Ministry of Health, State of Kuwait Kuwait Pediatric CouncilCOMMON & EMERGENCY CARE
⬇ Download
·
Front cover: Neonatal & Pediatric Common & Emergency Care Guide. Ministry of Health, State of Kuwait. By pediatricians, for pediatricians. First Edition.
Ministry of Health, State of Kuwait
QR code linking to the electronic versions of this guideScan for the
electronic versions
Kuwait Pediatric Council · Bedside reference

Neonatal & Pediatric
Common & Emergency Care Guide

Version 1.95 · Updated 20 October 2026

A searchable, algorithmic bedside companion for pediatricians and primary care physicians — every medication listed separately with weight‑based dosing, first- to third‑line therapy, and the can't‑miss diagnoses. Tap any topic to open it.

Panel of Reviewers

Kuwait Pediatric Council · 69 reviewers · alphabetical by first name
Dr. Abdulaziz AlosaimiSpecialist, General Pediatrics, Pediatric Cardiology & Critical Care
Dr. Abdulla AlfraijConsultant, General Pediatrics & Pediatric Critical Care
Dr. Abdullah Abd Alhussain Taqi AliConsultant, Pediatric Hematology & Oncology
Dr. Abdullah AlDuwaisanAssistant Professor of Orthopedic Surgery, Kuwait University
Dr. Abdullah RajabConsultant, Adult & Pediatric Surgery
Dr. Aceel AlawadiConsultant, General Pediatrics & Pediatric Pulmonology, LTV and Sleep Medicine
Dr. Ahlam MustafaConsultant in Pediatric Gastroenterology, Hepatology, Endoscopy and Nutrition
Dr. Ahmad AlhajConsultant, General Pediatrics & Pediatric Critical Care
Dr. Ahmad AlmosawiConsultant, General Pediatrics & Pediatric Pulmonology and Critical Care
Dr. Ahmad JaafarSenior Specialist, General Pediatrics & Pediatric Complex and Palliative Care
Dr. Aisha AlTerkaitConsultant, General Pediatrics & Pediatric Nephrology
Dr. Alaa ShehabSenior Specialist, General Pediatrics, Pediatric Rheumatology & Systemic Auto‑inflammatory Disease
Dr. Alya Hasan Askar HasanConsultant, Pediatric Neurosurgery
Dr. Amaar MarefiSpecialist, Pediatric Neurology & Neuroimmunology
Dr. Anfal TaherSenior Specialist, General Pediatrics & Pediatric Emergency
Dr. Basma Al‑TawariSpecialist, General Pediatrics
Dr. Bibi AlamiriConsultant Child and Adolescent Psychiatrist
Dr. Dalal MohammadSpecialist, General Pediatrics & Pediatric Rheumatology
Dr. Dana MarafiAssistant Professor of Pediatrics, Kuwait University; Pediatric Neurology, Epilepsy & Neurogenetics
Dr. Eiman Al‑HashemiSpecialist, General Pediatrics & Pediatric Critical Care
Dr. Eman BuhamrahConsultant, General Pediatrics & Pediatric Gastroenterology and Hepatology
Dr. Esmaeel TaqiConsultant Pediatric Surgery
Dr. Fahed AljaserConsultant, General Pediatrics & Pediatric Endocrinology
Dr. Fajer AltammarSenior Specialist, General Pediatrics, Pediatric Emergency & Pediatric Critical Care
Dr. Fanar FaridounSenior Specialist, General Pediatrics
Dr. Fares AlFaresAssistant Professor of Pediatrics, Kuwait University; General Pediatrics & Pediatric Hematology / Oncology
Dr. Fatemah BukhalafConsultant, General Pediatrics & Adolescent Medicine
Dr. Fatoumah AlabdulrazzaqConsultant, General Pediatrics & Pediatric Emergency; Clinical Pharmacologist & Toxicologist
Dr. Fawaz AlbaghliConsultant, General Pediatrics & Neonatology
Dr. Fawaz AlRefaeeConsultant, General Pediatrics & Pediatric Gastroenterology
Dr. Hanan AlsalehConsultant, Pediatric Ophthalmology
Dr. Hashem AlhashemiConsultant, General Pediatrics & Pediatric Critical Care
Dr. Hessah AlsunaienConsultant, General Pediatrics
Dr. Hussain SadeqSenior Specialist, General Pediatrics
Dr. Ibrahim AlqattanSenior Registrar, General Pediatrics
Dr. Khaled KalandarConsultant, General Pediatrics
Dr. Khalid AlothmanConsultant, General Pediatrics & Pediatric Infectious Diseases
Dr. Lujain AbulSpecialist, General Pediatrics & Pediatric Emergency
Dr. Mariam AyedConsultant, General Pediatrics & Neonatology and Neonatal Neuro‑Critical Care
Dr. Marwan AlqunaeeSenior Specialist, Otorhinolaryngology (ENT)
Dr. Maryam AlhajeriSpecialist, General Pediatrics & Pediatric Nephrology
Dr. Maysoon Al‑MusallamConsultant, General Pediatrics
Dr. Maysoun Al RushoodAssociate Professor of Pediatrics; Consultant, General Pediatrics & Pediatric Allergy and Clinical Immunology
Dr. Meshal AleneziConsultant, General Pediatrics & Pediatric Emergency
Dr. Mohammad AlghounaimConsultant, General Pediatrics & Pediatric Infectious Diseases; Medical Microbiologist
Dr. Mohammad AlHumaidanConsultant, General Pediatrics & Pediatric Emergency
Dr. Moneerah AlbesharahSenior Registrar, General Pediatrics
Dr. Muna AlmutairiConsultant, General Pediatrics & Pediatric Rheumatology
Dr. Munirah AlYaseenSpecialist, General Pediatrics, Pediatric Critical Care & Pediatric Neuro‑Critical Care
Dr. Mustafa AlQbandiConsultant, General Pediatrics & Pediatric Interventional Cardiology
Dr. Osama Shalaby AbdulazizConsultant, General Pediatrics & Pediatric Neurology
Dr. Rasha AlsafiConsultant, General Pediatrics, Clinical Genetics & Metabolic Disorders
Dr. Rashed AlAhmedSpecialist, Orthopedic Surgery; Pediatric & Adult Spine
Dr. Rawan AlFouzanSenior Specialist, General Pediatrics & Pediatric Pulmonology
Dr. Rehab BekhitPractitioner, General Pediatrics & Pediatric Critical Care
Dr. Saadoun Bin‑HasanConsultant, General Pediatrics & Pediatric Pulmonology and Sleep Medicine
Dr. Saleh AlsaifiConsultant Adult & Pediatric Orthopedics
Dr. Samir Mohammed Sanad El MesadyConsultant, Pediatric Emergency Medicine
Dr. Sara AliSpecialist, General Pediatrics
Dr. Sarah AltamimiSenior Registrar, General Pediatrics & Pediatric Critical Care
Dr. Suha AtyaniConsultant, General Pediatrics
Dr. Taiba AlmousawySenior Registrar, General Pediatrics
Dr. Taibah AlansariSenior Registrar, General Pediatrics
Dr. Talal AlsaleemConsultant, General Pediatrics
Dr. Tawa SaharSenior Specialist, Dermatology
Dr. Wafaa LaymounSenior Specialist, General Pediatrics & Pediatric Endocrinology and Diabetes
Dr. Waleed AldeeweliConsultant, Pediatric Dentistry
Dr. Yaqoub JafarSenior Specialist, Pediatric Surgery and Urology
Dr. Zainab MustafaSpecialist, Pediatrics, Neonatology & Neonatal Echocardiography and Haemodynamics
Preparation. This guide was drafted, edited, and formatted with the assistance of an AI‑based large language model used under direct human supervision. The tool was not an author and made no clinical judgments. All clinical recommendations, medication names and doses, diagnostic thresholds, and references were written by the author, checked against the primary sources and current guidelines, and reviewed by the review panel named below; the content is their work, not the AI tool's. Prepared in line with ICMJE guidance on the use of AI‑assisted technologies and with the Ministry of Health Practical Guide for the Use of Language‑based Artificial Intelligence Tools in Healthcare Practice, adopted and published as a guiding framework for staff of all MOH health facilities by Administrative Decision No. 6189 of 2026 of the Undersecretary of the Ministry of Health (issued under Law No. 70/2020 and Ministerial Decision No. 373/2025 on the code of ethics for health‑sector workers).
Author: Dr. Athari Almajed — Consultant, General Pediatrics & Pediatric Pulmonology, LTV and Sleep Medicine.
Reviewers: the review panel named above — reviewed the final version.
The author and reviewers have read this version and support its use as a reference alongside clinical judgment.
Every effort has been made to ensure that the information in this guide is accurate and current at the time of issue. Errors or omissions may nevertheless occur; readers are asked to report them to the address below so that they can be corrected.
Inquiries, input, or corrections: ayalmajed@moh.gov.kw
Conflicts of interest: none declared. Funding: none.
© 2026 Kuwait Pediatric Council. This guide may be reproduced for non‑commercial educational use with attribution.
No matches. Try a different term or clear the filter.

What the colors mean

01 · Resuscitation — cardiopulmonary arrest & the universal approach
02 · Behavioral & Psychiatric — agitation, self‑harm, drug‑induced syndromes
03 · Cardiac & Shock — arrhythmias, all types of shock, hypercyanotic spell
04 · Common Acute Conditions — everyday clinic & ED infections and presentations
05 · Complex & Technology‑Dependent Care — tracheostomy, feeding tubes, ECMO, post‑ICU, transport
06 · Endocrine & Metabolic — diabetes, adrenal, inborn errors, electrolytes
07 · Focused Specialty Emergencies — eye, dental, dermatologic, ENT & neurosurgical
08 · Gastroenterology & Hepatology — liver failure, GI bleeding, pancreatitis, hepatitis, cholestasis
09 · Hematologic & Oncologic — neutropenia, tumor lysis, sickle cell, bleeding
10 · Neonatal — newborn‑specific emergencies
11 · Neurologic — seizures & status epilepticus
12 · Orthopedic & Musculoskeletal — the limping child, SCFE, compartment syndrome, fractures
13 · Pediatric Trauma & TBI — primary/secondary survey, traumatic brain injury
14 · Renal & Urology — AKI, HUS, hypertensive emergency, acute scrotum & testicular torsion
15 · Respiratory, Allergy & Immunology — airway, breathing, anaphylaxis, allergy & immunology
16 · Rheumatologic — cytokine storm (HLH/MAS) & Kawasaki
17 · Surgical Emergencies — recognize, resuscitate, refer
18 · Toxicology & Environmental — poisoning, burns, heat, drowning, smoke inhalation
Each topic also carries an urgency tag showing how fast to act:
MINUTES immediately life‑threatening — act now HOURS urgent — stabilize and treat early ASSESS evaluate and manage on its own pathway
Call vs refer — in a hospital, call the in‑house specialist team (on site); in a polyclinic — or any facility where the specialty is not available — refer the patient to a facility that has it.

Abbreviations

CPS — Canadian Pediatric Society
GINA — Global Initiative for Asthma
KDIGO — Kidney Disease: Improving Global Outcomes
KNCPP — Kuwait National Child Protection Program
NASPGHAN — North American Society for Pediatric Gastroenterology, Hepatology and Nutrition
PES — Pediatric Endocrine Society
PIDS — Pediatric Infectious Diseases Society
NTSP — National Tracheostomy Safety Project
AAP — American Academy of Pediatrics
NRP — Neonatal Resuscitation Program
AARC — American Association for Respiratory Care
AUA — American Urological Association
BTF — Brain Trauma Foundation
CDC — Centers for Disease Control and Prevention
ELSO — Extracorporeal Life Support Organization
EMA — European Medicines Agency
ESPGHAN — European Society for Pediatric Gastroenterology, Hepatology and Nutrition
EULAR — European Alliance of Associations for Rheumatology
FDA — US Food and Drug Administration
AHA — American Heart Association
IDSA — Infectious Diseases Society of America
ASHP — American Society of Health‑System Pharmacists
ANMF — Australasian Neonatal Medicines Formulary
ESC — European Society of Cardiology
ISMP — Institute for Safe Medication Practices
SIDP — Society of Infectious Diseases Pharmacists
AES — American Epilepsy Society
EAN — European Academy of Neurology
PNS — Peripheral Nerve Society
RCPCH — Royal College of Paediatrics and Child Health (UK)
ILAE — International League Against Epilepsy
ISPAD — International Society for Pediatric and Adolescent Diabetes
MOH — Ministry of Health
BTS — British Thoracic Society (UK)
NAEMSP — National Association of EMS Physicians (US)
NICE — National Institute for Health and Care Excellence (UK)
WHO — World Health Organization
DRACMA — Diagnosis and Rationale for Action against Cow's Milk Allergy (WAO)
WAO — World Allergy Organization
ACR — American College of Rheumatology
APSA — American Pediatric Surgical Association
BSH — British Society for Haematology
CSTE — Council of State and Territorial Epidemiologists (US)
EAACI — European Academy of Allergy and Clinical Immunology
EAU — European Association of Urology
ECCO — European Crohn’s and Colitis Organisation
ESPID — European Society for Paediatric Infectious Diseases
ILCOR — International Liaison Committee on Resuscitation
NAEPP — National Asthma Education and Prevention Program (US)
NCS — Neurocritical Care Society
NHLBI — National Heart, Lung, and Blood Institute (US)
RCS — Royal College of Surgeons (UK)
SSC — Surviving Sepsis Campaign
UHMS — Undersea and Hyperbaric Medical Society
AAO‑HNS — American Academy of Otolaryngology–Head and Neck Surgery
BNF — British National Formulary (UK)
LITFL — Life in the Fast Lane (clinical education site)
ATLS — Advanced Trauma Life Support (course)
APLS — Advanced Paediatric Life Support (course)
AAF — amino acid formula
ABC — airway, breathing, circulation
ABCDE — airway, breathing, circulation, disability, exposure
ABG — arterial blood gas
ABO — ABO blood‑group system
ACE — angiotensin‑converting enzyme (inhibitor)
ACS — acute chest syndrome; also American College of Surgeons (trauma)
ADAMTS13 — von Willebrand factor‑cleaving protease (ADAMTS13)
ADHD — attention‑deficit / hyperactivity disorder
AED — automated external defibrillator; also antiepileptic drug
aEEG — amplitude‑integrated electroencephalography
AEIOU — alcohol, epilepsy, insulin, opioids/overdose, uremia (coma mnemonic)
AGEP — acute generalized exanthematous pustulosis
AHI — apnea–hypopnea index
AHO — acute hematogenous osteomyelitis
AHT — abusive head trauma
aHUS — atypical hemolytic uremic syndrome
AKI — acute kidney injury
ALT — alanine aminotransferase
ALTE — apparent life‑threatening event
AMPLE — allergies, medications, past history, last meal, events (history mnemonic)
AMR — antimicrobial resistance
AMS — altered mental status
ANC — absolute neutrophil count
AOM — acute otitis media
APGAR — Appearance, Pulse, Grimace, Activity, Respiration (score)
APML — acute promyelocytic leukemia
aPTT — activated partial thromboplastin time
ARDS — acute respiratory distress syndrome
ARF — acute rheumatic fever
ASD — atrial septal defect
AST — aspartate aminotransferase
ATOMAC — Arizona‑Texas‑Oklahoma‑Memphis‑Arkansas Consortium (pediatric trauma guidelines)
ASH — American Society of Hematology
ASO — antistreptolysin O
ATA — American Thyroid Association
ATP — adenosine triphosphate
AUC — area under the (concentration–time) curve
AV — atrioventricular
AVM — arteriovenous malformation
AVPU — alert / voice / pain / unresponsive (conscious‑level scale)
AVSD — atrioventricular septal defect
B19 — parvovirus B19
BSA — body surface area
B symptoms — lymphoma constitutional symptoms (Ann Arbor staging): unexplained fever > 38 °C, drenching night sweats, weight loss > 10%
BCG — bacille Calmette–Guérin (vaccine)
BID — twice daily
BMI — body mass index
BNP — B‑type natriuretic peptide
BP — blood pressure
BRUE — brief resolved unexplained event
BSPED — British Society for Paediatric Endocrinology and Diabetes
BUN — blood urea nitrogen
BWPS — Burch–Wartofsky Point Scale (for thyrotoxicosis)
BXO — balanitis xerotica obliterans
C1‑INH — C1‑esterase inhibitor
C3, C4 — complement components 3 and 4
CAH — congenital adrenal hyperplasia
CAP — community‑acquired pneumonia
CBC — complete blood count
CCHD — critical congenital heart disease
CD46 — membrane cofactor protein (complement regulator)
CDH — congenital diaphragmatic hernia
CFU — colony‑forming units
CH50 — total hemolytic complement
CHD — congenital heart disease
CICO — can't intubate, can't oxygenate
CK — creatine kinase
CKD — chronic kidney disease
CMC — children with medical complexity
CMPA — cow's milk protein allergy
CMV — cytomegalovirus
CNO — chronic nonbacterial osteomyelitis
CNS — central nervous system
CO — carbon monoxide
COG — Children’s Oncology Group
COHb — carboxyhemoglobin
CPAP — continuous positive airway pressure
CPEG — Canadian Pediatric Endocrine Group
CPR — cardiopulmonary resuscitation
CRMO — chronic recurrent multifocal osteomyelitis
CRP — C‑reactive protein
CRASH‑2 / CRASH‑3 — Clinical Randomisation of an Antifibrinolytic in Significant Haemorrhage trials (tranexamic acid in trauma / head injury)
CRRT — continuous renal replacement therapy
CSF — cerebrospinal fluid
CT — computed tomography
CVC — central venous catheter
CVID — common variable immunodeficiency
CVS — cardiovascular system
CXR — chest radiograph (chest X‑ray)
CYP2D6 — cytochrome P450 2D6 (codeine/tramadol metabolism)
D10 — 10% dextrose
DAT — direct antiglobulin (Coombs) test
DDAVP — desmopressin
DEFG — don't ever forget glucose (coma mnemonic)
DIC — disseminated intravascular coagulation
DIVA — difficult intravenous access
DKA — diabetic ketoacidosis
DL — direct laryngoscopy
DMD — Duchenne muscular dystrophy
DNase — deoxyribonuclease (dornase alfa)
DOPES — displacement, obstruction, pneumothorax, equipment, stomach (sudden deterioration of a ventilated child)
DRESS — drug reaction with eosinophilia and systemic symptoms
DSD — difference / disorder of sex development
DTaP — diphtheria, tetanus, acellular pertussis (pediatric)
EBV — Epstein–Barr virus
ECG — electrocardiogram
ECMO — extracorporeal membrane oxygenation
ECPR — extracorporeal cardiopulmonary resuscitation
ED — emergency department
EEG — electroencephalogram
eGFR — estimated glomerular filtration rate
EHF — extensively hydrolyzed formula
EMLA — eutectic mixture of local anesthetics
ENT — ear, nose and throat (otolaryngology)
ERCP — endoscopic retrograde cholangiopancreatography
ESBL — extended‑spectrum β-lactamase
ESETT — Established Status Epilepticus Treatment Trial
ESC‑NOW — Eat, Sleep, Console approach for Neonatal Opioid Withdrawal (trial)
ESR — erythrocyte sedimentation rate
ET — endotracheal (route)
ETT — endotracheal tube
EVD — external ventricular drain
eFAST — extended Focused Assessment with Sonography for Trauma (adds lung views for pneumothorax)
FAST — Focused Assessment with Sonography for Trauma (bedside ultrasound for free fluid)
FBC — full blood count
FEIBA — factor eight inhibitor bypassing activity
FFP — fresh frozen plasma
FHH — familial hypocalciuric hypercalcemia
FiO₂ — fraction of inspired oxygen
FIS — flexible intubation scope
FN — febrile neutropenia
FPE — food protein‑induced enteropathy
FPIAP — food protein‑induced allergic proctocolitis
FPIES — food protein‑induced enterocolitis syndrome
FTT — failure to thrive
FVC — forced vital capacity
G6PD — glucose‑6‑phosphate dehydrogenase
GA²LEN — Global Allergy and Asthma European Network (anaphylaxis criteria)
GAS — group A Streptococcus
GBS — group B Streptococcus; also Guillain–Barré syndrome
GCS — Glasgow Coma Scale
GER — gastroesophageal reflux
GERD — gastroesophageal reflux disease
GFR — glomerular filtration rate
GGT — gamma‑glutamyl transferase
GH — growth hormone
GI — gastrointestinal
GIR — glucose infusion rate
GJ — gastrojejunal (tube)
GU — genitourinary
H2‑antagonist — histamine H2‑receptor antagonist
HA — hypoallergenic (partially hydrolyzed formula label)
HAE — hereditary angioedema
HAST — hypoxia‑altitude simulation test
HbA1c — glycated hemoglobin
HBO — hyperbaric oxygen
HBV — hepatitis B virus
HCN — hydrogen cyanide
HCO₃⁻ — bicarbonate
HCT — hematocrit
HDU — high‑dependency unit
HEEADSSS — Home, Education, Eating, Activities, Drugs, Sexuality, Suicide, Safety (adolescent interview)
HFNC — high‑flow nasal cannula
HHS — hyperosmolar hyperglycemic state
HHV‑6 — human herpesvirus 6
HIV — human immunodeficiency virus
HLA — human leukocyte antigen
HLH — hemophagocytic lymphohistiocytosis
HME — heat and moisture exchanger
HR — heart rate
HSP — Henoch–Schönlein purpura (IgA vasculitis)
HSV — herpes simplex virus
HUS — hemolytic uremic syndrome
IABP — intra‑aortic balloon pump
IBD — inflammatory bowel disease
IBI — invasive bacterial infection (bacteremia or bacterial meningitis)
ICP — intracranial pressure
ICU — intensive care unit
ID — infectious diseases
IDM — infant of a diabetic mother
IE — infective endocarditis
IEI — inborn errors of immunity
IEM — inborn error of metabolism
IgA — immunoglobulin A
IgE — immunoglobulin E
IgG — immunoglobulin G
IgM — immunoglobulin M
IGRA — interferon-γ release assay
IM — intramuscular
iNO — inhaled nitric oxide
INR — international normalized ratio
IO — intraosseous
IPNA — International Pediatric Nephrology Association
ITP — immune thrombocytopenia
IU — international units
IUGR — intrauterine growth restriction
IV — intravenous
IVA — isovaleric acidemia
IVIG — intravenous immunoglobulin
JAK — Janus kinase (inhibitor)
JIA — juvenile idiopathic arthritis
JVP — jugular venous pressure
KCl — potassium chloride
KCNQ2, SCN2A — neonatal‑onset epilepsy genes
KPCC — Kuwait Poison Control Center
LAD — leukocyte adhesion deficiency
LCHADD — long‑chain 3‑hydroxyacyl‑CoA dehydrogenase deficiency
LDH — lactate dehydrogenase
LFTs — liver function tests
LGMD — limb‑girdle muscular dystrophy
LGA — large for gestational age
LMA — laryngeal mask airway
LMWH — low‑molecular‑weight heparin
LP — lumbar puncture
LOC — loss of consciousness
LR — likelihood ratio
LRINEC — Laboratory Risk Indicator for Necrotizing Fasciitis (score)
LTV — long‑term ventilation
LV — left ventricle / ventricular
MAP — mean arterial pressure
MAS — macrophage activation syndrome
MCAD — medium‑chain acyl‑CoA dehydrogenase deficiency
MCP — membrane cofactor protein (CD46)
MDRO — multidrug‑resistant organism
MEDIF — airline Medical Information Form
MEN — multiple endocrine neoplasia
MenACWY — quadrivalent meningococcal conjugate vaccine (serogroups A, C, W, Y)
MenB — serogroup B meningococcal vaccine
MEP — maximal expiratory pressure
MIC — minimum inhibitory concentration
MIP — maximal inspiratory pressure
min — minutes
MIRM — Mycoplasma pneumoniae‑induced rash and mucositis
MIS‑C — multisystem inflammatory syndrome in children
MMA — methylmalonic acidemia
MMR — measles, mumps and rubella (vaccine)
MMRV — measles–mumps–rubella–varicella vaccine
MRCP — magnetic resonance cholangiopancreatography
MRI — magnetic resonance imaging
MRP — most responsible physician
MRSA — methicillin‑resistant Staphylococcus aureus
MSSA — methicillin‑susceptible Staphylococcus aureus
MTP — massive transfusion protocol
MSUD — maple syrup urine disease
NAAT — nucleic acid amplification test
NAC — N‑acetylcysteine
NaCl — sodium chloride
NAGS — N‑acetylglutamate synthase
NAI — non‑accidental injury
NEC — necrotizing enterocolitis
NEJM — The New England Journal of Medicine
NEWS2 — National Early Warning Score 2
NG — nasogastric
NGT — nasogastric tube
NICU — neonatal intensive care unit
NIF — negative inspiratory force
NIV — non‑invasive ventilation
NJT — nasojejunal tube
NK — natural killer (cell)
NMS — neuroleptic malignant syndrome
NPA — nasopharyngeal airway
NPO — nil per os (nothing by mouth)
NSAID — non‑steroidal anti‑inflammatory drug
NT‑proBNP — N‑terminal pro‑B‑type natriuretic peptide
NTM — nontuberculous mycobacteria
ODT — orally disintegrating tablet
OGT — orogastric tube
OHP — 17‑hydroxyprogesterone (17‑OHP)
OI — oxygenation index
OME — otitis media with effusion
OPA — oropharyngeal airway
OPV — oral poliovirus vaccine
OR — odds ratio
ORS — oral rehydration solution
ORT — oral rehydration therapy
OSA — obstructive sleep apnea
OSI — oxygenation saturation index
PA — propionic acidemia; also posteroanterior (radiograph view)
PALF — pediatric acute liver failure
PALS — Pediatric Advanced Life Support
PaO₂ — arterial partial pressure of oxygen
PARDS — pediatric acute respiratory distress syndrome
PAS — Pediatric Appendicitis Score
PAT — Pediatric Assessment Triangle
PCR — polymerase chain reaction
PCT — procalcitonin
PDA — patent ductus arteriosus
PE — phenytoin equivalents
PEA — pulseless electrical activity
PECARN — Pediatric Emergency Care Applied Research Network
PED‑TRAX — Pediatric Trauma and Tranexamic Acid study (observational)
PEEP — positive end‑expiratory pressure
PEG — percutaneous endoscopic gastrostomy
PEN‑FAST — penicillin‑allergy risk‑assessment score
PEP — post‑exposure prophylaxis
PEWS — Pediatric Early Warning Score
PH — portal hypertension
PICC — peripherally inserted central catheter
PICS‑p — post‑intensive care syndrome — pediatric
PICU — pediatric intensive care unit
PIGN — post‑infectious glomerulonephritis
PJP — Pneumocystis jirovecii pneumonia
PLP — pyridoxal‑5‑phosphate
PMA — postmenstrual age
PNPO — pyridox(am)ine 5′‑phosphate oxidase (deficiency)
PO — by mouth (oral)
POC — portable oxygen concentrator
POCUS — point‑of‑care ultrasound
PPHN — persistent pulmonary hypertension of the newborn
PPI — proton pump inhibitor
PPV — positive‑pressure ventilation
PR — per rectum (rectal route); also PR interval on ECG
PRAM — Pediatric Respiratory Assessment Measure
PRBC — packed red blood cells
PRN — as required (pro re nata)
PROPPR — Pragmatic, Randomized Optimal Platelet and Plasma Ratios trial
PSG — polysomnography
PSGN — post‑streptococcal glomerulonephritis
PT — prothrombin time
PTH — parathyroid hormone
PTHrP — parathyroid hormone‑related peptide
PTSD — post‑traumatic stress disorder
PTU — propylthiouracil
PUCAI — Pediatric Ulcerative Colitis Activity Index
PVC — premature ventricular contraction
PVR — pulmonary vascular resistance
pVT — pulseless ventricular tachycardia
QID — four times daily
QRS — QRS complex (ECG)
QT — QT interval (ECG)
QTc — corrected QT interval
RADT — rapid antigen detection test
RAPD — relative afferent pupillary defect
RBC — red blood cell
RBS — random blood sugar
RBUS — renal and bladder ultrasound
RCA — right coronary artery
RCT — randomized controlled trial
RDS — respiratory distress syndrome
rFVIIa — recombinant activated factor VII
RIG — rabies immunoglobulin
RIME — reactive infectious mucocutaneous eruption
RLQ — right lower quadrant
ROSC — return of spontaneous circulation
ROTEM — rotational thromboelastometry
RR — respiratory rate
RSI — rapid sequence intubation
RSV — respiratory syncytial virus
RT — respiratory therapist
RV — right ventricle
s — seconds
SA — septic arthritis
SBP — systolic blood pressure
SC — subcutaneous
SCAR — severe cutaneous adverse reaction (RegiSCAR / J‑SCAR criteria)
SCFE — slipped capital femoral epiphysis
sCD25 — soluble CD25 (soluble interleukin‑2 receptor‑α)
SCID — severe combined immunodeficiency
SCIWORA — spinal cord injury without radiographic abnormality
SGA — small for gestational age
SIADH — syndrome of inappropriate antidiuretic hormone secretion
SIDS — sudden infant death syndrome
SIP — spontaneous intestinal perforation
SIPA — shock index, pediatric age‑adjusted
sJIA — systemic juvenile idiopathic arthritis
SJS — Stevens–Johnson syndrome
SOPA — suction, open mouth, pressure increase, airway alternative (NRP corrective steps)
SpO₂ — peripheral oxygen saturation
SPUR — severe, persistent, unusual, recurrent (immunodeficiency pattern)
SSSS — staphylococcal scalded skin syndrome
SSTI — skin and soft‑tissue infection
STAT — immediately (statim)
STEC — Shiga toxin–producing E. coli
STI — sexually transmitted infection
SVC — superior vena cava
SVR — systemic vascular resistance
SVT — supraventricular tachycardia
T1DM — type 1 diabetes mellitus
T2DM — type 2 diabetes mellitus
T3 / T4 — triiodothyronine / thyroxine
TB — tuberculosis
TBI — traumatic brain injury
TBSA — total body surface area
TBW — total body water
TCA — tricyclic antidepressant
TcB — transcutaneous bilirubin
Tdap — tetanus, diphtheria, acellular pertussis (adolescent/adult)
TEN — toxic epidermal necrolysis
TEN‑4‑FACESp — bruising clinical decision rule (Torso, Ears, Neck in a child ≤ 4 y or any bruise < 4 months; Frenulum, Angle of jaw, Cheek, Eyelid, Sclera; patterned)
TEG — thromboelastography
TFI — total fluid intake
TID — three times daily
TIF — tracheo‑innominate fistula
TIPS — transjugular intrahepatic portosystemic shunt
TLS — tumor lysis syndrome
TM — tympanic membrane
TMA — thrombotic microangiopathy
TMP‑SMX — trimethoprim‑sulfamethoxazole
TOF — tetralogy of Fallot
tPA — tissue plasminogen activator
TRAb — TSH‑receptor antibody
TREC — T‑cell receptor excision circle
TREKK — Translating Emergency Knowledge for Kids
TSB — total serum bilirubin
TSH — thyroid‑stimulating hormone
TSI — thyroid‑stimulating immunoglobulin
TTE — transthoracic echocardiography
TTP — thrombotic thrombocytopenic purpura
TTS — tight‑to‑shaft (tracheostomy cuff)
TWIST — Testicular Workup for Ischemia and Suspected Torsion (score)
TXA — tranexamic acid
UCD — urea cycle disorder
ULN — upper limit of normal
UTI — urinary tract infection
Vd — volume of distribution
VA — venoarterial (ECMO)
VAD — ventricular assist device
VATS — video‑assisted thoracoscopic surgery
VCUG — voiding cystourethrogram
VF — ventricular fibrillation
VKDB — vitamin K deficiency bleeding
VL — videolaryngoscopy
VLCADD — very‑long‑chain acyl‑CoA dehydrogenase deficiency
VP — ventriculoperitoneal (shunt)
VRE — vancomycin‑resistant enterococci
VSD — ventricular septal defect
VT — ventricular tachycardia
VTE — venous thromboembolism
VUR — vesicoureteral reflux
VV — venovenous (ECMO)
VZV — varicella‑zoster virus
WBC — white blood cell (count)
WOB — work of breathing
WPW — Wolff–Parkinson–White (syndrome)

