, ideally via venepuncture to avoid
sampling haemolysis which will result in an inaccurately high potassium.
– Stop all IV infusions containing potassium immediately.
– Avoid potassium-rich foods (e.g. bananas, oranges, raisins, tomatoes, avocados, dried fruits
and nuts).
– Use only fresh blood for transfusion (if required).

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– Monitor and record vital signs as often as required using an early warning system (see MSF
Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign charts).
– If hyperkalaemia with K+ ≤ 6 mmol/L, continue with above measures only and monitor
serum potassium again after 2 hours.
– If hyperkalaemia with K+ > 6 mmol/L, especially if there are signs of hyperkalaemia on ECG
(peaked T waves, wide QRS complex, arrythmias), actively treat as follows:
• Administer nebulised salbutamol to promote potassium uptake into cells:
< 5 years: 2.5 mg nebuliser, repeated after 1 to 2 hours if necessary
≥ 5 years: 5 mg nebuliser, repeated after 1 to 2 hours if necessary
• Administer calcium gluconate 10% IV 0.5 mL/kg (max. 10 mL) over 3 minutes to stabilise
cardiac muscle excitability.
• If central venous access in situ, and the patient can be cared for in an ICU environment with
adequate monitoring and staffing levels, administer a mixed infusion of glucose (dextrose)
50% 2 mL/kg and short-acting insulin 0.05 IU/kg in the same syringe over 5-10 minutes,
using a syringe pump, to promote intracellular potassium shift. Close monitoring of BGL
is required before, during and after infusion (within an hour of administration), as insulin
can cause a rapid fall in BGL.
• Repeat serum potassium hourly until stable and within therapeutic range.

15.3.4 Calcium disorders


Hypocalcaemia
Low serum calcium can be due to hypoparathyroidism or vitamin D deficiency and may occur
secondary to sepsis, hyperphosphatasemia, hypomagnesemia and ingestion of toxins or
poisons.

Clinical features
– Tetany
– Neuromuscular irritability with weakness
– Paraesthesia, cramps, fatigue
– Altered level of consciousness
– Seizures
– Cardiac arrhythmias
– Trousseau’s sign: carpopedal spasm after arterial occlusion of an extremity for 3 minutes
– Chvostek’s sign: muscle twitching on percussion of the facial nerve

Investigations
– Blood UE
– Blood gas, if available
– Electrocardiogram (ECG), if severe hypocalcaemia

Management
Specific treatment of hypocalcaemia depends on severity and is required if iCad < 4 mg/dL
(< 1 mmol/L).

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d iCa = ionized calcium is physiologically active (or free) calcium and makes up 40 to 45% of total serum calcium.

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– If mild or asymptomatic, treat with oral calcium and vitamin D supplementation:

calcium carbonate PO: 10 - 25 mg/kg 3 times daily with meals


+
colecalciferol (vitamin D3) PO:
• < 3 months: 2000 IU once daily for 3 months
• 3 to < 12 months: 2000 IU once daily for 3 months or 50 000 IU single dose
• 12 months to < 12 years: 3000 to 6000 IU once daily for 3 months or 150 000 IU single
dose
• ≥ 12 years: 6000 IU once daily for 3 months or 300 000 IU single dose

– If severe or symptomatic with signs of tetany:


• Monitor and record vital signs as often as required using an early warning system (see
MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign
charts).
• Administer calcium gluconate IV (see MSF Paediatric Injectables Handbook for more
detailed administration guidance):

calcium gluconate 10% solution by slow IV injection over 5-10 minutes:

• < 20 kg:
0.5 mL/kg (max. 10 mL) by slow IV injection over 5-10 minutes, then 2 to 4 mL/kg
(max. 40 mL) by continuous IV infusion over 24 hours
(dilute in 100 mL of glucose (dextrose) 5%, NaCl 0.9% or Ringer lactate)
• ≥ 20 kg:
10 mL by slow IV injection over 5-10 minutes, then 40 mL by continuous IV infusion
over 24 hours
(dilute in 250 mL or 500 mL of glucose (dextrose) 5%, NaCl 0.9% or Ringer lactate)

• Repeat calcium 3-4 hours after loading dose administered.


• Begin supplementation with colecalciferol (vitamin D3) PO as above.

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15.4 Pain management

Pain is an unpleasant sensory and emotional experience associated with actual or possible
tissue damage. Assessing the presence and severity of pain in children can be challenging,
especially in infants and younger children. Being unable to communicate verbally about pain
does not exclude that the child is experiencing pain and needs appropriate analgesia. Pain
assessment should be routine in all paediatric hospital care and treatment adequately tailored
and adapted.

15.4.1 Assessment
– Take a history and examine the child.
– Try to assess where the pain is (adjust to child’s age and understanding).
– In older children, ask to describe the pain:
• Character: sharp, dull, stabbing, burning, cramping, spasmodic, radiating, etc.
• Pattern: sudden, intermittent, chronic; at rest, at night, on movement, etc.
• Aggravating or relieving factors
• Associated symptoms.
– Assess intensity with a validated pain assessment tool to rate the ‘pain score’, recording
the score and the tool used. Use a self-reporting tool as preference, but where necessary a
behavioural assessment tool can be used, both in accordance to age, cognitive ability, and
level of consciousness or sedation. Choose the pain tool that is most adapted and accepted
according to context.
– Assess adequacy of treatment: use same pain assessment tool for consistency and re-
evaluate and record pain intensity after every treatment to monitor and adjust analgesia
adequately.
– If not already known, identify the underlying cause of the pain and treat if possible.

Self-reporting pain assessment tools


– Use in children who can quantify the level of pain and rate or score it.
– Note that as pain is always subjective, that how the child rates or scores their pain should be
accepted and respected.
– Numerical rating scale: 6 years and above.
– FACES® rating scale can be tried in 3 years and above.
– Ask the child to select the number (Figure 15.6) or facial expression (Figure 15.7) that best
corresponds to the intensity of their pain. Note the corresponding score.

Figure 15.6 - Numerical pain rating scale (6 years and above)


Numeric Rating Scale

0 1 2 3 4 5 6 7 8 9 10
No Moderate Worst
Pain Pain Possible
Pain
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Figure 15.7 - Wong-Baker FACES® Pain Rating Scalea (3 years and above)

Behavioural assessment tools4


For children unable to self-report (too young, cognitive impairment, unconscious or severely
sick), assess child’s behaviour to score intensity of pain. Various tools exist for different ages:
– Neonatal Facial Coding System (NFCS) recommended for infants ≤ 3 months.
– Face Limb Activity Cry Consolability (FLACC) scales recommended for children > 3 months.
– EVENDOL (Evaluation Enfant Douleur) scale recommended for young children from birth to
7 years.

Neonatal Facial Coding System (NFCS)


Recommended for infants ≤ 3 months.
– Assess for all 4 facial signs and add total score (see Table 15.9 and Figure 15.8)
– Total score: > 2 is moderate to severe pain, 0 is no pain.
Table 15.9 - NFCS Scoring system Figure 15.8 - NFCS facial signs

Scoring
Items
0 1
Brow bulge no yes
Eye squeezed shut no yes
Accentuated nasolabial fold no yes
Open mouth no yes

FLACC (Face Limb Activity Cry Consolability) scale


Recommended for > 3 months, acute pain and for post-operative care (see Table 15.10).
– Each category is scored from 0 to 2, giving a final score between 0 and 10.
– Corresponding pain intensity:
• 0 to 3: mild pain
• 4 to 6: moderate pain
• 7 to 10: severe pain

a Reprinted with permission from Wong Baker FACES Foundation.

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Table 15.10 - FLACC scoring scale

Scoring
FLACC Scale
0 1 2
Occasional grimace Frequent to constant
No particular
Face or frown, withdrawn, frown, clenched jaw,
expression or smile
disinterested quivering chin
Normal position Kicking,
Legs Uneasy, restless, tense
or relaxed or legs drawn up
Lying quietly, normal Squirming, shifting
Activity Arched, rigid or jerking
position, moves easily back and forth, tense
Crying steadily,
No cry Moans or whimpers,
Cry screams or sobs,
(awake or asleep) occasional complaint
frequent complaints
Reassured by
occasional touching, Difficult to console
Consolability Content, relaxed
hugging or being or comfort
talked to, distractible

EVENDOL (Evaluation Enfant Douleur)


The EVENDOL behavioural score was developed by a multi-professional group of experts in child
pain, to better identify and assess the intensity of pain in young children, from birth to 7 years
of age; studies have validated this scale in emergencies (medical or traumatic), in pre-hospital
medical transport, in post-operative and neonatal care and for newborns in maternity wards5,6.
– Five features are assessed:
• Vocal or verbal expression
• Facial expression
• Movements
• Postures
• Interaction with the environment
– Refer to EVENDOL chart in Appendix 21. Give a score for each feature and calculate total out
of maximum 15. Can be used at rest (R) or with movement (M).
– Score rating:
• Score 1/15 to 3/15: mild pain
• Score 4/15 to 7/15: moderate pain
• Score 8/15 to 15/15: severe pain

15.4.2 Management
– Relieve pain according to type (acute or chronic) and intensity.
– Where possible and appropriate, treat underlying cause.
– Non-pharmacologic measures (e.g. cognitive, behavioural, physical and supportive therapies)
help control pain by providing comfort or an element of distraction from the physical pain
(see Table 15.11). Two interventions are more effective than one. Use in combination with
pharmacologic treatment. See also MSF Manual of Nursing Care Procedures, Procedure:
Pain management.
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Table 15.11 - Examples of non-pharmacologic pain management measures

Infants and young children Older children


• Breastfeeding • Listening to music or singing
• Non-nutritive sucking e.g. use of dummy • Distraction: recalling of favourite place;
to promote sucking for comfort counting backwards by serial sevens
• Physical comfort: Kangaroo Care, • Blowing soap bubbles
swaddling, facilitated tucking • Breathing exercises: quiet, calm
• Oral sucrose/expressed breastmilk environment; slow inhalation and long
(usually reserved for pre-procedure exhalation
analgesia)
Drawing and playing
Physical measures: massage, applying ice locally, occasionally heat

– Give appropriate pharmacologic treatment (see below).


– Reassess pain and response to treatment regularly, at least every time vital sign measurements
are taken.

Analgesics
– Use oral analgesics whenever possible (better tolerated, fewer side effects, safer).
– Identify step on the three-step ladder that corresponds to pain score (see Table 15.12).
Table 15.12 -Three-step ladder

Ladder step Analgesia


Step 1: mild pain
Paracetamol +/- ibuprofen
Pain score 1-3
Step 2: moderate pain Paracetamol +/- ibuprofen + low-dose oral morphine or
Pain score 4-6 (4-7 EVENDOL) tramadolb
Step 3: severe pain
Paracetamol +/- ibuprofen + morphine IV, IM, SC
Pain score 7-10 (8-15 EVENDOL)

– Select analgesia corresponding to step on the three-step ladder (see Table 15.13 for analgesic
drug dosing). For moderate and severe pain, give regular analgesia over 24 hours, including
sufficient analgesia to allow the child to sleep through the night and to avoid breakthrough
pain:

Step 1: mild pain


– Give paracetamol and consider adding ibuprofen if necessary.

Step 2: moderate pain


– Add a low-dose oral strong opioid to step 1 analgesia.
– First line is morphine. Use tramadol as an alternative only if oral morphine is not available
or feasible, exercising particular caution in children < 12 yearsb.

b Tramadol is not approved for use in children < 12 years in some countries due to the risk of increased opioid
toxicity including life-threatening respiratory depression. If oral morphine is not available, tramadol may be
considered in hospitalised children < 12 years under close medical supervision at a dose of 1 to 2 mg/kg every
6 to 8 hours (max. 400 mg/day).

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– Adjust choice of opioid according to age and by monitoring efficacy of the analgesia given.
– For acute pain, start with immediate-release oral morphine.
– For chronic pain, low doses of sustained-release oral morphine are preferred.

Step 3: severe pain


– Add IV, IM or SC morphine to step 1 analgesia.
– For acute severe pain and in emergencies, administer morphine by IV titration (Table 15.14).
– IV morphine use requires:
• Adequate monitoring of pain, sedation, and vital signs (HR, RR, BP).
• Staff to recognise and treat respiratory depression as a result of an overdose of morphine.
• Immediate availability of naloxone and a basic airway kit (see Chapter 2, Section 2.9.5 for
management of morphine toxicity).
Table 15.13 - Analgesic drug dosing

Drug Route Dose

Paracetamol PO 15 mg/kg every 4 to 6 hours (max. 60 mg/kg/day)

IV (over • < 10 kg: 10 mg/kg every 6 hours


15 mins) (max. 30 mg/kg/day)
• 10 kg to 49 kg: 15 mg/kg every 6 hours
(max. 60 mg/kg/day)
• ≥ 50 kg: 1 g every 6 hours
(max. 4 g/day, or 3 g/day if risk of hepatotoxicity).

Ibuprofen PO • 3 months to 11 years: 5 to 10 mg/kg every 6 to 8 hours


(max. 30 mg/kg/day)
• ≥ 12 years: 200 to 400 mg every 6 to 8 hours
(max. 1200 mg/day)

Tramadolc PO, IM, IV • ≥ 12 years: 50 to 100 mg every 4 to 6 hours


(max. 400 mg/day)

Morphine PO immediate • 1 to 5 months: 0.1 mg/kg every 4 hours


release (MIR) • 6 months to 1 year: 0.2 mg/kg every 4 hours
• 2 to 11 years: 0.2 to 0.3 mg/kg every 4 hours
• ≥ 12 years: 5 to 10 mg every 4 hours
To be adjusted in relation to pain intensity.

PO sustained • ≥ 6 months: 0.5 mg/kg every 12 hours


release (MSR) To be adjusted in relation to pain intensity.

SC or IM • 1 to 5 months: 0.1 to 0.2 mg/kg every 6 hours


• 6 months to 11 years: 0.1 to 0.2 mg/kg every 4 hours
• ≥ 12 years: 2.5 to 10 mg every 4 hours
To be adjusted in relation to pain intensity.

c Tramadol is not approved for use in children < 12 years in some countries due to the risk of increased opioid
toxicity including life-threatening respiratory depression. If oral morphine is not available, tramadol may be
considered in hospitalised children < 12 years under close medical supervision at a dose of 1 to 2 mg/kg every
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Table 15.14 - IV morphine titration

Age/weight 1st dose Following doses Interval

< 6 months 0.05 mg/kg 0.05 mg/kg 5 to 10 mins until pain controlled

≥ 6 months
0.1 mg/kg 0.05 mg/kg 5 to 10 mins until pain controlled
< 50 kg

≥ 50 kg 2 to 3 mg 2 to 3 mg 5 to 10 mins until pain controlled

Dilution: see MSF Paediatric Injectables Handbook for details on dilution and administration.

– Move up or down the pain ladder depending on pain intensity and type of pain (Figure 15.9):
• Acute pain, surgical or trauma-related pain: intensity of pain higher initially but will then
decrease. Strategy is to move down the ladder.
• Chronic pain, cancer-associated pain: background pain with increase in intensity. Strategy
is to move up the ladder.

Figure 15.9 - Strategy for use of pain ladder

Step 3: severe pain


Chronic pain: Pain score 7-10
Cancer pain (8-15 EVENDOL)
Paracetamol +/- ibuprofen
+ morphine IV, IM, SC
Step 2: moderate pain
Pain score 4-6
(4-7 EVENDOL)
Paracetamol +/- ibuprofen
+ low-dose oral morphine
or tramadol
Step 1: mild pain
Pain score 1-3
Acute pain:
Paracetamol +/- ibuprofen
Trauma pain
Surgical pain

– Anticipate and treat adverse effects of analgesia. Constipation is especially common when
opioids are used, give laxatives routinely to prevent constipation when opioids are used for
> 3 days.
– Be aware of contraindications to analgesic medications.

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Contraindications

Bleeding or coagulation defects, history of severe asthma or severe hepatic


Ibuprofen
or renal impairment.

Severe respiratory distress and the risk of or known seizures (epilepsy, head
Tramadol injury, meningitis)
Do not give tramadol with or shortly before or after morphine.

Severe respiratory distress, severe liver failure, non-stabilised epilepsy and


raised intracranial pressure. It should not be given in combination with other
Morphine opioid analgesics (tramadol) or with other drugs that actively affect the CNS
(benzodiazepines, neuroleptics, antihistamines, phenobarbital, phenytoin)
because of the increased risk of sedation.