How to Open & Save This Guide

Which file? The EPUB resizes the text and is best for reading on phones and e‑readers. The PDF keeps the exact page layout. Use whichever you prefer — the steps are the same.
QR code linking to the electronic versions of this guide
Scan to download any format. Opens kpc-guide.com/downloads — the full guide as Print PDF (A4 and A5), Phone PDF and EPUB. The address stays the same when the files are updated.
QR code linking to the installable KPC Guide app
Scan to install the app. Opens the guide at kpc-guide.com — then Share → Add to Home Screen (iPhone) or ⋮ → Install app (Android). Works offline after the first open; updates install automatically.
Apple Books
iPhone · iPad · Mac
  1. Open the EPUB or PDF file.
  2. Tap the Share icon, then Copy to Books.
  3. On a Mac, drag the file onto the Books app.
  4. Find it any time in your Library.
Kindle
App or e‑reader
  1. Install the Send to Kindle app, or visit sendtokindle.amazon.com.
  2. Add the EPUB file — Amazon turns it into a Kindle book.
  3. It appears on all your Kindle apps under Library → Docs.
Android
Phones & tablets
  1. Open the Google Play Books app.
  2. Go to Library and tap Upload.
  3. Choose the EPUB or PDF — it syncs to all your devices.
Any e‑reader app or Adobe Acrobat also opens the files from Downloads.
Install as an App
Offline · home‑screen icon
  1. Open kpc-guide.com in Chrome (Android) or Safari (iPhone).
  2. Android: menu ⋮ → Install app. iPhone: Share → Add to Home Screen.
  3. Open it from your home screen — it works offline.
Screen looks dark? The pages are white. If they appear black, your reader's night / dark mode is on — switch it off in the app to see the guide as designed.
→

Find It by Symptom

The front door — start here: a presentation routes you to the card

Presentation → card index

NAVIGATORPresentation → card

You see a presentation, not a diagnosis. Start here and jump to the card.

▸
Chip colour = the guide section the card is inSolid chip = MINUTES card — act now
Fever & infection
◈ How to use
  • This routes the commonest bedside presentations to the relevant cards — it is a starting point, not a differential.
  • Tap a card name to jump straight to it. Chip colour shows the section the card is in; a solid chip is a MINUTES card (act now).
  • The full alphabetical index and the section colors remain the other two ways in.
Can’t‑miss patterns — recognition mapSee it → name the danger → act. Each branch ends in a sentinel pattern — tap it to jump to the full card (workup + doses). Not exhaustive; the section cards remain the source of truth.
HEART / NEONATE FEVER, RASH & SEPSIS SURGICAL / ABDOMEN BRAIN, CORD & BP METABOLIC, BONE & BLOOD Duct‑dependent CHD / IEMNeonate collapse / shock Cyanotic CHDCyanosis unresponsive to O₂ MyocarditisTachycardia + gallop, hepatomegaly Meningococcal sepsisFever + non‑blanching rash Serious bacterial infectionFever, infant < 90 days ITP vs meningococcemiaPetechiae — well or unwell? Epiglottitis / deep‑neckDrooling + tripod + stridor Malrotation + volvulusBilious (green) vomiting, infant Testicular torsionAcute scrotal pain / swelling Caustic injuryButton / lithium battery Raised ICP / brain tumorMorning headache + vomiting Cord compressionNight back pain + leg weakness Neuromuscular / botulismFloppy infant, weak cry Hypertensive emergencyVery high BP + seizure DKA ± cerebral edemaVomiting + polyuria + high glucose Septic arthritisLimp + fever, won't bear weight Acute hemolysisSudden pallor + jaundice Inflicted injuryBruise, non‑mobile infant Reconsider diagnosis“Gastroenteritis”, no diarrhea CAN'T‑MISSPATTERNSSEE → NAME → ACT
01

Resuscitation

PALS 2025 (AHA/AAP)
Time‑critical emergencies at a glanceSolid bar = clock starts at a knowable moment (a real deadline). Dashed bar = onset usually unknown — prognosis, act on suspicion.
The Golden WindowWhat must be done — and by when — for the guide’s time‑critical emergencies. The intervention above each bar is what the window governs.▸ Red “now” = a step that starts immediately, before any window applies (e.g. 100% O₂ in CO poisoning).Solid = clock starts at a knowable moment (recognition / arrival) — a real deadline to beat.Dashed = onset usually unknown — the window is prognosis; act on suspicion, do not treat it as a countdown.MINUTES1–2 HOURSWITHIN HOURS5 min15 min30 min1 h2 h4 h6 h8 hCardiac arrestHigh‑quality CPR + early defibrillationstart immediately AHA / ILCORAnaphylaxisIM epinephrinegive immediately EAACI / WAOConvulsive status epilepticusBenzodiazepine (then escalate)by 5 min NCS / ILAESickle vaso‑occlusive crisisParenteral analgesiawithin 30–60 min ASH / NHLBIMajor traumaHemorrhage control + definitive carewithin the 'golden hour' ATLS / RCSSeptic shock / meningococcemia▸ now: O₂ + IV/IO access nowIV fluid boluses + broad‑spectrum antibioticswithin 1 h Surviving Sepsis 2026Chemo‑induced febrile neutropeniaEmpiric antibioticswithin 1 h IDSA / NICEBacterial meningitisAntibiotics — LP first unless it delays themwithin 1 h IDSAButton / lithium battery▸ now: Honey if ≥12 mo & <12 hEndoscopic removalwithin ~2 h NASPGHAN / ESPGHANIschemic priapismAspiration ± phenylephrineafter ~4 h risk climbs AUA / EAUCO poisoning (severe)▸ now: 100% O₂ immediatelyHyperbaric O₂ (if indicated)greater benefit within ~6 h UHMSTesticular torsion▸ now: Manual detorsion (temporizing)Surgical detorsionsalvage falls after ~6 h EAU / AUAMidgut volvulus (bilious vomiting)Emergency laparotomyinfarcts within hours APSA / ACSAcute compartment syndromeFasciotomyirreversible by ~6–8 h Orthopedic consensusSolid‑bar windows are consensus targets for starting the named intervention; dashed‑bar figures are prognostic. Always act as early as possible. Immediate ABC resuscitation is assumed for every row. Built from the guide’s own time‑critical cards.

Cardiopulmonary Arrest

MINUTES

Unresponsive, apneic, pulseless within 10 seconds → CPR now.

▸
◣ High‑quality CPR is the priority
  • Rate 100–120 per minute; depth ⅓ of chest depth (~4 cm infant, ~5 cm child); full recoil; minimal interruptions.
  • Ratio 30:2 (single rescuer) · 15:2 (two rescuers). Adolescent (post‑pubertal): 30:2 for both single and two rescuers (adult BLS),.
  • With an advanced airway (all ages): continuous chest compressions with 1 breath every 2–3 seconds (20–30 breaths/min), without pausing compressions.
During CPR
  • Attach a monitor/defibrillator; establish access — immediate IO in cardiac arrest if an IV is not already in place (for other emergencies, limit peripheral IV attempts — ERC 2021: at most 2 attempts / 5 min — then go IO); consider an advanced airway (then continuous compressions with one breath every 2–3 s); give oxygen.
  • Do not delay epinephrine or defibrillation for access or intubation.
Rhythm on the monitor?
SHOCKABLE · VF / pVT
Defibrillate as early as possible — 2 J/kg → 4 J/kg → ≥4 J/kg (subsequent shocks; up to 10 J/kg or the adult dose, ≈ 200 J biphasic / 360 J monophasic).
  • Resume high‑quality CPR immediately after every shock.
  • Check the rhythm every 2 min, pausing compressions ≤ 10 s; check a central pulse (brachial in infants; femoral/carotid in children) only if an organized rhythm or signs of return of circulation appear. If VF/pVT persists, shock again and resume CPR.
  • Epinephrine during CPR after the 2nd shock (don't pause compressions), then every 3–5 min.
  • Amiodarone (or lidocaine) after the 3rd shock for refractory VF/pVT.
Sequence (a continuous cycle): shock → shock → epinephrine → shock → amiodarone → ↻ back to shock — keep repeating the 2‑min CPR–shock cycle, epinephrine every 3–5 min and a further amiodarone dose as needed.
NON‑SHOCKABLE · asystole / PEA
Give epinephrine during CPR as soon as possible, then every 3–5 minutes. Continue high‑quality CPR without unnecessary interruptions; check rhythm every 2 minutes. If a shockable rhythm appears, cross over to the shockable (VF/pVT) pathway and defibrillate.
Every cycle — reversible causes
  • 6 H's: hypoxia, hypovolemia, hydrogen ion (acidosis), hypo-/hyperkalemia, hypoglycemia, hypothermia.
  • 5 T's: tension pneumothorax, tamponade (cardiac), toxins, thrombosis (pulmonary), thrombosis (coronary).
ROSC
Post‑arrest: start post‑arrest care · secure the airway · wean oxygen to target SpO₂ 94–99% (avoid hyperoxic reperfusion injury) and normal carbon dioxide · systolic and/or mean arterial BP > 10th centile for age · targeted normothermia (36–37.5 °C) · correct metabolic derangements · treat seizures (EEG if persistent encephalo­pathy).
Medications & energy
Drug / actionDoseRoute & notes
Epinephrine (adrenaline)0.01 mg/kg (max 1 mg)IV/IO, 0.1 mg/mL (1:10,000) concentration; give during CPR without pausing compressions, every 3–5 min
Amiodarone5 mg/kg (max 300 mg)IV/IO bolus for refractory VF/pVT; may repeat up to twice (3 doses total; repeat doses max 150 mg each — PALS 2025; max 15 mg/kg). Avoid in prolonged QT (further prolongs QT)
Lidocaine1 mg/kgIV/IO alternative to amiodarone
Defibrillation2 → 4 → ≥4 J/kgUnsynchronized; up to 10 J/kg or adult dose (≈ 200 J biphasic / 360 J monophasic)
⚠ Remember
  • Respiratory failure is the leading cause of cardiac arrest in pediatrics — oxygenate and ventilate early.
  • Intraosseous access is fast — in cardiac arrest go straight to IO if an IV is not already in place (in other emergencies, IO if IV fails after 2 attempts / 5 min — ERC 2021); do not delay epinephrine waiting for a vein.
◈ Algorithms
  • Full AHA PALS flowcharts (cardiac arrest
  • bradycardia
  • tachycardia
  • post‑arrest) — cpr.heart.orgQR.
◣ Admit · Discharge · Refer
  • Admit — every child with return of circulation → start post‑arrest care (oxygenation/ventilation targets, hemodynamic support, treat the cause, neuroprotection, avoid fever and hypo/hyperglycemia).
  • Home from the emergency department — not applicable — care after unsuccessful resuscitation follows the death‑confirmation and bereavement pathway.
  • Refer — now — the specialty for the reversible cause (6 Hs / 5 Ts): cardiology, surgery, toxicology, or metabolic; involve the resuscitation team early.
Code Blue — team roles & positionsAssign each role out loud and close the loop: Team Leader (hands‑off), Airway Manager, Compressor, Defib Operator / CPR Coach, Medications & Vascular Access (×2), and Recorder / Documenter.
Code Blue resuscitation team roles and positions around the bed
Human‑prompted, AI‑generated image, reviewed and approved by the panel.
02

Behavioral & Psychiatric

Agitation · self‑harm · drug‑induced syndromes

Acute Severe Agitation

MINUTES

Keep child and staff safe; look for a treatable cause.

▸
① Exclude an organic cause first Check glucose, oxygenation, head injury, intoxication/withdrawal, pain. Agitation is a symptom — treat the cause where present.
② Non‑drug measures first Calm low‑stimulation environment, verbal de‑escalation, familiar caregiver; offer oral medication, including the child's own regular medication, when available.
severe / unsafe
③ Pharmacologic (per local pathway) Choose by cause (BETA): delirium → second‑generation antipsychotic (avoid benzodiazepines/anticholinergics); intoxication/withdrawal or anxiety → benzodiazepine (± haloperidol if severe); autism/developmental delay → extra dose of the child's own medication, avoid IM where possible; psychiatric/unknown, severe → olanzapine alone, or haloperidol + lorazepam. Prefer PO before IM. Physical restraint = brief last resort, continuous monitoring.
DrugDose (approximate)Route & notes
Olanzapine2.5–5 mg (< 40 kg); 5–10 mg (≥ 40 kg); IM dose ½–¼ of the oral dosePO/IM/ODT; the ODT (orally disintegrating — Zyprexa Zydis) is easiest in an agitated child. Do not give within 1 h of a benzodiazepine (respiratory depression)
Risperidone0.25–1 mgPO; well tolerated
Lorazepam0.05–0.1 mg/kg (max 2 mg)PO/IM/IV; for substance- or anxiety‑driven agitation
Haloperidol0.5–5 mg (IM dose half the oral dose); max 6 mg/day at 15–40 kg, 15 mg/day > 40 kgPO/IM; watch for dystonia/QT — second‑generation agents preferred
Diphen­hydramine1 mg/kg/dose (12.5–50 mg)IV/IM/PO; antidote for an acute dystonic reaction from an antipsychotic (haloperidol/risperidone). BETA also lists it as an option for mild agitation/anxiety in younger children, but it is not preferred here (avoid in delirium; paradoxical disinhibition)
⚠ Caution with benzodiazepines
  • Avoid benzodiazepines and diphenhydramine in delirium — can worsen confusion (paradoxical disinhibition).
  • Also avoid or use with caution in developmental delay and autism, where benzodiazepines commonly cause paradoxical reactions (more agitation).
◣ Admit · Discharge · Refer
  • Admit — ongoing risk, a medical cause, or need for continued sedation/monitoring.
  • Home — settled, medically cleared, with a safety plan and follow‑up.
  • Refer — now — psychiatry; medical/toxicology for organic causes.

Self‑Harm / Intentional Ingestion

HOURS

Stabilize the patient medically first, then address psychological safety.

▸
① Medical stabilization ABCDE, glucose, ECG, and a pregnancy test (β-hCG) in all post‑menarchal females. For any ingestion: identify agent and timing, check an acetaminophen level at ≥ 4 h after ingestion (if drawn earlier, repeat at 4 h before plotting on the nomogram) and a salicylate level, and contact poisons information (Kuwait Poison Control Center) for agent‑specific advice. Treat per the specific antidote pathway.
② Safety Continuous one‑to‑one observation, safe environment, involve a trusted adult/caregiver. Do not discharge before a mental‑health assessment.
Refer for psychiatric/psychosocial assessment; arrange follow‑up and support before discharge.
◈ Cross‑reference General approach, antidotes, and Kuwait Poison Control hotline: see Poisoning & Toxic Ingestion (Toxicology, Trauma & Environmental).
◣ Admit · Discharge · Refer
  • Admit — medical risk from the ingestion/injury, or ongoing suicidality → admit and monitor.
  • Home — medically cleared AND psychiatrically assessed as safe, with follow‑up and means restriction.
  • Refer — now — psychiatry (risk assessment), social work/safeguarding, and toxicology.

Drug‑Induced Hyperthermia Syndromes

MINUTES

Three look‑alikes with different triggers — and different antidotes.

▸
SyndromeClueKey treatment
Neuroleptic malignant syndromeAntipsychotic; "lead‑pipe" rigidity, slow onset, high creatine kinaseStop drug; cool; fluids; benzodiazepine; dantrolene; bromocriptine
Serotonin syndromeSerotonergic drug; clonus & hyperreflexia, rapid onset, agitationStop drug; cool; benzodiazepine; cyproheptadine
Malignant hyperthermiaVolatile anesthetic / succinylcholine; rigidity, rising CO₂Stop trigger; dantrolene 2.5 mg/kg IV rapid bolus, repeated until hypercarbia, tachycardia, rigidity and temperature are controlled (no fixed upper limit; reconsider the diagnosis if > 10 mg/kg is needed); aggressive cooling; treat hyperkalemia/rhabdomyolysis; urgent PICU/anesthesia
⚠ All three
  • Active cooling, IV fluids; treat hyperkalemia and rhabdomyolysis.
  • Secure airway; transfer to PICU.
◣ Admit · Discharge · Refer
  • Admit — all → PICU (cooling, sedation, dantrolene as indicated).
  • Home from the ward — not acutely; after resolution and review of the causative agent.
  • Refer — now — toxicology/PICU; psychiatry/pharmacy for a medication review.
03

Cardiac & Shock

Shock recognition & types · septic shock · arrhythmias · myocarditis / heart failure · congenital heart disease · hypercyanotic spell

Shock — Recognition & Type

MINUTES

Circulatory failure: tissues not getting enough oxygen. Hypotension is a late sign.

▸
◣ Recognize early (before hypotension)
  • Tachycardia, prolonged or flash capillary refill, cool or mottled skin, weak pulses, altered mental status, reduced urine output, rising lactate.,
Universal first steps Start with ABCDEs · Oxygen · IV/IO access · monitor · check glucose & lactate · identify the type below.
Which type of shock?
TypeCauseKey treatment
HypovolemicVomiting/diarrhea, hemorrhage, burnsCrystalloid or balanced solution 10–20 mL/kg boluses; blood products (packed red cells) early if hemorrhage,; stop ongoing losses
DistributiveSepsis, anaphylaxis, neurogenicFluids + early vasoactive; treat the cause (see Septic shock, Anaphylaxis)
CardiogenicMyocarditis, arrhythmia, heart diseaseCautious fluid 5 mL/kg slowly; inotrope/inodilator; treat arrhythmia; early cardiology consult and PICU escalation
ObstructiveTension pneumothorax, tamponade, duct‑dependent lesion, pulmonary embolismRelieve the obstruction (decompress a tension pneumothorax, drain a tamponade, and — for example — prostaglandin for a duct‑dependent lesion; massive/high‑risk PE → thrombolysis + heparin, specialist‑directed)
⚠ Mimics shock — not circulatory failure
  • Carbon monoxide, cyanide, hydrogen sulfide, and methemoglobinemia impair oxygen delivery or use at the hemoglobin / cellular level, not the circulation — so this is not true shock, and the usual endpoints (blood pressure, capillary refill) can look normal. Suspect it when perfusion and BP appear adequate but there is unexplained lactic acidosis / tissue hypoxia with a suggestive history (fire / smoke, enclosed space, oxidizing drugs). SpO2 is unreliable — confirm with co‑oximetry / blood gas,.
  • It will not respond to fluids or vasopressors: give 100% oxygen and the specific antidote,,, (see Smoke Inhalation & CO and Poisoning).
Resuscitation drugs
DrugDoseNotes
Balanced crystalloid10–20 mL/kg (5 mL/kg if cardiogenic)Ringer’s lactate preferred; normal saline if a balanced fluid is unavailable. Bolus; reassess for fluid overload after each
Epinephrine (adrenaline) infusion0.05–0.3 mcg/kg/minTitrate to response; first‑line vasoactive — epinephrine or norepinephrine (neither is preferred). May start peripherally with close observation for extravasation until central access is obtained
Norepinephrine (noradrenaline) infusionStart 0.05–0.1 mcg/kg/min
titrate with the PICU
a second agent is commonly considered once norepinephrine reaches ~0.1–0.3 mcg/kg/min (American and Asian/Middle‑East practice; European units often wait until ~0.3–1 mcg/kg/min)
Titrate to response; first‑line alternative — either epinephrine or norepinephrine is acceptable first‑line; choose by physiology (epinephrine if low cardiac output/myocardial dysfunction, norepinephrine if vasodilated/low vascular resistance), local practice and clinician preference. May start peripherally with close extravasation monitoring until central access is obtained
⚠ Fluid caution
  • Reassess after every bolus.
  • Vasoactives may start alongside fluids if evidence of life‑threatening end‑organ hypoperfusion.
  • Slow or stop fluids at first signs of fluid overload — new crackles, enlarging liver, gallop, worsening work of breathing, or overload on POCUS, — especially suspected cardiogenic shock.
◈ Therapeutic endpoints (aim for)
  • Heart rate and blood pressure normal for age, capillary refill ≤ 2 s, warm extremities with normal pulses,, normal mental status, urine output ≥ 1 mL/kg/h, falling / normalizing lactate (central venous O₂ saturation ≥ 70% where available).
  • Reassess after every fluid bolus and every change in vasoactive support.
◣ Admit · Discharge · Refer
  • Admit — any child in shock → call the PICU team to evaluate (high‑dependency/PICU); begin resuscitation before the type is confirmed.
  • Home from the ward — only once the cause is treated and perfusion is normal off vasoactive support.
  • Refer — now — by type — septic → PICU/infectious diseases; cardiogenic → cardiology; obstructive → treat the cause (tension pneumothorax, tamponade); hypovolemic/hemorrhagic → surgery/trauma. Involve PICU in parallel for any child in shock.

Septic Shock

MINUTESSSC

Infection + circulatory dysfunction. Defined by the Phoenix Sepsis ScoreQR in a child with suspected infection (≥ 2 points = sepsis; sepsis with ≥ 1 cardiovascular point = septic shock).

▸
⚠ The Phoenix score is not a screening tool
  • The Phoenix Sepsis Score identifies organ dysfunction — by the time it is positive, sepsis is already established.
  • It is not an early‑screening tool.
  • Keep using your standard pediatric early‑warning / sepsis‑screening triggers to catch the child before organ dysfunction develops.
FIRST HOUR — every minute counts
Resuscitate
  • Impaired perfusion = altered mental status; tachycardia with weak or bounding pulses and wide pulse pressure (± hypotension); capillary refill > 2 s, mottled cool skin or pallor; oliguria < 1 mL/kg/h (adolescents < 0.5 mL/kg/h),.
  • 100% oxygen via non‑rebreather mask during resuscitation. Once shock has resolved (continuous monitoring/PICU), SSC 2026 suggests titrating oxygen to SpO₂ 88–92% rather than > 94% (conditional) — not during active resuscitation, and individualize in sickle cell disease/severe anemia, cyanotic heart disease, low cardiac output or ongoing oxygen debt, and neurological dysfunction.
  • If intubating, avoid etomidate
  • two IV/IO
  • antibiotics within 1 hour
  • Probable sepsis without shock: rapid assessment; if sepsis is still likely, antibiotics ideally within 3 hours
  • IV fluid boluses.
  • Labs: glucose, CBC + differential, PCT or CRP, electrolytes, ionized calcium, renal and liver function, coagulation, blood gas, lactate, cultures (blood ± urine).
  • Hypotension (late sign) = systolic BP below, by age:
  • < 60 mmHg — neonate
  • < 70 mmHg — 1–12 mo
  • < 70 + 2 × age(yr) — 1–10 yr
  • < 90 mmHg — ≥ 10 yr (PALS age‑based thresholds; manual text).
Fluids
  • Balanced crystalloid (Ringer's lactate preferred over 0.9% saline, except with hyponatremia or raised‑ICP concern) 10–20 mL/kg boluses; reassess after each, up to 40–60 mL/kg in the first hour. Ringer's lactate contains calcium — never run ceftriaxone through the same line or Y‑site as Ringer's lactate or IV calcium: use the second IV/IO, or flush thoroughly with 0.9% saline before and after (age > 28 days).
  • Use crystalloids rather than albumin for initial resuscitation.
  • Watch for fluid overload — new hepatomegaly, crackles, gallop, or B‑lines on lung POCUS. Give further boluses only while shock persists without overload — titrate each bolus to markers of cardiac output and stop if shock resolves or overload develops; FEAST showed harm from liberal boluses in children without ICU access.
  • Use cardiac and lung point‑of‑care ultrasound (POCUS) to guide resuscitation where trained staff are available.
  • Start vasoactives if shock persists after fluid boluses — no evidence‑based volume threshold (before or after 40 mL/kg) — or earlier if overload develops.
fluid‑refractory
Vasoactive
  • Call PICU immediately.
  • Start epinephrine or norepinephrine (either is acceptable first‑line) — choose by physiology (epinephrine if low cardiac output/myocardial dysfunction, norepinephrine if vasodilated/low vascular resistance), local practice and clinician preference; a well‑sited peripheral IV is acceptable, with close extravasation monitoring while central access is arranged.
  • High‑dose catecholamines → add vasopressin or keep titrating the catecholamine.
  • Catecholamine‑resistant shock → consider hydrocortisone, especially with adrenal‑insufficiency risk (purpura fulminans, recent/chronic steroids, hypothalamic–pituitary–adrenal disease),; ACCM 2017 dosing ranges from 1–2 mg/kg/day (stress cover) up to 50 mg/kg/day titrated to shock reversal
  • Give stress‑dose hydrocortisone for suspected/documented adrenal insufficiency. In catecholamine‑resistant shock, hydrocortisone may reduce catecholamine requirements, but pediatric evidence remains limited,. Call PICU.
  • Do not start IV hydrocortisone for shock that fluids and vasoactives have already reversed — except in known or suspected adrenal insufficiency, where stress dosing is given (and continued) regardless of hemodynamics.
  • Refractory shock — persisting despite fluids, ≥ 2 vasoactives, and hydrocortisone, or low cardiac output on high inotropic support → consider VA‑ECMO as rescue therapy and contact an ECMO center early.
Medications
DrugDoseNotes
Ceftriaxone (empiric)100 mg/kg (max 4 g)IV; empiric regimen by focus (immunocompetent, community‑acquired): no obvious focus → ceftriaxone ± vancomycin ± amikacin; meningitis/encephalitis → ceftriaxone + vancomycin ± acyclovir; pneumonia → ceftriaxone ± vancomycin; skin/soft‑tissue → cefotaxime + vancomycin ± clindamycin; toxic shock or necrotizing fasciitis → piperacillin‑tazobactam + vancomycin + clindamycin; intra‑abdominal → piperacillin‑tazobactam; neonate → cefotaxime + ampicillin (± acyclovir if HSV suspected, ± vancomycin if MRSA suspected). Immunocompromised or hospital‑acquired: add antipseudomonal cover and consider antifungal. Send MRSA screening swabs. Agent choice by focus follows local practice (Kuwait Pediatric Council antibiotic policy). Meningitic ceftriaxone dose 50 mg/kg/dose every 12 h (100 mg/kg/day, max 4 g/day) ⚠ Calcium: do not give ceftriaxone simultaneously with calcium‑containing fluids (Ringer's lactate, calcium gluconate, parenteral nutrition) — separate line or flush. Neonates ≤ 28 days: ceftriaxone is contraindicated if calcium‑containing IV fluids are or will be given, and in premature or jaundiced neonates — use cefotaxime (see Must‑Avoid Drugs).
Balanced crystalloid10–20 mL/kgRinger’s lactate preferred; normal saline if unavailable. Bolus, reassess after each
Epinephrine (adrenaline)Start 0.05–0.1 mcg/kg/minIV/IO infusion; escalate every 5–10 min to target — escalation and titration must be done by the PICU team. Central line preferred; peripheral is a bridge only with close extravasation monitoring until central access
Norepinephrine (noradrenaline)Start 0.05–0.1 mcg/kg/min
titrate with the PICU
a second agent is commonly considered once norepinephrine reaches ~0.1–0.3 mcg/kg/min (American and Asian/Middle‑East practice; European units often wait until ~0.3–1 mcg/kg/min)
IV/IO infusion; escalate every 5–10 min to target — escalation and titration must be done by the PICU team. Central line preferred; peripheral is a bridge only with close extravasation monitoring until central access
Hydro­corti­sone1–2 mg/kg (max 100 mg)IV; give for suspected/documented adrenal insufficiency. No clear evidence for or against in catecholamine‑resistant shock
◈ Vasoactive infusions — how to give them safely
  • Epinephrine and norepinephrine infusions should be given via a central venous catheter wherever possible. Do not delay initiation of vasoactive support to obtain central access (SSC Pediatric 2026).
  • Peripheral use is a bridge only — via a large vein, a dedicated dilute infusion, with site review every 15 minutes for the first hour then hourly, and conversion to central access as soon as feasible.
  • Doses above your unit's approved central or peripheral maximum require consultant approval, documented in the notes. Escalation beyond 1 mcg/kg/min should prompt reassessment of the shock phenotype and consideration of vasopressin and hydrocortisone, rather than relying solely on dose escalation.
◈ Preparing the infusion — where you have no local formulary
  • Ampoules (Gulf/ME): epinephrine (adrenaline) 1 mg/mL (1:1,000) is the stock ampoule (0.1 mg/mL / 1:10,000 is the pre‑filled code syringe),,; norepinephrine (noradrenaline) 1 mg/mL ampoules (2 mg/2 mL, 4 mg/4 mL). The strength printed on the ampoule is norepinephrine base: a 4 mg/4 mL ampoule contains 4 mg — dose from the label strength.,
  • Rule of 6 (weight‑based): put 0.3 mg/kg in 50 mL (or 0.6 mg/kg in 100 mL) of glucose 5% → 1 mL/h = 0.1 mcg/kg/min (0.05 = 0.5 mL/h; 0.3 = 3 mL/h).
  • Standard concentration (safety‑preferred): epinephrine 10 / 20 / 40 mcg/mL; norepinephrine (base) 16 / 32 / 64 mcg/mL., Rate (mL/h) = dose (mcg/kg/min) × weight (kg) × 60 ÷ concentration (mcg/mL). Use the most dilute for a peripheral bridge.,
  • Diluent & safety: dilute in glucose 5% (0.9% saline alone: permitted by the UK norepinephrine label, not recommended by US epinephrine and norepinephrine labels) — not with bicarbonate/alkaline fluids; protect from light and discard if discolored,,; dedicated line; never bolus or flush a vasoactive line; independent double‑check of drug, concentration, weight, and rate.,
◣ Admit · Discharge · Refer
  • Admit — all → PICU/high‑dependency; fluid‑refractory or vasoactive‑requiring shock is always PICU.
  • Home from the ward — not from the acute episode — step down once off vasoactives with a controlled source.
  • Refer — now — infectious diseases for source control and antimicrobials; surgery for a drainable focus; an ECMO center if refractory.
Septic shock — the first hourThe first hour, step by step: recognize → access + labs → fluids → reassess → vasoactive → hydrocortisone/PICU, with antibiotics inside the hour. Details in the card above.
!ANTIBIOTICS within 60 minutesBroad‑spectrum antibiotic(s) IV/IO by focus (see table), after cultures — do not delay for the lab.RECOGNIZEPoor perfusion — altered mentation, CRT > 2 s,mottled/cool skin, oliguria < 1 mL/kg/h.10 minACCESS + LABS100% O₂ (non‑rebreather) · two IV/IO. Draw glucose,lactate, ionized calcium, cultures, gas.2≤ 5 minFIRST FLUID BOLUSBalanced crystalloid 10–20 mL/kg, reassess after each. Cardiac: 5 mL/kgslowly. No ICU: bolus only if hypotensive (10–20 mL/kg, max 40 mL/kg).3≤ 15 minREASSESS + REPEATRepeat to 40–60 mL/kg in 1st hour — STOP at overload (hepatomegaly,crackles, gallop, B‑lines). Correct glucose + calcium.415–40 minSTART VASOACTIVEEpinephrine or norepinephrine, by physiology — notdopamine. Peripheral IV acceptable while central accessarranged.5fluid‑refractorySTILL SHOCKEDCatecholamine‑resistant → hydrocortisone(adrenal‑insufficiency risk). Call PICU; reassessperfusion continuously.6≤ 60 min