15.4.3 Chronic pain


Defined as pain that lasts or recurs for longer than 3 months and is associated with significant
emotional distress and/or functional disability7. Most chronic pain in children is secondary to
an underlying condition and requires long-term management in an outpatient setting.
Management requires a combination of non-pharmacologic measures, cognitive behavioural
therapy and analgesics, with goals set with the child and family (regarding learning to live with
a level of background pain, managing crises or breakthrough pain, mental health support,
etc.).

15.4.4 Considerations for children with severe acute malnutrition (SAM)


Despite limited pharmacological evidence, as renal and hepatic function may be significantly
altered in a child with severe acute malnutrition, it is currently recommended to reduce dosing
by 50% or to increase the interval between doses.
Recommended analgesic dosing for children with SAM:

Drug Route Dose

Paracetamol PO, IV 10 mg/kg every 8 hours (max. 30 mg/kg/day)

Ibuprofen PO 5 mg/kg every 8 hours (max. 15 mg/kg/day)

Tramadold PO, IV, IM ≥ 12 years: 1 mg/kg every 6 to 8 hours maximum

PO 0.2 mg/kg every 8 hours maximum


Morphine
IM/SC 0.1 mg/kg every 4 to 8 hours

d Tramadol is not approved for use in children < 12 years in some countries due to the risk of increased opioid
toxicity including life-threatening respiratory depression. If oral morphine is not available, tramadol may be
15
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15.4.5 Neuropathic pain


Pain due to a lesion, disease or injury of the somatosensory nervous system. This primary
lesion can be peripheral or central and has a protective function as well. Neuropathic pain can
occur acutely but can become a chronic pain that has a substantial burden on the patient with
psychological distress, physical disability and reduced overall quality of life. It is often the most
severe and most difficult persistent pain to manage. Rehabilitation and psychological therapies
such as cognitive-behavioural therapy (CBT) should be provided alongside pharmacological
treatment.
Causes in children include trauma, phantom limb pain following amputation, spinal cord
injury, tumours, abscesses, post-surgical, viral nerve damage (e.g HIV, HSV), autoimmune or
metabolic diseases, or drugs (e.g. ARVs, ethambutol, isoniazid)8.
Diagnosis is clinical and based on features described of an unusual pain, such as burning,
shooting, electric shocks or other sensations that may be difficult to describe, and the area of
the skin near the pain may be numb or very sensitive that even light touch or clothes may be
painful.

Management
gabapentin PO
– 6 to 11 years: 5 mg/kg/day once daily. Titrate dose over 3 days, increasing 5 mg/kg/day.
Maximum dose: 15 mg/kg/day given in three divided doses.
– ≥ 12 years: D1: 300 mg once daily; D2: 300 mg 2 times daily; D3: 300 mg 3 times daily.
After D3: titrate dose as required, increasing by 300 mg/day at 2-day intervals until D10 and
subsequently at 3 day intervals up to a maximum of 3600 mg in three divided doses.
amitriptyline PO
– 6 to 11 years: start at 0.5 mg/kg at bedtime. Gradually titrate up once a week up to maximum
of 1 mg/kg. Maximum dose: 75 mg daily.
– ≥ 12 years: week 1: 25 mg once daily at bedtime; week 2: 50 mg once daily at bedtime;
week 3: 75 mg once daily at bedtime. Maximum dose: 75 mg daily. Avoid in patients at risk
of self-harm.
Dual treatment is recommended9,10. In cases of mild neuropathic pain, clinicians may consider
starting gabapentin or amitriptyline in isolation depending on patient risk factors. Monitor
closely for the development of suicidal thoughts and evaluate response to treatment after 2 to
4 weeks. Neither medication should be stopped abruptly.

15.4.6 Sedation or analgesia before a painful procedure


Consider prophylactic analgesia before painful procedures.
– For minor procedures such as IV catheter insertion, non-pharmacological measures are
usually sufficient.
– Start with step 1 analgesics: paracetamol +/- ibuprofen, given at least 30 minutes before the
procedure.

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– Local topical anaesthetics can be used in inpatient and emergency care settings:
• Dermal creame: use with planned procedures e.g. lumbar puncture.
▹ Apply half of a 4 g tube of EMLA cream (lidocaine/prilocaine) to the skin. Cover the
cream with an occlusive dressing and wait for 45 to 60 minutes. Analgesic effects last
for up to 4 hours after removal of the cream.
▹ Adverse reactions: transient skin irritation
• Subcutaneous injection of lidocaine 1% may be used for minor surgical procedures by
staff trained in the procedure.
▹ Infiltrate lidocaine 1% SC: 3 mg/kg/injection (max. 5 mg/kg/injection) in the area
involved with a small-bore needle (e.g. 25 Gauge needle). Do not use as IV.
– For procedures that require a stronger analgesia/sedation, such as ketamine, trained
staff and protocols need to be available (refer to MSF Standards for Paediatric Procedural
Sedation).

15
e Transitory Z code DEXTZFR0063; mixture of lidocaine 2.5% and prilocaine 2.5% in a cream base

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15.5 Nutritional support for the critically unwell child

Nutritional support is an essential element of paediatric critical care for all children, both non-
malnourished and malnourished, following initial resuscitation. Ideally, nutritional support in
hospital should be provided orally (i.e. eating and drinking), but this is not feasible in critically
unwell children. Enteral nutrition via oro/nasogastric tube (O/NGT)a is therefore used to
allow timely introduction of nutritional support. O/NGTs should be used for as short a time as
possible, as the goal is to get the child back on a nutritionally appropriate oral diet as soon as
safely possible (see MSF Hospital Food Service Management Protocol).
Early introduction of enteral nutrition has been shown to be beneficial in critically unwell
children, leading to reduced infections (particularly pneumonia), and a likely reduction
in mortality11,12,13. Enteral nutrition should therefore be started as soon as the child is
haemodynamically stable i.e. has received appropriate fluid resuscitation for circulatory
impairment.
Intravenous fluids have limited nutritional value and maintain adequate hydration, blood sugar
levels and electrolyte balance in the short term only. Children recovering from critical illness
have a considerable risk of developing nutritional deficiencies, therefore the use of exclusive
IV fluids should be limited to the first 24-48 hours of critical illness.
While the principles of nutritional support for critically unwell children are the same for both
malnourished and non-malnourished children, the enteral nutrition products and volume
of feeds are not. Ensure that nutritional assessment is carried out before starting enteral
feeding in critically unwell children, if not already done at admission. This chapter will focus
on nutritional support for the non-malnourished critically unwell child. For advice on enteral
feeding in critically unwell malnourished children from 1-59 months, refer to the MSF ITFC
Nutrition Care Protocol 2021b. For older critically unwell malnourished children, refer to local
protocols.

15.5.1 Indications for enteral nutrition


Enteral feeds should be started in the first 24 to 48 hours of admission13 if the following
conditions are met:
– Haemodynamically stable
– No signs of acute abdomen (see Chapter 5, Section 5.4)
– No imminent surgery
– Unable to tolerate oral intake
Although not contraindicated, a cautious approach should be taken when introducing enteral
feeds in children with severe respiratory distress, as increasing stomach volume may cause
deterioration. These children should be closely monitored for signs of worsening distress and
have an OGT inserted in preference to an NGT to minimise respiratory obstruction.

a In some contexts, naso-duodenal, jejunostomy and gastrostomy tubes may be used, though much less
common.
b Specific advice on the management of children with moderate acute malnutrition in Note 5.6 of this protocol.

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Children with a reduced level of consciousness have reduced protective airway reflexes (e.g.
gagging/coughing) therefore are at greater risk of regurgitation of gastric contents. This is
not a contraindication to the introduction of enteral feeds but necessitates close monitoring
and a more cautious approach to avoid aspiration of stomach contents into the airway and
lungs, causing an aspiration pneumonia. The position of the O/NGT should be verified after
insertion and before each use (see MSF Manual of Nursing Care Procedures, SOP – Gastric
Tubes: Maintenance).

15.5.2 Enteral nutrition products


The choice of enteral nutrition product depends on the child’s age, their calorie and fluid
requirements, and availability of the product. For all critically unwell children, expressed
breastmilk should be encouraged if the child is still breastfeeding. Remaining energy and
fluid requirements can be provided with the chosen appropriate enteral nutrition product.
Isocaloric enteral nutrition products are usually used to meet energy needs, but hypercaloric
enteral nutrition products may be preferred in specific cases e.g. if the child is fluid restricted
or for conditions with extreme increases in energy needs such as burns. See Table 15.15 for
calorie and water content of various enteral products.
Table 15.15 - Calorie and water content of enteral nutrition products

Calorie content Free water content


Type of enteral nutrition
(kcal/100 mL) (mL water/100 mL milk)

Breastmilk 70 90

Standard infant formula 70 90

F-100 diluted (F-100d) 70 –

F-100 100 8614

Enteral nutrition product, isocaloric,


100 83
childc: 1 kcal/mL

Enteral nutrition product,


150 73
hypercaloric, childd: 1.5 kcal/mL

Enteral nutrition products in order of preference for non-malnourished critically unwell


children:
– 1 to 6 months:
• Expressed breastmilk
• Standard infant formula
• F-100 diluted (F-100d)e
c Isocaloric, normoprotein, ready to use enteral nutrition available in MSF catalogue with code NFOSENICNPW05.
This is adequate for most children requiring enteral feeds. Semi-elemental drink/enteral powder also available
as NST with code NFOSDEICSEWV4 but is reserved for exceptional cases and is not available in all projects.
d Hypercaloric, normoprotein, ready to use enteral nutrition available in MSF catalogue with code
NFOSERHCNPF05. This is typically reserved for patients with extremely increased energy requirements such
as in children with severe burns.
e Only to be used if neither of the first two products are available. See MSF ITFC Nutrition Care Protocol 2021 for
15
preparation guidance.

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– > 6 months to 1 year:


• Expressed breastmilk
• Standard infant formula
• F-100f
– > 1 year:
• Expressed breastmilk (if still breastfeeding)
• Appropriate enteral nutrition product
• F-100f

15.5.3 Daily fluid requirements


Total daily fluid requirement
The total daily fluid requirement is the amount of fluid that the body needs to maintain
hydration each day. This fluid requirement can be met either intravenously (IV) or enterally,
or as a combination of the two. All fluids given to the child should be accounted for in the
total daily fluids, including IV flushes, medication infusions and enteral feeds. Total daily
fluid requirement is typically calculated using the Holliday-Segar formula which calculates
maintenance fluid requirements (see Section 15.2). Critically unwell patients are often fluid
restricted, which should be considered when calculating total daily fluid requirement (see
Section 15.2.2). If fluid restriction is considered necessary, the restriction is applicable to both
IV and enteral fluid volumes.

Enteral fluid volumes


In children, enteral fluid volume is equivalent to total daily fluid requirement15,16,17. This
volume meets hydration and nutritional requirements, as enteral nutrition products in this
age group are isocaloric. In infants, however, while total daily fluid requirements calculated
using Holliday-Segar will meet hydration needs, they are likely to be nutritionally inadequate,
since infant feeds are hypocaloric. Standard enteral fluid volumes for nutritional purposes in
infants are outlined in Table 15.16.
Table 15.16 - Standard enteral fluid volumes for the provision of nutrition in infants11

Age Fluids (mL/kg/day)

1-3 months 150 (140-160)

4-6 months 140 (130-155)

7-12 months 130 (120-145)

15.5.4 Energy requirements in critical illness


The volume of enteral nutrition to be administered during critical illness is based on calorie
(energy) requirements per kg of body weight, which vary depending on the phase of critical
illness. In the acute phase (lasting hours to days), there may be a significant reduction in energy
expenditure due to decreased activity and reduced insensible losses e.g. in comatose patients

f Only to be used if neither of the first two products are available. See MSF ITFC Nutrition Care Protocol 2021 for
preparation guidance.

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while in other patients stress factors during the acute phase can lead to hypermetabolism and
significantly increased energy expenditure, especially with fever or burns. It is therefore difficult
to accurately estimate energy requirements without risking either over- or underfeeding,
both of which can have adverse effects on recovery13. Overfeeding in particular during the
acute phase can exacerbate the catabolic stress response and impair recovery. Resting energy
expenditure is therefore used as a proxy for energy requirement during the acute phase of
critical illness. In the stable and recovery phases of critical illness, energy provision should be
gradually increased to ensure minimal loss of lean body mass.

Calculation of energy requirements in the acute phase of critical illness


In the absence of known resting energy expenditure, it is recommended that the Schofield
equation, which measures basal metabolic rate (BMR), is used to estimate energy requirements
in the acute phase of illness11,12 (see Table 15.17). Weight at admission should be used for
calculations to ensure that the nutritional support is appropriate.
Table 15.17 - Schofield energy equations (modified from AUSPEN11)

Age Gender kcal

Male BMR = 59.5 x W* – 30


0 to < 3 years
Female BMR = 58.3 x W – 31
Male BMR = 22.7 x W + 504
3 to < 10 years
Female BMR = 20.3 x W + 486
Male BMR = 17.7 x W + 658
10 to 15 years
Female BMR = 13.4 x W + 692
*W = weight (kg)
These calculations are only valid for the acute phase of critical illness (up to maximum 7 days).

15.5.5 Calculating target daily enteral feed volumes in the acute phase of critical
illness
Use the following steps to calculate the target volume of enteral feed required daily to meet
energy needs during the acute phase of critical illness (up to maximum 7 days).
Step 1: Calculate the estimated daily energy requirements according to weight (see Schofield
energy equation, Table 15.17).
Step 2: Choose the most appropriate/available enteral nutrition product (see Table 15.15). If
the patient is fluid restricted, consider hypercaloric feeds (children) or fortification of breastmilk
(infants) to meet energy needs without exceeding target enteral fluid volumes.
Step 3: Calculate and prescribe the target daily acute phase enteral feed volume according to
the calorie content of the chosen enteral nutrition product.

Target daily acute phase enteral feed volume =


estimated daily energy requirement ÷ calorie content of chosen enteral nutrition product
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Example: 3.5-year-old female weighing 12 kg


– Step 1: Estimated daily energy requirement (kcal/day) = 20.3 x 12 + 486 = 730 kcal/day
– Step 2: Chosen enteral nutrition product = F-100 = 1 kcal/mL
– Step 3: Target daily acute phase enteral feed volume (mL/day) = energy requirement (kcal/
day) ÷ calorie content of chosen enteral nutrition product (kcal/mL) = 730 ÷ 1 = 730 mL/day
See Appendix 22 for pre-calculated tables of target daily enteral feed volumes according to age
and weight in the acute phase of illness (up to maximum 7 days).

15.5.6 Administration of enteral feeds


Enteral feeds should be started slowly and increased as quickly as tolerated (see below for
signs of feed intolerance), aiming for delivery of two-thirds of total calculated target daily
acute phase requirements within 7 days at the latest13. If the child improves rapidly, full feeds
can be established within a few days. Ensure 4-hourly blood glucose monitoring for the first
24-48 hours after introduction of enteral feeds18. Until enteral feeds are established, critically
unwell children should receive IV maintenance fluids (see Section 15.2), which should be
gradually reduced as enteral feeds are increased to maintain the same total daily fluid intake.
Enteral feeds should be administered according to prescription either by gravity or using an
enteral feeding pump, if available (see MSF Manual of Nursing Care Procedures, SOP – Enteral
Nutrition Administration Methods). The preference for feed delivery is intermittent feeds
every three hours. If intermittent feeds are not tolerated, increase feed frequency to every
two hours or hourly, reducing volumes accordingly. If there is still intolerance on hourly bolus
feeds, start continuous feeding.

Signs of enteral feed intolerance


Signs of feed intolerance can be non-specific and include:
– Clinical signs of shock or haemodynamic instability
– Increasing respiratory distress
– Vomiting
– Diarrhoea
– Blood in stool
– Abdominal distension (abdominal girth increased for two consecutive measurements)
– Temperature instability
– Hyperglycaemia
– Large gastric residuals (seen on checking for correct placement of O/NGT)
– Reduced bowel sounds
Consider refeeding syndrome (See Chapter 12, Section 12.3) in children who deteriorate after
the introduction of enteral feeds after a prolonged period of starvation, even if they do not
meet the anthropometric criteria for acute malnutrition.

Stepwise approach to introducing and increasing enteral feeds


Step 1: Start at 30% of target daily acute phase enteral feed volume (as calculated above). If
tolerated, reduce IV fluids accordingly and continue for 6-12 hours.
Step 2: Increase to 50% of target daily acute phase enteral feed volume and reduce IV fluids
accordingly. If tolerated, continue for 6-12 hours.

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Step 3: Increase to 70% of target daily acute phase enteral feed volume and reduce IV fluids
accordingly. If tolerated, continue for 6-12 hours.
Step 4: Increase to target daily acute phase enteral feed volume. If tolerated, stop IV fluids
and provide remaining daily enteral fluid intake in the form of water via O/NGT in 30-60 mL
aliquotsg.

Total enteral fluid requirement = enteral feed volume + IV fluids + water

Example: 3.5-year-old non-malnourished child weighing 12 kg, no fluid restriction in place.


Current IV maintenance fluids: 45 mL/hr
Chosen enteral nutrition product: F-100
Target daily acute phase enteral feed volume = 730 mL
Target 3-hourly acute phase enteral feed volume = 730 ÷ 8 = 90 mL
– Step 1: Start at 30% of target acute phase enteral feed volume = 90 x 0.3 = 30 mL every
3 hours. Reduce IV fluids to 35 mL/hr and continue for 6-12 hours.
– Step 2: Increase to 50% of target acute phase enteral feed volume = 90 x 0.5 = 45 mL every
3 hours. Reduce IV fluids to 30 mL/hr and continue for 6-12 hours.
– Step 3: Increase to 70% of target acute phase enteral feed volume = 90 x 0.7 = 60 mL every
3 hours, reduce IV fluids to 25 mL/hr for 6-12 hours.
– Step 4: Increase to 100% of target acute phase enteral feed volume = 90 mL every 3 hours
and give 45 mL water via O/NGT every 3 hours.

15.5.7 Advancing enteral feeds


Target enteral feed volumes calculated for the acute phase of critical illness should be used up
to a maximum of 7 days. If the child is improving and target acute phase enteral feed volumes
are tolerated, feed volume can be cautiously increased to full enteral fluid volume.
The child should be advanced to full oral intake as soon as they are well enough, i.e. when fully
conscious and able to safely tolerate oral feeds. In infants, re-establish breastfeeding as soon as
possible, or give expressed breastmilk or infant formula via mouth. In children, introduce food
according to usual eating habits. In the first few days after re-establishing oral feeds, record
food and fluid intake to ensure that it is adequate. For further advice on nutrition requirements
for hospitalised children, please refer to MSF Hospital Food Service Management Protocol.
If the child remains critically unwell after 7 days, an individualised enteral nutrition plan
should be devised with the input of a nutrition specialisth, as the target enteral feed volumes
calculated for the acute phase will be inadequate to meet their increasing daily energy needs
(see Section 15.5.3 and Section 15.5.4 above).

g Do not give water to infants under 6 months old. In infants under 6 months old, continue to gradually increase
enteral feeds as tolerated until full enteral feed volume has been reached (see Table 15.16 for standard enteral
feed calculations in infants) and continue to reduce IV fluids accordingly until they can be stopped.
15
h Consider consulting the MSF telemedicine platform for specific case by case advice.

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15.6 Palliative care

Paediatric palliative care aims to relieve suffering and improve the quality of life for children
with life-threatening illnesses, as well as to provide support to their families. Although
palliative care is often started when curative options have been exhausted, it can also be
provided alongside potentially curative treatments. It is not synonymous with end-of-life care
and should be a component of any care plan for children with significant life-limiting illnesses.
The aim of palliative care is to promote comfort and dignity to children with serious health
problems, regardless of whether their illness can be cured or not, and palliative care may take
place in hospital or at home. It encompasses physical, psychosocial, and spiritual support and
requires the input of a multidisciplinary team. End-of-life care is a component of palliative care
that occurs in the last hours or days of life.
In humanitarian and low-resource settings, palliative care may be required more frequently for
conditions that may be curable in other contexts with more advanced healthcare. Common
conditions in children that require palliative care include congenital cardiac anomalies and
other congenital anomalies, malignancies, critical illness or injury where recovery is unlikely,
chronic or degenerative conditions for which there is no definitive treatment (e.g. HIV,
muscular dystrophies), and severe neurological conditions. Palliative care should be integrated
into care early in paediatric critical illness, as it is often difficult to predict prognosis and
eventual outcome in children. A child’s developmental stage will heavily influence all aspects
of palliative care.
This chapter will briefly outline the main components of paediatric palliative care – symptom
management; communication; and psychosocial support. For a comprehensive guide to
paediatric palliative care, refer to MSF OCBA Palliative Care Programmatic and Clinical
Guidelines. For more guidance on psychosocial support in palliative care, refer to MSF Mental
Health and Psychosocial Support Guideline, Chapter 13.

15.6.1 Symptom management


Children may not be able to express what is distressing them. It is important to look for
non-verbal cues and listen to family members when assessing for symptoms, especially pain.
Common symptoms that may affect children requiring palliative care include:
– Pain (see Section 15.4 for the assessment and management of pain in children)
– Breathlessness
– Secretions
– Nausea, with or without vomiting
– Constipation
– Anxiety
– Spasticity and muscle spasm
– Seizures

Examination
Carry out a complete physical examination, paying particular attention to inside the mouth
and ears, presence of lymph nodes and skin problems (especially nappy area and scalp).

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Management
Symptom management should be holistic, including both pharmacological and non-
pharmacological options. Ensure thorough assessment of symptoms, treat any treatable
causes, give medications to control symptoms at age-appropriate dosing (preferably via oral
route), and consider social, psychological or spiritual factors which may impact symptom
management. If palliative care will take place at home, adequate planning is required to ensure
that good-quality care is provided.

Specific symptom management includes:


– Respiratory care:
• Ensure regular mouth hygiene (nursing care using mouth swabs, treating mouth sores
etc).
• Gentle suctioning can relieve distress from secretions in the mouth and airway.
• Modify positioning to minimise breathlessness.
• Oxygen for comforta, as required.
– Pain relief (see also Section 15.4):
• Assess pain regularly and ensure that pain relief is adequate.
• Use adjuvant therapy if indicated, e.g. for neuropathic pain.
• Ensure non-pharmacological measures are used in combination with medications, e.g.
allow presence of parents/carers and encourage physical comforting such as cuddling,
breastfeeding; bring familiar objects from home; encourage play, music and drawing;
provide access to physical measures such as massage, heat/cold therapy; teach breathing
exercises to calm.
– Nausea, with or without vomiting:
• Treatment with antiemetic should be short-term.
• In children over 1 year old, consider metoclopramideb PO or slow IV, 100 to
150 micrograms/kg (max. 10 mg) repeated as required up to 3 times daily.
– Constipation:
• Common side effect of opioid analgesia.
• Treat with lactulose PO:
▹ 1-11 months, 2.5 mL 2 times daily
▹ 1-4 years, 2.5-10 mL 2 times daily
▹ 5-17 years, 5-20 mL 2 times daily
– Anxiety:
• Try non-pharmacologic methods to calm anxiety in the first instance, e.g. breathing
exercises, distraction, music, psychosocial support.
• Consider diazepam PO in children over 1 year old, 2 mg 2 or 3 times daily.
– Spasticity and muscle spasm:
• Use pillows or other supports to maintain normal joint position.
• Prevent contractures through gentle physiotherapy and passive movement of limbs.
• Consider the use of diazepam PO as a muscle relaxant:
▹ 1 month - 2 years: 0.1 to 0.3 mg/kg once or 2 times daily
▹ > 2-4 years: 2.5 mg once or 2 times daily
▹ 5-12 years: 5 mg once or 2 times daily
▹ ≥ 12 years: 5 to 10 mg once or 2 times daily

a The provision of oxygen in palliative care is for comfort only, i.e. to minimise symptoms of respiratory distress.
It is not necessary to target a certain saturation level or to administer high flows which may cause discomfort.
b Metoclopramide can induce severe extra-pyramidal side-effects in children therefore should be used with
15
caution and for maximum of 5 days. It is contraindicated in children less than 1 year old.

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• Baclofen PO may be used as an alternative, if available:


75 micrograms/kg 4 times daily, increased gradually at weekly intervals until satisfactory
response up to a maintenance dose of maximum 0.75 to 2 mg/kg daily (max. 40 mg/day
< 8 years; max. 60 mg ≥ 8 years).
– Seizures:
• Seizures cause stress and discomfort to the child, therefore it is important that they are
adequately controlled in children receiving palliative care.
• Manage according to advice in Chapter 7, Section 7.2.

15.6.2 Communication
Communication with the child
Good communication is essential when providing palliative care. Language and methods of
communication should be adapted to the child’s level of development and understanding.
Important discussions and sharing of sensitive information should only take place after
consultation and agreement with parents/carers/families. Honesty is a key component of
communication with children, and it is important not to lie, even when faced with difficult
questions. Children are often aware that they are dying, even if no-one tells them directly,
and they will pick up on the worried faces of their parents/carers and healthcare team. We
may inadvertently cause more worry and anxiety by failing to talk about this, as children may
imagine a situation that is worse than reality when faced with uncertainty.
Some important points to remember when communicating with children:
– Engage with children non-verbally before starting to speak to them to build trust, e.g. smile,
offer a toy, engage in play/drawing with them.
– Get down to their level to make them feel more comfortable, e.g. sit on the bed or floor.
– Maintain a distance that allows the child to feel safe, leaving them to come closer when they
are ready.
– Use language that is appropriate for their developmental age.
– Talk to the child with their parents/carers unless otherwise requested and allow them to sit
on their parent’s/carer’s lap or stay near them if they want to.
– Ensure that you speak directly to the child as well as the parents/carers.
– Be honest and don’t make promises that are unrealistic.
– Listen to the child when they speak and don’t rush them or interrupt if they are unable to
express themselves easily.
– Don’t give information to the child without their parent’s/carer’s permission.

Communication with families


It can be difficult to discuss palliative care for a seriously unwell child with their families, and
any such conversation requires great sensitivity. Ensure that you allocate the time required
to speak to family members, and that discussions take place in a quiet location that allows
privacy. Involve other members of the multidisciplinary team who are closely involved in the
care of the child, such as the nurse or the mental health team, to provide additional support to
families. It is important to be honest with families so that they can prepare for what lies ahead,
and in turn prepare other family members, especially siblings. It will usually be the family who
will talk to their child to explain what is happening, so they need to have all the information
required to do this in the best way possible and to allow them to make decisions regarding

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care. Reassure families that palliative care does not mean that there that is nothing more that
can be done, but that it aims to make the child more comfortable by treating pain and other
symptoms. Explain to families if options are available for providing palliative care at home, so
that they can decide if this would be best for their child and their family. Provision of palliative
care at home may not be possible, but families should still be offered the option of taking their
child home to provide whatever care they can in their home environment, if this is what they
feel is best for them and their child.
If it seems likely that the child will not survive, there are key steps that should be followed to
inform a family that death is expected:
1) Open the conversation by introducing yourself and asking permission to talk about their
child’s current condition.
2) Assess their understanding of the illness and their child’s condition.
3) Ask about how much information they would like to know about their child’s condition and
likely prognosis, both short- and long-term.
4) Share the prognosis sensitively but clearly and allow the family time to process this
information.
5) Assess goals by asking the family what they would like to do for their child, considering the
information they have just received.
6) Establish a plan, recommending a focus on symptom control, comfort and allowing the
child to be close to their loved ones.
7) Close the conversation by reassuring the family that you are available for support or further
information and ensure that they have a way to contact a member of the team whenever
they need to.
8) Record all conversations with families and patients in the patient’s medical file and
communicate to the rest of the team during handover processes so that all medical staff
are aware of the plan.

Communication within the multidisciplinary team


Good communication amongst members of the multidisciplinary team is essential to ensure
that all staff are aware of conversations and decisions regarding palliative care. Where feasible,
all members of the multidisciplinary team should be involved in discussions about the palliative
care plan. Ensure good record of discussions and decisions in the patient’s medical file, and
handover of key information during shift changes.

15.6.3 Psychosocial support


Support for the child
Children with life-limiting illnesses need emotional and psychosocial support to understand
their illness and what it may mean for them. It is important that they are able to talk to people
they trust to be able to share their worries. Common worries for children include pain and
other symptoms, changes to their daily life, school and other activities, concern for their
parents/carers, guilt and changes in relationships with siblings and friends. Activities such as
art and music may help children to express how they feel and find strategies to cope with their
worries and all children should continue to play and learn even when they are ill. As children
are still growing and developing, their understanding of their illness may change over time,
and they may have new questions or require new strategies to cope with their illness. Involve
the mental health team in the child’s care to evaluate and provide support where required.
15

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Support for family members


Caring for sick children is very challenging, especially when the child may not get better.
Parents/carers have many worries related to this including how they will cope; their new role
as a medical carer for a sick child; how they will explain things to siblings and other family
members and support them; the financial implications of being unable to work; and feelings
of guilt. Support families by listening to their fears and challenges and involving them in their
child’s care and any decisions that must be made. They should be treated as part of the team
caring for their child and given positive encouragement that they are making the right choices
for their child. Encourage the family to draw on support from wider family, the community,
and religious leaders, where relevant.
Siblings will need additional support as they may feel neglected due to the attention that is
given to the sick child and may experience conflicting emotions. They also need consistent
and honest information about their sick brother or sister and to be able to ask questions
or talk about any fears that they may have. They usually want to be close to their parents/
carers and their sick sibling, and older children may want to help care for them which should
be encouraged. All siblings should be able to play and spend time with their sick brother or
sister if desired. Encourage parents/carers to maintain normal routines for siblings as much as
possible, and to ensure that appropriate care is available for siblings if their parents/carers are
away from home caring for the sick child.

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14. Therapeutic milk technical bulletin | UNICEF Supply Division. Accessed November 29, 2023.
https://www.unicef.org/supply/documents/therapeutic-milk-technical-bulletin
15. Nager AL, Wang VJ. Comparison of Nasogastric and Intravenous Methods of Rehydration in
Pediatric Patients With Acute Dehydratio. Pediatrics. 2002;109(4):566-572.
https://doi.org/10.1542/peds.109.4.566
16. Oakley E, Borland M, Neutze J, et al. Nasogastric hydration versus intravenous hydration for
infants with bronchiolitis: a randomised trial. Lancet Respir Med. 2013;1(2):113-120.
https://doi.org/10.1016/S2213-2600(12)70053-X
17. Mackenzie A, Barnes G. Randomised controlled trial comparing oral and intravenous
rehydration therapy in children with diarrhoea. BMJ. 1991;303(6799):393-396.
https://doi.org/10.1136/bmj.303.6799.393
18. Singer P, Blaser AR, Berger MM, et al. ESPEN guideline on clinical nutrition in the intensive
care unit. Clin Nutr. 2019;38(1):48-79.
https://doi.org/10.1016/j.clnu.2018.08.037

426
Appendices

1. Developmental milestones....................................................................................... 429


2. WHO growth charts for children.............................................................................. 432
3. Paediatric vital signs................................................................................................. 436
4. Oropharyngeal airway insertion............................................................................... 438
5. Intraosseous needle insertion.................................................................................. 439
6. Performing a lumbar puncture................................................................................. 443
7. Clinical Respiratory Score (CRS)................................................................................ 446
8. Asthma action plan................................................................................................... 447
9. How to make a spacer with a plastic bottle..............................................................448
10. Inhaler technique using a spacer............................................................................ 449
11. Sputum specimen collection in children................................................................451
12. WHO rehydration plans A, B and C......................................................................... 453
13. Glasgow and Blantyre Coma Scales........................................................................ 454
14. Urinary collection procedures................................................................................ 457
15. Suprapubic aspiration of urine............................................................................... 463
16. Body surface area estimation in children...............................................................466
17. Blood pressure centiles for age.............................................................................. 467
18. F-75 feed volumes in Phase 1................................................................................. 468
19. ARV prophylaxis in PMTCT...................................................................................... 469
20. Causes of fever of unknown origin (FUO)...............................................................471
21. EVENDOL chart....................................................................................................... 477
22. Daily enteral feed volumes and administration in critically unwell children..........478
Appendix 1. Developmental milestones

2 Months 4 Months
Physical & Movement Cognitive Communication/Language Social & Emotional Physical & Movement Cognitive Communication/Language Social & Emotional

Holds head up when Follows past midline Laughs and vocalises Smiles responsively and Holds head steady without Looks at their hands with Makes sounds back when Smiles on his own to get
on tummy (sounds other than crying) spontaneously support when held. interest. caregiver talks to them. caregiver’s attention.
Watches caregiver as
Moves both arms and they move Reacts to loud sounds Looks at caregiver’s face Brings hands to mouth. Turns head towards the Looks at caregiver, moves,
legs sound of caregiver’s voice. or makes sounds to get or
Pushes up on keep their attention.
Opens hands briefly elbows/forearms when on
tummy
© OCP Paediatrics, L&D and BKL 2023 © OCP Paediatrics, L&D and BKL 2023

6 Months 9 Months
Physical & Movement Cognitive Communication/Language Social & Emotional Physical & Movement Cognitive Communication/Language Social & Emotional

Leans on hands to support Puts things in their mouth Takes turns making Knows familiar people. Gets to a sitting position by Bangs two things together. Lifts arms to be picked up. Looks when you call their
themselves when sitting. to explore them. sounds with caregiver . themselves. name.
Laughs. Looks for objects when
Pushes up with straight Reaches to grab a toy Moves things from one hand dropped out of sight Reacts when caregiver
arms when on tummy. they want. to their other hand. (like toy). leaves (looks, reaches for
caregiver, cries).
Rolls from tummy to back. Closes lips to show they Sits without support
don’t want more food.
© OCP Paediatrics, L&D and BKL 2023 © OCP Paediatrics, L&D and BKL 2023
Appendix 1

429
Reprinted with permission from OCP Paediatrics, L&D and BKL
430
12 Months 15 Months
Appendix 1

Physical & Movement Cognitive Communication/Language Social & Emotional Physical & Movement Cognitive Communication/Language Social & Emotional

Tries to say one or 2 words Copies other children while


besides “mama” or “dada”, like playing, like taking toys out of
“ba” for ball or “da” for dog. a container when another
child does.
Pulls up to stand. Puts blocks in and out Understands “NO” Plays games with you, Takes a few steps on their Tries to use things the Looks at a familiar object, when
Shows you an object they like.
of cup. (pauses briefly or stops, like pat-a-cake. own. right way, like a phone you name it.
Pincer grasp: picks up when you say it). cup or book. Claps when excited.
Uses fingers to feed Follows directions given with
things between thumb and Looks for things they both a gesture and words
themselves some food. Hugs stuffed doll or other toy.
pointer finger like small bits see you hide, like a toy Calls a parent “mama” or e.g. They give you a toy when
of food. under a blanket. “dada” or another special you hold out your hand and say, Shows affection (hugs,
name. “Give me the toy!”. cuddles or kisses caregiver).
© OCP Paediatrics, L&D and BKL 2023 © OCP Paediatrics, L&D and BKL 2023

18 Months 24 Months
Physical & Movement Cognitive Communication/Language Social & Emotional Physical & Movement Cognitive Communication/Language Social & Emotional

e
Give It to m

Mu
aw
!