Myocarditis / Acute Heart Failure

HOURS

The "gastroenteritis" or "asthma" that is really the heart — look for it.

▸
◢ Recognize
  • Viral prodrome, then tachycardia out of proportion to the fever, poor feeding, lethargy, grunting or respiratory distress.
  • Hepatomegaly, gallop rhythm, weak pulses, cool peripheries. Older child: chest pain, syncope, palpitations.
  • Commonly mislabeled as gastroenteritis, sepsis, asthma, pneumonia, or bronchiolitis.
Confirm ECG (sinus tachycardia, low voltages, ST/T changes, arrhythmia, or heart block), chest X‑ray (cardiomegaly, pulmonary edema), troponin and BNP raised, echocardiogram for reduced function.
⚠ Resuscitate with care
  • Oxygen and close monitoring. Intubation is high‑risk in ventricular dysfunction (cardiac arrest at induction): do not intubate electively outside PICU; if unavoidable — most experienced operator, inotrope running and resuscitation drugs drawn up, PICU/cardiology (and the ECMO team where available) informed beforehand — call PICU.
  • Do not give large fluid boluses (expert consensus).
  • Use 5 mL/kg slowly and reassess for signs of fluid overload (worsening hepatomegaly, new crackles, a gallop, or respiratory distress).
  • Start inotropes early (cardiology/PICU‑directed) — milrinone (preferred if blood pressure allows — an inodilator that lowers afterload and can drop BP) or dobutamine.
  • Tailor to hemodynamics: normotensive with cold peripheries and rising lactate → dobutamine or milrinone; hypotensive with poor perfusion → epinephrine.
  • Check and correct electrolytes (calcium, potassium, magnesium, phosphate).
  • Treat arrhythmia, give oxygen and ventilatory support.
  • Early PICU and pediatric cardiology; refractory shock needs urgent PICU/cardiology transfer — advanced mechanical circulatory support is a specialist/PICU decision.
Inotropes / vasoactives
DrugDoseNotes
Milrinone0.25–0.75 mcg/kg/min IV infusionInodilator — first‑line inotrope (AHA 2021), if the blood pressure allows. Many units omit the 50 mcg/kg loading dose in acute shock to avoid hypotension (expert practice; not stated in the AHA statement).
Dobutamine2–20 mcg/kg/min IV infusionNormotensive with cold peripheries and rising lactate.
Epinephrine0.05–0.3 mcg/kg/min IV infusionHypotensive with poor perfusion — reserve vasopressor‑inotropes (epinephrine, dopamine) for hypotension or cardiogenic shock (more chronotropic and arrhythmogenic); calcium chloride or vasopressin can raise perfusion pressure without extra cardiac stimulation. Consider mechanical circulatory support (ECMO/VAD) early.
◣ Admit · Discharge · Refer
  • Admit — all suspected cases → PICU/cardiology; arrhythmia, low output, or a troponin/BNP rise mandates continuous monitoring.
  • Home from the ward — only after cardiology review, recovered function, and a heart‑failure plan.
  • Refer — now — cardiology urgently (echo, rhythm); a transplant/ECMO/mechanical‑support center if low output or refractory arrhythmia.

Bradycardia + Poor Perfusion

MINUTES

Slow heart rate with shock — usually hypoxic.

▸
First 100% oxygen, support airway & breathing, monitor, IV/IO. Ventilation corrects most pediatric bradycardia.
HR < 60 with poor perfusion despite oxygenation & ventilation? Poor perfusion = acutely altered mental status, signs of shock, or low BP.
YES
Start CPR. Give epinephrine. Atropine for a vagal cause or heart block; consider pacing. Treat the reversible cause; call PICU/cardiology early.
NO
Support, observe, treat the cause, seek cardiology input.
◣ Look for the cause
  • Hypoxia is the commonest — oxygenate and ventilate first. Also: hypothermia; drugs/toxins; raised intracranial pressure (Cushing's triad — hypertension, bradycardia, irregular breathing) (see Raised ICP); increased vagal tone (e.g., suctioning, intubation); AV / heart block.
  • A well, athletic, or sleeping child may be physiologically bradycardic.
DrugDoseNotes
Epinephrine (adrenaline)0.01 mg/kg (max 1 mg)IV/IO, 0.1 mg/mL (1:10,000) concentration, every 3–5 min
Atropine0.02 mg/kg (min 0.1 mg, max single dose 0.5 mg); may repeat onceIV/IO; for increased vagal tone or primary AV block. Organophosphate/carbamate poisoning needs larger, escalating doses (0.02 mg/kg, doubled every 5 min until secretions dry) — see Poisoning
◣ Admit · Discharge · Refer
  • Admit — all → PICU with continuous monitoring, including any child needing atropine, epinephrine, or pacing.
  • Discharge — only after a reversible cause is corrected, the rhythm is stable, and cardiology has reviewed.
  • Refer — cardiology for pacing or structural/conduction disease; treat reversible causes (hypoxia, vagal, raised ICP, toxins, electrolytes).
◈ Reading the tracing

Supraventricular Tachycardia

MINUTES

Narrow QRS, no rate variability. HR > 220 infant / > 180 child.

▸
◣ Throughout
  • Run a continuous ECG rhythm strip during every intervention — documents the moment of conversion; can unmask underlying WPW.
Hemodynamically unstable (shock, poor perfusion, reduced consciousness)?
UNSTABLE
Synchronized cardioversion; sedate only if it will not delay — use an agent that gives amnesia, not fentanyl alone (see sedation note). If IV/IO access is already in place, one rapid adenosine dose may be given while the defibrillator charges — never delay the shock.
STABLE
Vagal maneuvers first — ice to the face in infants; Valsalva in older children (modified/postural Valsalva: pediatric experience is very limited) — then adenosine.
✦ Modified Valsalva
  • Sit child semi‑recumbent; blow into a 10 mL syringe hard enough to just move the plunger (~15 s); then immediately lay flat and raise legs to ~45° for 15 s.
  • More effective than standard strain in the adult REVERT trial and a 2025 pediatric randomized trial.,
Drug / actionDoseNotes
Adenosine (1st dose)0.1 mg/kg (max 6 mg)⚠ Technique is critical: use the most proximal IV; two‑syringe or 3‑way‑stopcock method — rapid push, then an instant 5–10 mL saline flush while raising the arm. Often needs two people.
Adenosine (2nd dose)0.2 mg/kg (max 12 mg)If no response to the first dose.
If the 2nd dose failsConsult cardiologyNext steps (with cardiology): synchronized cardioversion, or one antiarrhythmic infusion — amiodarone 5 mg/kg over 20–60 min OR procainamide 15 mg/kg over 30–60 min; PALS 2025 adds IV sotalol as an option when SVT with compromise has failed vagal maneuvers, adenosine and cardioversion and no expert is reachable (dose and infusion time from the 2025 guideline/pharmacy protocol; it prolongs QT and depresses contractility). Never mix antiarrhythmics.
Synchronized cardioversion0.5–1 → 2 J/kgFor the unstable child. If it will not delay the shock, sedate with an agent that provides amnesia — do not rely on fentanyl alone (see the sedation note below).
⚠ Sedation for cardioversion — amnesia, not just analgesia
Fentanyl alone is a pitfall: it gives analgesia but no amnesia (pharmacology; PALS says only “consider sedation”), so the child may be awake and remember the shock; pushed rapidly it can cause chest‑wall rigidity. Ketamine’s myocardial depression matters mainly in prolonged, catecholamine‑depleted shock; in most children it is a net sympathomimetic (positive inotrope), and ketamine or etomidate is standard for brief pediatric procedural sedation — there are no RCTs for this ~60‑second window. Involve a pediatric anesthesiologist / follow your procedural‑sedation protocol.
◣ Admit · Discharge · Refer
  • Admit — first presentation, hemodynamic instability, or need for adenosine/cardioversion → monitored bed/PICU.
  • Home from the emergency department — a stable child who reverts and stays in sinus rhythm, feeding and well, with cardiology follow‑up and a clear return plan.
  • Refer — clinic — cardiology for all confirmed SVT (WPW screen, ablation planning) and for recurrent episodes.
◈ Reading the tracing

Ventricular Tachycardia (with a pulse)

MINUTES

Wide‑QRS tachycardia. Pulseless VT → use the arrest algorithm.

▸
Stable or unstable?
UNSTABLE
Synchronized cardioversion 0.5–1 → 2 J/kg. Sedate if it will not delay the shock — use an agent that gives amnesia, not fentanyl alone (see the sedation note in the Supraventricular Tachycardia card). Expert input.
STABLE
If regular and monomorphic, consider adenosine (diagnostic/therapeutic — may unmask SVT with aberrancy; not for irregular or polymorphic rhythms). Polymorphic VT / torsades → magnesium sulfate 25–50 mg/kg IV (max 2 g) and avoid QT‑prolonging antiarrhythmics. Contact cardiology before starting antiarrhythmics — a single infusion of amiodarone or procainamide (not both: additive QT prolongation).
DrugDoseNotes
Amiodarone5 mg/kg (max 300 mg)IV over 20–60 min if perfusing; monitor BP & QT
Procainamide15 mg/kgIV over 30–60 min; do not combine with amiodarone
◣ Admit · Discharge · Refer
  • Admit — all → PICU with continuous monitoring and a defibrillator at the bedside.
  • Home from the ward — not from the acute episode — only after cardiology work‑up and a management plan.
  • Refer — now — cardiology urgently (structural disease, channelopathy, QT/electrolytes).
  • Refer — clinic — consider genetics and family screening.
◈ Reading the tracing

Neonatal & Infant CHD

MINUTESRECOGNIZE BY PRESENTATION

Three ways congenital heart disease declares itself in the newborn — cyanosis, shock, or heart failure.

▸
① Cyanosis — cyanotic CHD ("5 T's + 1"); duct‑dependence varies
  • Transposition of the great arteries (duct‑dependent for mixing)
  • Truncus arteriosus (not duct‑dependent)
  • Total anomalous pulmonary venous drainage (not duct‑dependent; obstructed type = surgical emergency — alprostadil does not relieve the obstruction)
  • Tricuspid atresia
  • Tetralogy of Fallot — only the critical / pulmonary‑atresia type is duct‑dependent (ordinary TOF presents with tet spells; see below).
  • + 1: critical pulmonary stenosis / atresia.
  • Assess the response to oxygen — a formal hyperoxia test is no longer routinely recommended. High FiO₂ can accelerate ductal closure, dangerous in a duct‑dependent lesion. Use pre-/post‑ductal SpO₂, chest X‑ray + blood gas, and echocardiography instead. In suspected duct‑dependent CHD, do not delay alprostadil while waiting for a hyperoxia test.
② Cardiogenic shock / collapse — duct‑dependent systemic flow (left‑heart obstruction)
  • Hypoplastic left heart
  • critical coarctation
  • interrupted aortic arch
  • critical aortic stenosis.
  • Gray, mottled shock with weak/absent femoral pulses, a pre-/post‑ductal saturation & blood‑pressure gap, and metabolic acidosis. Avoid high inspired oxygen — it lowers pulmonary vascular resistance and steals from systemic flow. Start alprostadil.
③ Heart failure — left‑to‑right shunts
  • VSD
  • AVSD
  • PDA
  • (large ASD — rarely).
  • Present after the first weeks as pulmonary vascular resistance falls — not as immediate newborn emergencies; ASD rarely causes neonatal heart failure.
  • Tachypnea, poor feeding, sweating with feeds, hepatomegaly, faltering growth.
Suspect a duct‑dependent lesion → start Prostaglandin E1 (alprostadil) before the echocardiogram
Anticipate Apnea (be ready to intubate), hypotension, fever. Urgent cardiology + transfer; carry the infusion on transfer.
DrugDoseRoute & notes
Alprostadil (prostaglandin E1)Collapsed, acidotic or known left‑heart obstruction: start 0.05 mcg/kg/min (50 ng/kg/min), up to 0.1 (rarely 0.1–0.2 on specialist advice).
Suspected, well and not acidotic: start 0.005–0.015 mcg/kg/min (5–15 ng/kg/min); double every 20 min if no response, to max 0.1.
Maintenance: lowest effective dose (often 0.01–0.02 mcg/kg/min)
IV infusion (peripheral or central); two IV lines; never interrupt — not even for apnea. Apnea is the commonest side effect, mostly within the first hour and with doses above ~15 ng/kg/min; also hypotension, fever. Be ready to support ventilation.
⚠ Don't be caught out
  • The collapsed neonate labeled “sepsis,” “bronchiolitis,” or a “cyanotic spell” may be a closing duct.
  • If shock or cyanosis does not respond to oxygen and fluids, start alprostadil empirically while arranging an urgent echocardiogram — do not wait for imaging.
  • SpO₂ targets: 75–85% in duct‑dependent systemic or pulmonary lesions (accept down to 70% if lactate stays < 2 mmol/L); > 75% in transposition.
  • TGA or hypoplastic left/right heart with SpO₂ persistently < 70% and rising lactate → urgent tertiary cardiology call (emergency balloon atrial septostomy may be needed). Persistent acidosis or cyanosis (SpO₂ < 70%) despite maximum alprostadil → time‑critical transfer.
◈ Availability
  • Prescribe and label as ALPROSTADIL (the single unambiguous name — avoid the ambiguous "prostaglandin E1" and any trade name).
  • Stocked in neonatal and cardiac units.
◈ Arrhythmia
  • Tachycardia — SVT (narrow QRS) and ventricular tachycardia (wide QRS): see the Supraventricular Tachycardia and Ventricular Tachycardia cards; adenosine dosing is given on the SVT card.
  • Screen every well newborn before discharge — see Critical CHD — Pulse Oximetry Screening (Neonatal).
◣ Admit · Discharge · Refer
  • Admit — any duct‑dependent lesion or cyanosis/shock → NICU/PICU; keep the duct open with alprostadil.
  • Home — only under cardiology, with a feeding/oxygen/weight plan and clear red‑flag advice.
  • Refer — now — pediatric cardiology urgently (echo) and a cardiac‑surgical center; arrange safe transfer.
◈ See also Newborn screening & pulmonary hypertension: Critical CHD — Pulse Oximetry Screening · Persistent Pulmonary Hypertension (PPHN) (Neonatal).

Hypercyanotic (Tet) Spell

MINUTESTETRALOGY OF FALLOT

Sudden deep cyanosis, distress, and a quieter murmur in Tetralogy of Fallot.

▸
① Position & calm Knee‑to‑chest position (or let the child squat). Keep calm — minimal handling. Give 100% oxygen.
② Increase RV preload Morphine to settle the cycle; fluid bolus to increase filling.
③ Increase systemic resistance / slow the heart
  • Phenylephrine; IV beta‑blocker (esmolol or propranolol) only on PICU/cardiology advice — watch for hypotension and myocardial depression. Avoid agents that increase contractility — they worsen the outflow obstruction.
  • Phenylephrine, IV beta‑blocker, and bicarbonate (for persistent acidosis) are specialist‑supported — call PICU/cardiology early.
④ Still hypercyanotic Anesthesia/PICU: paralyze, intubate and ventilate; continue phenylephrine; urgent cardiac‑surgical referral.
DrugDoseNotes
Morphine0.1–0.2 mg/kgIV/IM/subcut; settles the spell
Crystalloid bolus10–20 mL/kgIV, increases preload
Phenylephrine5–20 mcg/kgIV; raises systemic vascular resistance (formulary dosing)
Propranolol0.05–0.1 mg/kgslow IV; alternative to esmolol (formulary dosing)
Esmolol500 mcg/kg IV load over 1 min, then 50–300 mcg/kg/min infusionIV beta‑blocker alternative to propranolol (formulary dosing)
Sodium bicarbonate1 mmol/kgIV, if significant metabolic acidosis
◣ Admit · Discharge · Refer
  • Admit — any spell → monitored bed/PICU; recurrent or severe spells need urgent intervention.
  • Home from the ward — only after cardiology review, a spell‑management plan (knee‑chest, hydration, propranolol as advised), and caregiver education.
  • Refer — now — pediatric cardiology urgently — a spell often brings surgical repair forward.
◈ See also Neonatal & Infant CHD for duct‑dependent lesions and alprostadil.

Blocked Systemic‑to‑Pulmonary Shunt (BT / Sano)

MINUTESShunt‑dependent CHD

Sudden cyanosis with a lost shunt murmur — the shunt is occluding; a peripheral‑hospital emergency.

▸
◣ Recognize it — the shunt is blocking
  • Known shunt‑dependent cyanotic CHD (modified Blalock–Taussig or Sano shunt) with acute, severe cyanosis., Modified Blalock–Taussig shunt: a tube graft from the subclavian or innominate artery to the pulmonary artery. Sano shunt: a tube graft from the right ventricle to the pulmonary artery, used in the first‑stage (Norwood) operation for hypoplastic left heart syndrome.
  • Loss of the continuous shunt murmur (a patent shunt has continuous turbulent flow; an occluded shunt has no flow).
  • Sudden desaturation, then hypotension and metabolic acidosis; falling PaO2, rising lactate, falling cerebral NIRS from baseline.,
  • Echo: reduced or absent flow across the shunt confirms it — but do not delay treatment for imaging.,
⚠ Call for help now
  • Call cardiac ICU/PICU + cardiothoracic surgery + cardiology immediately, and activate your retrieval service.,
  • The physiology to fix it: drive more blood across the shunt — raise systemic vascular resistance (SVR) and lower pulmonary vascular resistance (PVR) — while you anticoagulate.
① RESUSCITATE (airway & oxygen) — Secure the airway and ventilate; give 100% oxygen and optimize oxygenation. Urgent echo — but do not delay treatment.,
② RAISE SVR (push flow across the shunt) — Fluid bolus 5 mL/kg aliquots (4% albumin), reassessing; add a vasoconstrictor — phenylephrine 5–20 mcg/kg IV bolus (infusion 0.1–0.5 mcg/kg/min), or norepinephrine 0.025–0.3 mcg/kg/min, or epinephrine infusion.
③ LOWER PVR (unload the lungs) — Deepen sedation + paralysis; hyperventilate to lower PaCO2 (mild respiratory alkalosis); keep well oxygenated. On cardiac‑center advice, magnesium sulfate 0.4 mmol/kg (≈ 100 mg/kg = 0.2 mL/kg of the 50% solution; max 2 g) may be added: dilute to ≤ 20% and infuse over 20–30 min — never as an IV push; continuous BP monitoring with vasopressor support running (magnesium also lowers SVR).
④ ANTICOAGULATE (stop the clot) — Heparin 50–100 units/kg IV bolus (AHA 2018, class IIa), then 20 units/kg/h infusion (infants: 25–30 units/kg/h). Restart prostaglandin (alprostadil) if the arterial duct has not been surgically ligated.
⑤ DEFINITIVE RESCUE — cardiac catheterization (balloon angioplasty, stent, or thrombolysis) or emergency surgical shunt revision; ECMO to bridge a deteriorating child.,, Confirm with echo and transfer to the cardiac center.,
Medications — heparin, phenylephrine and norepinephrine doses per AHA 2018 (Marino); albumin, epinephrine and magnesium doses are expert practice; confirm against your cardiac center's protocol
Drug / productDoseNotes
▮ SVR Phenylephrine5–20 mcg/kg IV bolus; infusion 0.1–0.5 mcg/kg/minRaises SVR; dilute before use (e.g., 10 mg in 100 mL, then 1 mL made up to 10 mL)
▮ SVR Norepinephrine (noradrenaline)0.025–0.3 mcg/kg/min infusionRaises SVR; central line preferred, peripheral as a bridge,
▮ SVR Epinephrine (adrenaline)up to 0.05 mcg/kg/min infusionInotrope/vasopressor support
▮ SVR Albumin 4%5 mL/kg aliquotsVolume to support preload/SVR; reassess after each
▮ PVR Magnesium sulfate 50%0.4 mmol/kg (≈ 100 mg/kg = 0.2 mL/kg of 50%; max 2 g) IV over 20–30 minPulmonary vasodilator — helps lower PVR. Dilute to ≤ 20% before infusion; never IV push; monitor BP (systemic vasodilator).
▮ CLOT Heparin50–100 units/kg IV bolus
→ 20 units/kg/h (infants: 25–30 units/kg/h)
Prevents clot propagation; monitor APTT / anti‑Xa,,
▮ DUCT Prostaglandin E1 (alprostadil)per unit protocolIf the duct is not ligated — may reopen ductal pulmonary flow
✦ The trap
The instinct to give a vasodilator, or deep vasodilating sedation without vasopressor support, drops SVR and worsens shunt flow. Do the opposite — raise SVR, lower PVR, heparinize, and get the child to the cath lab or operating room. A lost shunt murmur in a cyanotic child is the shunt occluding until proven otherwise.,

Acute Rheumatic Fever

DIAGNOSEAHA 2015 · AHA 2009 · RHDAustralia 2020

Prevent the second attack — every recurrence adds valve damage.

▸
◣ Diagnose — Jones 2015 (revised)
  • Need evidence of preceding group A strep (rising/elevated ASO or anti‑DNase B, a positive throat culture, or a positive rapid antigen test in a child with a high pre‑test probability of streptococcal pharyngitis — a recent scarlet fever history is supportive but is not one of the 2015 criteria) plus either 2 major or 1 major + 2 minor.
  • Recurrence also allows 3 minor. Chorea and indolent carditis can be diagnostic on their own.
  • Get an echo in every suspected case (repeat even if first is normal) — subclinical valve regurgitation counts as carditis.
⚠ Use the moderate/high‑risk column
  • Kuwait has no recent ARF incidence data to show it meets the AHA low‑risk definition (< 2 per 100,000 school‑age children per year), and many children seen here come from high‑incidence regions — so this guide applies the moderate/high‑risk column (local consensus), accepting lower specificity.
  • In this group a single joint (mono‑arthritis or even mono‑arthralgia) and a lower fever/ESR threshold already count.
Jones 2015Low‑risk populationModerate / high‑risk (Gulf)
MajorCarditis (clinical or subclinical on echo) · migratory polyarthritis (flitting, large joints) · chorea · erythema marginatum · subcutaneous nodulesSame, except joints = mono‑arthritis or polyarthritis, or polyarthralgia only after other causes have been excluded — exclude septic arthritis before counting a single inflamed joint
MinorPolyarthralgia · fever ≥ 38.5 °C · ESR ≥ 60 mm/h and/or CRP ≥ 3.0 mg/dL (30 mg/L) · prolonged PR (if carditis not a major)Mono‑arthralgia · fever ≥ 38 °C · ESR ≥ 30 mm/h and/or CRP ≥ 3.0 mg/dL (30 mg/L) · prolonged PR (if carditis not a major)
A manifestation counts once — polyarthritis as a major cannot also be counted as a minor.
Treat
TargetWhat to give
Eradicate GAS (everyone, even if swab negative)Benzathine penicillin G IM once: ≤ 27 kg → 600,000 units; > 27 kg → 1,200,000 units. Alt: penicillin V PO ×10 d; if allergic, azithromycin 12 mg/kg/day (max 500 mg) ×5 d.
Arthritis / mild carditisUntil the diagnosis is confirmed: acetaminophen alone (15 mg/kg/dose every 4 h; max 60 mg/kg/day or 4 g/day) — NSAIDs mask evolving joint signs and fever. Then first‑line naproxen 10–20 mg/kg/day PO in 2 divided doses (max 1,250 mg/day) or ibuprofen 5–10 mg/kg/dose PO every 8 h (max 2,400 mg/day). Second‑line: aspirin 50–60 mg/kg/day PO in 4–5 divided doses (may be escalated to 80–100 mg/kg/day), continued until symptoms and inflammatory markers settle, then tapered; watch for tinnitus/hyperpnea (salicylate toxicity).
Moderate–severe carditis / heart failureConsider prednisone/prednisolone 1–2 mg/kg/day (max 80 mg) in selected severe carditis, then taper, overlapping aspirin — overall benefit in meta‑analyses is not evident. Diuretic + ACE inhibitor for heart failure; bed rest.
Sydenham choreaUsually self‑limited — quiet environment, protect from injury. If disabling: carbamazepine (first‑line) or valproate (off‑label); a corticosteroid may be added for very severe chorea. Salicylates do not treat the chorea itself.
Secondary prophylaxis — benzathine penicillin G IM every 3–4 weeks (≤ 27 kg 600,000 units; > 27 kg 1,200,000 units)
Category (from last attack)Duration
ARF without carditis5 years or until age 21 (whichever longer)
Carditis, no residual valve disease10 years or until age 21 (whichever longer)
Carditis with residual valve disease10 years or until age 40 (whichever longer), sometimes lifelong. WHO 2024: evidence on duration is limited — follow national/professional guidance; in children with mild isolated regurgitation and a normal echocardiogram, stopping after 1–2 years may be reasonable
◈ When to use oral penicillin instead IM benzathine remains preferred for most patients. Exception — severe valve disease (severe mitral stenosis, aortic stenosis or aortic regurgitation), LVEF < 50%, or NYHA III–IV heart‑failure symptoms (including severe acute carditis with heart failure): sudden cardiovascular collapse has followed the injection, so prefer oral penicillin V, decided with cardiology (AHA advisory 2022; WHO 2024). WHO also accepts oral penicillin where IM delivery cannot be assured, or when recurrence risk is low (e.g., age ≥ 40), decided jointly with the patient. Oral penicillin V 250 mg twice daily is also the accepted alternative if the IM injection is declined (sulfadiazine if penicillin‑allergic), although adherence is worse and it is less effective. For any IM dose: give lying down, fed and hydrated, and observe ≥ 30 min with epinephrine at hand.
✦ The point of the card
  • Treatment settles the attack; prophylaxis prevents rheumatic heart disease.
  • Recurrences are cumulative valve damage — document the injection schedule and hand it over so it is never missed.