Walks without holding on to Copies you doing Tries to say three or more words Moves away from you but looks Walks up steps Plays with more than Says at least two words together, Notices when others are hurt or
anyone or anything. chores, like sweeping besides “mama” or “dada”. to make sure caregiver is close. one toy at the same like “More milk”. upset, like pausing or looking
sad when someone is crying.
with a broom. Points to show something Kicks a ball time, like putting toy
Feeds themselves with Follows one-step directions food on a toy plate. Points to at least two body parts
interesting. Looks at caregivers face to see
their fingers. Plays with toys in a without any gestures, like giving when you ask them to show you. how to react in a new situation.
you the toy, when you say, Helps caregiver to dress
simple way, like “Give it to me!” Uses more gestures than just
Climbs on and off a couch pushing a toy car. themselves by pushing arm
through sleeve or lifting up foot. waving and pointing, like blowing
or chair without help a kiss or nodding “YES”.
© OCP Paediatrics, L&D and BKL 2023 © OCP Paediatrics, L&D and BKL 2023

Reprinted with permission from OCP Paediatrics, L&D and BKL


30 Months 36 Months
Physical & Movement Cognitive Communication/Language Social & Emotional Physical & Movement Cognitive Communication/Language Social & Emotional

My
n
is An ame
Duck ton Ruumm
Rummm
Cuac
!

Takes some clothes off by Uses things to pretend, Says two or more words, with Plays next to other children
themselves, like loose like feeding a block to a one action word, like “Doggie and sometimes plays with Puts on some clothes by Draws a circle when Speech all understandable Interactive play
pants or an open jacket. doll as if it were food. run!”. them. themselves, like loose you show them how.
pants or a jacket.
Jumps off the ground with Follows two-step Names things in a book when
both feet. instructions like “Put you point and ask, “What is
the toy down and close this?”.
the door!”.
© OCP Paediatrics, L&D and BKL 2023 © OCP Paediatrics, L&D and BKL 2023

48 Months 60 Months
Physical & Movement Cognitive Communication/Language Social & Emotional Physical & Movement Cognitive Communication/Language Social & Emotional

...an
ok d th
Mama lo .. the en,
af ! ca
at my le ...4. flew t
...3. awa
1...2 y!

Counts to 10.
Pretends to be something
Holds pencil or crayon Draws a person with Talks about at least one thing else during play (teacher, Hops on one foot. Uses words about time, like Tells a story they heard or Follows rules or takes turns
between fingers and three parts that happened during their day, superhero, dog). “yesterday”, “tomorrow” or made up with at least two when playing games with
like “I played soccer!”. other children.
thumb, not a fist. “morning” and “night”. events
Tells what comes next Asks to go play with children, e.g., a cat was stuck in a
if none are around, like ”Can I Sings, dances or acts for you.
Catches a large ball in a well-known story. Answers simple questions like, Pays attention for 5 to 10 tree and a man saved it.
“What is a coat for?” or “What is play with Alex?”.
most of the time. minutes during activities
a crayon for?”.
Names four colours Avoids danger, like not jump (e.g., during story telling time
from tall heights. or making arts and crafts)
© OCP Paediatrics, L&D and BKL 2023 © OCP Paediatrics, L&D and BKL 2023

Reprinted with permission from OCP Paediatrics, L&D and BKL


Appendix 1

431
Appendix 2

Appendix 2. WHO growth charts for children


Full list of growth standards available to download at https://www.who.int/tools/child-growth-
standards/standards.

2.1 Weight for age – girls (birth to 6 months and birth to 5 years)

432
Appendix 2

2.2 Length/height for age – girls (birth to 5 years)

2.3 Head circumference for age – girls (birth to 5 years)

433
Appendix 2

2.4 Weight for age – boys (birth to 6 months and birth to 5 years)

434
Appendix 2

2.5 Length/height for age – boys (birth to 5 years)

2.6 Head circumference for age – boys (birth to 5 years)

435
Appendix 3

Appendix 3. Paediatric vital signs

Respiratory and heart rate


Normal respiratory rate and heart rate for children according to age

Respiratory rate Heart rate


Age
Normal range (breaths/min) Normal range (beats/min)

< 2 months 30-60 100-160

2 to 11 months 30-50 90-160

1 to 5 years 25-40 80-140

6 to 12 years 20-30 70-120

> 12 years 14-20 60-100

Temperature and oxygen saturations


Thresholds for temperature and oxygen saturations for children

Oxygen saturation
Temperature (⁰C)
Normal range %

Location Fever Hypothermia

Axillary > 37.5 < 35 SpO2 ≥ 92%

Core > 38 < 35.5

AVPU
AVPU to assess level of consciousness in childrena

A Alert

V Voice: responds to vocal stimuli

P Pain: responds to painful stimulib

U Unresponsive

a Blantyre and Glasgow Coma Scales can also be used to assess conscious level in children but are more complex
and less useful in emergency situations (see Appendix 13).
b A painful stimulus can be given by applying supra-orbital pressure at the supraorbital notch or by applying
pressure to the nailbed.

436
Appendix 3

AVPU is used for emergency assessment of neurological status as it is a quick and simple tool.
It is used to screen for any deviation from normal level of consciousness. Any score below ‘A’
is abnormal and should prompt a more detailed neurological assessment and evaluation of
conscious level e.g. Glasgow Coma Scale (see Appendix 13). Scores of ‘P’ or ‘U’ indicate coma.

Blood pressure
Normal blood pressure for children according to agec

Blood pressure (mmHg)

Systolic Diastolic
Systolic
Age (50th to 90th (50th to 90th
hypotension
percentile for age) percentile for age)

1 to 11 months 72-104 37-56 < 70

1 to 2 years 86-104 40-61

3 to 5 years 89-108 46-68


< 70 +
(age in years x 2)
6 to 8 years 93-111 55-72

9 years 97-112 59-74

10 to 11 years 98-116 59-75


< 90
12 to 15 years 103-129 61-80

c BP ranges correspond to an average of male and female data for children with height between 25th and
75th centile for age. Data adapted from Tables 4 and 5 of reference:
Flynn JT, Kaelber DC, Baker-Smith CM, et al. Clinical Practice Guideline for Screening and Management of High
Blood Pressure in Children and Adolescents. Pediatrics. 2017;140(3):e20171904.
https://doi.org/10.1542/peds.2017-1904

437
Appendix 4

Appendix 4. Oropharyngeal airway insertion

An oropharyngeal airway can be used in an unconscious child to lift the tongue and pharyngeal
soft tissues off the posterior pharynx to maintain a patent airway.
To choose the correctly sized oral airway, hold it along the side of the child's face with the
flange at the corner of the mouth (Figure 4.1). The tip of the airway should reach the angle of
the mandible. It should be inserted in the same direction as its final position, using a tongue
depressor to push the tongue to the floor of the mouth to avoid pushing the device into the
base of the tongue. Once in place, it allows air to flow into the airway unobstructed (Figure 4.2).

Figure 4.1 - Sizing of oropharyngeal airway

Figure 4.2 - Position and airflow of oropharyngeal airway

438
Appendix 5

Appendix 5. Intraosseous needle insertion


Copied with permission from MSF Manual of Nursing Care Procedures, SOP – Intraosseous
Needle: Insertion.

MSF Library of Nursing Resources

SOP - Intraosseous Needle: Insertion


Refer to the full procedure Intraosseous Needle- Insertion, fixation and maintenance, removal for
rational and additional information on each step
Pre-procedure

1. Perform hand hygiene

2. Confirm the patient’s identity


3. Explain procedure to patient or caregiver in their preferred language and why they require the
procedure and the benefits and risks of receiving it. Allow the patient/caregiver to ask questions and
obtain verbal consent
4. Ensure the patient does not have any known allergies to medications

5. Provide privacy

6. Perform hand hygiene


7. Assess the patient and the patient’s limbs to determine:
a. what location to use
b. what size of intraosseous needle to use

In adults there are three appropriate


insertion sites: the proximal humerus,
proximal tibia and distal tibia.

In neonatal/paediatric patients, there are


three appropriate insertion sites; the
proximal tibia (preferred), the distal tibia and
the distal femur.
In newborns, an umbilical line should be first
attempted.
8. Perform hand hygiene

9. Clean/disinfect tray/trolley and intraosseous drill and allow to dry


10. Gather remaining equipment on dry tray/trolley:
a. For drill insertion:
i. Intraosseous drill
ii. EZ-IO intraosseous needle
The EZ-IO drill has 2 needle sizes:
paediatric : 15 mm long, pink (3 kg to 39 kg)
paediatric and adult : 25 mm long, blue (more than 39kg)
iii. L-shaped EZ-CONNECT extension tubing for motorized insertion
iv. EZ-IO stabilizing dressing for motorized insertion
v. Non-sterile gloves
b. OR for manual insertion:
i. Intraosseous needle with trocar for manual insertion
ii. Extension tubing for manual insertion
iii. Sterile gauze and clear adhesive
iv. Sterile gloves
c. Flush(s):
i. 0.9% sodium chloride
ii. 19G needle(s)
Intraosseous Needle: Insertion_SOP_v1.0-2021 1

439
Appendix 5

MSF Library of Nursing Resources


iii. 10ml syringe(s)
d. 5ml syringe to attempt aspiration
e. 5ml syringe if drawing blood
f. Antiseptic skin solution
g. Alcohol-based hand rub
h. Detergent/disinfectant for surfaces
i. Sharps container
j. Waste bin(s)
11. Obtain assistance if needed

Procedure

12. Perform hand hygiene


13. Using a non-touch technique, draw up 10ml of 0.9% sodium chloride into the syringe
Prime the appropriate extension tubing with 0.9% sodium chloride.
Leave the syringe attached to the extension tubing and place on general aseptic field
14. If using a drill, using a non-touch technique, connect the needle set to the driver on the powered drill,
leaving the needle cap on until ready to insert
15. Relocate the insertion site of the needle by palpating the anatomical landmarks
16. Perform hand hygiene
a. For drill insertion: apply non-sterile gloves
b. For manual insertion: apply sterile gloves
17. Disinfect the skin in a back and forth, up and down movement for 30 seconds with appropriate
antiseptic. ALLOW TO AIR DRY
Do NOT re-palpate the area for insertion
18. Stabilize the limb of the insertion site
19. Remove the needle cap and identify the black needle markings

The needle needs to be long enough so that the distal


mark on the needle is visible once the needle is inserted
into the skin.

20. Place the needle at a 90° angle from the bone and
insert the intraosseous needle with a rotating
mechanism through the skin/subcutaneous
tissue until bone is reached.
Then STOP

Intraosseous Needle: Insertion_SOP_v1.0-2021 2

440
Appendix 5

MSF Library of Nursing Resources


21. If using a drill:
Press the driver trigger whilst applying minimal pressure, driving
through the bone until a ‘give’ is heard or felt

Release the driver trigger when the proximal mark on the


needle is level with the skin

Remove the power driver from the needle set while


stabilizing the needle hub
22. If using a manual intraosseous needle:
Elevate elbow so that it is in line with the needle and
grasp the needle in the palm of the dominant hand, index and
middle fingers approximately 2 cm from the tip.

Ensure the bevel is facing towards the foot.

Use a screwing motion applying steady downward

Pressure perpendicular to bone but slightly away from the


physeal (or growth) plate and advance the needle into
the bone until a ‘give’ is heard or felt
23. Remove the stylet by holding the plastic base
of the needle hub with one hand whilst turning
the upper part of the needle counter clockwise.

The catheter should feel secure in the bone.

24. Safely discard of stylet in a sharps container


25. Using a non-touch technique, connect the 5ml syringe and aspirate 0.5-1ml of bone marrow.
If needed, withdraw blood for blood sampling.
Disconnect the 5ml syringe and attach 10ml syringe primed with 0.9% sodium chloride.
26. Flush with 1-2 mL of 0.9% of sodium chloride. If no tissue swelling observed flush with 0.9% of sodium
chloride:
• 3ml in neonates
• 5-10ml in paediatrics
• 10 ml in adults
27. Disconnect the 10ml syringe access as needed using a non-touch technique
28. Clean and dry surrounding skin, if bloody or wet from insertion, then
apply a stabilizing dressing with a transparent adhesive
using a non-touch technique

CAUTION: The stabilizer dressing must be applied


before the extension set. The stabilizer dressing will
not fit over the extension line.

Intraosseous Needle: Insertion_SOP_v1.0-2021 3

441
Appendix 5

MSF Library of Nursing Resources


Post-procedure
29. Ensure all sharps are disposed of in a safety box and other waste disposed of correctly according to
local procedures
30. Remove gloves and clean/disinfect tray/trolley and motorized drill, if used

31. Perform hand hygiene


32. Document in the patient’s file:
a. date and time of insertion,
The intraosseous vascular access can only remain in site for a maximum of 24 hours or for 8
hours in neonates. It is recommended to write the date and time of insertion on the dressing
for appropriate monitoring of the site.
b. size and length of the needle,
c. number of attempts,
d. location of the device,
e. whether it was a manual or drill insertion
f. the name of the healthcare worker who inserted the needle

Intraosseous Needle: Insertion_SOP_v1.0-2021

Intraosseous Needle: Insertion_SOP_v1.0-2021 4

442
Appendix 6

Appendix 6. Performing a lumbar puncture

A lumbar puncture (LP) is a relatively simple and safe procedure, but it is frightening for most
children and their parents/carers. Be sure to explain the procedure and urgent indications to
the parent/carer and provide reassurance to both the child and parents/carers.
LP is indicated to confirm a diagnosis of meningitis or encephalitis and should only be performed
if a laboratory is available and capable of analysing any cerebrospinal fluid (CSF) collected for
microscopy and biochemistry as a minimum. If available, culture and GeneXpert should also
be performed. LP should only be carried out by a clinician trained to do so.
Treatment with antibiotics should not be delayed in order to perform an LP. Ideally an LP
should be performed before antibiotic administration but if there are any contraindications
or if performing the procedure is likely to delay antibiotic administration by more than 30
minutes, administer antibiotics first. Results of an LP performed up to 2-3 days after antibiotic
administration can still be useful.

Contraindications
Ensure that there are no contraindications to LP and that consent has been obtained from the
patient or parent/carer.
Contraindications to LP are:
– Severe cardiopulmonary instability that potentially requires prompt resuscitation measures
(e.g. shock)
– Obvious signs of increased intracranial pressure (ICP), other than bulging fontanelle:
decerebrate or decorticate posturing, absent doll’s eye reflex, abnormal respiratory pattern,
unequal pupil size or dilatation of pupils
– Focal neurological signs
– Focal seizures or seizures within the last 30 minutes
– Bradycardia, hypertension
– Obvious bleeding disorder and/or low platelet count (< 80 000 platelets/microlitre)
– Skin infection over the site for LP

Equipment
You will need two people to perform this procedure – one trained clinician to carry out the LP,
and one assistant to hold the child in the correct position.
Equipment includes:
– Spinal needle for LP, 22 G (0.7 x 40 mm)
– Antiseptic solution for skin
– Sterile gloves
– Surgical mask
– 4 x 4 sterile compresses
– Lidocaine 1% (without epinephrine)
– Tubes for collection of CSF (non-sterile red-top blood tubes can be used if you are not
obtaining a CSF culture).

443
Appendix 6

Analgesia and anaesthesia


Give prophylactic analgesia before carrying out a lumbar puncture, which can be a painful
and uncomfortable procedure. Non-pharmacological measures should be used for all children,
regardless of age, in addition to analgesia. Local anaesthesia should be used in children older
than 3 months to numb the area e.g., lidocaine. If the LP is planned and non-emergent, local
anaesthetic cream e.g. EMLA can be used, if available. See Chapter 15, Section 15.4.6 for
details of pre-procedure analgesia.

Positioning
The most important determinant of a successful lumbar puncture is how well the child is held.
Ensure that the child is held firmly enough to keep them still but comfortable. The spine should
be curled as much as possible to open the vertebral spaces, with attention to avoid over-
flexion of the neck which can cause respiratory compromise. Watch the patient carefully to
ensure that their breathing remains regular and calm. Monitor oxygen saturations throughout
the procedure.
Young children should be held lying down (Figure 6.1), while an older child can be held either
lying down or sitting up (Figure 6.2). Feel for the posterior-superior iliac crests on each side
and visualise an imaginary line running between the iliac crests – this line intersects the spine
at approximately the fourth lumbar vertebrae (L4). Feel for the intervertebral spaces of L3-4
and L4-5 and mark the chosen space by pressing the fingernail lightly into the skin overlying
the space to leave a small indentation.
Figure 6.1 - Positioning and holding a child on their side for LP

Figure 6.2 - Positioning and holding an older child sitting up for an LP

444
Appendix 6

Procedure
Wash and disinfect your hands with an alcohol-based solution. Put on sterile gloves and take
standard precautions. Disinfect the insertion site in a large circular motion from centre to
periphery using antiseptic solution. Carefully palpate again the chosen intravertebral space
(either L3-4 or L4-5) without touching any non-sterilised skin. Administer local anaesthetic
(see Chapter 15, Section 15.4.6).
Needle insertion and CSF collection
– Hold the needle in your dominant hand.
– Advance the needle slowly through the spinous ligaments, aiming slightly towards the
umbilicus (see Figure 6.3).
– Once a slight “pop” is felt, remove the stylet slowly.
– Place the stylet on a sterile surface for later reinsertion.
– Let CSF drip out slowly and collect 1–2 mL, according to laboratory capabilities.
– If no CSF comes out, rotate the needle slowly; if there still is no CSF, reinsert the stylet and
advance very slowly (1 mm) and repeat the procedure.
– Note the pressure, colour, and clarity of the CSF flow.
– Once CSF has been collected, replace the stylet prior to removing the needle.
– Apply compression to the area and apply a small protective dressing.
Figure 6.3 - Needle insertion for LP

Monitoring
Monitor the child for 1–3 hours post-procedure. Vital signs, including AVPU, should be taken
immediately post-procedure and then as often as required using an early warning system
(see MSF Manual of Nursing Care Procedures, Assessment and vital signs, Charts: Vital sign
charts). Ensure the sterile dressing is in place, clean and intact. The dressing should stay on
at least for 48 hours. The child should lie down for few hours after the procedure, then can
remain in a position of comfort. They should not be too active (no running, jumping, dancing,
excitement), but movement is not limited. Advise the parent/carer to call for help if any of
the following occur: fever, altered level of consciousness or abnormal behaviour, headache,
nausea/vomiting.

Complications of lumbar puncture


– Headache: most common, minimised by having the child lie down after the procedure.
– Cerebral herniation: most serious complication, it can occur when LP is performed in a
patient with raised ICP. Most cases occur within the first 12 hours after LP.
– Infection: meningitis can be induced if the LP is performed through a soft tissue infection at
the site of puncture or if unsterile equipment/procedure is used.

445
Appendix 7

Appendix 7. Clinical Respiratory Score (CRS)

The Clinical Respiratory Score (CRS) is a simple scoring system that can be used to guide
the assessment of respiratory distress and response to treatment. Based on the total score
obtained, the child can be classified as having mild, moderate or severe respiratory distress.

Clinical Respiratory Score (CRS)1,2

Assess Score 0 Score 1 Score 2

Respiratory rate Age < 2 months: < 50 Age < 2 months: 50-60 Age < 2 months: > 60
(breaths/minute) Age 2-11 months: < 40 Age 2-11 months: 40-50 Age 2-11 months: > 50
Age 1-5 years: < 30 Age 1-5 years: 30-40 Age 1-5 years: > 40
Age > 5 years: < 20 Age > 5 years: 20-30 Age > 5 years: > 30

Auscultation Good air movement, Depressed air movement Diminished or absent


expiratory scattered inspiratory and expiratory breath sounds, severe
wheezing or loose rales/ wheezes or rales/crackles wheezing or rales/
crackles crackles or marked
prolonged expiration

Use of accessory Mild to no use of Moderate intercostal Severe intercostal and


muscles accessory muscles, retractions, mild to subcostal retractions,
mild to no retractions moderate use of nasal flaring
or nasal flaring on accessory muscles, nasal
inspiration flaring

Mental status Normal to mildly Irritable, agitated, restless Lethargic


irritable

Room air SpO2 > 95% 90-95% < 90%

Colour Normal Pale to normal Cyanotic, dusky

Based on the total score obtained, 3 categories of respiratory distress are possible:
Mild (≤ 3), Moderate (4-7), Severe (8-12)

1. Nayani K, Naeem R, Munir O, et al. The clinical respiratory score predicts paediatric critical care disposition in
children with respiratory distress presenting to the emergency department. BMC Pediatr. 2018;18(1):339.
https://doi.org/10.1186/s12887-018-1317-2
2. Asthma/Recurrent Wheezing Clinical Guideline | Clinical Standards | Texas Children’s Hospital. Texas Children’s
Hospital. Published January 2019. Accessed November 20, 2023.
https://www.texaschildrens.org/sites/default/files/uploads/documents/outcomes/standards/AcuteAsthma.
pdf

446
Appendix 8

Appendix 8. Asthma action plan

ASTHMA
ACTION PLAN
all inhalers should
be used
with a SPACER

Your child is in the GIVE THE DAILY MEDICINE


GREEN ZONE if ALL of that has been prescribed:
these are true:
F Beclomethasone OR ______ colour inhaler
_____ puffs twice a day

F Salmeterol OR _______ colour inhaler


• Able to do all their regular ACTIVITIES NORMALLY ____ puffs twice a day
• Has NO SIGNS OF A COLD (congestion, runny nose)
F Budesonide/Formoterol OR _______ colour
• Able to sleep through the night WITHOUT BREATHING inhaler ____ puffs twice a day
PROBLEMS
F Montelukast ___ mg once a day
• Breathing well with NO COUGH OR WHEEZE
F No daily Medications

Your child is in the


YELLOW ZONE if they • Continue to give medications from
green zone
have ANY of these:

• Salbutamol 2 puffs every 4 hours


• COUGHING during the day or night
until better
• SIGNS OF A COLD (congestion, runny nose) (Give up to 4 puffs for older/bigger
• Wheezing or having TROUBLE BREATHING children)

• Complaining of a TIGHT CHEST

• Able to do some but not all of their usual activities


• If no improvement after 1 day
without BREATHING PROBLEMS
go to clinic/hospital

Your child is in
RED ZONE if they have
• Seek medical care immediately
ANY of these: at the clinic/hospital

• BREATHING VERY HARD or fast or with difficulty


• UNABLE TO STOP COUGHING
• NEEDS SALBUTAMOL inhaler treatments more often than
every 4 hours • Give salbutamol treatments 2-4 puffs
• Obvious LOUD WHEEZING (Give up to 4 8 or 10 puffs for severe
symptoms or older/bigger children)
• NOT ABLE TO TALK WELL due to breathing difficulty
as often as needed for relief on the
• NOT ABLE TO DO ANY USUAL ACTIVITIES due to breathing
way to the health facility
difficulty
• They are NOT GETTING BETTER despite use of salbutamol
every 4 hours x 1 day

©MSF Paediatric International Working Group -Sept 2023/Graphic Design:A.Filot

447
Appendix 9

Appendix 9. How to make a spacer with a plastic bottle

Copied with permission from MSF Manual of Nursing Care Procedures, Annex – How to make
a spacer with a plastic bottle.

MSF Manual of Nursing Care Procedures

How to make a spacer with a plastic bottle


Annex n 1 – Medication by inhalation using a spacer

If no commercially produced spacer available within the project, a plastic one can be made from a 500ml plastic
bottle.

• Cut the bottom of the bottle.


• Wash the bottle in a solution of one drop of dishwashing soap in
1 L of potable water to reduce the electrostatic charge within
the plastic spacer. Do NOT rinse and let air dry. Not rinsing
improves medication delivery of the spacer.
• Once air dried, tape the end to make the edges smooth before
applying to the patient’s face.
• Adapt the MDI to the nozzle of the bottle with tape.
• Prior to use, prime the spacer with two puffs of the medication Figure 1: Homemade spacer from 500ml plastic bottle
to be delivered.
Note that plastic spacers have electrostatic charges within the chamber that attract particles and significantly
reduce medication delivery to the lungs.

A very similar process can be followed for producing a plastic spacer with mouthpiece.

• Wash the bottle in a solution of one drop of dishwashing soap in 1 L


of potable water to reduce the electrostatic charge within the
plastic spacer. Do NOT rinse and let air dry. Not rinsing improves
medication delivery of the spacer.
• Once air dried, prepare an opening with the same shape and size of
the MDI connection at the end of the bottle
• Adapt the MDI to the opening with tape. Figure 2: Homemade spacer from 500ml plastic bottle
• Prior to use, prime the spacer with two puffs of the medication
to be delivered.
Note that plastic spacers have electrostatic charges within the chamber that attract particles and significantly reduce
medication delivery to the lungs

Annex 1 – Medication by inhalation using a spacer_v1.0-2020

448
Appendix 10

Appendix 10. Inhaler technique using a spacer

Copied with permission from MSF Manual of Nursing Care Procedures, SOP – Medication
administration by inhalation using a spacer.
MSF Manual of Nursing Care Procedures

Medication administration by inhalation using a spacer


SOP – Please refer to the full procedure for rational and additional information on each step

Pre-procedure

1. Perform hand hygiene

2. Confirm the patient’s identity

3. Explain procedure to patient or caregiver, ensuring the patient/caregiver understands why he/she is
receiving the treatment, the risks and benefits of receiving the medication and what the possible side
effects are. Allow patient/caregiver to ask questions and obtain verbal consent
4. Ensure the patient does not have any known allergies to medications

5. Perform any necessary assessment before administration of medication

6. Perform hand hygiene

7. Clean/disinfect tray/trolley and allow to dry

8. Verify the prescription and ensure:


a. The right patient e. The right date and time
b. The right medication f. The prescription is valid (legible and signed)
c. The right dose and dilution g. The medication has not already been administered
d. The right route h. The medication is appropriate for the patient’s condition
9. Gather equipment on dry tray/trolley:
a. Medication to be administered in an c. Alcohol-based hand rub
inhaler form d. Nurses watch or a clock with a second hand
b. Spacer with face mask OR with mouthpiece e. Waste bin (s)
Procedure

10. Perform hand hygiene

11. Confirm the patient’s identity and check that it matches the medical prescription

12. Position patient upright in a sitting position

13. If necessary, clear the upper airways by asking the patient to blow his/her nose or clearing the
patient’s nose
14. Remove mouthpiece cover from inhaler and shake the inhaler well for 2-5 seconds

15. Insert the inhaler upright into the spacer

16. Ask the patient to create a seal with their mouth over the mouthpiece or ensure that the mask
covers the nose and mouth and apply gently to the face to create a seal
17. Ask the patient to slightly tilt their head backwards while inhaling slowly and deeply. Press down on
the canister to deliver the medication
18. If possible, the patient should hold his/her breath for 10 seconds and then breathe out.
If this is not possible, follow the next step
19. If patient unable to hold breath, instruct the patient to breathe normally for 4-6 breaths

20. If more than one dose/puff is needed, wait 30 seconds while the patient breathes normally, shake
the inhaler and repeat steps 16-19

Medication administration by inhalation using a spacer _v1.0-2020 1 449


Appendix 10

MSF Manual of Nursing Care Procedures


21. If mask used, wipe patient’s face after administration

22. If the medication administered was a corticosteroid, ensure the patient rinses his/her mouth with
water 2 minutes after administration
Post-procedure

23. Perform hand hygiene

24. Take apart the spacer, clean the mouthpiece or facemask and spacer and allow to air dry
25. Document administration and assessment findings in the patient’s file

26. Follow-up patient


27. If the patient is going to be followed as an outpatient, ensure sufficient time for patient education,
(offer appropriate tools and allow the patient/caregiver to ask questions)

Medication administration by inhalation using a spacer_v1.0-2020

Medication administration by inhalation using a spacer _v1.0-2020 2

450
Appendix 11

Appendix 11. Sputum specimen collection in children

Selected relevant parts copied from Appendix 3, MSF Tuberculosis Guidelines.

Appendix 3. Collection, storage, and shipment of respiratory specimens

3.1 Respiratory specimen collection


Staff members (and attendants if necessary) present during sputum collection or collection of
any other respiratory specimen should wear a respirator to prevent bacilli inhalation.
When a patient cannot expectorate spontaneously, respiratory specimens can be obtained
by sputum induction (in children and adults) or by nasopharyngeal or gastric aspiration (in
children only). These procedures must be performed under close medical supervision and only
if the specimen is collected for molecular tests, culture, or genome sequencing.
They should be well explained to the patient and the person accompanying them beforehand.

3.1.4 Sputum induction


Patients should be observed for respiratory distress (including SpO2 monitoring) during the
procedure and for 15 minutes after the procedure. Oxygen must be ready at hand (risk of
bronchospasm).
Equipment
• Gloves
• Labelled sputum container
• Mask and tubing for nebulizer
• Holding chamber (spacer) with masks of different sizes (to be sterilised between each
patient)
• Sterile hypertonic solution of 3 to 6% sodium chloride
• Sterile solution of 0.9% sodium chloride (for the specimen)
• Salbutamol metered dose inhaler
• Pulse oximeter and oxygen
Procedure
Patients should fast for at least 2 hours before the procedure to reduce the risk of vomiting
and aspiration.
• Seat the patient comfortably. For young children, sit upright in an adult’s arms.
• Give the patient the sputum container.
• Administer 200 micrograms (2 puffs) of salbutamol via a holding chamber, 10 minutes before
nebulization.
• Fill the nebulizer with 5 ml of 3 to 6% hypertonic saline solution (sputum inducer).
• Place the nebulizer mask over the patient’s mouth.
• Leave the patient to inhale until the reservoir is empty.
• Encourage the patient to cough and spit at any time if they feel to urge to do so.
• Collect at least 2 ml of sputum and close the container tightly.
• Terminate the procedure if unsuccessful after 15 minutes.

451
Appendix 11

3.1.5 Nasopharyngeal aspiration


Equipment
• Gloves
• Suction catheter (CH6 for children 1-11 months; CH8 for children 1-10 years)
• 50 ml syringe or equipment for electric suction
• Sterile solution of 0.9% sodium chloride
• Labelled collection container
Procedure
Children should fast for at least 2 hours before the procedure to reduce the risk of vomiting
and aspiration.
• Do 1 to 2 minutes of clapping.
• Clean out the nasal cavity with 0.9% sodium chloride.
• Lie the child on their back or side.
• Lubricate the end of the suction catheter.
• Put 2 drops of 0.9% sodium chloride into each nostril.
• Measure the distance from the tip of the nose to the angle of the jaw, which represents the
depth to which the catheter should be inserted. Gently insert the suction catheter to this
depth without applying suction.
• Once the catheter is in the posterior nasopharynx, suction with the 50 ml syringe or the
electric suction devicea and slowly pull out the catheter whilst suctioning.
• Collect 2 to 3 ml of respiratory secretions. If insufficient (< 2 ml), put 2 drops of 0.9% sodium
chloride into each nostril, then suction on the other nostril.
• Close the container tightly.