Pericarditis & Cardiac Tamponade

MINUTESESC 2015 · ESC 2025

Tamponade is a clinical diagnosis — drain, don't wait for the scan.

▸
◣ Pericarditis — chest pain + additional criteria (ESC 2025)
  • Pleuritic chest pain relieved by sitting forward,
  • pericardial friction rub,
  • widespread ST elevation / PR depression on ECG (not one coronary territory)
  • new/worsening pericardial effusion on echo.,
  • raised CRP — now a formal criterion
  • pericardial edema or late gadolinium enhancement on cardiac MRI
  • ESC 2025: pleuritic/positional chest pain plus the additional criteria above (rub · ECG changes · raised CRP · new/worsening effusion · CMR findings): definite = pain + more than 1 additional criterion; possible = pain + 1; unlikely = pain alone. (ESC 2015: any 2 of 4 — chest pain, rub, ECG changes, effusion.)
  • Causes — viral/idiopathic (commonest), purulent, post‑pericardiotomy, autoimmune (SLE, JIA), uremic, TB, malignancy,.
⚠ Tamponade — recognize and act
  • Beck's triad (hypotension, muffled heart sounds, and raised JVP) + tachycardia and a narrow pulse pressure; pulsus paradoxus > 10 mmHg (inspiratory drop in systolic BP).
  • Children compensate then crash — tachycardia is the early sign. A small effusion can tamponade if it accumulates fast — volume on echo does not equal severity; the clinical picture does.
  • Beck's triad and pulsus are often incomplete — their absence does not exclude it.
Hemodynamic compromise (tamponade)?
YES
Emergency echo‑guided pericardiocentesis — removing even a small volume rescues output. IV fluid 10–20 mL/kg is a bridge only, never a substitute (expert consensus — not guideline‑stated). Maintain systemic vascular resistance with a vasopressor — norepinephrine (± vasopressin) — as a temporizing bridge to support coronary and systemic perfusion; keep the circulation full, fast, and tight (preload, avoid bradycardia, support afterload; expert consensus — not guideline‑stated). Avoid intubation / positive‑pressure ventilation — it drops preload and can cause arrest; if unavoidable, drain first, low tidal volume/PEEP, keep volume‑loaded (expert consensus — not guideline‑stated). Avoid diuretics/vasodilators.
NO
Uncomplicated pericarditis: high‑dose NSAID (ibuprofen) until symptoms resolve; add colchicine for recurrent pericarditis — it halved recurrences in children (in adults it is also given for a first episode). Treat the cause; restrict strenuous exercise until symptom‑free with normal CRP/ECG/echo. No corticosteroids in children unless there is a specific indication such as autoimmune disease (growth and other side effects; they also increase recurrence); no aspirin (Reye syndrome, hepatotoxicity). Anti‑IL‑1 therapy (anakinra) may be considered for recurrent, especially steroid‑dependent, pericarditis.
DrugPediatric doseNotes
Ibuprofen30–40 mg/kg/day divided every 6–8 h (max ~2.4 g/day)First‑line anti‑inflammatory; give with gastroprotection, taper on CRP.
Colchicine< 5 yr: 0.5 mg/day · > 5 yr: 1–1.5 mg/day dividedAdjunct for recurrent pericarditis in children (ESC class IIa) — halves recurrence; reduce in renal impairment.,
Purulent pericarditisUrgent drainage + IV vancomycin + 3rd‑gen cephalosporin, ~3–4 weeks (antibiotic choice and duration: expert consensus — not guideline‑stated)Surgical emergency — NSAIDs alone are inadequate; narrow to culture.
✦ The trap
Don't reach for the ventilator in a crashing tamponade — positive‑pressure ventilation can be the last straw. Drain first. And treat purulent pericarditis as the surgical emergency it is.,

Infective Endocarditis (incl. Subacute)

HOURSDuke‑ISCVID 2023 / AHA

Fever + a new murmur + positive cultures — think endocarditis; diagnose by the Duke‑ISCVID 2023 criteria.

▸
◣ Suspect it — subacute clues
  • Persistent/unexplained fever with a new or changed regurgitant murmur — the classic pairing.,
  • Subacute course over weeks: malaise, weight loss, night sweats, anorexia. Viridans‑group streptococci are the commonest cause in children with underlying heart disease (typically subacute native‑valve disease); S. aureus dominates in children without heart disease and in acute disease.
  • Peripheral stigmata (late; immune‑mediated or embolic): splinter hemorrhages, tender Osler nodes, painless Janeway lesions, Roth spots, splenomegaly, embolic phenomena.,
  • At‑risk: congenital heart disease, prosthetic valve/material, previous IE, indwelling central lines, IV drug use.,
◣ Duke‑ISCVID 2023 criteria — how to classify
  • DEFINITE (clinical) = 2 major, or 1 major + 3 minor, or 5 minor.,
  • POSSIBLE = 1 major + 1 minor, or 3 minor.,
  • REJECTED = firm alternative diagnosis, or resolution with ≤ 4 days of antibiotics.
The three MAJOR domains (Duke‑ISCVID 2023)
MICROBIOLOGY
Typical organism in ≥ 2 separate blood‑culture sets (S. aureus, S. lugdunensis, E. faecalis, all streptococci except S. pneumoniae/S. pyogenes, Granulicatella, Abiotrophia, Gemella, HACEK; with intracardiac prosthetic material also coagulase‑negative staphylococci, Corynebacterium striatum/jeikeium, Serratia marcescens, Pseudomonas aeruginosa, Cutibacterium acnes, non‑tuberculous mycobacteria, Candida) or a non‑typical organism in ≥ 3 sets; or Coxiella burnetii phase I IgG > 1:800 (or one positive culture), Bartonella IgG ≥ 1:800, or blood PCR positive for Coxiella, Bartonella or T. whipplei.
IMAGING · SURGICAL
Imaging: echocardiography, cardiac CT or [18F]FDG PET/CT evidence of endocardial involvement — on echo: vegetation, abscess, new partial dehiscence of a prosthetic valve, or new valvular regurgitation (worsening of an existing murmur is not enough). Surgical: endocarditis documented at operation. Definite / possible / rejected thresholds are unchanged.
◣ The five MINOR criteria
  • Predisposition — predisposing heart condition or IV drug use.,
  • Fever > 38°C.,
  • Vascular phenomena — arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial or conjunctival hemorrhage, Janeway lesions.,
  • Immunologic phenomena — glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor.,
  • Microbiologic evidence not meeting a major criterion. (The 2023 Duke‑ISCVID update adds imaging and surgical criteria and new predispositions.)
⚠ Workup — get it right the first time
  • Draw ≥ 3 sets of blood cultures from separate venipunctures before starting antibiotics — the single most important step for diagnosis and tailoring therapy.,
  • Echo: TTE first; proceed to TEE if TTE is non‑diagnostic, a prosthetic valve is present, or suspicion stays high.,
  • Add ESR/CRP, CBC, and urinalysis (microscopic hematuria supports it). Do not delay antibiotics in a septic/unstable child once cultures are drawn.
◈ Endocarditis prophylaxis (AHA / ESC 2023) — who
Prophylaxis needs both a highest‑risk cardiac condition and a high‑risk procedure., The highest‑risk cardiac conditions:
  1. Prosthetic heart valve (surgical or transcatheter) or prosthetic material used for valve repair.,
  2. Previous infective endocarditis.,
  3. Unrepaired cyanotic CHD (including palliative shunts/conduits).,
  4. Completely repaired CHD with prosthetic material/device — during the first 6 months after the procedure.
  5. Repaired CHD with a residual defect at or adjacent to the prosthetic patch/device.
  6. Cardiac transplant recipients who develop valvulopathy.
  7. Left ventricular assist device (LVAD) or implantable heart (AHA 2021; also ESC 2023).,
  8. Surgical or transcatheter pulmonary artery valve or conduit (e.g., Melody valve, Contegra conduit) — no 6‑month limit.
◆ ESC 2023 emphasis: for all intermediate- and high‑risk patients, good oral hygiene and regular dental review prevent more endocarditis than any single antibiotic dose.,
◈ Endocarditis prophylaxis (AHA) — which procedures
  • Dental — any procedure that manipulates gingival tissue or the periapical region of teeth, or perforates the oral mucosa (extractions, scaling, periodontal work, implants). Anesthetic injections through non‑infected tissue, radiographs, orthodontic appliance placement or adjustment, and shedding of deciduous teeth do not count.,
  • Respiratory tract — procedures with incision or biopsy of the respiratory mucosa (e.g., tonsillectomy, adenoidectomy, bronchoscopy with biopsy). If the airway procedure treats an established infection, add an anti‑staphylococcal agent when S. aureus is suspected.
  • Infected skin, skin structures, or musculoskeletal tissue — regimen should cover staphylococci and β-hemolytic streptococci.
  • Not recommended for GI or GU procedures, or for bronchoscopy/endoscopy without incision/biopsy, solely to prevent endocarditis.
  • ◆ ESC 2023 is less restrictive for non‑dental procedures — systemic prophylaxis may be considered (Class IIb) in high‑risk patients undergoing an invasive diagnostic or therapeutic respiratory, GI, GU, skin, or musculoskeletal procedure. Where the two guidelines differ, follow your local protocol.
Prophylaxis regimen — single dose 30–60 min before the procedure
SituationPediatric dose (single)Max
Able to take oralAmoxicillin 50 mg/kg PO2 g
Unable to take oralAmpicillin 50 mg/kg IM/IV, or cefazolin / ceftriaxone 50 mg/kg IM/IVAmpicillin 2 g · cefazolin/ceftriaxone 1 g
Penicillin allergy — oralCephalexin 50 mg/kg, or azithromycin / clarithromycin 15 mg/kg, or doxycycline (< 45 kg 2.2 mg/kg; ≥ 45 kg 100 mg)Cephalexin 2 g · azithromycin/clarithromycin 500 mg · doxycycline 100 mg
Penicillin allergy — no oralCefazolin or ceftriaxone 50 mg/kg IM/IV1 g
✦ The trap
Clindamycin is no longer recommended (dropped in the 2021 AHA update — C. difficile risk and adverse effects). Prophylaxis is not indicated for most CHD, nor for routine GI/GU procedures., Avoid cephalosporins if there is a history of anaphylaxis, angioedema, or urticaria to penicillin. Good oral hygiene and regular dental care prevent more endocarditis than any single antibiotic dose.,
04

Common Acute Conditions

Everyday clinic & ED infections and presentations

Fever in a Well‑Appearing Infant < 2 Months

HOURS≤ 60 DAYS · CPS 2026 / AAP 2021

Most are viral — but ~8–13% have a serious bacterial infection. Define fever as rectal ≥ 38.0°C; stratify risk and spare the low‑risk from over‑testing.

▸
◣ Scope & first move
  • This pathway is for the well‑appearing, full‑term (≥ 37 wk), previously healthy infant with a documented rectal temperature ≥ 38.0°C. Hypothermia < 36.0°C also signals an elevated risk of infection — manage identically.
  • This pathway does not apply to the ill‑appearing at any age.
  • Exclusions — an infant with any of these risk factors is outside this pathway (manage individually and conservatively): prematurity < 37 wk, prior or prolonged hospitalization, a chronic / genetic / technology‑dependent condition, immunodeficiency, recent antibiotics, or any focal bacterial infection (e.g., omphalitis, cellulitis).
⚠ Keep a high index of suspicion
  • Even a well‑appearing infant can deteriorate quickly.
  • The youngest (≤ 21–28 days) have the highest risk of invasive bacterial infection (IBI — bacteremia or bacterial meningitis) and the lowest threshold for full work‑up, LP, empiric antibiotics, and admission.
◣ Everyone gets
  • All ages: history + exam, urinalysis + urine culture (catheter or suprapubic; clean‑catch acceptable), blood culture, CBC + differential, and an inflammatory marker — procalcitonin (PCT) or CRP.
  • Risk‑stratify with a validated rule: PECARN or Step‑by‑Step (both use PCT), or Aronson when PCT is unavailable — keep a lower threshold for LP with Aronson.
  • CSF pleocytosis = > 15 cells/mm³ (≤ 28 d) or > 9 cells/mm³ (> 28 d) → treat as bacterial meningitis. Don't delay the LP if there are neurological signs.
Risk stratification — validated low‑risk rules
RuleLow risk if ALL criteria are met
PECARN (uses PCT)1) Urinalysis negative (leukocyte esterase, nitrite, ≤ 5 WBC/hpf); 2) ANC ≤ 4000/µL; 3) PCT ≤ 0.5 ng/mL,
Step‑by‑Step (uses PCT)1) Well‑appearing; 2) 22–90 days; 3) urinalysis negative for leukocytes; 4) PCT < 0.5 ng/mL; 5) CRP ≤ 20 mg/L and ANC ≤ 10,000/µL,
Aronson (no PCT — keep a lower LP threshold)Low risk if ≤ 1 point: age < 21 d (1) · ED temp 38.0–38.4°C (2) or ≥ 38.5°C (4) · ANC ≥ 5185/µL (2) · urinalysis positive (3),
◈ Applying the rules — PCT timing & alternatives
  • Where procalcitonin is not readily available, PECARN and Step‑by‑Step (both require PCT) cannot be fully applied. Use an alternative: the Aronson rule (no PCT needed) and keep a lower threshold for LP; CRP ≤ 20 mg/L with a normal ANC and urinalysis still support lower risk.
  • When PCT is obtained, draw it ≥ 2 h after fever onset — it rises ~3–4 h after a bacterial trigger, so very early samples can read falsely low. It typically stays low (< 0.5 ng/mL) in isolated viral illness.
  • Missed invasive infection with Step‑by‑Step clusters in the 22–28‑day group and in infants tested very early — keep a low threshold in these.
Fever pathway algorithms (well‑appearing, ≥ 37 weeks)
Algorithm 1 — infant 0–28 days with fever ≥ 38°C
Infant aged 0–28 days with fever ≥ 38 °CRisk Factors? prematurity < 37 wk, prior or prolonged hospitalization, a chronic /genetic / technology‑dependent condition, immunodeficiency, recent antibiotics, orany focal bacterial infection (e.g., omphalitis, cellulitis).Assess ClinicallyExit PathwayYESRisk StratificationPECARN, Step‑by‑Step, or AronsonLow riskfor IBIHigh riskfor IBIOPTION 1:•Perform LP•Hospitalization with or without Abx•Observe culture resultsOPTION 2:•LP refusal (shared decision withfamily; need to understand risks)•Hospitalization without Abx•Observe pending culturesAny positive culture•Perform LP•Start AntibioticsPerform LPEmpiric antibioticsHospitalization
Algorithm 2 — infant 29–60 days with fever ≥ 38°C
Infant aged 29–60 days with fever ≥ 38 °CRisk Factors? prematurity < 37 wk, prior or prolonged hospitalization, a chronic /genetic / technology‑dependent condition, immunodeficiency, recent antibiotics, orany focal bacterial infection (e.g., omphalitis, cellulitis).Assess ClinicallyExit PathwayYESRisk StratificationPECARN, Step‑by‑Step, or AronsonLow risk OR only urinalysis‑positiveYESNOLow riskfor IBIHigh riskfor IBINegative Urinalysis•No antibiotics•Observation in hospital or closefollow‑up (every 24 hours)Positive Urinalysis•Start Abx for UTI•LP only if clinically indicatedPositive Blood Culture•Repeat blood culture•Perform LP•Start antibiotics according to culturePerform LPEmpiric antibioticsHospitalization
Empiric antibiotics — well‑appearing, ≥ 37 weeks
AgeFirst‑line IVModifiers
0–7 daysAmpicillin 50 mg/kg/dose q8h (meningitis 100 mg/kg/dose q8h) + gentamicin 4 mg/kg/dose q24h,Meningitis: add — or replace the aminoglycoside with — cefotaxime 50 mg/kg/dose q8h. HSV risk: add acyclovir 20 mg/kg/dose q8h.
8–28 daysAmpicillin 50 mg/kg/dose q6h (meningitis 75 mg/kg/dose q6h) + gentamicin 5 mg/kg/dose q24h,Meningitis: add — or replace the aminoglycoside with — cefotaxime 50 mg/kg/dose q6h (200 mg/kg/day for meningitis at this age). HSV risk: add acyclovir 20 mg/kg/dose q8h.
29–60 daysCeftriaxone 100 mg/kg/dose q24hMeningitis: add vancomycin 15 mg/kg/dose q6h. HSV risk: add acyclovir 20 mg/kg/dose q8h. Low‑risk UTI: cefixime 8 mg/kg/dose q24h PO.,
◈ Beyond 60 days The well‑appearing infant 61–90 days falls outside this pathway: risk of invasive infection is lower and routine blood culture / full septic work‑up is not required. At minimum obtain a urinalysis and urine culture in every febrile infant 61–90 days; blood culture, CBC and PCT/CRP with risk stratification as for 29–60 days are optional (clinician's choice). Infants who are low‑risk, or have an isolated UTI and are clinically well, can go home with follow‑up in 24–48 h; escalate the ill‑appearing or those with abnormal results.
◈ See also For the ill‑appearing or septic neonate (≤ 28 days) use Neonatal Sepsis — Early‑Onset (rapid approach). Ampicillin uses one regimen throughout this guide — 50 mg/kg/dose, q8h in the first week and q6h from day 8, with the term‑neonate meningitis doses (100 mg/kg/dose q8h in the first week, then 75 mg/kg/dose q6h) from Lexicomp; CPS gives 75 mg/kg/dose q6h. Gentamicin and cefotaxime doses are the CPS regimen.

Gastroenteritis & Dehydration

HOURS

Assess hydration: alertness, eyes, mucosa, skin turgor, capillary refill, urine output.

▸
◣ Clinical signs of dehydration
  • Altered mental status
  • sunken eyes
  • dry oral mucosa
  • poor skin turgor
  • delayed capillary refill
  • decreased urine output
  • tachycardia
  • abnormal peripheral perfusion.
  • The more signs present, the greater the fluid deficit; no single sign is reliable alone.
Degree of dehydration?
NONE–MODERATE
Oral rehydration with ORS; a single ondansetron dose can reduce vomiting and the need for IV.
SEVERE / SHOCK
IV/IO crystalloid bolus, repeat to reverse shock; then deficit + maintenance. Check glucose & electrolytes.
Drug / fluidDoseRoute & notes
Oral rehydration solution~50–100 mL/kg over 4 hOral/NG + replace ongoing losses. First‑line for minimal–moderate dehydration.
0.9% sodium chloride (bolus)20 mL/kgIV/IO rapid bolus for hypovolemia/shock; reassess during & after each bolus and repeat until perfusion is restored. If shock seems out of proportion to the diarrhea/vomiting, consider sepsis, DKA, a surgical abdomen, or myocarditis. Balanced crystalloid (e.g., Ringer's lactate) is an acceptable alternative.
0.9% sodium chloride (moderate)10 mL/kg over 30–60 minModerate dehydration not tolerating oral — then reassess for a further bolus or transition back to ORT if tolerated.
Ondansetron0.15 mg/kg/dose — single dose, max 8 mg (either route). Weight‑based: 2 mg (8–15 kg) · 4 mg (15–30 kg) · 8 mg (> 30 kg)PO preferred; age ≥ 6 months only. Reduces vomiting and the need for IV. Restart ORT 15–30 min after the dose. Ondansetron prolongs the QT interval dose‑dependently — do not exceed 8 mg in a single pediatric dose (the 16 mg cap is an adult chemotherapy figure, not for gastroenteritis).
Zinc (adjunct to ORS)5 mg/dayOral, 10–14 days (WHO 2024, conditional recommendation — replaces the former 20 mg/day [10 mg/day < 6 months], which caused more vomiting). A WHO/UNICEF measure for low- and middle‑income settings where zinc deficiency is common — shortens diarrhea by ~½ day (~1 day if malnourished); the benefit is concentrated in children ≥ 6 months who are zinc‑deficient or malnourished. Not routine in high‑income, well‑nourished populations including Kuwait; reserve for malnutrition, documented zinc deficiency, or persistent / chronic diarrhea. Little benefit under 6 months. (ESPGHAN/ESPID acute‑gastroenteritis guideline: zinc not recommended for well‑nourished European children.)
Racecadotril — optional adjunct1.5 mg/kg/dose PO TID with ORS
sachets 10 mg (≤ ~12 kg) / 30 mg (> ~13 kg). Age > 3 months. Continue until diarrhea stops (2 normal stools), max 7 days.
Antisecretory enkephalinase inhibitor — reduces stool water loss without slowing gut motility (unlike loperamide, which is contraindicated). Adjunct to ORS, not a substitute. Licensed and used in Kuwait/Europe/Asia; not FDA/NICE/AAP/CPS/WHO‑endorsed. ESPGHAN/ESPID 2014: “may be considered” (II‑B, weak recommendation, moderate‑quality evidence; responder NNT ≈ 4). Cochrane 2019 found it safe with limited benefit (low‑certainty).
Pearls
  • Resume normal feeding (including breastfeeding) early. Antibiotics only for specific pathogens.
  • C. difficile (CPS 2026) — do not test healthy children < 2 years (colonization is common, disease rare); think of it with diarrhea after antibiotics, in IBD, immunocompromise or hospital stay. Non‑severe: oral vancomycin 40 mg/kg/day in 4 doses (max 125 mg/dose) for 10 days (preferred), or metronidazole 30 mg/kg/day in 4 doses (max 500 mg/dose) for 10 days; stop the precipitating antibiotic. Severe (systemic toxicity): oral vancomycin as above. Severe complicated (hypotension/shock, ileus, megacolon, peritonitis): vancomycin 40 mg/kg/day in 4 doses (max 125 mg/dose; 2 g/day) PO/NG — or rectally if ileus — plus IV metronidazole 30 mg/kg/day in 4 doses (max 500 mg/dose) for 10–14 days; surgical review. IV vancomycin does not treat C. difficile. Second or later recurrence: tapered/pulsed vancomycin, or fidaxomicin 200 mg PO twice daily for 10 days if ≥ 6 months and ≥ 12.5 kg — with infectious diseases.
  • Red flags: bilious or bloody vomit, severe pain/distension (think surgical), inability to tolerate ORS.
  • Zinc dosing & evidence: WHO guideline on management of pneumonia and diarrhoea in children up to 10 years of age (2024)QR.
◣ Admit · Discharge · Refer
  • Admit — shock or severe dehydration, failed oral/NG rehydration, intractable vomiting, dangerous electrolyte derangement, or diagnostic uncertainty.
  • Home from the emergency department — minimal or mild dehydration tolerating oral rehydration, with carers confident on fluids and red‑flag advice.
  • Refer — now — surgical review if a surgical abdomen is suspected; PICU for refractory shock or severe electrolyte disturbance.

Acute Otitis Media

ASSESSINFANT–CHILD · CPS 2016 / AAP 2013

Diagnose by the drum, not the symptoms — then choose between watchful waiting and antibiotics.

▸
◣ Clinical diagnosis — effusion + acute inflammation
  • Acute onset (otalgia, ear‑tugging, or non‑specific signs in the non‑verbal child) plus a middle‑ear effusion plus signs of acute inflammation.
  • A bulging tympanic membrane is the key sign — highest predictive value for bacterial AOM, especially if yellow, cloudy, or hemorrhagic. Acute perforation with purulent otorrhea also confirms a bacterial cause — distinguish from otitis externa, chronic drainage, or tube discharge.
  • Not AOM: a non‑bulging drum, or erythema / air‑fluid level alone without bulging. Effusion without inflammation is OME — do not give antibiotics.
  • Scope: the watchful‑waiting option applies only to healthy children ≥ 6 months (CPS 2016). AAP 2013 is narrower: observation only for unilateral non‑severe AOM at 6–23 months and for non‑severe AOM at ≥ 24 months — bilateral AOM at 6–23 months is treated at once, and moderate otalgia counts as severe,. Infants < 6 months are excluded from observation — treat all with antibiotics. Excludes tympanostomy tubes, craniofacial anomalies, immunocompromise, or recurrent AOM.
Decision by age & severity
How old is the child, and how severe?
< 6 MONTHS
Antibiotics for all — no watchful waiting (below the CPS/AAP observation range; the exam is less reliable and complications are more likely). In a febrile infant ≤ 90 days, do not attribute the fever to AOM alone — evaluate for invasive bacterial infection (see Fever in the Well‑Appearing Infant).
≥ 6 MO — TREAT NOW
Bulging, erythematous TM and any of: highly febrile (≥ 39°C), moderately‑to‑severely ill, severe otalgia, symptoms ≥ 48 h, perforation with otorrhea, bilateral AOM at 6–23 months (AAP), or complicated disease (mastoiditis, facial palsy).
≥ 6 MO — WATCHFUL WAITING (24–48 H)
Otherwise‑healthy child, mildly ill, alert, responding to antipyretics, low‑grade fever (< 39°C), mild otalgia — or when the diagnosis is uncertain. Needs assured follow‑up.
◈ How to watchful‑wait (choose one)
  • Reassess within 24–48 h to document the course; or have the caregiver return if no improvement or worsening by 48 h; or give a “safety‑net” prescription to fill only if not improved by 48 h.
  • Always give analgesia advice; ensure ready access to care.
DrugDoseRoute & notes
Amoxicillin (first choice)40–45 mg/kg/dose BID (max 4 g/day)PO. Drug of choice — covers S. pneumoniae; excellent middle‑ear penetration.
Amoxicillin‑​clavulanate40–45 mg/kg/dose BID (amoxicillin component; max 4 g/day amoxicillin)PO. If AOM + purulent conjunctivitis, amoxicillin in the last 30 days, or failure at 48–72 h. Specify the 14:1 suspension (for children up to 40 kg; above that use an adult formulation).
Cefuroxime‑​axetil15 mg/kg/dose BID (30 mg/kg/day; max 1 g/day)PO, twice daily. Non‑anaphylactic penicillin allergy (cefprozil is an alternative).
Ceftriaxone50 mg/kg IM/IV once daily × 3 daysIf oral not tolerated or amoxicillin‑clavulanate failed. Reserve.
◈ Duration — by age
  • < 2 years: 10 days. ≥ 2 years, uncomplicated: 5 days (CPS 2016; AAP 2013 gives 7 days for 2–5 years and 5–7 days for ≥ 6 years).,
  • Also 10 days for a perforated TM or recurrent AOM.
  • Symptoms should improve within 24 h and resolve in 2–3 days — reassess if they persist or worsen.
⚠ Analgesia is part of every plan
  • Pain control (acetaminophen or ibuprofen) is essential whether or not antibiotics are given — it is often the child's main need.
  • Persistent effusion after treatment does not warrant a change of antibiotic; a middle‑ear effusion can linger for months.
◣ Admit · Discharge · Refer
  • Admit — a complication (mastoiditis, intracranial spread, facial palsy), a toxic child, or failure of second‑line therapy.
  • Home from the emergency department — uncomplicated disease — analgesia, with observation or antibiotics per age and severity, and safety‑netting.
  • Refer — now — ENT for suspected mastoiditis or complicated disease.
  • Refer — clinic — ENT for recurrent disease or a non‑resolving effusion.

GAS Pharyngitis

ASSESS≥ 3 YR · IDSA 2025

Most sore throats are viral. Score first to decide who needs a test — then treat the confirmed case.

▸
◣ When to test — score first
  • Sore throat is usually viral, and clinician judgment alone is unreliable. GAS causes up to ~30% of childhood (and ~15% of adult) pharyngitis.
  • IDSA 2025 suggests a clinical scoring system to decide who to test. A score is most useful for spotting low‑probability patients in whom testing is unlikely to help — prefer a score that needs no lab (Centor / McIsaac).
  • Does not apply under 3 years — GAS in this age may not show the typical features; test only for an outbreak, scarlet fever, or a household case.
  • Score criteria point to GAS: fever, tonsillar swelling or exudate, tender anterior cervical nodes, and absence of cough. Cough, coryza, or hoarseness point to a virus.
Centor / McIsaac — one point eachPoint
Tonsillar exudate or swelling+1
Tender / swollen anterior cervical nodes+1
History of fever+1
No cough+1
Age 3–14 years (McIsaac)+1
◈ How to test
  • Read the score as a probability of GAS (IDSA 2025, Centor / McIsaac): 0–1 low (~7–13%) → testing can usually be deferred; 2–3 intermediate (~21–38%) → test; ≥4 high (~50–70%) → test, and still confirm before treating.
  • Test with a rapid antigen test (RADT), a molecular test (NAAT), or throat culture.
  • In children, confirm a negative rapid antigen test with culture, or use a molecular test.
  • The score selects who to test — never a treatment threshold.
  • Do not use ASO titers to diagnose acute pharyngitis.
  • Start treatment within 9 days of onset.
⚠ Test even if the score is low
Test regardless of a low score when the patient is high‑risk: a household GAS case (shared indoor living or sleeping space), prior rheumatic fever, or features of complicated or systemic GAS — peritonsillar or retropharyngeal abscess, scarlet fever, or toxic shock.
Lab‑confirmed GASDrug & doseDuration
First choiceAmoxicillin 50 mg/kg once daily (max 1 g) or 25 mg/kg/dose BID (max 500 mg/dose); or penicillin V 250 mg BID–TID (children), 250 mg QID or 500 mg BID (adolescents and adults)10 days
Poor adherence expectedBenzathine penicillin G IM — < 27 kg: 600,000 units; ≥ 27 kg: 1,200,000 units (deep IM only — never IV)1 dose
Non‑immediate (delayed / non‑IgE) penicillin allergyCephalexin 20 mg/kg/dose BID (max 500 mg/dose) ◈ if unavailable: cefuroxime‑axetil 20 mg/kg/day ÷ BID (max 500 mg/day) PO10 days
Documented penicillin anaphylaxis / IgE‑mediated (immediate) reactionAzithromycin 12 mg/kg on day 1 (max 500 mg)
then 6 mg/kg (max 250 mg) once daily on days 2–5 (IDSA, as corrected 2014) — the FDA‑labeled 12 mg/kg once daily × 5 days (max 500 mg/day) is an accepted alternative
or clarithromycin 7.5 mg/kg/dose BID (max 250 mg/dose) × 10 days
or clindamycin 7 mg/kg/dose TID (max 300 mg/dose) × 10 days
5–10 days
⚠ Why we treat
  • Antibiotics prevent suppurative complications and acute rheumatic fever (but not post‑streptococcal glomerulonephritis). All GAS is penicillin‑susceptible, but macrolide and clindamycin resistance is now common (about one in three invasive US isolates per CDC surveillance; 5–8% and ~1% when IDSA 2012 was written) and varies locally — reserve those for true penicillin anaphylaxis and confirm local susceptibility.
  • Acetaminophen or ibuprofen for pain and fever; corticosteroids are not recommended as analgesic adjuncts.
◣ Admit · Discharge · Refer
  • Admit — rarely — complications (peritonsillar abscess, dehydration, systemic illness).
  • Home from the emergency department — most, with antibiotics and safety‑net advice.
  • Refer — now — ENT for abscess.
  • Refer — clinic — ENT for recurrent tonsillitis.

Urinary Tract Infection

HOURS> 2 MONTHS

A common occult source of fever in infants — get a reliable sample before antibiotics.

▸
◁ When to suspect & test
  • Preverbal child with unexplained fever (> 39°C, no source) — especially fever > 48 h without another focus. A clear viral source (coryza, cough, diarrhea, rash) makes UTI unlikely.
  • Verbal child (≥ 3 yr): dysuria, frequency, hematuria, abdominal/back pain, or new daytime incontinence. Beware bubble‑bath / hygiene vulvovaginitis — sterile cultures, often mis‑treated as UTI.
  • Usual pathogens: E. coli (most), then Klebsiella, Enterobacter, Citrobacter, Serratia; S. saprophyticus in adolescent girls.
  • Do not over‑diagnose: low colony counts, mixed growth, or no pyuria usually mean contamination or asymptomatic bacteriuria.
Sampling — before antibiotics
  • Toilet‑trained: clean‑catch midstream. Not toilet‑trained: catheter or suprapubic aspirate for culture.
  • A bag specimen may screen the urinalysis but its culture is unreliable (contamination up to 63%) — never use it to diagnose.
  • A single antibiotic dose sterilizes urine; always collect first.
◈ Interpreting the urinalysis UTI is unlikely if the urinalysis is completely normal. Leukocyte esterase or nitrite positive ≈ 93% sensitive; nitrite alone is highly specific (~98%) but often falsely negative (frequent voiding, Gram‑positive / non‑nitrate organisms). Pyuria (AAP 2026, unspun urine): under 2 months ≥ 5 WBC/HPF or ≥ trace leukocyte esterase; 2 months to 5 y ≥ 10 WBC/HPF or ≥ 2+ leukocyte esterase to start treatment (once the culture is positive, ≥ 5 WBC/HPF or ≥ 1+ is enough). Nitrite does not show inflammation, so it cannot separate UTI from asymptomatic bacteriuria.
Diagnostic colony‑count thresholds
Collection methodMinimum count (CFU/mL)Note
Clean catch / midstream≥ 10⁵Mixed growth usually = contamination.
In‑and‑out catheter≥ 10⁴Single uropathogen plus pyuria (AAP 2026; lowered from 5 × 10⁴). Indwelling‑catheter specimens less reliable.
Suprapubic aspirate≥ 10⁴Single uropathogen plus pyuria (AAP 2026). Most reliable method.
◣ Admit · Discharge · Refer
  • Admit — young infants, ill/septic, unable to tolerate oral, or complicated/obstructive UTI.
  • Home — well child on oral antibiotics with follow‑up.
  • Refer — clinic — nephrology/urology for recurrent, atypical, or obstructive UTI, or abnormal imaging.

UTI — Treatment & Follow‑up

HOURSLOCAL SUSCEPTIBILITY

Oral is fine for most non‑toxic children — pick the empiric agent from your antibiogram; plan for ESBL.

▸
Cystitis or febrile UTI / pyelonephritis?
CYSTITIS · AFEBRILE LOWER TRACT
Dysuria/frequency, no fever (mainly post‑pubertal girls). 3 days (NICE NG109, to which NG224 refers) of an oral agent chosen by local E. coli susceptibility. No imaging needed.
FEBRILE UTI / PYELONEPHRITIS
Treat 5–7 days from 2 months of age (AAP 2026: a course of ≤ 7 days rather than longer). Give a longer course (> 7 days) to infants under 2 months and to children with a urinary tract anomaly, bacteremia, or no clinical response to the initial course. Oral is as effective as IV in non‑toxic children likely to tolerate every dose. Use IV initially if toxic, aged ≤ 28 days, vomiting, or unable to tolerate oral — then step down early once improving (AAP 2026: oral from > 28 days of age if well and tolerating).
◈ ESBL risk — plan for it
  • ESBL‑producing Enterobacterales are increasingly isolated even without prior antibiotics — often resistant to cephalosporins and many oral agents.
  • Where local ESBL rates are high or the child is high‑risk: amikacin (IV) is the most reliable aminoglycoside — active against the large majority of pediatric ESBL isolates, whereas gentamicin is variable (roughly half),,. TMP‑SMX (PO) is a useful oral step‑down once susceptibility is confirmed, though ESBL isolates are often co‑resistant.
  • Fluoroquinolones are not routine in prepubertal children but may be used if the isolate is resistant to other oral options and oral therapy is a reasonable alternative to parenteral treatment.
Antimicrobial options — if the isolate is susceptible
DrugDoseNotes
Amikacin (IV)15 mg/kg once daily (max 1.5 g/day)ESBL‑active empiric choice,,; once‑daily 15 mg/kg per the UK SmPC; monitor levels & renal function if > 48 h.
Gentamicin (IV/IM)5–7.5 mg/kg once dailyESBL activity variable (~half of isolates) — confirm susceptibility. Monitor levels / renal function > 48 h.
Ceftriaxone (IV/IM)50–75 mg/kg once daily (max 2 g)Less nephrotoxic but broader; not reliable if ESBL.
Ampicillin (IV)50 mg/kg/dose q6h (max 2 g/dose)± aminoglycoside; many E. coli now resistant. (Lexicomp)
TMP‑SMX (PO)4–5 mg/kg/dose (TMP) BID (max 160 mg TMP/dose)Preferred oral step‑down once susceptible — covers many ESBL isolates if tested S.
Cefixime (PO)8 mg/kg/dose once daily (max 400 mg/day)Common first oral choice pending susceptibilities (if low ESBL).
Cefdinir (PO)7 mg/kg/dose BID or 14 mg/kg once daily (max 600 mg/day)Palatable oral step‑down; not always on the MOH formulary. Like cefixime, not reliable against ESBL.
Cephalexin (PO)12.5 mg/kg/dose QIDOral cephalosporin option.
Amoxicillin‑​clavulanate (PO)13 mg/kg/dose (amoxicillin component; 7:1) TIDIf susceptible; amoxicillin alone often resisted.
Ciprofloxacin (PO) *15 mg/kg/dose BID (max 750 mg/dose)* Not routine in prepubertal children — reserve for resistant isolates.
◁ Complicated UTI — escalate & image early
  • Hemodynamic instability, rising creatinine, abdominal/bladder mass, poor urine flow, or no improvement by 24 h / fever not settling by 48 h on appropriate antibiotics.
  • Use IV until clearly improving; start with a renal & bladder ultrasound (RBUS) to look for obstruction or abscess.
⚠ Imaging & follow‑up
  • RBUS after a first febrile UTI in a child < 5 yr (AAP 2026). It need not be done during the acute illness — arrange it before discharge; scan acutely if the illness is severe or atypical.
  • VCUG is not routine — consider it after a first febrile UTI only if RBUS is abnormal (hydronephrosis, scarring, or findings suggesting high‑grade VUR or obstructive uropathy), with an atypical pathogen or complex course, or after a second febrile UTI,. AAP 2026: offer VCUG for a clinically relevant RBUS abnormality, for every child under 2 years with a second febrile UTI, and from 2 years with a second febrile UTI that has no other explanation. After a first febrile UTI with a normal RBUS it is an option only in selected groups (age < 1 month, organism other than E. coli, circumcised boys, septic shock or ICU admission, or unreliable follow‑up). No routine prophylaxis in low‑risk VUR (grade I–II without bladder–bowel dysfunction). A normal RBUS does not exclude VUR (VCUG grades reflux; DMSA for scarring).
  • Routine antibiotic prophylaxis is not recommended while awaiting RBUS.
  • Repeat urinalysis / culture to confirm cure is not recommended unless symptoms persist.
  • Counsel families to test urine early in any future unexplained fever.
  • Recurrent afebrile UTI is often driven by bladder–bowel dysfunction — assess and treat constipation (a major, modifiable risk factor).

Skin & Soft Tissue Infections

ASSESSCPS 2026

Match the antibiotic to the layer and the pathogen — most are oral, short‑course, and cephalexin‑first.

▸
◣ Types — by depth & morphology
  • Impetigo (epidermis): non‑bullous (honey‑crusted) or bullous; highly contagious. Mostly group A streptococcus (GAS) / S. aureus.
  • Erysipelas / cellulitis (dermis → subcutis): spreading erythema, warmth, tenderness. Non‑purulent cellulitis is more often GAS; purulent points to S. aureus.
  • Folliculitis / furuncle / carbuncle / abscess: discrete pus collections — S. aureus (methicillin‑susceptible, MSSA, or methicillin‑resistant, MRSA). Source control is the priority.
  • Necrotizing infection (fascia/muscle): pain out of proportion, rapid spread, necrosis, crepitus — surgical emergency. GAS ± polymicrobial.
How severe, and is there pus?
MILD / NON‑PURULENT
Impetigo or small localized lesion, systemically well — often resolves with skin/wound care alone. Limited: topical mupirocin 2% TID × 5 days. Widespread/multiple lesions or systemic features: oral cephalexin.
PURULENT — ABSCESS / FURUNCLE
Incision & drainage is the treatment. For a small, drained abscess in a healthy host without surrounding cellulitis, antibiotics are usually not needed; stop them once source control is achieved.
SEVERE / DEEP / NECROTIZING
Extensive or rapidly progressive, systemic toxicity, necrosis or crepitus → admit, urgent surgical debridement, and broad empiric IV therapy: piperacillin‑tazobactam (or ceftriaxone) + vancomycin + clindamycin (antitoxin); stop vancomycin once MRSA is excluded; consult infectious diseases.
Oral cephalexin is the antimicrobial of choice when antibiotics are warranted.
By pathogen / setting
TargetDrug & doseNotes
MSSA / GAS — oral, first‑lineCephalexin 50–100 mg/kg/day PO ÷ TID–QID (e.g., 25 mg/kg/dose QID or 33 mg/kg/dose TID; max 1 g/dose, 4 g/day)
upper end, TID for adherence, for moderate cellulitis managed as an outpatient
Drug of choice (CPS 2026). Covers MSSA and GAS. Upper‑range dosing enables outpatient treatment of moderate cellulitis.,
MSSA / GAS — IV (admitted)Cefazolin 33 mg/kg/dose IV q8h (max 2 g/dose)IV first‑line for non‑toxic inpatients. Step down to oral cephalexin on improvement.
GAS — streptococcalAmoxicillin 25 mg/kg/dose PO BID (max 4 g/day); penicillin G IV if severeFor confirmed/likely pure GAS (erysipelas, non‑purulent cellulitis).
MRSA — oral, first‑lineTrimethoprim-sulfamethoxazole 4–6 mg/kg/dose (trimethoprim component) PO BID (max 160 mg TMP/dose)Preferred oral MRSA agent — also covers GAS. Use when colonized or MRSA strongly suspected.
MRSA — alternativeClindamycin 10 mg/kg/dose PO/IV q8h (max 600 mg/dose PO [1.8 g/day], 900 mg/dose IV [2.7 g/day])Only where local clindamycin susceptibility is high. Anti‑toxin role in severe disease.
MRSA — IV (severe)Vancomycin 15 mg/kg/dose IV q6h (max 4 g/day before level‑guided adjustment)Add when MRSA suspected in toxic/deep infection; stop once MRSA excluded. K. kingae (the leading bone/joint pathogen at 6–48 months) is generally susceptible to β‑lactams, so cefazolin/cephalosporins — rather than vancomycin or clindamycin alone — are preferred empirically for bone/joint infection in under‑4s.,
◈ Duration & step‑down
  • 5–7 days is usually enough, even for many severe SSTIs (rarely > 7 days).,
  • Failure to improve → re‑evaluate diagnosis and source control, not simply broaden.
  • Avoid routine combination therapy (e.g., cephalexin + TMP‑SMX) and broad outpatient IV (ceftriaxone).
  • If a child improves on a non‑MRSA agent but is later found MRSA‑colonized/positive, do not switch — clinical response governs.
⚠ Preventing recurrence
  • Protect the skin barrier: optimize eczema control, diligent wound care, cover open lesions, treat scabies/lice, and encourage varicella vaccination.
  • Reserve decolonization (5‑day nasal mupirocin + chlorhexidine washes, or dilute bleach baths) for recurrent moderate–severe SSTIs or household clusters — success is variable and re‑colonization common.
◣ Admit · Discharge · Refer
  • Admit — systemic illness, rapid spread, an abscess needing drainage, immunocompromise, or failed oral therapy; suspected necrotizing infection → emergency.
  • Home — localized, well child on oral antibiotics with review.
  • Refer — now — surgery for drainage or necrotizing infection.

Cervical Lymphadenopathy

ASSESSCOMMON

Very common and usually reactive — your job is to separate the benign node from the few that need antibiotics, imaging, or a malignancy work‑up.

▸
◣ What counts as abnormal
  • A small, mobile, palpable node is normal in most healthy children. Treat a cervical node > 1 cm as enlarged (inguinal > 1.5 cm; epitrochlear > 0.5 cm).,
  • A supraclavicular node is never normal — it is the single highest‑risk site for malignancy. Image and investigate every one.,,
  • Sort by tempo & laterality — it points to the cause.,
Pattern → likely cause
PatternThinkAction
Acute, bilateral, tenderReactive viral URTI (commonest)
EBV / CMV if prolonged with splenomegaly
Supportive, no antibiotics, safety‑net. EBV serology if a glandular‑fever picture.,
Acute, unilateral, tender, warm ± fluctuantBacterial lymphadenitis — S. aureus (incl. MRSA) & group A strepEmpiric oral antibiotics 10 d; ultrasound if fluctuant → drain an abscess. Review at 48 h.,,
Subacute (2–6 wks) / chronic (> 6 wks), often non‑tenderNontuberculous (atypical) mycobacteria (violaceous, "cold", young child), cat‑scratch (Bartonella), TB, toxoplasma,Don't just re‑course antibiotics — investigate. NTM → complete surgical excision; cat‑scratch → usually self‑limited (azithromycin if bulky/symptomatic).,,,
⚠ Can't‑miss — red flags for malignancy (lymphoma / leukemia / metastasis)
  • Supraclavicular node; hard, matted, fixed, or painless / rubbery; > 2 cm and enlarging; persisting or progressive beyond 4–6 weeks; generalized nodes (≥ 2 non‑contiguous regions) or hepatosplenomegaly; B symptoms — unexplained fever > 38°C, drenching night sweats, weight loss > 10%; a mediastinal mass on chest X‑ray.,,,,
  • Any one → urgent bloods + imaging and refer., Strongest predictors: a larger node and older age — the risk rises with each — more nodal sites, a supraclavicular site, fixed nodes, and an abnormal chest X‑ray; fever, weight loss, and organomegaly may also raise the odds.,,
◣ Work‑up (when it isn't simple reactive)
  • Bloods: CBC + differential + blood film (blasts, cytopenias), ESR / CRP, LDH; EBV / CMV serology; a TB test (IGRA or tuberculin); Bartonella / toxoplasma serology if exposed.,,,
  • Imaging: ultrasound first‑line (size, abscess, architecture); chest X‑ray if any red flag (mediastinal mass).,,,
  • Biopsy (excisional preferred) for a red‑flag or supraclavicular node, failure to regress by 4–6 weeks, or progression despite treatment.,,,
Empiric antibiotics — acute bacterial lymphadenitis (10 days)
SettingOralNotes
Cover S. aureus + GASCephalexin 50–100 mg/kg/day ÷ 3–4 (max 4 g/day) OR amoxicillin-clavulanate,Review at 48 h; most settle within days. Add source control if an abscess forms.
MRSA risk / penicillin allergyClindamycin 20–40 mg/kg/day ÷ 3,Also covers GAS; use per local MRSA rates.,
Fluctuant / abscessIncision & drainage + cultureUltrasound‑guided if deep; send pus for routine and mycobacterial culture.,,
✦ Don't forget
  • A cervical node ≥ 1.5 cm is a clinical criterion of Kawasaki disease — reassess if fever has lasted ≥ 5 days.
  • Tender anterior nodes with exudative pharyngitis suggest GAS pharyngitis.
  • A firm supraclavicular or matted node in a child with pallor or bruising → treat as possible malignancy and refer same day.,,
✦ Your role — the general pediatrician
  • Most nodes are yours to manage. Do the first‑line assessment and reassurance; classify by duration (acute ≤ 2 wks · subacute 2–6 wks · chronic > 6 wks) and actively look for a red flag.,,
  • Treat acute bacterial lymphadenitis empirically and review at 48 h. Safety‑net every child and set a definite review point — a node that has not begun to shrink by ~4 weeks, or is growing, needs work‑up.,,
  • You can start the first‑line bloods and request the ultrasound yourself. Refer early rather than re‑course antibiotics for a persistent or red‑flag node: same‑day to hematology‑oncology for a hard/matted/supraclavicular node or systemic features; surgery/ENT for excision biopsy (persisting > 6 weeks or progressive); infectious diseases for suspected TB or atypical mycobacterial disease.,,,,
◣ Admit · Discharge · Refer
  • Admit — systemically unwell, a large / fluctuant node needing drainage, airway or deep‑space concern, or a strong malignancy suspicion.,,,
  • Home from the emergency department — the well child with a small, mobile, reactive node → safety‑net and review in 2–4 weeks.,,
  • Refer — clinic — surgery / ENT for excision (NTM, abscess, biopsy); hematology‑oncology for a red‑flag node; infectious diseases for TB or atypical infection.,,

Fever — Assessment & Antipyretics

ASSESSNICE NG143

Fever ≥ 38°C. Treat the child's discomfort and risk — not the number.

▸
◣ Risk‑assess by traffic light (and by age)
  • Any infant under 3 months with fever is high‑risk → use the Fever in the Young Infant pathway.
  • Red (high‑risk): pale/mottled/ashen/blue, no response to social cues, unrousable, weak/high‑pitched cry, grunting, respiratory rate > 60, reduced skin turgor, bulging fontanelle, neck stiffness, non‑blanching rash, focal seizures/neurology.
  • Amber (intermediate): pallor, decreased activity, poor feeding, dry mucous membranes, reduced urine, nasal flaring, tachycardia, fever ≥ 5 days, rigors, non‑weight‑bearing/limb swelling.
  • Green (low‑risk): normal color, responsive, content, moist membranes — manage at home with safety‑netting.
Antipyretic dosing
Drug · routeDoseMax · notes
Acetaminophen — PO10–15 mg/kg/dose every 4–6 h PRN≤ 1 g/dose, ≤ 5 doses/24 h; max 75 mg/kg/day (not > 4 g/day). Onset 30–60 min.
Acetaminophen — IV≥ 2 y: 15 mg/kg/dose every 6 h
29 days–2 y: 15 mg/kg/dose every 6 h
Neonate (birth–28 days): 12.5 mg/kg/dose every 6 h
≥ 2 y: max 750 mg/dose if < 50 kg, 1 g/dose if ≥ 50 kg; ≤ 75 mg/kg/day (not > 4 g/day). 29 days–2 y: max 60 mg/kg/day. Neonate: max 50 mg/kg/day. Daily maxima include acetaminophen by all routes.
Ibuprofen — PO5–10 mg/kg/dose every 6–8 hAge ≥ 6 months. Max 400 mg/dose, 40 mg/kg/day. Give with food + ensure hydration.
Ibuprofen — IV10 mg/kg/dose every 6–8 hAge ≥ 6 months. Max 400 mg/dose, 40 mg/kg/day.
◈ Avoid
  • Acetaminophen — severe liver failure.
  • Ibuprofen — dehydration / any poorly hydrated child, renal impairment, active GI bleeding / ulcer disease, and chickenpox (varicella) — associated with severe skin and soft‑tissue infection; use acetaminophen (see Must‑Avoid Drugs).
⚠ Use antipyretics for comfort, not the thermometer
  • Give only while the child is uncomfortable.
  • Giving both agents together (PITCH trial) gave more fever‑free time over 24 h than either alone, but cleared fever no faster than ibuprofen alone and did not improve comfort — so for comfort one agent is usually enough.
  • Switch agents if discomfort is not relieved; alternate only if discomfort recurs before the next dose; counsel carefully to avoid dosing errors.
  • Tepid sponging is not recommended; don't over- or under‑wrap. Antipyretics do not prevent febrile seizures. Encourage fluids; safety‑net for red/amber signs.

The Rash — Approach & Red Flags

MINUTES

Two questions first: does the child look unwell, and does the rash blanch?

▸
◣ Step 1 — Does the child look unwell? (before focusing on the rash)
  • Rapid ABCDE‑style screen: work of breathing; color and perfusion (capillary refill > 2–3 s, mottled, cold peripheries); heart rate and respiratory rate for age; mental status (irritable, lethargic); fever; neck stiffness, photophobia, bulging fontanelle in infants.
  • Any red flag → urgent assessment + empiric IV antibiotics (see Septic Shock), in parallel with the rash exam. Looks well → Step 2.
  • A blanching rash does not rule out sepsis — meningococcal disease often begins as a blanching maculopapular rash before turning petechial or purpuric, and the classic non‑blanching rash can be a late sign. Escalate an unwell child whatever the rash looks like.
  • Darkly pigmented skin: erythema, petechiae and purpura may appear dark brown or violaceous and be masked — check all over the body (including the nappy area), look for petechiae in the conjunctivae, and lower the threshold to escalate.
Step 2 — Does the rash blanch? (press a clear glass against it)
Does the rash blanch under glass?
NON‑BLANCHING
Petechiae (< 2 mm) or purpura (> 2 mm) — purpura carries higher risk. Unwell or febrile → treat as invasive meningococcal disease / sepsis until excluded. A well child still needs a diagnosis and follow‑up (see below) — do not dismiss just because they look well.
BLANCHING
Usually benign — viral exanthem, urticaria, or eczema. Treat symptomatically; safety‑net with clear advice to "come back if the child becomes unwell, even if the rash looks the same or fades."
Non‑blanching — sort the cause
CauseKey features
Meningococcal / invasive bacterialIll, febrile — emergency (identified at Step 1)
IgA vasculitis (Henoch–Schönlein)Palpable purpura on buttocks and legs in a well child; abdominal pain, arthralgia/arthritis; check urine for blood and protein (renal involvement)
Immune thrombocytopenia (ITP)Well child, isolated low platelets, bruising; often post‑viral; watch for mucosal bleeding (epistaxis, gums)
Mechanical purpuraForceful cough, vomiting or breath‑holding; classically above the nipple line (head and neck, SVC territory) — benign
LeukemiaPallor, hepatosplenomegaly, fatigue, bone pain, unexplained bruising
Blanching — sort the cause
CauseKey features
Viral exanthemsRoseola, measles, rubella, slapped‑cheek (parvovirus B19); hand‑foot‑and‑mouth and varicella are vesicular, not purely maculopapular
Scarlet feverSandpaper rash + strawberry tongue → penicillin
UrticariaTransient wheals → antihistamine; airway or systemic features → see Anaphylaxis
Kawasaki diseaseFever ≥ 5 days + rash + non‑purulent conjunctivitis + mucositis/strawberry tongue + extremity changes + cervical node — easily mistaken early for scarlet fever or a viral exanthem (see Kawasaki Disease)
⚠ Any unwell child is the emergency
  • Escalate immediately — with or without a rash, and whatever the rash looks like.
  • This alone is sufficient.
◣ Escalate urgently — regardless of blanching — also if
  • Non‑blanching rash with fever, ill appearance, or rapid spread.
  • Retiform purpura (branching, angulated, stellate) rather than round petechiae/purpura — suggests vascular occlusion (DIC, severe sepsis, vasculitis) and is higher‑acuity than ordinary purpura.
  • Mucosal involvement (eyes, mouth, genitals) with blistering or skin peeling → Stevens–Johnson syndrome / TEN or toxic shock syndrome. Superficial peeling with perioral crusting and radial fissures but mucous membranes spared, especially in young children → staphylococcal scalded skin syndrome (SSSS) — mucosal sparing is the classic clue that separates SSSS from SJS/TEN. The Nikolsky sign (gentle shearing pressure separates the epidermis) is positive in SJS/TEN, SSSS, and pemphigus.
  • Vesicles in a neonate → herpes simplex. Skin vesicles never appear in roughly 30–40% of neonatal HSV with CNS or disseminated disease (32% CNS, 39% disseminated) — keep the threshold low for a full sepsis + HSV workup (and empiric acyclovir) in any unwell neonate, even with no rash.
  • Fever ≥ 5 days with rash plus any Kawasaki features.
◈ Bedside tips
Faded or changed rash? Ask whether a parent photographed it — useful for evanescent eruptions like urticaria. Stroke test: a wheal along a tongue‑blade stroke = dermographism (common, benign); a wheal raised specifically over a pigmented lesion = Darier's sign (mastocytosis — worth recognizing in recurrent unexplained wheals). Herpes zoster in a dermatomal band is usually benign and immunocompetent in children, especially after early‑life varicella or vaccination; consider underlying immunodeficiency only if it is multidermatomal, sacral, recurrent, prolonged or treatment‑refractory, or has invasive features.

Preseptal & Orbital Cellulitis

HOURSCPS 2026

The orbital septum is the firewall — eye signs separate sight‑threatening orbital disease from benign preseptal swelling.

▸
◤ The distinction that drives everything
  • The orbital septum is the anatomic firewall. Preseptal (periorbital) = infection anterior to it — usually from skin trauma or sinusitis; mostly benign. Orbital = posterior to it — a complication of ethmoid sinusitis eroding the lamina papyracea; threatens vision and brain.
  • The distinction drives etiology, imaging, antibiotics, and disposition.
Differentiate at the bedside
Clinical featurePreseptalOrbital
Eyelid swelling & erythemaPresentPresent
Pain with eye movementAbsentPresent
Extraocular movementsNormalImpaired / restricted
ProptosisAbsentOften present
Chemosis / diplopia / ↓ acuity / RAPDAbsentMay be present
Fever / toxic appearanceMay be presentUsually present
◁ Etiology & microbiology
  • Preseptal — traumatic: skin flora after a bite/scratch → S. pyogenes, S. aureus.
  • Preseptal — atraumatic: a complication of bacterial rhinosinusitis.
  • Orbital: mirrors acute sinusitis — Streptococcus (anginosus, pyogenes, pneumoniae groups); S. aureus and oral anaerobes in chronic sinusitis / older children; H. influenzae if under‑immunized.
  • MRSA: generally low but rising — risk factors do not reliably predict it; a negative nasal MRSA swab reliably excludes it and guides the oral step‑down.
◈ Imaging — contrast CT orbits + sinuses
  • Well children with uncomplicated preseptal disease need no imaging.
  • Contrast CT is first‑line; MRI preferred if intracranial extension or cavernous sinus thrombosis is suspected.
  • Its job: find who needs surgery or has a complication.
  • Image if toxic appearance, optic‑nerve signs (abnormal vision, RAPD), intracranial signs (focal deficit, seizure), prominent forehead swelling, high‑risk labs (CRP > 120 mg/L, WBC > 20,000/µL or ANC > 10,000/mm³), or to resolve diagnostic uncertainty.
  • Blood count and CRP (± blood culture) for severe infection, uncertain preseptal vs orbital extent, or a limited examination (young child); conjunctival swabs are not recommended.
  • Otherwise reasonable to delay CT 24–36 h to judge response when ENT / ophthalmology are available.
◣ Admit · Discharge · Refer
  • Admit — orbital signs, systemic illness, age < 1, and all true orbital cellulitis → IV antibiotics.
  • Home from the emergency department — mild preseptal in a well child on oral antibiotics with 24 h review.
  • Refer — now — ophthalmology and ENT for orbital involvement; surgery for an abscess.