3.1.6 Gastric aspiration


Equipment
• Gloves
• Nasogastric tube (CH6 for children 1-11 months; CH8 for children 1-10 years)
• 50 ml syringe
• Sterile water
• Labelled collection container
Procedure
Children should fast for 4 to 8 hours before the procedure. The specimen should be collected
early in the morning in order to collect the sputum swallowed during the night.
• Place the child in a half-sitting or sitting position in the adult’s arms.
• Insert a nasogastric tube and check that it is correctly placed.
• Suction with a 50 ml syringe.
• Collect 5 to 10 ml of gastric fluid. If insufficient (< 5 ml), rinse the stomach with 10 ml of
sterile water and suction again.
• Close the container tightly.
• Start culture within 4 hours of collecting the specimen. If there will be more than 4 hours
delay, neutralize with an equal volume of sodium bicarbonate.

a If an electric suction device is used, the suction pressure should be 80-100 mmHg for children 1-11 months;
100-120 mmHg for children 1-10 years.

452
Appendix 12

Appendix 12. WHO rehydration plans A, B and C

WHO Plan A for no dehydration


Give ORS PO, 10 ml/kg after each loose stool to prevent dehydration:
Weight (kg) <5 5 to < 10 10 to 20 > 20
ORS (mL) to be given
50 100 200 300
after each loose stool

WHO Plan B for some dehydration


Give ORS PO, 75 mL/kg over 4 hours:
Weight (kg) <6 6 to < 10 10 to < 12 12 to < 19 19 to < 30
Total ORS (mL)
200-400 400-700 700-900 900-1400 1400-2200
over 4 hours
Volume of ORS
50-100 100-175 175-225 225-350 350-550
per hour (mL/hr)

– In addition, give extra ORS to replace fluids lost with each loose stool according to plan A
(above).
– Reassess degree of dehydration after 4 hours and continue with appropriate treatment plan.
If dehydration has resolved, management with plan A can continue at home.

WHO Plan C for severe dehydration


Administer Ringer lactate IV (alternatively sodium chloride 0.9%), 100 mL/kg over 3 hours (or
over 6 hours if < 12 months) as follows:
First administer 30 mL/kg* Then administer 70 mL/kg
Age
over: over:
< 12 months 1 hour 5 hours
≥ 12 months 30 minutes 2½ hours
* Repeat this volume if radial pulse remains weak or absent.
– As soon as the child is awake, alert, and can tolerate a nasogastric tube or take oral fluids,
start ORS at 5 mL/kg/hour in addition to the ongoing IV fluid resuscitation and encourage
breastfeeding (if relevant).
– In addition, if tolerated, give extra ORS to replace fluids lost with each loose stool according
to plan A (above).
– Assess the degree of dehydration at the end of the fluid resuscitation (3 hours for children,
6 hours for infants). Continue further rehydration according to degree of dehydration
following the appropriate treatment plan (A, B or C).

453
Appendix 13

Appendix 13. Glasgow and Blantyre Coma Scales

13.1 Glasgow Coma Scale


The Glasgow Coma Scale (GCS) is widely used to assess brain injury and neurological status
in children and adults. Young children should be assessed using an adapted version of the
GCS which takes into account their relatively immature verbal and motor developmental level.
There is no universally accepted Paediatric Glasgow Coma Scale and variations exist in practice.
It is generally recommended that children 2 years and younger should use an adapted GCS,
and children 5 years and older should use the conventional adult GCS. For children between
the ages of 2 and 5 years (i.e. 3- and 4-year-olds), either scale can be used depending on their
level of development and verbal abilities.
Both the GCS and Paediatric GCS have a minimum score of 3 and a maximum score of 15. It
is useful to give a score for each criterion as well as the total score e.g. E4 + V3 + M5 = 12/15.
Table 13.1 - Paediatric Glasgow Coma Scale (infants and children ≤ 2 years old)
CRITERIA BEST RESPONSE SCORE
Opens eyes spontaneously 4
Opens eyes in response to speech/noise 3
Eye opening
Opens eyes in response to painful stimulus* 2
response
Does not open eyes 1
TOTAL EYE OPENING SCORE _/4
Coos, babbles, alert 5
Irritable cries, but consolable 4
Cries/wails in response to painful stimulus*, persistently
3
Verbal response irritable
Moans in response to painful stimulus*, inconsolable 2
No verbal response 1
TOTAL VERBAL SCORE _/5
Moves spontaneously and purposefully 6
Withdraws from touch 5
Withdraws from painful stimulus* 4
Motor response Abnormal flexion to painful stimulus* (decorticate response) 3
Extension to painful stimulus* (decerebrate response) 2
No motor response 1
TOTAL MOTOR SCORE _/6
GCS TOTAL SCORE = E__+ V__+ M__ __/15
* A painful stimulus can be given by applying supra-orbital pressure at the supraorbital notch or by applying
pressure to the nailbed.

454
Appendix 13

Table 13.2 - Glasgow Coma Scale


CRITERIA BEST RESPONSE SCORE
Opens eyes spontaneously 4
Opens eyes in response to speech 3
Eye opening
Opens eyes in response to painful stimuli* 2
response
Does not open eyes 1
TOTAL EYE OPENING SCORE _/4
Orientated, words or sentences to usual ability 5
Confused, disorientated, words or sentences less than usual
4
ability

Verbal response Inappropriate words 3


Incomprehensible sounds, moaning 2
No verbal response 1
TOTAL VERBAL SCORE _/5
Obeys commands 6
Localises painful stimuli 5
Flexion withdrawal to painful stimuli* 4
Motor response Abnormal flexion to painful stimuli* (decorticate response) 3
Extension to painful stimuli* (decerebrate response) 2
No motor response 1
TOTAL MOTOR SCORE _/6
GCS TOTAL SCORE = E__+ V__+ M__ __/15
* A painful stimulus can be given by applying supra-orbital pressure at the supraorbital notch or by applying
pressure to the nailbed.

Interpretation of GCS and Paediatric GCS score


Score 13-15 Mild brain injury/insult
Score 9-12 Moderate brain injury/insult
Score 3-8 Severe brain injury/insult.
All patients with a score of ≤ 8 are in a comatose state while those with a score of 3 are in a
deep coma and completely unresponsive.

455
Appendix 13

13.2 Blantyre Coma Scale


The Blantyre Coma Scale is a modification of the original GCS, originally designed to measure
coma in cerebral malaria. It is suitable for use in pre-verbal children and has a minimum score
of 0 and a maximum score of 5.
Table 13.3 - Blantyre Coma Scale
CRITERIA BEST RESPONSE SCORE

Eye opening Watches or follows 1


response Fails to watch or follow 0
Cries appropriately with painful stimulus*, or, if verbal,
2
speaks
Verbal response
Moan or abnormal cry with painful stimulus* 1
No vocal response to painful stimulus* 0
Localises painful stimulus* 2
Motor response Withdraws limb from painful stimulus* 1
No response or inappropriate response 0
TOTAL SCORE __/5
* A painful stimulus can be given by applying supra-orbital pressure at the supraorbital notch or by applying
pressure to the nailbed.

Interpretation of Blantyre Coma Scale score


5 Normal conscious level
3-4 Abnormal conscious level
<3 Coma
0 Deep coma

456
Appendix 14

Appendix 14. Urinary collection procedures

14.1 Midstream urine specimen collection


Copied with permission from MSF Manual of Nursing Care Procedures, SOP – Specimen
Collection: Midstream Urine.

MSF Library of Nursing Resources

SOP - Specimen Collection: Midstream Urine


Refer to the full procedure Specimen Collection – Urine for rational and additional information on
each step
Pre-procedure

1. Perform hand hygiene

2. Confirm the patient’s identity and check that it matches the medical request
3. Explain procedure to patient or caregiver in their preferred language and why they require the
procedure and the benefits and risks of receiving it. Allow the patient/caregiver to ask questions and
obtain verbal consent
4. Obtain a history of the illness

5. Ask whether the patient/caregiver is able to collect the sample on their own

6. Perform hand hygiene

7. Clean/disinfect tray/trolley and bedpan or urinal and allow to dry


8. Gather remaining equipment on dry tray/trolley:
a. Urine collection pot
b. Bedpan or urinal (if no latrine/toilet available)
c. Soap and water or 0.9% sodium chloride
d. Transport bag
e. Non-sterile gloves (if patient requires assistance)
f. PPE (according to risk assessment)
g. Alcohol-based hand rub
h. Detergent/disinfectant for surfaces
i. Waste bin (s)
9. Using a permanent marker, label the sample pot (on the container and not the lid) with:
a. the patient’s name (first and last name)
b. date of birth
c. patient identification number
d. Date and time of collection
Procedure

10. Perform hand hygiene. If patient requires assistance, put on non-sterile gloves and other PPE

11. Ask the patient/caregiver to wash their own hands before urine collection

12. If the patient can do the collection independently, explain the procedure and collection process
13. Allow the patient to use the latrine/toilet. If none are available, provide privacy and give the patient a
bedpan or urinal
14. Retract the foreskin (if patient male) or separate the labia (if patient female) and clean the skin
surrounding the urethral meatus with soap and water or 0.9% sodium chloride
15. Ask the patient to begin voiding first stream of urine into the toilet or bedpan/urinal

457
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MSF Library of Nursing Resources


16. Without interrupting the urine flow, place the urine container into the urine stream

17. Once the urine container is sufficiently full, allow the patient to continue voiding in the latrine/toilet or
bedpan/urinal. Close the urine pot, touching only the outside
18. Allow the patient to perform personal and hand hygiene

19. If needed, transfer the urine from the urine pot into a labelled analysis tube

Post-procedure
20. If excess urine was collected in a bedpan/urinal/pot, dispose of urine correctly in the dirty utility (sluice
room)/toilet or as per local procedure
21. Clean/disinfect tray/trolley, urine pot and bedpan/urinal, if needed

22. Remove non-sterile gloves/PPE and discard. Perform hand hygiene


23. Put sample in a transport bag and ensure the laboratory request is filled by the treating clinician and
completed by healthcare worker collecting the sample
24. Follow local procedure for transportation of specimens to the laboratory
25. Document in the patient’s file:
a. procedure date and time
b. any urine observations
c. volume of urine voided (if collected in bedpan/urinal) and if strict fluid balance is required

Specimen Collection: Midstream Urine_SOP_v1.0-2021

Specimen Collection: Midstream Urine_SOP_V1.0-2021 2

458
Appendix 14

14.2 Urine collection bag


Copied with permission from MSF Manual of Nursing Care Procedures, SOP – Specimen
Collection: Paediatric Urine Collection Bag.

MSF Library of Nursing Resources

SOP - Specimen Collection: Pediatric Urine Collection Bag


Refer to the full procedure Specimen Collection - Urine for rational and additional information on
each step
Pre-procedure

1. Perform hand hygiene

2. Confirm the patient’s identity and check that it matches the medical request
3. Explain procedure to patient or caregiver in their preferred language and why they require the
procedure and the benefits and risks of receiving it. Allow the patient/caregiver to ask questions and
obtain verbal consent.
4. Obtain a history of the illness

5. Provide privacy

6. Perform hand hygiene

7. Clean/disinfect tray/trolley and allow to dry


8. Gather remaining equipment on dry tray/trolley:
a. Non-sterile urine collection pot
b. Urine collection bag (boy, girl or premature)
c. Soap and water or 0.9% sodium chloride
d. Transport bag
e. Non-sterile gloves
f. PPE (according to risk assessment)
g. Alcohol-based hand rub Urine collection bags available in MSF
h. Detergent/disinfectant for surfaces male (left) female (right)
i. Waste bin (s)
9. Using a permanent marker, label the sample pot (on the container and not the lid) with:
a. the patient’s name (first and last name)
b. date of birth
c. patient identification number
d. date and time of collection
Procedure

10. Perform hand hygiene. Apply non-sterile gloves and PPE


11. Retract the foreskin (male) or separate the labia (female). Clean the skin surrounding the urethral
meatus with soap and water or 0.9% sodium chloride and allow to dry.
12. With the help of an assistant, keep the genitals exposed. Unwrap the bag and expose the adhesive on
the bottom half of the urine bag.

Specimen Collection: Pediatric Urine Bag_SOP_V1.0-2021 459


1
Appendix 14

MSF Library of Nursing Resources


13. Apply the adhesive starting between the anus and the genitals and then over the genitals, ensuring
there are no wrinkles.

Reapply nappy to help secure the bag in place.


Post-procedure

14. Ensure waste disposed of correctly according to local procedures

15. Clean/disinfect tray/trolley

16. Remove non-sterile gloves/PPE and discard. Perform hand hygiene.

17. Check every 20-30 minutes if the patient has urinated to obtain fresh sample and avoid overfilling.

18. Once 10-15 ml of urine in the bag, perform hand hygiene and apply non-sterile gloves/PPE

19. Using a non-touch technique, carefully remove the bag from the skin and transfer sample into the
urine pot and close the lid

20. Remove non-sterile gloves/PPE and discard. Perform hand hygiene.


21. Place sample in a transport bag and ensure the laboratory request is filled by the treating clinician and
completed by healthcare worker collecting the sample
22. Follow local procedure for transportation of specimens to the laboratory
23. Document in the patient’s file:
a. procedure date and time
b. any urine observations
c. volume of urine collected, especially if strict fluid balance is required

Specimen Collection: Pediatric Urine Bag_SOP_v1.0-2021

Specimen Collection: Pediatric Urine Bag_SOP_V1.0-2021 2

460
Appendix 14

14.3 In-out catheter specimen collection


Copied with permission from MSF Manual of Nursing Care Procedures, SOP - Intermittent
Urinary Catheterisation.

MSF Library of Nursing Resources

SOP – Intermittent Urinary Catheterization


Refer to the full procedure Urinary Catheterization for rational and additional information on each step

Pre-procedure
1. Perform hand hygiene

2. Confirm the patient’s identity

3. Provide privacy
4. Explain procedure to patient or caregiver in his/her preferred language, including what the urinary catheter
is for, why they require it and the benefits and risks of inserting one. Agree on a stop signal with the patient
that can be used to indicate that he/she wishes to stop the procedure.

Allow the patient/caregiver to ask questions and obtain verbal consent


5. Ensure the patient does not have any allergies (including to latex)
6. Ask the patient to perform peri-urethral cleaning with soap and water independently. If patient unable to
do so, the caregiver or healthcare provider should perform the cleaning
7. Perform hand hygiene

8. Clean/disinfect trolley and allow to air dry


9. Gather equipment and position on BOTTOM shelf of dry trolley
- Sterile urine catheter in appropriate size for patient - Oral sucrose solution (for infants <6 months)
(preferable intermittent nelaton catheter, if not - Sterile gloves
available use a foley catheter without inflating the - Alcohol based hand rub
balloon. ) - Apron (according to risk of exposure)
- Sterile urine collection pot (if needed for analysis) - Waterproof towel or disposable drawsheet)
- Sterile lubricant sachet - Sterile kidney dish
- x2 sterile drapes (1 critical aspetic field on trolley and - Bed pan to collect the urine
1 to cover gential area) - Antiseptic for meatal disinfection
- sterile gauze - Detergent/disinfectant for surfaces
- sterile gallipot - Sims speculum (FGM patients only)
- sterile dressing forceps (if available) - Waste bin (s)

10. Obtain assistance if needed.

Procedure
11. Perform hand hygiene

12. Bring trolley to patient’s bedside and position waste bin

13. Place the sterilie drape on the top shelf of the dry trolley. Using a non-touch technique, open and prepare
the equipment onto the sterile drape.