Preseptal & Orbital — Management

HOURSRISK‑BASED

Preseptal is mostly oral outpatient; orbital is admitted, IV, and shared with ENT + ophthalmology.

▸
Preseptal or orbital?
PRESEPTAL — MOSTLY OUTPATIENT
Well, immunized child, eyelid erythema/edema with normal painless eye movements, normal vision, no proptosis → oral antibiotics + review. Admit the very young, severe, or not‑improving.
ORBITAL — ADMIT, EMERGENCY
Pain/restriction on eye movement, proptosis, chemosis, diplopia, reduced acuity, or RAPD → admit: CBC/CRP, blood cultures, IV antibiotics, same‑day ENT + ophthalmology, CT per criteria. Do not swab the conjunctiva (contamination).
What to send
  • Uncomplicated preseptal, well child: no work‑up.
  • Severe / uncertain / young child: CBC + CRP. Severe disease: blood cultures before antibiotics. Drained pus / abscess → culture ± PCR. MRSA nasal swab where available — a negative result reliably excludes MRSA and guides the oral step‑down.
Empiric antimicrobial therapy
ScenarioFirst‑lineDose (max) · MRSA / notes
Traumatic preseptal (bite / broken skin)PO cephalexin
IV cefazolin
Cephalexin 25 mg/kg/dose q6h (100 mg/kg/day, max 4 g/day); cefazolin 33 mg/kg/dose q8h (100 mg/kg/day). MRSA suspected → TMP‑SMX 4–6 mg/kg/dose (TMP) q12h (max 160 mg TMP/dose) or clindamycin.
Atraumatic preseptal (from sinusitis)PO cephalexin
IV cefazolin
Doses as above (local adaptation on infectious‑disease review — CPS 2026 recommends amoxicillin PO / ampicillin IV here). Escalate to / add amoxicillin‑clavulanate (co‑amoxiclav 30 mg/kg [= amoxicillin 25 mg/kg + clavulanate 5 mg/kg] q8h) if no response by 24–48 h or the child is under‑immunized.
Orbital cellulitis (admitted)IV ceftriaxone + vancomycinCeftriaxone 50 mg/kg q12h (max 4 g/day) + vancomycin 15 mg/kg q6h (target levels). Alternative: ceftriaxone + clindamycin (adds anaerobe/MSSA cover) or amoxicillin‑clavulanate. PO step‑down by culture + MRSA swab.
Severe · toxic / intracranial / optic‑nerveIV ceftriaxone (or cefotaxime) + vancomycin + metronidazoleCeftriaxone 50 mg/kg q12h + vancomycin 15 mg/kg q6h + metronidazole 10 mg/kg q8h. CNS‑penetrating triple cover; consult ID; assess for surgery.
◈ Why these choices — adapted to local epidemiology (infectious‑disease review)
  • In Kuwait, near‑universal Hib and pneumococcal conjugate vaccination reduces the H. influenzae / S. pneumoniae contribution, so a first‑generation cephalosporin (cephalexin/cefazolin — strong streptococcal + MSSA cover) is a reasonable narrow empiric choice for skin- and sinus‑origin preseptal disease; escalate to amoxicillin‑clavulanate on non‑response or under‑immunization.
  • For orbital disease, vancomycin is included empirically as a local adaptation to the regional community‑associated MRSA rate, which is much higher than in Canada (infectious‑disease review — CPS 2026 adds vancomycin only when MRSA is suspected and notes a negative MRSA swab reliably excludes it); ceftriaxone covers sinusitis streptococci with good tissue/CNS penetration; metronidazole is added for intracranial extension.
  • Always tailor to immunization status, prior antibiotics, and the local antibiogram.
ConditionDuration
Preseptal cellulitis7 days (infectious‑disease review; CPS 2026 gives 5–7 days)
Orbital cellulitis (uncomplicated)10–14 days
Orbital + subperiosteal / orbital abscess (no intracranial)2–3 weeks
✦ Surgery, adjuncts & step‑down
  • Surgery: subperiosteal or orbital abscess → prompt ENT + ophthalmology for possible drainage (most small subperiosteal collections settle medically); intracranial complications → neurosurgery.
  • IV → oral once clearly improving, narrowed by cultures / MRSA swab.
  • Adjuncts: intranasal saline/steroids only with subspecialty input; systemic corticosteroids are not routinely recommended. Escalate to ID for systemic illness, non‑response, large abscess, or intracranial extension.
⚠ Sight & brain at risk — red flags
  • Falling visual acuity, a relative afferent pupillary defect, severe or bilateral proptosis, ophthalmoplegia, cranial‑nerve palsies, or altered consciousness → cavernous sinus thrombosis or intracranial spread.
  • Image urgently and escalate immediately.
  • Bilateral involvement or rapid progression despite IV therapy is an emergency.
◈ Difficult IV access? Reassess for an early IV→oral switch at every line failure rather than re‑sticking — see IV → Oral Switch & the DIVA Patient (Quick Reference).

BRUE (Brief Resolved Unexplained Event)

ASSESS< 1 YR · AAP 2016

A frightening but now‑resolved episode in a well‑appearing infant — a diagnosis of exclusion.

▸
◣ Define
  • An infant < 1 year, when an observer reports a sudden, brief, now‑resolved episode of one or more of: cyanosis or pallor; absent, decreased, or irregular breathing; a marked change in tone (hyper- or hypotonia); or altered responsiveness.
  • Diagnose a BRUE only when no explanation is found after appropriate history and examination.
◣ Lower‑risk — all of
  • Age > 60 days; gestation ≥ 32 wk and corrected (postmenstrual) age ≥ 45 wk.
  • First event (no prior BRUE, not in clusters); duration < 1 min; no CPR by a trained provider; no concerning history or examination findings.
◣ Lower‑risk — do
  • Should — educate caregivers about BRUEs and use shared decision‑making to guide evaluation, disposition, and follow‑up; offer resources for caregiver CPR training.
  • May — obtain pertussis testing and a 12‑lead ECG; briefly monitor with continuous pulse oximetry and serial observations.
✕ Lower‑risk — do not / need not
Should not: blood counts or cultures, CSF, electrolytes/renal panel/calcium, ammonia, blood gases, or metabolic screen (urine organic acids, plasma amino acids, acylcarnitine); chest X‑ray, echocardiogram, EEG, or studies for reflux; home cardiorespiratory monitoring; acid‑suppression or antiepileptic drugs. Need not: viral respiratory testing, urinalysis, glucose, bicarbonate, lactate, anemia work‑up, or neuroimaging; admission solely for cardiorespiratory monitoring.
⚠ Concerning features → not lower‑risk, evaluate
  • Toxic appearance, lethargy, vomiting, or respiratory distress at assessment; significant compromise / CPR during the event; recurrent or prior events; family history of sudden cardiac death, long‑QT syndrome, unexplained drowning or motor‑vehicle death, SIDS, or sibling BRUE; history suggesting seizure; paroxysmal cough or pertussis exposure; any trauma or concern for maltreatment; unexplained sibling death or dysmorphic features.
  • These mandate targeted evaluation — the testing restrictions above apply to lower‑risk infants only.
✦ Pearl — “lower‑risk” is not “no‑risk”
  • In the multicenter BRUE network, about 4% of infants had a serious underlying condition (most often a seizure disorder or an airway abnormality) — nearly half diagnosed only after the index visit — and return visits occurred after roughly 7% of ED discharges and 11% of hospital discharges.
  • The AAP criteria reliably identify low‑risk infants but over‑classify many as higher‑risk.
  • Safety‑net every family, offer CPR training, and consider asking carers to video any recurrence for diagnostic clarity.
◣ Admit · Discharge · Refer
  • Admit — higher‑risk BRUE (age < 2 months, prematurity, repeated events, or concerning features) for monitoring.
  • Home from the emergency department — lower‑risk BRUE with education, CPR resources, and follow‑up.
  • Refer — clinic — by cause (cardiology, neurology, safeguarding).

Adolescent Emergencies — Kuwait Context

HOURSADOLESCENT

Mental‑health crises and menstrual emergencies — within the Kuwait consent and confidentiality framework.

▸
◣ Mental health & self‑harm
  • Screen the psychosocial context in a calm, private setting — Home, Education, Eating, Activities, Drugs, Sexuality, Suicide/safety (HEEADSSS).
  • Acute self‑harm, suicidal ideation, or intentional ingestion → manage per the Self‑Harm / Intentional Ingestion card (continuous one‑to‑one observation, remove the means, treat the ingestion, mental‑health assessment before discharge). This card adds the adolescent consent, confidentiality, and safeguarding framework below.
◣ Menstrual emergencies
  • Heavy menstrual bleeding: assess for hemodynamic compromise and anemia. Check CBC, ferritin, coagulation screen and von Willebrand studies (especially at menarche), thyroid function, and a pregnancy test — performed within the local legal/ethical and safeguarding framework, and discussed with a senior clinician where culturally sensitive.
  • Severe dysmenorrhea: first‑line is a scheduled NSAID; escalate to hormonal therapy for a menstrual indication if refractory, and reassess for secondary causes (endometriosis) if no improvement after 3–6 months.
  • Amenorrhea: investigate primary amenorrhea if no menarche by age 15 (or within 3 years of thelarche), or by 13 with no secondary sexual characteristics; in secondary amenorrhea, exclude pregnancy first.,
DrugDoseRoute & notes
Tranexamic acidPO 1.3 g three times daily for up to 5 days (US label dose, post‑menarchal; not studied < 18 y) or 15–25 mg/kg/dose (max 1.5 g) two to three times daily (SmPC) · IV 10 mg/kg/dose (max 1 g) every 8 hAcute heavy menstrual bleeding,,. The weight‑based PO dose and the IV maximum are the pediatric doses (4 weeks–18 years, Perth Children’s Hospital monograph citing BNF for Children 2024) and equal the Cyklokapron SmPC adult doses.,
Combined oral contraceptive / oral progestogenper gynecology protocolHormonal control of acute bleeding or refractory dysmenorrhea
NSAID (ibuprofen / mefenamic acid)ibuprofen 10 mg/kg/dose every 6–8 h (max 400 mg/dose, 40 mg/kg/day); mefenamic acid per protocolDysmenorrhea; also reduces menstrual blood loss
Iron3–6 mg/kg/day elemental ironIron‑deficiency anemia from chronic loss
⚠ Safeguarding overrides confidentiality
  • Confidentiality with an adolescent is real but not absolute.
  • When there is imminent risk of serious harm — self‑harm, suicide, abuse, or exploitation — override it: involve the guardian and escalate through the hospital safeguarding pathway.
  • Treat life- or limb‑threatening conditions immediately, with or without consent.
◈ Kuwait legal framework
  • Under Law No. 70/2020 (Medical Profession & Patients’ Rights), informed consent is required before any intervention and, for a minor, is given by the legal guardian (wali).
  • Confidentiality (Article 13): the practitioner must not disclose a patient’s secret — whether it came to their knowledge, was discovered through practice, or was entrusted to them — except in defined circumstances: a written order from a court, the public prosecution, or a competent investigating authority; disclosure to prevent or report a crime; notification of a communicable disease to the authority designated by the Ministry; the patient’s written consent; information exchange required between the care team for the patient’s management; or reporting of child abuse (Law 21/2015) or elder abuse/neglect (Law 18/2016).
  • Under the Mental Health Law No. 14/2019, a physician may hold a patient for up to 72 hours for psychiatric assessment when there is danger to self or others or an inability to self‑care/consent (Art. 11); involuntary referral is also permitted by judicial order or at the request of a relative (to second kinship), the treating physician, or an investigator. Disclosing a patient’s psychological information is a criminal offense.
  • Confirm exact article wording against the official gazette text and current Kuwait MOH circulars.

The Child with Obesity

ASSESSAAP 2023

Obesity reshapes acute care — weight‑based dosing, a harder airway, and comorbidities that present as emergencies.

▸
◣ Define
  • Obesity = BMI ≥ 95th percentile for age and sex; severe obesity ≥ 120% of the 95th percentile (or BMI ≥ 35). A chronic disease with genetic, physiologic, and environmental contributors — not a failure of willpower.
  • Focuses on how obesity modifies acute care — drug dosing, the airway, resuscitation, and the comorbidities that present as emergencies.
◣ Approach & work‑up
  • Confirm the BMI percentile; targeted history (diet, activity, sleep/snoring, family history, medications) and exam for comorbidity signs — acanthosis nigricans, hypertension (correct‑size cuff), hepatomegaly, hip/knee findings, papilledema.
  • Screen ≥ 10 years: fasting glucose/HbA1c (T2DM), ALT (fatty liver), and a lipid panel; blood pressure with an appropriately sized cuff.
Management — drug dosing is the key bedside trap
DrugDoseRoute & notes
Resuscitation drugs · defibrillationActual (total) body weight — but cap at the adult doseLength‑based tapes (Broselow) estimate weight poorly — only about half of estimates fall within 10% of actual weight — weigh the child.
General ruleNo universal scalar — dosing is drug‑specificThere is no valid one‑size default; the correct weight basis depends on each drug's pharmacokinetics. Confirm with clinical pharmacy / the formulary. Never exceed the adult dose (PPAG: weight‑based dosing from 40 kg only until the adult dose is reached); scaling a hydrophilic drug to total body weight can cause overdose.,
Lipophilic drugs, large VdLoading dose nearer total body weightThen maintain on lean/adjusted weight (e.g., some sedatives, induction agents).
CefazolinTotal body weight (TBW)Cap at the adult dose. TBW dosing is supported for cefazolin.
AntineoplasticsBody surface area calculated from actual weight, per oncology protocolChemotherapy is dosed by body surface area; do not empirically cap or reduce without the oncologist/pharmacist.
Amino­glycosides · hydrophilic drugsAdjusted body weightVolume of distribution altered; gentamicin is dosed on adjusted body weight in obesity, level‑guided.
◈ Rule of thumb When total body weight exceeds ~120% of ideal body weight, choose the weight basis deliberately — per drug, not by a blanket rule. Never exceed the recommended adult dose for the indication, regardless of weight. For any drug not listed above, or with a narrow therapeutic index, involve clinical pharmacy.
⚠ Airway & ventilation
  • Anticipate difficult bag‑mask ventilation and intubation and rapid desaturation (reduced functional residual capacity).
  • Pre‑oxygenate well, position ramped/HELP (ear‑to‑sternal‑notch), and have adjuncts ready.
  • Higher risk of OSA and obesity‑hypoventilation.
◣ Red flags — don't‑miss acute comorbidities
  • T2DM → DKA or HHS — hyperglycemic hyperosmolar state is increasingly reported in youth with T2DM (up to ~2% present with HHS at T2DM onset) and obesity makes dehydration hard to assess.
  • SCFE — hip, thigh, or knee pain with a limp in an adolescent (see the SCFE card).
  • Idiopathic intracranial hypertension — headache, papilledema, visual change.
  • Cholelithiasis / pancreatitis, VTE in adolescents, worsening asthma control.
✦ Pearl — weigh the choice, not just the child
Document both actual weight and ideal body weight, pick the scalar per drug class, and avoid codeine (and tramadol) — the FDA recommends against their use in adolescents 12–18 with obesity, OSA or severe lung disease because of CYP2D6 ultra‑rapid metabolism and respiratory depression.

Pertussis (Whooping Cough)

MINUTESAAP Red Book 2024 · CDC

In the young infant, the danger is apnea and cyanosis — the “whoop” is often absent.

▸
◣ Recognize
  • Paroxysmal coughing fits ± inspiratory whoop or post‑tussive vomiting, worse at night, with well periods in between; often marked lymphocytosis.
  • Infants < 6 months / unimmunized: may present with apnea, cyanosis or bradycardia and little cough — a low threshold to admit and monitor.
⚠ Severe / malignant pertussis
Extreme leukocytosis (WBC > 50 ×10⁹/L), pneumonia, pulmonary hypertension and refractory hypoxemia carry high mortality in young infants — escalate early to critical care; exchange transfusion/leukoreduction is considered in specialist units.
◣ Workup
  • Nasopharyngeal PCR — test of choice in the first 3–4 weeks of cough; culture (< 2 weeks) for confirmation/typing; serology in later/adolescent disease.
  • CBC — marked lymphocytosis; extreme leukocytosis predicts pulmonary hypertension and death in young infants.
  • Chest X‑ray if respiratory distress.
AgeAzithromycinNotes
< 6 months10 mg/kg once daily for 5 daysMacrolide of choice — lowest risk of infantile pyloric stenosis
≥ 6 months10 mg/kg (max 500 mg) day 1, then 5 mg/kg (max 250 mg) days 2–5PO
◈ Public‑health & contacts
  • Pertussis is notifiable — inform public health.
  • Droplet precautions until 5 days of macrolide.
  • Offer post‑exposure prophylaxis (same macrolide dosing) to close contacts, prioritizing households with infants < 12 months or pregnant women,, and check the family’s immunization status.
  • Reinforce maternal Tdap each pregnancy (27–36 weeks) as the main protection for young infants.
◣ Admit · Refer
  • Admit — any infant < 6 months, apnea/cyanosis, feeding difficulty, pneumonia or extreme leukocytosis.
  • Refer — now — call critical care for severe pertussis.
05

Complex & Technology‑Dependent Care

Technology‑dependent & medically complex children — tracheostomy, feeding tubes, ECMO, post‑ICU, transport

The Child with Medical Complexity

ASSESS

When a Child with Medical Complexity presents unwell — start from their baseline, and treat the carer as the expert.

▸
◢ Who — and why they decompensate fast
  • Children with Medical Complexity (CMC) have chronic conditions with medical fragility, multiple coexisting problems needing multidisciplinary care, and often medical technology dependence — a tracheostomy, long‑term ventilation, enteral feeding tubes and pumps, a central venous catheter, a ventriculoperitoneal shunt, or an intrathecal baclofen pump. They usually have polypharmacy, coordinated care needs, and frequent healthcare use.
  • They have little reserve, present atypically, and the carer knows the baseline — when they say “this is not normal for him,” believe it and look hard.
◢ The unwell child — a structured approach
  • Start from baseline: their usual saturations, tone, secretions, feeds, alertness, and seizure pattern. Deviation from baseline is the alarm, not the absolute number.
  • Read the emergency care plan first — diagnosis, baseline, devices and sizes, drugs, allergies, and the agreed goals of care.
  • Think the common six:
  • infection
  • device malfunction
  • constipation
  • pain / dystonia
  • seizures
  • medication problem (including withdrawal).
  • These cause most acute presentations.
Technology problem — where to look
DeviceRed flag → action
Tracheostomy / home ventilatorDesaturation, distress, or alarm → blocked or displaced tube, tracheitis → see Tracheostomy Emergencies. Ventilator alarm → think DOPES (displacement, obstruction, pneumothorax, equipment, stomach),
Gastrostomy / jejunostomyDislodged or blocked tube, leak, or peritonism → see Gastrostomy (Feeding) Tube Problems
a fresh stoma can close within hours
Central venous catheterFever = line infection until proven otherwise — paired cultures (line + peripheral) before antibiotics
do not pull a tunneled line lightly. Occlusion or breakage → specialist
VP shuntVomiting, headache, drowsiness, irritability, or a bulging fontanelle = shunt malfunction / raised ICP until proven otherwise → urgent imaging + neurosurgery
Baclofen pumpItch, rigidity, fever, agitation, autonomic instability = acute withdrawal (can be life‑threatening) → urgent specialist
bridge with benzodiazepines ± oral baclofen
⚠ Polypharmacy & do‑not‑stop drugs
  • Do not abruptly stop chronic medications — most should be continued — including anticonvulsants, baclofen, and long‑term steroids, or long‑term oxygen / ventilation.
  • If on long‑term steroids and acutely unwell, give stress‑dose steroids (see Adrenal Crisis).
  • Reconcile every drug, check interactions, and bring the child’s own equipment and ventilator settings with them.
◈ Plan before the crisis Agree and document the baseline, the emergency care plan, and the goals of care with the family and the medical home in advance — and make sure it travels with the child.

Tracheostomy Emergencies

MINUTES

The deteriorating child with a tracheostomy — oxygenate both ways, then work the algorithm: patent, obstructed, or displaced?

▸
🖨 Printable tracheostomy tools
  • Ward cards — elective tube change (2 sides), bedside emergency box, the 5 R’s of routine care · print on A5
    Open / print ward cards (A5 PDF) kpc-guide.com/print/KPC-Tracheostomy-Ward-Cards-A5.pdf
  • Bedhead signs — tracheostomy (upper airway patent) and neck breather (laryngectomy) · print on A4
    Open / print bedhead signs (A4 PDF) kpc-guide.com/print/KPC-Tracheostomy-Bedhead-Signs-A4.pdf
◢ First moves — call for help, oxygenate both ways
  • Call for help. Apply high‑flow oxygen to both the stoma and the face as soon as it is available — use two sources if you have them; with a single oxygen source, apply it to the airway the child is breathing through (face or stoma). Attach pulse oximetry ± waveform capnography (exhaled CO₂ = a patent or partly patent airway). Bring the tracheostomy emergency kit: same‑size and one‑size‑smaller tubes, a suction machine + catheters, water‑based lubricant, a cuff syringe, and a bag‑valve‑mask.,,, Use the bedside emergency card (tube type and size, cuff status, suction depth); suction with a premarked catheter to the pre‑determined depth on the card — just past the tube tip, no deeper. Routine humidification (HME / “Swedish nose”) helps prevent the thickened secretions and mucus plugs that obstruct the tube.,
  • Rapid airway assessment: look, listen, and feel at BOTH the mouth and the stoma — assess chest rise, breath sounds (air entry), airflow, and exhaled CO₂ (if available).
① Is the tracheostomy tube in place?
NO
Accidental decannulation. If trained, reinsert the tracheostomy tube. If not trained or reinsertion fails, ventilate via whichever route achieves chest rise (upper airway or stoma). Continue ventilation and await expert airway support.
YES
Tube is in place — proceed to the steps below.
② Remove what may be causing the problem
  • Remove any speaking valve or cap, remove the inner cannula (if present), and check the ventilator / circuit (if ventilated) — this alone may relieve the obstruction.
  • (Some inner cannulas must be reinserted to connect a breathing circuit.)
③ Can you pass a suction catheter?
PASSES
Tube is patent — suction to clear secretions (a partially obstructed tube may still need replacing — if suction does not clear it, change the tube; do not persist). Ventilate via the tracheostomy if not breathing. Continue ABCDE.
WON’T PASS
Tube is obstructed or displaced. Deflate the cuff (if present — adult NTSP algorithm step; most pediatric tubes are uncuffed) — if this improves things, air is moving around the tube → remove the tracheostomy tube.
after tube removal / still not ventilating
④ Ventilate — via whichever route achieves chest rise
  • Upper airway (if patent): cover the stoma (gauze / finger) and bag‑mask via the mouth/nose (± oral or nasal airway), or an LMA.
  • Stoma (if the upper airway is not patent or oral/nasal ventilation is ineffective — e.g., laryngectomy, subglottic stenosis): ventilate over the stoma with an appropriately sized pediatric face‑mask, or an LMA.
at once if trained — otherwise when trained help arrives
⑤ Re‑establish the airway
  • Emergency tube change — maximum 3 attempts: (1) the same‑size tube on its obturator; (2) a tube half a size (0.5 mm ID) smaller, with shoulder roll/neck extension and stay sutures lifted if present; (3) a half‑size smaller tube passed over a soft suction catheter as a guide. After each attempt confirm patency (suction catheter passes to the marked depth, capnography); remove any replacement tube that is not patent — do not ventilate through it. After three failed attempts do not force — stop: oxygenate/ventilate via the upper airway (stoma occluded) or over the stoma and await expert airway support; rescue intubation — oral (uncut ETT half a size smaller than the tracheostomy tube, advanced beyond the stoma) or via the stoma (tube half a size smaller),,
  • Confirm with capnography. A shoulder roll (pillow or rolled towel under the shoulders) may improve airway patency and access to the stoma.
◣ DOPES — causes of deterioration
  • D — Displacement (accidental decannulation),
  • O — Obstruction (mucus plug, blood, granulation tissue),
  • P — Pneumothorax,
  • E — Equipment failure (ventilator / circuit, speaking valve, cap, inner cannula, oxygen failure),,
  • S — Stomach (distended stomach / abdominal compartment),
✦ Keep the obturator at the bedside
  • Keep the tracheostomy obturator at the bedside at all times.,
  • In an emergency it may be needed to reinsert the child's existing tube when a new tube is unavailable or there is no time to open one — a dedicated obturator eases insertion, reduces trauma and protects the stoma.
⚠ No upper airway? (laryngectomy / fixed obstruction)
  • If the child cannot be ventilated or intubated from above (fixed upper‑airway obstruction such as severe subglottic stenosis or bilateral vocal‑cord palsy; laryngectomy is rare in children), the stoma is the only airway — do not waste time on face‑mask ventilation; oxygenate via the stoma (face mask or laryngeal mask over it) and re‑cannulate, or intubate the stoma with a tube one half‑size smaller than the tracheostomy tube.
  • Know this from the care plan before the emergency.,
⚠ Bleeding — exclude tracheo‑innominate fistula (TIF)
  • Massive bleeding — or a brief “sentinel” bleed — 3 days to 6 weeks after tracheostomy is TIF until proven otherwise (adult‑derived window),; in children TIF also occurs late in long‑term tracheostomies, and most reported pediatric cases had neurological comorbidity.
  • This is an airway/ENT/surgical emergency — call expert help (ENT, surgery, anesthesia/ICU) immediately.
  • As an expert‑performed bridge while help arrives: overinflate the cuff to tamponade (controls bleeding in > 80% in adult series); if it fails, orally intubate past the stoma (ETT cuff distal to the bleed) and apply the Utley maneuver — a finger through the stoma compressing the artery against the back of the sternum — then activate massive transfusion, call ENT + surgery, and go to OR.,
  • Any tracheostomy bleeding needs ENT review before discharge.
◢ Tracheitis
  • Increasingly purulent / copious secretions, fever, plugging, rising work of breathing — can obstruct. Send a tracheal aspirate to guide antibiotics; empiric cover usually includes S. aureus (including MRSA) and Pseudomonas, the organisms most often reported, guided by prior cultures and the local antibiogram; step up humidification and suction.
⚠ When NOT to change the tube yourself — call ENT / the tracheostomy team
As a general pediatrician, do not attempt an elective tube change when: it is the first change (the surgical / ENT team performs or directly supervises the first change, usually at day 3–7 post‑formation, to confirm a patent tract); the stoma is fresh / immature (< 7 days, especially percutaneous) — high risk of a false passage or an unrecoverable airway,; you are not trained in that specific tube, or the correct‑size tubes and suction are not at hand,; the child is unstable, on high ventilator / oxygen support, or has a known difficult airway — change only where ENT / anesthesia and airway rescue are immediately available; or there is active bleeding or suspected tracheo‑innominate fistula (an emergency, not a routine change); the tracheostomy was placed for critical upper airway obstruction — the upper airway is not a reliable rescue route, so a lost or displaced tube can mean a lost airway (treat the stoma as the only airway and change only with ENT / anesthesia and airway rescue at the bedside),; or the child has had major airway / tracheal reconstruction (laryngotracheal reconstruction, slide tracheoplasty, tracheal resection & anastomosis) — the tube may cross or protect a fresh repair, so changes are done by the surgical team only (risk of disrupting the anastomosis or a false passage; expert consensus). Otherwise keep the current tube, oxygenate, and get expert help.
Elective tube change (routine)
  • Two people.
  • Supine with a shoulder roll, neck extended; suction.
  • Load the obturator, lubricate, deflate the cuff.,
  • Remove the old tube along its curve; insert the new one on the obturator in a downward, inward arc — never force. Remove the obturator immediately, insert the inner cannula, inflate the cuff, and confirm (chest rise, breath sounds, capnography, suction catheter passes),,
  • Secure ties to a one‑finger gap.
⚠ Call ENT / anesthesia early
  • Any bleeding · suspected TIF (emergency) · failed or difficult reinsertion · obstructing granulation · accidental decannulation with a fresh stoma (< 7 days) — lift the stay sutures ‘up and out’ to aid reinsertion; if it fails, intubate orally.,
  • An established stoma can still narrow within hours of decannulation, so if the tube has been out for several hours and the child is stable, call ENT before repeated attempts (dilation may be needed) — expert consensus, not guideline‑stated.
◣ Admit · Discharge · Refer
  • Admit — any airway compromise → ED/PICU.
  • Home — after the tube is secure and patent and the caregiver is confident.,
  • Refer — now — ENT and the home‑ventilation/tracheostomy team.,
◎ Learn more — open‑access pediatric resources (no login required)
  • Cincinnati Children’s — Tracheotomy Care — caregiver handbook (Arabic available) plus short videos including an emergency tube change: cincinnatichildrens.orgQR
  • AboutKidsHealth (SickKids) — Tracheostomy & ventilation — home care, suctioning and emergency management: aboutkidshealth.ca/trachventQR

Tracheostomy Tubes & Cuff Types

REFERENCE

Know the exact tube before you change or ventilate — same stated size from different manufacturers is not interchangeable.

▸
Tube — what it is and when
TubeMaterial & featuresNotes
PVC tubePVC, firm, thermosensitive, radiopaque line
neonatal / pediatric / pediatric‑long
cuffed (soft air cuff) or uncuffed. Pediatric sizes are single‑lumen (no inner cannula).
Single‑patient, disposable. Sized by inner diameter (ID, mm).
Silicone tubeSilicone, soft and flexible, reusable
cuff options tight‑to‑shaft (TTS), air, or foam
extended‑proximal and adjustable‑length (wire‑reinforced) variants exist.
Bivona silicone tubes, including wire‑reinforced variants, are labeled MR‑conditional (≤ 3 T) — check the specific tube’s labeling before MRI. Sized by ID.
Cuff types — inflate with what, watch what
CuffInflate withUse / caution
Uncuffed—Most children; airflow around the tube (speech), least mucosal injury.
Air cuffAirPositive‑pressure ventilation or aspiration protection; keep cuff pressure < 20–25 cmH₂O (minimal‑leak) — over‑inflation causes mucosal ischemia.
Tight‑to‑shaft (TTS)Sterile water (never air)Deflated, it sits flush like an uncuffed tube (speech / airflow); inflate only when needed. Air diffuses out of silicone — use water.
Foam cuffSelf‑inflating (pilot open to air)For a difficult seal or tracheomalacia; actively deflate and cap the pilot to insert / remove, then release to self‑inflate.
⚠ Cuff safety
  • Never use a speaking valve or cap with the cuff inflated — no route to exhale (can be fatal); deflate cuff first.
  • Deflate cuff whenever a seal is not needed, to protect mucosa and allow speech.
◢ Before any tube change
  • Same‑size tubes from different manufacturers differ in outer diameter and length — not interchangeable; if you must substitute in an emergency, be ready to downsize.
  • Keep a same‑size and one‑size‑smaller spare at the bedside; know the exact tube from the bedside emergency card.
  • After insertion, confirm airway — chest rise, capnography, suction catheter passes.
◎ Learn more — open‑access pediatric resources (no login required)
  • Cincinnati Children’s — Tracheotomy Care — caregiver handbook (Arabic available) plus short videos including an emergency tube change: cincinnatichildrens.orgQR
  • AboutKidsHealth (SickKids) — Tracheostomy & ventilation — home care, suctioning and emergency management: aboutkidshealth.ca/trachventQR

Gastrostomy (Feeding) Tube Problems

HOURS

A dislodged tube is time‑critical — the stoma can close within hours. Tract age decides who replaces it.

▸
◣ Dislodged tube — the clock is the stoma
  • Empty tract narrows within hours — per ESPGHAN the fistula can close spontaneously within 6 h; if no replacement is at hand, the same tube or a Foley catheter can be inserted gently and taped to keep it open. By 24 h it is usually lost (expert consensus). Keep it open now, then replace.
  • Tract age decides the route — ask when the tube was first placed.
How old is the stoma tract?
IMMATURE < 6 WEEKS
High risk of a false tract / intraperitoneal placement → do NOT insert a tube into the stoma. Cover stoma with gauze, keep nil‑by‑stoma, get to hospital for guided replacement by pediatric surgery / gastroenterology / interventional radiology.
MATURE ≥ 6 WEEKS
Epithelialized tract → bedside replacement usually safe. Replace promptly with a same‑size balloon tube; lubricate, advance gently, inflate the balloon with water. Caveat: ESPGHAN notes centres wait at least 6 weeks before the first change; maturation may be delayed with immunosuppression, corticosteroids, obesity or diabetes (and, by extension, malnutrition or chemotherapy) — if unsure, treat as immature.
If the same size will not pass
  • Place the largest Foley catheter that passes atraumatically to hold the stoma open, then serially dilate in 2‑Fr steps to the target size.
  • Do not inflate a Foley balloon inside the tract to dilate (expert consensus — not guideline‑stated).
  • If > 24 h out, or any resistance / false‑passage concern → stop and refer.
◈ Confirm before feeding
  • Verify intragastric position before use: aspirate gastric contents (pH ≤ 5.5 — the nasogastric‑tube threshold, applied by extension) — beware a false pH on proton‑pump inhibitors (expert consensus).
  • After any difficult or uncertain replacement, confirm with a water‑soluble contrast study before first use (expert consensus — not stated in the ESPGHAN paper). Never use air insufflation to confirm.
  • Document tube type, French size, and balloon volume.
◣ Blocked tube & stoma issues
  • Blocked: flush gently with warm water; do not force. Hold feeds until patency is confirmed.
  • Buried bumper: suspect if the tube will not rotate or advance freely, or pain, leakage, or resistance on feeding — prevented by avoiding traction and rotating + advancing the tube regularly. Buried bumper or suspected peritonitis (pain, feed intolerance, fever, rigidity) → stop feeds, urgent surgical review.
  • Granulation, leak, redness, excoriation: see Enteral Feeding Tubes — Types & Complications.
⚠ Admit / escalate
  • Admit — peritonitis or systemic infection; buried bumper syndrome; uncertain or difficult placement; concern of a false passage; any immature‑tract dislodgement; tube out > 24 h.
  • Refer — now — surgery / gastroenterology.
◣ Admit · Discharge · Refer
  • Admit — peritonitis, a dislodged tube with a lost tract, or inability to replace it.
  • Home — a replaced, patent tube with feeds tolerated.
  • Refer — now — surgery/gastroenterology for tract problems or any immature‑tract dislodgement (< 6 weeks, or longer if healing is impaired).
◎ Learn more — open‑access pediatric resources (no login required)
  • Cincinnati Children’s — G‑Tube Home Care — caregiver handbook + procedure videos (Arabic available): cincinnatichildrens.orgQR
  • Together by St. Jude — Types of Tubes & Devices — illustrated visual guide to NG / ND / NJ and G / GJ / J tubes and low‑profile buttons: together.stjude.orgQR

Enteral Feeding Tubes — Types, Delivery & Complications

REFERENCE

Know the route before you feed or give a drug — the stomach tolerates boluses, the jejunum does not.

▸
Tube types — route, how to feed, and what not to give
TubeRoute & how to feedDo NOT
NGT / OGTStomach
short‑term
bolus or continuous. Nasogastric vs orogastric route is a unit / clinical choice — evidence favors neither (in preterm infants). Choose by expected duration, gag strength, and respiratory status: prefer OGT when nasal airflow matters (preterm, CPAP, respiratory distress) or the gag is weak
NGT is more secure for a stronger gag or longer use (preterm rationale: nasal tubes may compromise respiration, oral tubes displace more easily; otherwise expert consensus). Confirm gastric aspirate pH ≤ 5.5 before each use (x‑ray if in doubt; local policy: confirm by x‑ray).
Never feed with position unconfirmed. Use OGT (not NGT) in suspected base‑of‑skull injury.
NJTNose → jejunum (post‑pyloric)
for gastroparesis or high aspiration risk. Continuous feeds only.
No bolus (dumping). pH is unreliable — confirm position by imaging (expert consensus — not guideline‑stated).
Gastrostomy
(PEG / high‑profile / button)
Abdominal wall → stomach; long‑term. Bolus or continuous.Force or over‑rotate a PEG bumper (buried bumper). A low‑profile button needs an extension set to feed.
Gastro­jejunostomy (GJ)Through the gastric stoma, tip in jejunum
gastric + jejunal ports. Jejunal port = continuous only
gastric port = venting / medicines.
Blind replacement — needs fluoroscopy. No bolus down the jejunal port.
Jejunostomy (J)Abdominal wall → jejunum. Continuous feeds only, small volumes.Bolus feed. Attempt a bedside change — refer (surgical tract).
⚠ Medicines through a feeding tube
  • Use liquid formulations where possible; never crush enteric‑coated or modified / sustained‑release tablets (blocks the tube, alters the drug).
  • Give each drug separately and flush with water before, between, and after. The route matters: down a jejunal (post‑pyloric) tube avoid hypertonic or large‑volume drugs (dumping, perforation), and some medications cannot be given jejunally at all — check with pharmacy.
  • Some parenteral (injectable) preparations can be given enterally when no oral liquid exists (e.g., clonidine, glycopyrrolate) — confirm suitability and dose with pharmacy first.
◢ Differentiate the tube at the bedside
  • Where it enters — nose / mouth (NGT/OGT) vs the abdomen (gastrostomy / GJ / J).
  • Profile — an external bumper with a balloon port (water valve) = balloon gastrostomy; flush to the skin needing an extension = low‑profile button; a firm internal flange that resists gentle traction = PEG.
  • Ports — two labeled ports (GASTRIC + JEJUNAL) = GJ; a single feed port plus a balloon port = gastrostomy.
  • Read the French size, length, and brand off the tube and the care plan. Unsure of the route? Confirm with contrast — do not feed to find out.
Manage the common stoma complications
ProblemWhat & whyManagement
Granulation (granuloma)Red, moist, friable overgrowth from friction and moisture.Stop the movement (secure the tube, correct balloon volume); saline soaks; topical silver nitrate (protect surrounding skin with a barrier) or a short topical steroid; silver / foam / hydrocolloid dressing.
LeakGastric contents track around the tube.Do not just upsize the tube (enlarges the stoma). Correct balloon volume; treat constipation, retching, delayed emptying (vent, prokinetic, slow the feed); treat granulation / infection; barrier cream. Consider buried bumper.
RednessIrritation vs infection.< 5 mm erythema is usually irritation — barrier protection. Spreading redness, pain, swelling, or pus = infection → swab, then topical or systemic antibiotics (cover skin flora).
ExcoriationEnzymatic burn from leaked feed and acid.Stop the leak at source; barrier products (zinc or dimethicone cream, pectin barrier ring / powder); keep dry; involve the stoma nurse.
◈ Golden rules
  • Confirm route before feeding or giving a drug; gastric tolerates boluses, jejunal is continuous only; flush to keep patent.
  • A fresh gastrostomy stoma can close within hours if the tube falls out — see Gastrostomy (Feeding) Tube Problems.
◎ Learn more — open‑access pediatric resources (no login required)
  • Together by St. Jude — Types of Tubes & Devices — illustrated visual guide to NG / ND / NJ and G / GJ / J tubes and low‑profile buttons: together.stjude.orgQR
  • Cincinnati Children’s — G‑Tube Home Care — caregiver handbook + procedure videos (Arabic available): cincinnatichildrens.orgQR

ECMO — What the General Pediatrician Needs to Know

ASSESSKNOW WHEN TO CALL · ELSO

Temporary heart–lung support for severe but reversible failure — your job is to recognize the candidate and call early.

▸
◣ What it is
  • Temporary machine support that oxygenates the blood and removes CO2 (± supports the circulation) to buy time for potentially reversible heart or lung failure. It is a bridge — to recovery, a decision, or transplant — not a cure, and is run only in a specialized PICU / ECMO center.,
  • VV (veno‑venous) = lung support (the heart still works); VA (veno‑arterial) = heart ± lung support, and covers ECPR (ECMO during a refractory but reversible cardiac arrest).,
⚠ When to think ECMO — call early
Severe cardiac or respiratory failure not responding to maximal conventional therapy, in a child with a reversible cause (e.g., fulminant myocarditis, ARDS / severe pneumonia, PPHN; neonatal MAS or CDH). Call the PICU / ECMO center early — before catastrophic deterioration or irreversible brain injury; timely referral improves outcomes, so do not wait for arrest. The center decides candidacy, thresholds, and timing.,,,
⚠ Usually not a candidate
  • An irreversible condition with no exit strategy · severe irreversible brain injury · a lethal chromosomal / congenital anomaly (e.g., trisomy 13 or 18 — not 21) · uncontrolled bleeding.,,
  • Extreme prematurity, very low birth weight, and many days of prior ventilation lower the chance of benefit.,,
  • The final decision rests with the ECMO team.
✦ Your role — before and after
  • You are not expected to run ECMO — you recognize the failing‑yet‑reversible child and escalate.,
  • Resuscitate and support maximally, protect the brain and other organs, avoid irreversible injury, and call the PICU / ECMO center early.,
  • Afterwards, survivors need long‑term multidisciplinary follow‑up: about 1 in 4 neonatal survivors has neuropsychological deficits (more after cardiac ECMO) and new problems can appear later — track development and arrange hearing tests (sensorineural loss can be progressive / late).
  • Support the family through a high‑risk, uncertain course (major complications include bleeding, clots, and stroke).,,
◣ Admit · Discharge · Refer
  • Admit — refractory cardiac or respiratory failure with a reversible cause → PICU / ECMO center now.,
  • Refer — now — discuss early — call before the child is in extremis; deterioration is often rapid.

Post‑PICU Syndrome (PICS‑p)

ASSESSAFTER CRITICAL ILLNESS

Surviving the PICU is only the start — new physical, cognitive, emotional, and social problems can follow the child and family for years.

▸
◣ What it is
  • Post‑Intensive Care Syndrome — pediatric (PICS‑p): new or worsening impairment across four domains after critical illness — physical, cognitive, emotional, and social — affecting the child and the family. It emerges over the months after discharge and can persist for years.,,
  • You, the general pediatrician, are the one who sees these children back — so you screen for it, coordinate care, and reassure.,,
The four domains — what to look for
DomainWatch for
PhysicalICU‑acquired weakness, fatigue, pain, poor feeding / growth, reduced exercise tolerance, poor sleep
residual respiratory or organ problems.,
CognitiveAttention, memory, and executive difficulties
developmental regression in the young
declining school performance.,
EmotionalPTSD, anxiety, depression, nightmares / delusional memories, fear, irritability or aggression, behavioral change.,,
SocialTrouble reintegrating at school, absenteeism, withdrawal from peers and activities, identity and participation problems.,
◣ Higher risk after…
  • Longer PICU stay, mechanical ventilation, sedation and delirium, renal replacement, ECMO, cardiac arrest, sepsis, ARDS, or major trauma; oncology / neurology diagnoses; an unscheduled admission; younger age and pre‑existing conditions.,
⚠ Don't forget the family (PICS‑F)
  • Parents and siblings are affected too: screened before PICU discharge, ~60% of parents were at risk of PTSD and ~75% of depression (single‑center study), alongside anxiety, financial strain, and impaired family functioning.,,
  • Ask how the family is coping, and support them.,
✦ Your role
  • At the first post‑discharge visits and beyond: screen every domain (development, school, mood / sleep, physical function) and the family's wellbeing; coordinate multidisciplinary follow‑up — physiotherapy / occupational therapy / speech‑language therapy, psychology, neurodevelopmental assessment, and school liaison; reconcile medications; and treat the family as part of the patient.,
  • Normalize and follow up rather than dismiss — recovery is a trajectory, not an event.,,
◣ Admit · Discharge · Refer
  • Screen — every child at follow‑up after a significant PICU admission.,
  • Refer — now — escalate new severe mental‑health symptoms (e.g., self‑harm risk) or acute physical deterioration.,
  • Refer — clinic — neurodevelopment / rehabilitation, psychology / psychiatry, and the relevant specialty for persistent domain‑specific problems; social work for family support.,

Aeromedical Transport — Neonatal & Pediatric

ASSESSPRE‑FLIGHT ASSESSMENT · MOH A‑ADM‑014

Match the transport tier to clinical risk — two predictable cabin stresses (hypoxia, gas expansion) drive the pre‑flight assessment.

▸
◣ Two cabin stresses — assess before every flight
  • Hypobaric hypoxia — cabins are pressurized to a maximum 8,000 ft equivalent (≈ breathing 15% oxygen at sea level); a healthy PaO2 falls to ~60–75 mmHg (8–10 kPa; SpO2 ~89–94%). Limited cardiopulmonary reserve desaturates further. Resting SpO2 alone is insensitive. If available, a HAST (hypoxia‑altitude simulation test) best predicts in‑flight oxygen need in a child with chronic lung or cardiac disease. If HAST is not available, use the practical alternative: base the decision on resting oximetry, the diagnosis and trajectory, and any prior flight tolerance, and — when in doubt — give empiric in‑flight oxygen (double an existing flow) or choose a sea‑level cabin / air ambulance for higher‑risk children.,,,
  • Trapped‑gas expansion — gas in a closed space expands ~38% from sea level to 8,000 ft. Pneumothorax, recent surgery with retained gas, and intracranial or intraocular gas need a sea‑level cabin (air ambulance) when the gas cannot be excluded. A current pneumothorax requires a chest drain before any urgent flight — even if it is minimal.
⚠ Neonatal & infant air transport — stability, not age, governs
  • Term neonate (> 37 weeks): defer non‑urgent flying for the first 7 days after birth to confirm feeding, thermoregulation, and no undiagnosed cardiorespiratory problem or silent pneumothorax.,
  • Preterm (< 37 weeks) not yet at the expected date of delivery: avoid non‑essential flying; if travel is essential, in‑flight oxygen must be available (low flow, e.g. 1 L/min; a hypoxic challenge test is not reliable at this age). Infants < 1 year with chronic respiratory problems: discuss with a respiratory pediatrician and consider HAST — SpO₂ < 85% on HAST = in‑flight oxygen; 85–90% = pediatrician discretion.
  • Preterm without chronic lung disease: the “~3 months corrected age” figure is a soft guide, not a fixed cutoff — fitness depends on gestational maturity + demonstrated cardiorespiratory stability + being apnea‑free, judged individually. Avoid flying during a respiratory infection until ~6 months corrected age (apnea risk). Former preterms with BPD / neonatal chronic lung disease: discuss with a respiratory pediatrician and, where available, a HAST before flying — advised if oxygen was needed within the last 6 months; sea‑level SpO₂ does not predict in‑flight desaturation, and SpO₂ < 85% on the test means in‑flight oxygen at 1–2 L/min. Preterm infants who have not yet reached their due date do not need the test (unreliable) but should have in‑flight oxygen available.,,
  • An incubator is not mandatory for a stable infant — a physiologically stable infant may travel in an aircraft bassinet / in‑arms. A transport incubator is needed for thermal instability, continuous monitoring, controlled oxygen/humidity, or mechanical ventilation.,,
  • Respiratory support changes the route, not by age: a ventilated or monitoring‑dependent infant goes by dedicated air ambulance (incubator/transport platform, continuous SpO2 + ECG, capnography if ventilated, altitude‑appropriate settings, sea‑level‑cabin option). A stable, monitored, ventilated infant can still be flown for urgent surgery with a specialist team.,,
  • Tier by stability: stable, self‑ventilating, thermally stable → bassinet/in‑arms commercial (after the term deferral / individualized preterm assessment); oxygen‑dependent or apnea‑risk → commercial + medical clearance + in‑flight O2 (roughly double the flow at cruise); unstable/ventilated/monitoring‑dependent → dedicated air ambulance.,,
In‑flight oxygen — infants & young children
Current support / statusAction
Already on oxygenDouble the flow rate in flight as a starting point; confirm it is deliverable in the cabin.,,
Needs > 4 L/min at baselineCommercial flight not advised → escalate to air ambulance.,
◎ Oxygen logistics
  • Carriers supply oxygen at fixed flows (often 2–4 L/min, set rates or none).,
  • A need for precise or higher flow, or a corrected requirement > ~4 L/min, cannot be reliably managed on a scheduled flight.,
  • Carry an airline‑approved portable oxygen concentrator (POC) with battery for ≥ 150% of journey time; the US prohibits passenger oxygen cylinders (use a POC or carrier oxygen).,,
Transport tier — assign the lowest tier that safely covers the whole journey
TierMode & escortTypical pediatric patient
0Commercial seat, no escortStable, self‑caring; PEWS low.
1Commercial seat + non‑medical attendantMinor / vulnerable; needs help with mobility, not clinical care.
2Commercial seat + a competent trained caregiver
a nurse/RT is required only if oxygen- or ventilation‑dependent, or other risk is expected
Stable tracheostomy on room air (with a trained caregiver competent in the device), stable oxygen, or pump feeding.
3Commercial seat or stretcher + physician + nurse (add RT for home‑vent)Stable established home ventilation, or a fragile child with deterioration potential.
4Dedicated air ambulance + critical‑care teamCritically ill or unstable (meets air‑ambulance criteria below).
◎ Scoring & personnel (per policy)
  • The policy stratifies patients by Level of care 0–4 and a NEWS‑based risk level (Low = 1–4 · Medium = 5–6 · High = ≥ 7, as printed in the policy; a score of 0 is also low risk). In children, substitute an age‑appropriate PEWS (NEWS2 is not for use under 16 yr).
  • If findings fall between tiers, choose the higher tier. A low score with high deterioration potential (end‑stage lung disease, potential airway/hemodynamic compromise) is classified up by the accompanying physician.
  • At least two competent personnel escort any patient; for a child, include a parent/legal guardian where possible.
◎ Local availability (Kuwait) A dedicated pediatric / neonatal aeromedical transport team is not yet established — transfers are currently staffed by the accompanying pediatric / treating team. Confirm current MOH capability early and coordinate through the A‑ADM‑014 pathway (Directorate of Treatment Abroad).
⚠ Dedicated air ambulance (sea‑level cabin) — when commercial carriage will not do
Any one absolute criterion mandates it: acute / unstable ventilation or a credible need to intubate or escalate in transit; hemodynamic instability needing vasoactive / inotropic infusion; a trapped‑gas condition needing sea‑level cabin (unresolved pneumothorax, recent intracranial / intraocular gas, significant bowel obstruction); need for invasive monitoring or mechanical support (arterial‑line titration, ICP monitoring, IABP, ECMO, VAD, external pacing); refractory hypoxemia or oxygen need beyond carrier capability; status epilepticus / uncontrolled seizures; or a communicable disease needing isolation. Under the policy, Medevac (air ambulance) also applies to priority 1–2 cases, expedited transfer of an unstable patient, brain‑death repatriation, or when the commercial route/port is not cleared. Absolute contraindications to flight until treated: untreated pneumothorax, hemothorax or a compromising effusion, cardiac tamponade, recent abdominal surgery / immediate post‑op, or a penetrated eye injury.
✦ Airway & cuffs at altitude
  • The cabin is a poor place to rescue a failing airway — secure a difficult or unstable airway definitively before departure, not aloft; do not defer a foreseeable intubation to the aircraft.,
  • Air in an endotracheal / tracheostomy cuff expands as cabin pressure falls — cuff pressure rises on ascent and falls (with a leak) on descent; measure cuff pressure with a manometer and adjust the cuff volume as needed during ascent and descent, or consider filling the cuff with saline/water.
  • Confirm the ventilator and oxygen are airline‑approved with battery for ≥ 150% of journey time.,
◣ Team, clearance & handover
  • Escort competence: current pediatric / neonatal resuscitation (PALS / NRP) and competence with the child's devices; the accompanying physician is the MRP en route.
  • Clearance: pre‑flight medical report + risk assessment reviewed and approved by the MRP (senior registrar or above) 7–14 days and again 48–72 h before departure; airline MEDIF for commercial carriage. A return/repatriation reassessment is mandatory before flying home.
  • Handover: document status before, during and on arrival, and give a structured handover to the receiving team using the policy's handover tools.
◣ Admit · Discharge · Refer
  • Escalate — any air‑ambulance criterion, or a deteriorating trajectory → critical‑care transport team + treatment‑abroad / transport committee.
  • Proceed commercial — stable child at Tier 0–3 with a completed pre‑flight clinical assessment (HAST where available) and confirmed oxygen/device support.,,
  • Refer — now — the MOH Directorate of Treatment Abroad (DTA) decides transport type; involve the relevant clinical council for team and equipment.
06

Endocrine & Metabolic

Diabetic Ketoacidosis

HOURSISPAD 2022 · TREKK 2023

Glucose > 11 mmol/L (200 mg/dL) + pH < 7.3 or bicarbonate < 18 + ketonemia (β-hydroxybutyrate ≥ 3 mmol/L).

▸
Diabetic Ketoacidosis — bedside algorithmAdapted from TREKK; aligned with the Kuwait PICU Task Force · ISPAD 2022.
Pediatric DKA algorithm flowchart
◈ Fluids — the ISPAD 2022 method
  • After the bolus, replace the estimated deficit (5% mild · 7% moderate · 10% severe, minus the bolus) plus maintenance evenly over 24–48 h; the weight‑band rates in the algorithm equal a 7% deficit (minus a 10 mL/kg bolus) plus maintenance over 24 h. Use the DKA calculator for the patient‑specific rate. Rapid versus slow rehydration and 0.45% versus 0.9% saline did not change neurological outcomes in the 1,389‑episode PECARN FLUID trial.,
◈ Severity & PICU
  • For DKA managed in the PICU, follow the latest Kuwait PICU Task Force DKA guideline — the local task‑force protocol governs fluid, insulin and electrolyte targets in the unit.
  • Consider PICU for severe DKA, young children (age < 5 y), reduced consciousness, long symptom duration, compromised circulation, or high‑risk features (pH < 7.1, pCO₂ < 21 mmHg, urea > 7 mmol/L).
⚠ Cerebral injury — further detail
  • If focal neurological deficits develop, obtain an urgent CT to exclude cerebral venous thrombosis or intracranial hemorrhage. Do not postpone treatment to obtain a CT. Perform hourly GCS so cerebral injury is caught early — it is the leading cause of death in pediatric DKA.
◈ Avoid where possible
Intubation (ventilation removes the child's respiratory compensation for the acidosis), central venous catheters (thrombosis risk; a large dead space can make insulin delivery erratic if insulin runs through the CVC), and routine urinary catheterization.
✦ Pearl — the masquerades of new‑onset DKA
  • First‑presentation diabetes is missed when DKA wears a disguise: abdominal pain and vomiting taken for gastroenteritis or appendicitis, Kussmaul breathing taken for pneumonia or an asthma attack, and polyuria taken for a urinary tract infection or, in a younger child, secondary enuresis.
  • A bedside glucose and ketones settle it in seconds.
◣ Admit · Discharge · Refer
  • Admit — all children with DKA; level of care follows severity: mild DKA → general pediatric ward with hourly monitoring; moderate/severe, young age (< 5 y), reduced consciousness, or high‑risk features → high‑dependency/PICU.
  • Home from the ward — not from DKA; after transition to subcutaneous insulin with diabetes‑team education.
  • Refer — now — pediatric endocrinology/diabetes team for all; PICU for cerebral‑injury risk.

Hyperglycemic Hyperosmolar State (HHS)

MINUTESISPAD 2022

Not “severe DKA” — very high glucose, very high osmolality, little ketosis, and higher mortality.

▸
◣ Define (differs from DKA)
  • Glucose > 33 mmol/L (600 mg/dL), serum osmolality > 320 mOsm/kg, venous pH > 7.25 (arterial > 7.30) and bicarbonate > 15 mmol/L, only mild ketosis, with altered consciousness/profound dehydration. Increasingly seen in adolescents with obesity/type‑2 diabetes.
⚠ Manage it differently from DKA
  • Fluid deficits are larger (~12–15%) and fluid — not insulin — is the priority first.
  • Start insulin later and lower (only once glucose stops falling with fluids alone, ~0.025–0.05 unit/kg/h).
  • Watch for rhabdomyolysis, malignant‑hyperthermia‑like fever, thrombosis and arrhythmia from potassium/phosphate shifts. Fever with a rising creatine kinase may be treated with dantrolene (mortality is high even with treatment).
  • Mortality is higher than DKA.
✦ Mixed pictures exist
  • Some children have features of both HHS and DKA.
  • When ketoacidosis coexists, follow DKA fluid/insulin caution but expect a bigger fluid requirement and monitor osmolality and creatine kinase closely.
◣ Workup
  • Glucose, venous blood gas, beta‑hydroxybutyrate/ketones.
  • Electrolytes with corrected sodium, potassium, phosphate, magnesium, calcium; BUN/creatinine.
  • Calculated effective osmolality; ECG + continuous cardiac monitoring.
  • Creatine kinase — screen for rhabdomyolysis.
StepApproachNotes
Fluids first0.9% saline bolus ≥ 20 mL/kg, repeated until perfusion is restored; then 0.45–0.75% saline to replace the deficit (assume 12–15%) over 24–48 h, and replace urinary lossesAim to lower glucose gradually with fluid alone initially
Insulin (delayed)0.025–0.05 unit/kg/h once glucose plateaus on fluidsNo bolus; avoid rapid osmolar shifts
MonitorOsmolality, K⁺, PO₄, Ca²⁺, creatine kinase, neuro obsAnticipate rhabdomyolysis and hyperthermia
◣ Admit · Refer
  • Admit to high‑dependency/PICU.
  • Call pediatric endocrinology and critical care.

Adrenal Crisis / Salt‑Wasting CAH

MINUTESBSPED 2023

Shock + low sodium + high potassium + low glucose; collapse with illness.