14. Perform hand hygiene


15. For infants 0-6 months, consider giving oral sucrose solution analgesia 2-3 minutes before the procedure.
16. Assist patient to lie in supine position in bed. Position towel/draw sheet under patient’s buttocks
17. For female patients: have the patient bend their knees, hips flexed and feet resting about 60cms apart

For male patients: the legs can be extended on the bed


18. Using a non-touch technique, apply sterile drapes over genitals & between legs

Intermittent Urinary Catheterization SOP_V1.0_2021 1


461
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19. Apply apron and other PPE according to risk assessment and perform hand hygiene

20. Apply sterile gloves


21. Open the sterile plastic protective wrapping of the catheter and dip the tip into the small amount of sterile
water or water-based lubricant. Ensure the catheter remains sterile by only placing it on sterile surface or
sterile kidney basin.
22. For female patients: with the non-dominant hand, spread the labia minora so that the urethral meatus is
visualized. This hand will remain here throughout the rest of the procedure

For male patients: with the non-dominant hand, lift the penis at a 60-90° angle and retract the foreskin (if
present). This hand will remain here throughout the rest of the procedure
23. Using a non-touch technique, use the dominant hand to disinfect the insertion site with the appropriate
antiseptic and sterile gauze. If available, use sterile forceps
24. Place the open end of the catheter inside the sterile kidney dish and place the sterile kidney dish between
the patients legs, holding the tip of the catheter to remain sterile
25. For female patients: using the dominant hand introduce the tip of the catheter into the urethra in an
upward and backward direction. Advance the catheter until urine drains and then advance another 6-8cm

For male patients: with the non-dominant hand holding the penis firmly at a 60-90° angle, insert the tip of
the catheter into the urethra and slowly advance the catheter. Once urine flows, advance catheter another
6-8 cm. If resistance is felt at the external sphincter, pause for 10-20 seconds and instruct the patient to
breathe deeply and evenly. Increase the traction on the penis slightly and apply steady, gentle pressure on
the catheter while the patient exhales or while giving a cough
26. If no urine flows, or resistance is still felt, stop the procedure, remove catheter and discard. Re- attempt
with a new sterile catheter that has been lubricated as above.
27. Use the bed pan to collect large amounts of urine from the bladder
28. If collecting urine for laboratory analysis, use sterile collection pot and obtain sample from the end of
catheter
29. Note the colour, odour, clarity and quantity of urine drained into the kidney dish

30. Once urine flow stops, gently remove the catheter

Post-procedure
31. Remove towel/draw sheet, assist patient to replace underwear or gown over genitals and ensure the bed
linen is not soiled (if soiled or wet, replace with clean dry linen)
32. Ensure waste is disposed of according to local procedure.
Remove sterile gloves and PPE, discard single-use items.
33. Perform hand hygiene

34. Clean/disinfect trolley

35. Perform hand hygiene


36. Document the procedure in the patients file detailing:
- Date/time of intermittent cathereterization - Quality (colour, odour, clarity) and quantity of urine drained
- Type and size of the catheter used at insertion
- Any difficulties during insertion - Name of nurse/clinican

37. Follow-up as required with clinical team.


Inform the patient/caregiver to notify when the first urine is passed after catheterisation

Intermittent Urinary Catheterization_SOP_v1.0-2021


Intermittent Urinary Catheterization SOP_V1.0_2021 2

462
Appendix 15

Appendix 15. Suprapubic aspiration of urine

Suprapubic bladder aspiration (SPA) is a safe and effective method for obtaining urine specimens
in infants and children younger than 2 years when a urinary tract infection is suspected. It is
the most reliable way to obtain an uncontaminated urine sample for culture and avoids delay
in administration of antibiotics for unwell febrile children while awaiting a clean-catch sample.
SPA should be performed by an experienced clinician who is trained in the procedure, ideally
with the support of ultrasound to maximise success.

Contraindications
Ensure that there are no contraindications to SPA and that consent has been obtained from
the patient or parent/carer.
Contraindications to SPA are:
– Obvious or unexplained bleeding disorder
– Abdominal distension
– Massive organomegaly
– Skin infection over the site for SPA

Equipment
You will need two people to perform this procedure – one trained clinician to carry out the
SPA, and one assistant to hold the child in the correct position.
Equipment includes:
– 22G or 23G needle
– 3 mL or 5 mL syringe
– Antiseptic solution for skin
– Sterile gloves
– 4 x 4 sterile compress
– Urine specimen pot
– POCUS machine, if available and staff trained in its use

Analgesia and anaesthesia


Non-pharmacological measures should be used for all children, regardless of age, prior to and
during the procedure. If the SPA is not urgent, local anaesthetic cream e.g. EMLA can be used,
if available. See Chapter 15, Section 15.4.6 for details.

Preparation
To ensure maximum success, ensure that the child has not urinated in the last 30 minutes.
If they have, give fluids (water by mouth or IV maintenance fluids if unable to drink, see
Chapter 15, Section 15.2) and wait 30 minutes before performing the procedure. Check that
the bladder is dull to percussion before starting the procedure or use POCUS, if available, to
confirm that the bladder is full. If the bladder is empty, SPA is not recommended.

463
Appendix 15

Position
With the child in the supine position, use one arm to hold the legs extended in a frog-leg
position and the other on the upper abdomen/torso to keep the child still. Only get the child
into position and remove the nappy immediately before the procedure to avoid stimulating
urination. Occlude the urethral opening just before needle insertion because the procedure
will stimulate urination in many children.

Procedure
– Identify the puncture site by visualising a line between the umbilicus (belly button) and
pubic symphysis. The site for needle insertion is in the midline, about 1-2 cm above the
pubic symphysis, approximately at the lower abdominal crease (see Figure 15.1).
Figure 15.1 - Landmarks to identify needle insertion site

– Wash and disinfect your hands with an alcohol-based solution.


– Put on sterile gloves and take standard precautions.
– Disinfect the abdomen around the insertion site in a large circular motion from centre to
periphery using antiseptic solution.
– Attach a 22G or 23G needle to a 3 mL or 5 mL syringe.
– Angle the needle 10 to 20 degrees towards the head, keeping it perpendicular to the skin
(see Figure 15.2).
– Insert the needle into the skin using a quick puncture motion.
– Advance the needle while pulling the plunger of the syringe, creating suction in the syringe
to aspirate urine as soon as the bladder is reached.
– If urine is obtained, remove needle and place sample in urine specimen collection pot.
– If unsuccessful, partially withdraw the needle to just below the skin and angle slightly more
perpendicular to the frontal plane before advancing the needle under suction again.
– Do not repeat this manoeuvre more than once if unsuccessful.

464
Appendix 15

Figure 15.2 - Needle insertion

Post-procedure care
– Apply a light dressing to cover the puncture site.
– No specific post-procedure care is required.

Complications
– Microscopic haematuria is common and not a concern.
– Rare complications include bladder haematoma, macroscopic haematuria, bladder
haemorrhage, intestinal perforation.

465
Appendix 16

Appendix 16. Body surface area estimation in children

Body surface area can be estimated based on weight alone using the following tables,
reproduced from reference1.

Body weight Surface area Body weight Surface area Body weight Surface area
(kg) (m2) (kg) (m2) (kg) (m2)
2 0.16 17 0.71 40 1.3
2.5 0.19 18 0.74 41 1.3
3 0.21 19 0.77 42 1.3
3.5 0.24 20 0.79 43 1.3
4 0.26 21 0.82 44 1.4
4.5 0.28 22 0.85 45 1.4
5 0.3 23 0.87 46 1.4
5.5 0.32 24 0.9 47 1.4
6 0.34 25 0.92 48 1.4
6.5 0.36 26 0.95 49 1.5
7 0.38 27 0.97 50 1.5
7.5 0.4 28 1.0 51 1.5
8 0.42 29 1.0 52 1.5
8.5 0.44 30 1.1 53 1.5
9 0.46 31 1.1 54 1.6
9.5 0.47 32 1.1 55 1.6
10 0.49 33 1.1 56 1.6
11 0.53 34 1.1 57 1.6
12 0.56 35 1.2 58 1.6
13 0.59 36 1.2 59 1.7
14 0.62 37 1.2 60 1.7
15 0.65 38 1.2
16 0.68 39 1.3

Values calculated using the Boyd equation.


The same calculations and tables are used in the British National Formulary for Children (BNFC).

1. Sharkey I, Boddy AV, Wallace H, et al. Body surface area estimation in children using weight alone: application
in paediatric oncology. Chemotherapy Standardisation group of the United Kingdom Children’s Cancer Study
Group. Br J Cancer. 2001;85(1):23-28.
https://doi.org/10.1054/bjoc.2001.1859

466
Appendix 17

Appendix 17. Blood pressure centiles for age1

Reproduced with permission from:


1. Coulthard MG. Single blood pressure chart for children up to 13 years to improve the recognition of hypertension
based on existing normative data. Arch Dis Child. 2020;105(8):778-783.
https://doi.org/10.1136/archdischild-2019-317993

467
Appendix 18

Appendix 18. F-75 feed volumes in Phase 1

Copied with permission from MSF ITFC Nutritional Care Protocol 2021, Children 1-59 months:
ANNEXInpatient,
5 – QU ICK158.
page TABLE: CALCULATING AMOUNTS OF F-75 IN PHASE 1

Nutritional Care Protocol – Children 1-59 months – Inpatient – MSF June 2021 158
468
Appendix 19

Appendix 19. ARV prophylaxis in PMTCT

Adapted from MSF Prevention of mother to child transmission of HIV guidelines.

19.1 Low-risk HIV-exposed infants


Low risk infants are infants whose mothers:
– Have been on successful ART for more than 4 weeks prior to deliverya.
Start nevirapine (NVP) syrup once daily as soon as possible after birth for 6 weeks (see
Table 19.1).
Table 19.1 - Daily ARV prophylaxis for low-risk neonates and infants

Birth weight NVP syrup (10 mg/mL)

≥ 1.5 to < 2 kg and ≥ 35 weeks GA 2 mg/kg once daily

2 to < 2.5 kg 10 mg once daily

≥ 2.5 kg 15 mg once daily

19.2 High-risk HIV-exposed infants


High-risk infants include infants whose mothers:
– Have received less than 4 weeks of ART at the time of delivery, or
– Are on ART but with recorded antenatal viral load of > 1000 copies/mL at delivery, or
– Have incidental HIV infection during pregnancy or breastfeedingb, or
– Were first identified as HIV-positive at delivery, or
– Were first identified during the breastfeeding period with or without a negative HIV test
during pregnancy.
Start combination ARV prophylaxis as soon as possible after birth.

Simplified ARV prophylaxis regimen for high-risk neonates and infants


The simplified regimen should be used unless national protocols recommend the standard
WHO ARV prophylaxis regimen (see below). From birth to 6 weeks, give one quarter of
AZT/3TC/NVPc fixed dose combination (FDC) dispersible tablet two times daily. Teach the
parents/carer how to use a cutter to obtain 4 equal parts.
At 6 weeks, switch to AZT 60 mg/3TC 30 mg dispersible tablet: 1 tab two times daily plus NVP
50 mg dispersible tablet: ½ tablet once daily, or NVP alone for 6 weeks (see also Table 19.2).

a Treatment success is best defined by maternal viral load < 1000 copies/mL during the last 6 months of
pregnancy, at delivery and during breastfeeding.
b Defined as a new HIV diagnosis in a pregnant or breastfeeding woman with a previous negative test during
pregnancy.
c AZT = zidovudine; 3TC = lamivudine; NVP = nevirapine.

469
Appendix 19

Table 19.2 - Simplified ARV prophylaxis for high-risk neonates and infantsd
Age Simplified prophylaxis for high-risk neonate and infant
AZT 60 mg/3TC 30 mg/NVP 50 mg:
Birth to 6 weeks
¼ tab, two times daily
AZT 60 mg/3TC 30 mg: Plus NVP 50 mg:
> 6 to 12 weeks 1 tab, two times daily ½ tab, once daily
Or NVP 50 mg alone: ½ tab, once daily

Standard WHO recommended (2016) ARV prophylaxis regimen for high-risk neonates
To be used if part of the national recommendation. Where available, give NVP and AZT
combined regimen from birth to 12 weeks. Adjust dose according to birth weight for LBW
neonates receiving ARV prophylaxis at or around birth (see Table 19.3).
Table 19.3 - WHO recommended ARV prophylaxis for high-risk neonates and infants
NVP 10 mg/mL syrup AZT 10 mg/mL syrup
Birth weight or age
or 50 mg tablet or 60 mg tablet
≥ 1.5 to < 2 kg 2 mg/kg*, 4 mg/kg*,
and ≥ 35 weeks GAe once daily two times daily
1 mL syrup, 1 mL syrup,
≥ 2 to < 2.5 kg
once daily two times daily
≥ 2.5 kg 1.5 mL syrup, 1.5 mL syrup,
Birth to 6 weeks once daily two times daily
½ tab or 2 mL syrup, 1 tab,
> 6 to 12 weeks once daily two times daily
Or NVP alone, according to weight
* For low birthweight (LBW) neonates, the dose is expressed in mg/kg in order to be very precise (less than 1 mL).

– If this is too complicated for the mother, choose the simplified regimen above.
– If appropriate formulations are not available, give NVP alone from birth to 12 weeks.
In addition, for all HIV-exposed neonates and infants start cotrimoxazole prophylaxis from
4 to 6 weeks of age and continue until HIV infection has been excluded (see Chapter 13,
Section 13.4.4).

d This simplified prophylactic regimen has not been formerly evaluated yet but has been discussed with WHO
experts who recognize the importance of simplicity for success.
e Note: Very preterm neonates will need further reduced doses.

470
Appendix 20. Causes of fever of unknown origin (FUO)

Table 20.1 - Typical pathogens causing FUO according to clinical diagnosis. Adapted from reference1
Infectious causes
Clinical diagnosis Non-infectious causes
Bacterial Viral Parasitic Fungal
Systemic; sepsis; shock Gram-positive: S. pyogens, Dengue, HIV, VHF Malaria HLH
S. aureus, Pneumococcus. MAS
Gram-negative: N. meningitidis, Acute leukaemia/
enteric Gram-negatives, lymphoma
Pseudomonas spp. Neuroblastoma
Rickettsial agents (RMSF, Drug fever
Ehrlichiosis) Lupus
Meningitis; Leptospirosis, M. tuberculosis, Lymphocytic Naegleria spp., Cryptococcus, Ruptured
parameningeal C. tetani choriomeningitis, HIV Baylisascaris, coccidiodomyses, craniopharyngioma
infection (mastoiditis, Trypanosoma brucei histoplasma, IVIG use
subdural/epidural gambiense or blastomyces NSAID use
abscess) rhodesiense
Cervical lymphade- Non-group A Streptococcus: EBV, CMV, HIV, Toxoplasmosis, Kikuchi-Fujimoto
nopathy (predominant); Groups C and G Adenovirus African and American disease
pharyngitis/tonsillitis; Arcanobacterium; trypanosomiasis HLH
peritonsillar or Fusobacterium, other Kawasaki disease
parapharyngeal abscess anaerobes ALPS
Endocarditis; HACEK bacteria, Bartonella, American Kawasaki disease
pericarditis; peripheral Coxiella, Legionella, CONS, trypanosomiasis Rheumatic disease
venous infection Streptobacillus, Enterococci, PAN
enteric gram-negative bacteria, Postinfectious
S. aureus, pyogenic organisms, SLE
Mycobacteria
Appendix 20

471
472
Infectious causes
Clinical diagnosis Non-infectious causes
Bacterial Viral Parasitic Fungal
Appendix 20

Pneumonitis Legionella, Nocardia, HIV, measles Blastomyces, Sarcoid


C. pneumoniae or C. psittaci; Histoplasma, Wegener syndrome
P. jiroveci, M. tuberculosis Cryptococcus, Aspiration
Coccidiodomyces, Foreign body
Aspergillus, Mucor Sequestered lobe
Hepatitis; Bartonella, Leptospira, Borrelia, Hepatitis B, C, E, EBV, Toxoplasmosis, Histoplasma, Cholecystitis/cholangitis
hepatomegaly; CMV, HSV, HIV, Lassa Malaria, Visceral Candida IBD
splenomegaly Leishmaniasis, Autoimmune hepatitis
Schistosomiasis, Drug hypersensitivity
Q fever
Gastroenteritis; peri- S. typhi, Yersinia, C. difficile, Adenovirus Giardia, IBD
appendiceal or pelvic E. coli, Brucella, Aeromonas Cryptosporidium, Pancreatitis
abscess; pyelonephritis; Mycobacterial: M. bovis and Entamoeba
renal abscess tuberculosis, S. hominis,
anaerobes
Osteomyelitis; Group B Streptococcus, Influenza A and B Dengue, Chikungunya Rheumatic disease, JIA
pyomyositis; myositis K. kingae, Salmonella spp., Histiocytosis
M. tuberculosis, S. aureus, Ankylosing spondylitis
gram-negative enteric agents Relapsing multifocal
osteomyelitis
Malignancy
Skin infections Streptobacillus, S. aureus, HIV, measles Lupus
(pustular, necrotic, Pseudomonas spp., JIA
bullous); eruptions N. meningitidis, Group A Kawasaki disease
Streptococcus, Rickettsiosis IBD

Abbreviations: VHF, viral hemorrhagic fever; RMSF, Rocky Mountain spotted fever; CONS, coagulase negative staphylococci; HACEK, Haemophilus, Aggregatibacter, Cardiobacterium,
Eikenella, Kingella; HSV, Herpes simplex virus; UTI, Urinary tract infections, ALPS, autoimmune lymphoproliferative syndrome; GABS, Group AB hemolytic Streptococcus; IBD,
Inflammatory bowel disease; HLH, Hemophagocytic Lymphohistiocytosis, MAS, macrophage activation syndrome; IVIG, intravenous immune globulin, NSAID, Non-steroidal anti-
inflammatory drugs, PAN, polyarteritis nodosa, JIA, Juvenile idiopathic arthritis, HIB, Haemophilus influenzae type B.
Table 20.2 - Vector-borne and zoonotic causes of FUO
Epidemiology/
Cause History Clinical findings Laboratory Treatment
exposures
Brucella Sustained fever Worldwide, mainly Hepato- Rose-Bengal test Children < 8 years:
Brucella patterns, night sweats, rural areas animal splenomegaly, and/ (RBT), co-trimoxazole PO, 20 mg/kg
chills, asthenia, joint or animal products or lymphadenopathy mild elevation of SMX (max. 800 mg) + 4 mg TMP/
and muscle pain. (unpasteurized milk/ hepatic enzymes, kg (max. 160 mg), 2 times daily
Osteoarticular pain: cheese, insufficiently lymphocytopenia + rifampicin PO, 15-20 mg/kg
sacroiliitis, arthritis, cooked/raw meat) (max. 600 mg) once daily for
orchitis. 6 weeks (or gentamicin IM,
Meningoencephalitis 5 mg/kg once daily for 2 weeks).
Children ≥ 8 years:
doxycycline PO, 2-2.2 mg/kg
(max. 100 mg) 2 times daily for
6 weeks
+ rifampicin (or gentamicin), as
above.
Leptospirosis Mild form: high Animal urine Relative bradycardia, Thrombocytopenia Mild form:
Leptospira fever, rigors, myalgia, (rodents), bulbar conjunctivitis, Proteinuria doxycycline PO, 2-2.2 mg/kg
headache, anorexia, contaminated soil pharyngeal Pyuria (max. 100 mg) 2 times daily for
abdominal pain, nausea, or water, infected hyperemia Granular casts 7 days.
vomiting, cough, chest animal tissue Alternatively, azithromycin PO,
pain. Chest X- ray: small 10 mg/kg (max. 500 mg) once
Flooding nodular densities on D1, then 5 mg/kg (max.
Severe form (Weil’s 250 mg) once daily on D2
syndrome): onset and D3, especially in children
same as mild + < 8 years old.
acute hepatorenal
manifestations, Severe form:
jaundice, oligo-anuria, ceftriaxone IV, 80-100 mg/kg
purpura, ecchymosis, (max. 2 g) once daily for 7 days.
epistaxis, hemoptysis, Alternatively, benzylpenicillin
myocarditis, pericarditis. IV, 50 000 IU (30 mg)/kg (max.
2 MIU or 1200 mg) every
6 hours for 7 days.
Appendix 20

473
474
Epidemiology/
Cause History Clinical findings Laboratory Treatment
exposures
Appendix 20

Schistosomiasis Acute infection Contaminated water Lymph-node Eosinophilia, Children over 4 years old:
Schistosoma (Katayama fever): enlargement Hematuria praziquantel PO, 40 mg/kg
(haematobium, sudden onset of single dose. Give pre-treatment
mansoni, japonicum) fever, urticaria and prednisolone for 7 days in
angioedema, chills, Katayama fever.
myalgias, arthralgias,
dry cough, diarrhea,
abdominal pain, and
headache.
Borrelia/Relapsing Febrile episodes Body lice, Splenomegaly, Blood smear for doxycycline PO, 4 mg/kg (max.
fever separated by Cold climate/season, bleeding signs, spirochetes 100 mg) single dose
afebrile periods of Overcrowding, jaundice, or
Louse borne
approximately 7 days. Poor sanitation neurological erythromycin PO
(epidemic): Borrelia
symptoms 250 mg single dose (< 5 years
recurrentis High fever, headache, old);
asthenia, diffuse pain, 500 mg single dose (≥ 5 years
anorexia, abdominal old)
pain, vomiting, diarrhea or
azithromycin PO, 10 mg/kg (max.
500 mg) single dose
Borrelia/Relapsing Fever, headache, Temperate/ warm Splenomegaly Blood smear for doxycycline PO, 2-2.2 mg/kg
fever asthenia, muscle regions Hepatomegaly spirochetes, (max. 100 mg) 2 times daily for
and bone pain, Rural areas in SSA Conjunctival CSF analysis for 7-10 days
Tick borne (epidemic):
photophobia, cough hyperemia spirochetes if CNS or
Borrelia duttoni
Cranial nerve palsies, Lymphadenopathy involvement azithromycin PO, 10 mg/kg
meningitis (max. 500 mg) once daily for
7-10 days, especially in children
Fever lasts 3-6 days < 8 years old
and re-appears after or
7-10 days ceftriaxone IV, 50-75 mg/
kg (max. 2 g) once daily for
10-14 days, if CNS involvement
Epidemiology/
Cause History Clinical findings Laboratory Treatment
exposures
Q Fever Flu-like symptoms Contact with farm Minimal auscultatory Elevated liver doxycycline PO, 2-2.2 mg/kg
Coxiella burnetii (fatigue, headache, animals (cattle, abnormalities, enzymes, (max. 100 mg) 2 times daily for
myalgias) with a goats, sheep) Hepatomegaly thrombocytopenia 14 days or
prolonged fever or
(1-3 weeks), Consumption of raw co-trimoxazole PO, 2-10 mg/kg
hepatitis, pneumonia, milk of the trimethoprim component
endocarditis 2 times daily (max. 320 mg/
24 hours) for 14 days (especially
in children < 8 years old)
Amoebic abscess Right upper quadrant More frequent young Hepatomegaly Leukocytosis, tinidazole PO, 50 mg/kg (max.
Entamoeba histolytica pain, fever (38.5 to adults elevated alkaline 2 g) once daily for 5 days
39.5ºC) phosphatase and or
hepatic enzymes metronidazole PO, 15 mg/kg
Cough, sweating, 3 times daily for 5-10 days
malaise, weight loss,
anorexia, and hiccup
Cat scratch disease Cutaneous lesion at Scratch or bite from Regional Nonspecific tests, azithromycin PO, 10 mg/kg
Bartonella henselae the site of inoculation an infected cat, lymphadenopathy, Serology (max. 500 mg) once on D1, then
that evolves through exposure to cat fleas, hepato- 5 mg/kg (max. 250 mg) once
vesicular, erythematous, contact with cat splenomegaly, or daily for 4 days
and papular phases saliva through broken ocular manifestation
with enlarged lymph skin or mucosal
nodes proximal to the surfaces (i.e., mouth
inoculation site. and eyes).
Visceral involvement
(liver, spleen) is rare but
presents with persistent
fever, abdominal pain,
and/or weight loss
Parinaud oculo-
glandular syndrome,
Neuroretinitis,
encephalopathy.
Appendix 20

475
476
Epidemiology/
Cause History Clinical findings Laboratory Treatment
exposures
Appendix 20

African tick bite fever Mild headache, Rural Africa Patients with severe Liver function tests doxycycline PO, 2.2 mg/kg
Rickettsia africae fever, myalgias, infections may have mildly abnormal, (max. 100 mg) 2 times daily for
solitary or multiple neurologic, cardiac, thrombocytopenia 5-7 days (or until 3 days after
eschars with regional ocular, or renal disappearance of fever).
lymphadenopathy complications.
Generalized rash In severe infections, add a
Mediterranean (vesicular or Mediterranean area loading dose of doxycycline PO,
spotted fever maculopapular) 4.4 mg/kg (max. 200 mg) on D1
Ricketssia conorii overlooked or before continuing twice daily
completely absent. dosing as above.
Long-lasting subacute
neuropathy and
myocarditis
Fever, headache,
maculopapular rash
with eschar or black
necrotic scabbed lesion
(tache noire) at the site
of the inoculating tick
bite.

1. Chusid MJ. Fever of Unknown Origin in Childhood. Pediatr Clin North Am. 2017;64(1):205-230.
https://doi.org/10.1016/j.pcl.2016.08.014
Appendix 21

Appendix 21. EVENDOL chart

The EVENDOL behavioural score was developed by a multi-professional group of experts in


child pain, to better identify and assess the intensity of pain in young children, from birth to
7 years of age; studies have validated this scale in emergencies (medical or traumatic), in pre-
hospital medical transport, in post-operative and neonatal care and for newborns in maternity
wards.

A pain scale validated


A pain scale for children from birth
for children to 7 years
under 7 Score ranges from 0 to 15.
Treatment threshold: 4/15.

Note everything you observe, even if you think the symptoms are not due to pain but to fear, tiredness or illness severity.

Analgesic
Name sign sign Following assessments
sign Assessment at admission
moderate strong and/or after analgesic3
sign weak
or present or present
absent or at rest 1 during examination2
about half almost R R R R
transient
the time all the time (R) or mobilization (M) M M M M
Vocal or verbal expression
cries and/or screams and/or moans
0 1 2 3
and/or complains of pain
Facial expression
furrowed forehead and/or frown, furrowed
0 1 2 3
or bulging brow and/or tense mouth
Movements
restlessness, agitation and/or rigidity
0 1 2 3
and/or muscular tenseness
Postures
unusual and/or antalgic posture and/or
0 1 2 3
protection of the painful area and/or immobility
Interaction with the environment
can be comforted and/or interested in normal low very low absent
playing and/or interacts with people 0 1 2 3
Remarks Total /15

Date & Time

Signature
1
At rest (R): observe the child from a distance, before performing any examination or procedure, at rest, ensuring the best possible conditions of safety and comfort, for example with his/her parents, when he/she is playing.
2
During examination or mobilization (M): assess pain during examination or mobilization or palpation of the painful area by nurse or by doctor.
3
Reassess pain regularly after analgesic administration: wait 30 to 45 minutes if analgesic is administered by oral or rectal route, 5 to 10 minutes if administered by IV route. Note whether the child is at rest (R) or mobilized (M).
Pain 2012, 153: 1573-1582. Contact: elisabeth.fournier-charriere@bct.aphp.fr - © 2011 - Evendol Group Graphic design: Zid et Zen communication - zidetzen@club-internet.fr

Reprinted with permission from authors of original paper1. Copyright Evendol Group. More
information at https://pediadol.org/.

Score rating:
– Score 1/15 to 3/15: mild pain
– Score 4/15 to 7/15: moderate pain
– Score 8/15 to 15/15: severe pain

1. Fournier-Charrière E, Tourniaire B, Carbajal R, et al. EVENDOL, a new behavioral pain scale for children ages
0 to 7 years in the emergency department: Design and validation. Pain. 2012;153(8):1573-1582.
https://doi.org/10.1016/J.pain.2012.02.024

477
Appendix 22

Appendix 22. Daily enteral feed volumes and


administration in critically unwell children

The following tables give target daily enteral feed volumes during the acute phase of critical
illness only (up to maximum of 7 days), calculated using the Schofield energy equations which
estimate basal metabolic rate (BMR). All volumes have been rounded for ease of administration.
Enteral feeds using these calculations should only be continued in infants and children who are
unable to eat and drink by mouth, up to a maximum of 7 days. As soon as they improve, feeds
should be increased in infants and children should be commenced on full oral feeds as per
usual diet.

22.1 Infants < 1 year old


a) Target daily enteral feed volumes according to weight in the acute phase of critical illness

Weight Target daily acute phase


Feed
(kg) enteral feed volume (mL)a
3 210
4 295
5 375
Expressed breastmilk/ 6 460
standard infant formula 7 545
8 630
9 715
10 800

b) Titrated administration of 3-hourly feeds in the acute phase of critical illness

Acute phase
Weight 30% of 50% of 70% of Target
Feed
(kg) 3-hourly feed 3-hourly feed 3-hourly feed 3-hourly feed
volume (mL) volume (mL) volume (mL) volume (mL)
3 8 15 18 30
4 12 20 28 40
Expressed 5 15 25 35 50
breastmilk/ 6 18 30 42 60
standard
infant 7 20 35 50 70
formula 8 24 40 56 80
9 28 45 62 90
10 30 50 70 100

a For standard enteral fluid volumes in infants, see Chapter 15, Table 15.16.

478
Appendix 22

22.2 Children 1 to < 3 years old

a) Target daily enteral feed volumes according to weight in the acute phase of critical illness

Weight Target daily acute phase


Feed
(kg) enteral feed volume (mL)

8 440

9 500

10 555

11 620
Isocaloric enteral nutrition
product (1 kcal/mL)/F-100
12 675

13 740

17 790

15 850

b) Titrated administration of 3-hourly feeds in the acute phase of critical illness

Acute phase
Weight
Feed 30% of 50% of 70% of Target
(kg)
3-hourly feed 3-hourly feed 3-hourly feed 3-hourly feed
volume (mL) volume (mL) volume (mL) volume (mL)

8 15 28 40 55

9 20 32 45 65

Isocaloric 10 20 35 50 70
enteral
11 25 40 55 80
nutrition
product
12 25 42 60 85
(1 kcal/mL)/
F-100 13 28 48 65 95

14 30 50 70 100

15 32 52 75 105

479
Appendix 22

22.3 Children 3 to < 10 years old

a) Target daily enteral feed volumes according to weight in the acute phase of critical illness

Target daily acute phase


Weight enteral feed volume (mL)
Feed
(kg)
Male Female

12 775 730

13 800 750

14 825 770
Isocaloric enteral
nutrition product 15 845 790
(1 kcal/mL)/F-100
16-19 900 840

20-24 1000 930

25-30 1125 1050

b) Titrated administration of 3-hourly feeds in the acute phase of critical illness

Acute phase

30% of 50% of 70% of Target


Weight
Feed 3-hourly feed 3-hourly feed 3-hourly feed 3-hourly feed
(kg)
volume (mL) volume (mL) volume (mL) volume (mL)

Male Female Male Female Male Female Male Female

12 30 30 50 45 70 65 95 90

13 30 30 50 50 70 70 100 95
Isocaloric
enteral 14 30 30 55 50 75 70 105 95
nutrition
15 30 30 55 50 75 70 105 100
product
(1 kcal/ 16-19 35 30 60 55 80 75 115 105
mL)/F-100
20-24 40 35 65 60 90 85 125 120

25-30 45 40 70 65 100 90 140 130

480
Appendix 22

22.4 Children 10 to 15 years old

a) Target daily enteral feed volumes according to weight in the acute phase of critical illness

Target daily acute phase


Weight enteral feed volume (mL)
Feed
(kg)
Male Female

25-30 1150 1050

31-35 1240 1130


Isocaloric enteral
nutrition product 36-40 1330 1200
(1 kcal/mL)/F-100
41-45 1420 1270

46-50 1510 1330

b) Titrated administration of 3-hourly feeds in the acute phase of critical illness

Acute phase

30% of 50% of 70% of Target


Weight
Feed 3-hourly feed 3-hourly feed 3-hourly feed 3-hourly feed
(kg)
volume (mL) volume (mL) volume (mL) volume (mL)

Male Female Male Female Male Female Male Female

25-30 45 40 70 65 100 90 145 130


Isocaloric
enteral 31-35 50 40 80 70 110 100 155 140
nutrition
36-40 50 45 85 75 115 105 165 150
product
(1 kcal/ 41-45 55 50 90 80 125 110 180 160
mL)/F-100
46-50 60 50 95 85 135 115 190 165

481
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Fax: +31 (0)20 62 05 170
E-mail: office@amsterdam.msf.org

Spain Medicos Sin Fronteras


Calle Zamora 54, 08005 Barcelona
Tel.: +34 933 046 100
Fax: +34 933 046 102
E-mail: oficina@barcelona.msf.org

Switzerland Médecins Sans Frontières


Route de Ferney 140 - Case postale 1224 - 1211 Genève 1
Tel.: +41 (0)22 849 84 82
E-mail: office-gva@geneva.msf.org

Achevé d’imprimer en France par ISI Print, 93120 La Courneuve


Mars 2024

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