▸
◣ Recognize
  • Known adrenal insufficiency/CAH under stress, or a neonate (1–4 weeks) with vomiting, poor feeding, weight loss, hyperpigmentation, ambiguous genitalia (in females).
  • Labs: low sodium, high potassium, metabolic acidosis, low glucose.
① Steroid — don't wait Hydro­corti­sone immediately (draw 17‑OHP/cortisol first only if no delay).
② Fluids + glucose Saline 10 mL/kg bolus, repeat as needed; treat low glucose; maintenance with dextrose‑saline.
③ Electrolytes & cause High potassium usually corrects with fluids + steroid (ECG for peaked T waves). Treat the trigger (often infection); cover empirically for sepsis if suspected. Endocrine + PICU.
Drug / fluidDoseRoute & notes
Hydro­corti­sone< 1 yr 25 mg
1–5 yr 50 mg
> 5 yr 100 mg
IV/IM, then 50–100 mg/m²/day divided every 6 h
Sodium chloride 0.9%10 mL/kgIV bolus over 5–10 min; reassess and repeat as needed (BSPED 2023)
Dextrose 10%2 mL/kgIV, for low glucose; recheck glucose at 15 min, repeat if needed
Fludro­corti­sone0.1 mg once dailyOral — maintenance only, not for the acute crisis
⚠ Do not use dexamethasone for salt‑wasting crisis
  • It has no mineralocorticoid effect.
  • Give hydrocortisone immediately — do not delay it for lab results.
  • High‑dose hydrocortisone (> 50 mg) covers the mineralocorticoid need acutely; fludrocortisone is added later for maintenance.
◣ Admit · Discharge · Refer
  • Admit — all → monitored bed; hydrocortisone before labs, treat hypoglycemia/hyponatremia.
  • Home from the ward — only after stabilization, endocrine review, and stress‑dosing/emergency‑injection education.
  • Refer — now — pediatric endocrinology (the "endocrine review" required before discharge).

Hypoglycemia (Beyond the Newborn)

MINUTESPES 2015

Plasma glucose < 3.3 mmol/L (60 mg/dL), or symptomatic (Whipple triad) — treat now; in a child with a known hypoglycemia disorder keep glucose > 3.9 mmol/L (70 mg/dL); draw the critical sample first only when it will not delay treatment.

▸
◣ Recognize
  • Autonomic: sweating, tremor, tachycardia, hunger, pallor, anxiety. Neuroglycopenic: lethargy, irritability, poor feeding, behavior change, confusion, seizures, coma.
  • Whipple triad confirms it: low plasma glucose + consistent symptoms + resolution with glucose. Confirm any bedside reading with a laboratory plasma glucose (glucometers are unreliable when low).
  • Red‑flag context: hepatomegaly (glycogen storage / fatty‑acid oxidation defect), midline defects or micropenis (hypopituitarism), hyperpigmentation (adrenal insufficiency), fasting- or illness‑triggered episodes, or a high glucose‑infusion requirement.
⚠ Draw the critical sample — but never delay treating severe or symptomatic hypoglycemia
Obtain the sample before glucose whenever it can be drawn immediately. If the child is symptomatic or severely hypoglycemic, treat first and take the sample as soon as access allows — do not delay treatment for the sample. At the moment of hypoglycemia (ideally glucose < 2.8 mmol/L): lab glucose, venous gas/bicarbonate, insulin + C‑peptide, β-hydroxybutyrate + free fatty acids (the pivotal branch point), lactate, ammonia, cortisol + growth hormone, acylcarnitine profile + carnitine, plasma amino acids; and the first‑void urine for ketones, organic acids ± toxin/sulfonylurea screen. One missed sample can cost the diagnosis.
① Correct now IV D10 2 mL/kg (200 mg/kg) slow push — avoid large hyperosmolar boluses. If alert with a safe airway: oral rapid carbohydrate ~0.3 g/kg.
② Maintain
  • Continue D10 at maintenance and titrate the glucose‑infusion rate to keep glucose > 3.9 mmol/L (central line for > D12.5)
  • A requirement > 8–10 mg/kg/min strongly suggests hyperinsulinism (a hallmark — confirm on the critical sample); maintain euglycemia with escalating dextrose as an initial measure until the endocrinology team advises.
Glucagon 0.5–1 mg IM/SC (fixed dose, independent of weight) when there is no IV access or hyperinsulinism is suspected; 0.03 mg/kg (max 1 mg) only if given IV — a rise > 1.7 mmol/L (30 mg/dL) suggests hyperinsulinism. It fails in glycogen‑depleted states (ketotic hypoglycemia, fatty‑acid oxidation defects).
◣ Read the ketones/free‑fatty‑acids branch
  • Low ketones + low free fatty acids (non‑ketotic) with detectable insulin → hyperinsulinism (congenital KATP, Beckwith‑Wiedemann, exogenous insulin/sulfonylurea, dumping).
  • Low ketones + high free fatty acids (hypoketotic) → fatty‑acid oxidation defect (e.g. VLCADD or LCHADD) — abnormal acylcarnitines ± hyperammonemia/cardiomyopathy.
  • High ketones + high free fatty acids (appropriate) → ketotic hypoglycemia of childhood (commonest, 1–5 yr, illness‑triggered, diagnosis of exclusion), GH/cortisol deficiency, or glycogen storage disease (hepatomegaly, high lactate).
◣ Admit · Discharge · Refer
  • Admit — unexplained symptomatic or persistent hypoglycemia → until fasting safety is documented and a cause established.
  • Home — only after a documented safe fast and a sick‑day/emergency plan (home glucagon where indicated).
  • Refer — now — pediatric endocrinology/metabolic; hyperinsulinism or a glucose infusion rate > 8–10 mg/kg/min → consult endocrinology with congenital hyperinsulinism (CHI) expertise.

Acute Electrolyte Emergencies

MINUTES

Stabilize the heart, stop the seizures, then correct at a safe rate.

▸
◢ Hyperkalemia — get an ECG first
  • Hyperkalemia = serum K⁺ > 5.5 mmol/L (ERC 2021 bands: mild 5.5–5.9 · moderate 6.0–6.4 · severe ≥ 6.5 or ECG changes; Lehnhardt 2011 uses 5.5–6.5 · 6.5–7.5 · > 7.5); hypokalemia = K⁺ < 3.5 mmol/L (severe < 2.5).
  • ECG progression: peaked T waves → flattened P / prolonged PR → widened QRS → sine wave → arrest. Treat urgently if there are ECG changes or potassium > 6.5 mmol/L.
  • If the child is well with a normal ECG, repeat a free‑flowing venous sample first — hemolysis causes pseudohyperkalemia. Stop all potassium intake and potassium‑raising drugs.
Hyperkalemia — stabilize, shift, remove
Step / drugDoseRoute & notes
STABILIZE · Calcium gluconate 10%0.5 mL/kg (max 20 mL) IV over 5–10 minCardiac monitor; protects the heart, does not lower potassium. Repeat after 15 min if ECG still abnormal. Not in the same line as bicarbonate (precipitates); caution in digoxin toxicity
SHIFT · Insulin (soluble) + glucose0.1 unit/kg (max 10 units) + glucose 0.5 g/kg IV (= 5 mL/kg of dextrose 10%)Onset 10–20 min; monitor glucose closely — early and late hypoglycemia
SHIFT · Salbutamol (nebulized)2.5 mg if < 25 kg; 5 mg if ≥ 25 kgAdditive to insulin; may cause tachycardia
SHIFT · Sodium bicarbonate1 mmol/kg IVOnly if acidotic; modest, adjunctive effect
REMOVE · Potassium binder0.5–1 g/kg (max 30 g) oral / rectalSodium/calcium polystyrene sulfonate; slow onset — not for immediately life‑threatening hyperkalemia; avoid with ileus, bowel obstruction, or NEC risk
REMOVE · Furosemide1 mg/kg IVIf making urine
REMOVE · Dialysis—Refractory or severe; involve renal / PICU early
◈ The logic
  • Calcium and the shifters (insulin, salbutamol, bicarbonate) only buy time; only binders, loop diuretics, and dialysis actually remove potassium from the body.
  • Recheck potassium and glucose after treating.
Sodium — correct at a safe rate
◎ Definitions Hyponatremia = Na⁺ < 135 mmol/L (severe < 125); hypernatremia = Na⁺ > 145 mmol/L (> 150 is often used for hypernatremic dehydration — expert consensus, not guideline‑stated).
ProblemTreatmentNotes
Hyponatremia with seizures / encephalo­pathy3% saline 2 mL/kg (max 100 mL) IV over 10 min
repeat once or twice until symptoms improve
Each bolus raises sodium by about 2 mmol/L; stop boluses once symptoms improve and keep the rise ≤ 12 mmol/L in 24 h; many experts aim for a 5–6 mmol/L rise in the first 1–2 h and no more than 10 mmol/L in the first 5 h and 15–20 mmol/L in 48 h (expert consensus — not guideline‑stated).
Hyponatremia (no severe symptoms)Treat the cause; correct slowlyDo not exceed 8 mmol/L per 24 h (a conservative expert limit; NICE pediatric ceiling 12 mmol/L per 24 h) — osmotic demyelination. Volume depletion → 0.9% saline; SIADH → fluid restriction
Hypernatremic dehydrationResuscitate shock with isotonic fluid first, then rehydrate over ~48 hLower sodium ≤ 0.5 mmol/L per hour (≤ 10–12 per 24 h) — faster risks cerebral edema,
Calcium & magnesium
◎ Definitions Hypocalcemia = total calcium < 2.1 mmol/L or ionized < 1.1 mmol/L (neonate < 2.0 mmol/L; correct total calcium for albumin). Hypomagnesemia = Mg²⁺ < 0.7 mmol/L (blocks correction of low K⁺ and Ca²⁺).
ProblemTreatmentNotes
Symptomatic hypocalcemiaCalcium gluconate 10% 0.5 mL/kg (max 20 mL) IV over 5–10 min, diluted 1:5–1:10 in 0.9% saline or 5% dextrose unless via central access; may repeat once if symptoms persist (local practice — the UK label gives age‑banded doses of 0.1–0.9 mL/kg, up to 2 mL/kg in severe neonatal hypocalcemia), cardiac monitor
then infusion
Tetany, seizures, prolonged QT, Chvostek / Trousseau signs. Monitor heart rate / ECG during injection; avoid extravasation (tissue necrosis)
Refractory hypocalcemia or hypokalemiaCheck and replace magnesiumLow magnesium blocks correction of both — replace it first (it makes hypokalemia refractory to potassium and impairs parathyroid hormone secretion),
⚠ The safe‑rate rule
Move fast to stabilize the heart (calcium) and stop seizures (3% saline), but correct chronic sodium slowly: overcorrecting low sodium causes osmotic demyelination, and dropping high sodium too fast causes cerebral edema.
◣ Admit · Discharge · Refer
  • Admit — symptomatic or severe derangements, or those needing infusions/monitoring → high‑dependency/PICU.
  • Home from the emergency department — mild, asymptomatic, correctable causes, with a follow‑up recheck.
  • Refer — now — nephrology/endocrinology by cause; PICU for arrhythmia risk or rapid shifts.

Hypercalcemia

HOURS

Corrected calcium > 2.6 mmol/L (10.5 mg/dL); > 3.5 mmol/L (14 mg/dL) is a crisis.

▸
◣ Recognize
  • Stones, bones, groans & psychiatric moans: nephrocalcinosis/stones; bone pain; constipation, nausea, anorexia, pancreatitis; lethargy, confusion, weakness, hypotonia, coma. Infants: poor feeding, failure to thrive, irritability.
  • Polyuria → dehydration (nephrogenic diabetes insipidus) — vicious cycle worsening the calcium. Cardiac: short QT, bradyarrhythmia; monitor ECG when severe/symptomatic.
  • Correct for albumin: add 0.8 mg/dL per 1 g/dL albumin below 4.0; confirm with ionized calcium.
  • Mild 2.6–3.0
  • moderate 3.0–3.5
  • severe > 3.5 mmol/L.
◣ Find the cause — PTH is the branch point
  • High or inappropriately normal PTH → primary hyperparathyroidism (think MEN) or familial hypocalciuric hypercalcemia (low urine Ca/Cr — benign, do not operate).
  • Suppressed PTH → malignancy (PTHrP/osteolysis), vitamin D intoxication, granulomatous disease, immobilization, thiazides, milk‑alkali. Send PTHrP, 25‑OH & 1,25-(OH)₂ vitamin D, phosphate, magnesium, urine Ca/Cr.
  • Infants: subcutaneous fat necrosis, Williams syndrome, idiopathic infantile hypercalcemia, neonatal severe hyperparathyroidism.
Lower the calcium — hydrate, then remove
Step / drugDoseRoute & notes
Stop intake—Stop all calcium & vitamin D (diet, fluids, supplements); stop thiazides, lithium, vitamin A/D
0.9% saline (cornerstone)10–20 mL/kg bolus, then ~2–3× maintenance (~3000 mL/m²/day)IV; restores volume then drives calciuresis; target brisk urine output
Furosemide1 mg/kg IVOnly after volume repletion; for fluid overload; monitor K⁺/Mg²⁺
Calcitonin (salmon)4 IU/kg SC/IM every 6–12 h (up to 8 IU/kg q6h)Rapid onset (2–6 h), modest; tachyphylaxis by 48 h — a bridge. Salmon is the potent form used clinically (≈40× human calcitonin).
Zoledronic acid (preferred)0.025–0.05 mg/kg as a single IV dose (max 4 mg; pediatric dose: local practice) — do not repeat within 7 days; check creatinine, calcium and vitamin D first
4 mg/5 mL vial, dilute 1:20 in 0.9% saline, infuse over 15 min
Preferred bisphosphonate for high bone turnover (malignancy, immobilization) — higher response rate (complete response ~88% vs ~70%) and a much shorter infusion (5 min vs 2 h in the trial) than pamidronate in adult hypercalcemia of malignancy (Major, J Clin Oncol 2001). Onset 24–48 h; ensure volume replete; watch for hypocalcemia; reduce/withhold in renal impairment
Pamidronate (alternative)0.5–1 mg/kg IV over 2–4 h (pediatric dose: local practice)Alternative where zoledronic acid is unavailable; same indications (adult comparative trial); onset 24–48 h; ensure volume replete; watch for hypocalcemia
GlucocorticoidPrednisone 1–2 mg/kg/dayFor vitamin D–mediated, granulomatous disease, or lymphoma/leukemia
Dialysis—Severe/refractory, renal failure, or cannot tolerate a saline load
◣ Admit · Discharge · Refer
  • Admit — moderate–severe, symptomatic, or > 3.5 mmol/L → monitored bed/PICU with ECG.
  • Home from the emergency department — mild & asymptomatic with an outpatient workup and offending agents stopped.
  • Refer — now — pediatric endocrinology ± oncology/nephrology.
  • Refer — clinic — parathyroidectomy for primary hyperparathyroidism (not for FHH).

Thyroid Storm (Thyrotoxic Crisis)

MINUTESATA 2016 · BWPS

Decompensated hyperthyroidism: fever, tachyarrhythmia and agitation, often with a trigger.

▸
◣ Recognize
  • Known/undiagnosed Graves’ disease with hyperthermia, marked tachycardia or tachyarrhythmia (atrial fibrillation/heart failure), agitation or reduced consciousness, and GI upset — usually with a trigger (infection, surgery, DKA, medication non‑adherence).
⚠ Treat on clinical suspicion
  • Do not wait for thyroid function results.
  • Provide supportive care (cooling, fluids, treat the trigger) and block the thyroid axis in the right order — β-blockade and a thionamide first, and give iodine only after the thionamide to avoid fueling hormone synthesis.
◣ Workup
  • TSH (suppressed), free T4, free T3, TRAb/TSI.
  • CBC, LFTs, glucose, electrolytes, calcium; ECG.
  • Diagnosis is clinical (Burch‑Wartofsky ≥ 45 highly suggestive) — do not delay treatment for labs.
Step / drugDoseRoute & notes
1 · Propranolol (β-block)0.25–0.5 mg/kg/dose PO/NG q6hControls heart rate, tremor and agitation; slows peripheral T4→T3. Caution in heart failure — treat failure alongside. Avoid propranolol in asthma/bronchospasm (seek senior advice on a cardioselective alternative),
2 · Methi­mazole (thionamide)0.5–1 mg/kg/day PO/NG/PR divided q8h (max 30 mg/day — local practice)Blocks new hormone synthesis; give the thionamide before iodine. Carbimazole is its prodrug — not mg‑for‑mg: 1 mg carbimazole ≈ 0.6 mg methimazole (carbimazole 0.75–1.3 mg/kg/day),
2 · PTU (thionamide — alternative)Dose per endocrinologyAlso blocks peripheral T4→T3. Either thionamide is acceptable — no difference in mortality (Lee, JAMA Netw Open 2023; adult ICU data); ATA 2016 has historically listed PTU first in storm. Pediatric guidance avoids PTU because of the risk of hepatic failure.
3 · Potassium iodide (saturated solution, SSKI)1–5 drops PO/NG q8h (local practice; pediatric pre‑operative SSKI regimen 1–4 drops three times daily); if only Lugol's (strong iodine) solution is available, 5–10 drops q8hBlocks hormone release,; give ≥ 1 h after the thionamide
4 · Hydro­corti­soneStress dose — per endocrinologyReduces peripheral T4→T3 conversion and covers relative adrenal insufficiency,
◣ Admit · Refer
  • Admit to PICU/HDU.
  • Call pediatric endocrinology and critical care.

Metabolic Crisis (Inborn Error)

MINUTESANY AGE

Suspected inborn error of metabolism — "sepsis that doesn't fit."

▸
◣ Recognize (think inborn error)
  • Encephalopathy, vomiting, seizures, or apnea after a symptom‑free interval or a catabolic trigger (fasting, intercurrent illness, surgery); poor feeding; tachypnea. Family history or parental consanguinity.
  • Mimics sepsis — “sepsis that doesn’t fit.” Presents at any age, not only the newborn. Not every metabolic crisis is hyperammonemic — the pattern points to the group:
PatternAcid–base · ammoniaPointers
Urea‑cycle (hyperammonemia)Respiratory alkalosis; very high ammonia; low ureaLittle or no acidosis; encephalo­pathy ± seizures
Organic acidemia (MMA / PA / IVA)High‑anion‑gap metabolic acidosis + ketosis; ammonia high (secondary)Hypoglycemia; offending acid on urine organic acids
MSUDKetosis with normal / near‑normal ammonia; acidosis variable (expert consensus)Maple‑syrup odor (urine/cerumen); high plasma leucine (alloisoleucine diagnostic)
Fatty‑acid oxidation disorder (MCAD, LC‑FAOD)Hypoketotic hypoglycemia after fasting or illness; ammonia normal or mildly raised; acidosis variableLethargy/encephalopathy, hepatopathy, cardiomyopathy or arrhythmia, rhabdomyolysis (check CK) — abnormal acylcarnitines. Reverse catabolism with high‑dextrose fluids (GIR as below); long‑chain fat restriction and medium‑chain fat sources only on metabolic advice.
① Stop catabolism Stop all protein — a temporary emergency measure (first ~24–48 h) until the metabolic team advises; prolonged protein restriction itself worsens catabolism, so protein is reintroduced on their guidance. Run high‑dextrose fluids; avoid hypotonic fluids (add enough sodium chloride; hyperammonemia causes brain edema) and, by common practice, lactated Ringer's. Treat low glucose. This card is initial stabilization pending specialist consultation.
② Immediate labs + call metabolic team
  • Ammonia (free‑flowing sample, on ice, run STAT and process immediately), blood gas, glucose, lactate, ketones, electrolytes/anion gap.
  • Send as confirmatory (not routine/STAT): plasma amino acids, urine organic acids, acylcarnitines.
high ammonia
③ Nitrogen scavengers + cofactors See drug table — coordinate with the metabolic service.
ammonia > 500 µmol/L (or 250–500 µmol/L with encephalopathy, onset on day 1–2 of life, or no fall within 3–6 h) / coma
Urgent hemodialysis or CRRT. Transfer to a metabolic center.
Drug / measureDoseRoute & notes
Dextrose 10%Dextrose 10% with electrolytes; glucose infusion rate: neonate 10 · infant 8 · older child 6 mg/kg/min. Higher rates only on metabolic adviceIV — reverses catabolism. Hyperglycemia is dangerous: add insulin, or reduce the rate if lactate is > 3 mmol/L.
Sodium benzoate + sodium phenylacetate≤ 20 kg: 250 mg/kg load over 90–120 min, then 250 mg/kg/day
> 20 kg: 5.5 g/m² load over 90–120 min, then 5.5 g/m²/day
Max 12 g/day of each scavenger
IV; must be diluted in dextrose 10% (≥ 25 mL/kg) — never undiluted; central line where possible (the product label specifies central access), peripheral only when life‑saving — ask pharmacy for an appropriately diluted preparation. In MMA / PA, phenylacetate/phenylbutyrate is not the primary scavenger (depletes glutamine) — benzoate ± carglumic acid per the metabolic team.
L‑arginine hydrochloride250 mg/kg (up to 400 mg/kg) over 90–120 min, then 250 mg/kg per 24 h. Argininosuccinic aciduria: 200–400 mg/kg load, then 200–400 mg/kg per 24 h; max 12 g/dayIV; omit in arginase deficiency
Carglumic acidAcute 100–250 mg/kg/day (2–4 divided doses)
then maintenance ~50 mg/kg/day (range 10–100) in 2 divided doses — titrate to plasma ammonia
Oral/NG; for NAGS deficiency & some organic acidemias,
L‑carnitine100 mg/kgIV / oral; for suspected organic acidemia
◈ Availability
  • Nitrogen scavengers, carglumic acid and L‑carnitine are specialist stock held in tertiary metabolic / PICU units, not general wards.
  • Phone the metabolic on‑call early — high‑dextrose fluids, protein cessation and dialysis access can start anywhere while drugs are sourced. Avoid valproate.
◣ Admit · Discharge · Refer
  • Admit — all suspected → PICU; stop protein, high‑dose dextrose, treat hyperammonemia.
  • Home from the ward — not acutely; under the metabolic team with an emergency regimen.
  • Refer — now — metabolic/genetics urgently and a center capable of ammonia scavengers/hemofiltration.
07

Focused Specialty Emergencies

Focused eye, dental, dermatologic, ENT & neurosurgical emergencies

Pediatric Eye Emergencies

MINUTESSIGHT‑THREAT

Chemical burn — irrigate before anything else. Leukocoria, orbital cellulitis, and a ruptured globe are the sight- and life‑threats not to miss.

▸
⚠ Chemical injury — irrigate FIRST
  • Immediate, continuous irrigation with normal saline or Ringer’s lactate (preferred) or tap water BEFORE examination, imaging or even registration; a topical anesthetic helps. Evert the lids and sweep out particles. Irrigate until the pH is neutral (7.0) on litmus/pH paper — up to 10–15 L may be needed — or for at least 30 min if pH cannot be measured. Alkali (drain/oven cleaner, cement, wet button batteries) penetrates deeper than acid.
  • Then urgent ophthalmology.
◣ The can't‑miss diagnoses
  • Orbital (post‑septal) cellulitis — proptosis, pain on or limited eye movement, reduced acuity or color vision, a relative afferent pupillary defect, chemosis → emergency. CT orbits + sinuses, IV antibiotics, ophthalmology + ENT. Distinguish from preseptal (lid swelling only, with normal movement, vision, and pupil) (see Preseptal & Orbital Cellulitis).
  • Ruptured / penetrating globe — after trauma with a distorted (teardrop) pupil, prolapsed dark uveal tissue, or marked subconjunctival hemorrhage → cover with a rigid shield (never a pad or any pressure), keep NPO, give analgesia + antiemetic, update tetanus, and refer urgently. No drops, no ointment.
  • Leukocoria (white pupil reflex), a new squint, or an absent red reflex → retinoblastoma until proven otherwise → urgent ophthalmology (a life‑threatening tumor).
  • Ophthalmia neonatorum — hyperacute purulent conjunctivitis in the first days of life → gonococcal risk (corneal perforation) → emergency: systemic ceftriaxone or cefotaxime is the main treatment (adequate systemic therapy makes topical antibiotics unnecessary; prefer cefotaxime in the jaundiced neonate or with calcium‑containing IV fluids), frequent saline irrigation of discharge, admit and swab; test for both N. gonorrhoeae and C. trachomatis. Doses (CDC 2021): gonococcal — ceftriaxone 25–50 mg/kg IV/IM once (max 250 mg), or cefotaxime 100 mg/kg IV/IM once if ceftriaxone cannot be given (calcium‑containing IV fluids; caution in hyperbilirubinemia, especially preterm); evaluate for disseminated infection. Chlamydial — oral erythromycin 12.5 mg/kg/dose every 6 h for 14 days (watch for pyloric stenosis).
  • Acute red painful eye with photophobia/reduced vision, or hyphema (blood layering in the anterior chamber after trauma) → same‑day ophthalmology.
  • Corneal ulcer (microbial keratitis) — red, painful, photophobic eye with a white/opaque corneal infiltrate or haze ± discharge; high risk in contact‑lens wearers and after trauma → sight‑threatening, same‑day ophthalmology. Do not patch; stop contact‑lens wear (expert consensus — not covered by the cited review).
  • Congenital / infantile glaucoma — the infant triad of watering (epiphora), photophobia, and blepharospasm with an enlarged or cloudy cornea (buphthalmos) → urgent ophthalmology (needs surgery); do not dismiss as a blocked tear duct.
  • New anisocoria (unequal pupils) — may signal a third‑nerve palsy, Horner syndrome, or raised ICP / herniation (see Raised ICP); with reduced consciousness, ptosis, or trauma it is a red flag → urgent assessment. Check pupils in both light and dark to localize (expert consensus — not covered by the cited review).
⚠ Safeguarding — retinal hemorrhages
Multilayered retinal hemorrhages extending to the periphery in an infant with encephalo­pathy suggest abusive head trauma — involve safeguarding and ophthalmology (see Fractures — Non‑Accidental Red Flags).
✦ Pearl — check the red reflex in every child
A symmetrical red reflex helps exclude retinoblastoma, cataract, and vitreous pathology; any white, asymmetric, or absent reflex needs urgent ophthalmology.
✦ Your role — the general pediatrician
  • You are the first responder, not the eye surgeon.
  • Three time‑critical moves are yours: (1) irrigate immediately for any chemical splash — don't wait for ophthalmology; (2) shield (never pad or press) a suspected ruptured globe, keep NPO, give analgesia + antiemetic; (3) check the red reflex in every child and treat leukocoria / an absent reflex as retinoblastoma.
  • Document visual acuity, pupils, and eye movements before referral. Avoid drops, ointment, or any pressure on a possibly open globe, and never patch a suspected corneal ulcer.
  • Then refer to ophthalmology (add ENT for orbital cellulitis) within the timeframe the diagnosis demands.
◣ Refer
  • Refer — now — ophthalmology urgently — chemical injury, suspected globe rupture, leukocoria/absent red reflex, orbital cellulitis (add ENT), acute vision loss, or hyphema.

Dental & Oral Emergencies

MINUTESTIME‑CRITICAL

An avulsed permanent tooth is a true emergency — reimplant within minutes. Never reimplant a primary tooth. Watch the swelling that threatens the airway.

▸
◣ Dental trauma
  • Luxation (displaced or mobile tooth) — do not attempt to reposition it; analgesia and same‑day dental referral.
  • Crown fracture — preserve any fragment and keep it moist (milk or saline); analgesia; prompt dental review — pulp exposure needs same‑day care.
  • Primary tooth avulsion — do NOT reimplant (risks of damaging the permanent successor); reassure and arrange dental review.
  • Post‑extraction bleeding — firm gauze pressure 15–20 min ± tranexamic acid; if it persists, consider an undiagnosed bleeding disorder.
⚠ Avulsed PERMANENT tooth — minutes matter
  • Reimplant as soon as possible. Hold the tooth by the crown — never touch or scrub the root (protect the periodontal ligament).
  • If dirty, rinse gently in milk, saline or the child’s saliva, reinsert, have the child bite on gauze.
  • If reimplantation isn't possible, transport the tooth at once in (in order of preference) milk, Hank's balanced salt solution, saliva (spat into a cup) or saline. Water is a poor medium but still better than letting the tooth dry.
  • Then urgent dental care for splinting; assess tetanus prophylaxis — indicated for a contaminated avulsion and guided by both the child's immunization status and the nature of the wound; consider antibiotics.
  • Prognosis falls sharply once extra‑oral dry time exceeds ~60 min, and periodontal‑ligament cells are then considered non‑viable — reimplant anyway.
✦ Pearl — milk beats water
If Hank's solution isn't to hand, cold milk is the best readily‑available storage medium; tap water is hypotonic and kills periodontal‑ligament cells, worsening the outcome. Time is tooth.
◣ Primary herpetic gingivostomatitis (HSV‑1)
  • The commonest cause of a painful mouth with fever in the 1–5‑year‑old: fever (usually 3–5 days, occasionally up to a week), swollen, friable, bleeding gingiva, and crops of painful vesicles → ulcers on the gingiva, tongue, lips, and buccal mucosa (often with perioral spread), drooling, and refusal to eat or drink. Tender cervical lymphadenopathy is usual and, being reactive, resolves as the illness settles. Self‑limited — the illness runs ~10–14 days.
  • Management is supportive — the priority is hydration and analgesia (acetaminophen ± ibuprofen); offer cold, bland fluids. Dehydration from poor intake is the main reason to admit. Avoid topical lidocaine/anesthetic gels in young children (toxicity).
  • Oral acyclovir — 20 mg/kg/dose 4×/day for 5–7 days (max single dose 800 mg); immunocompromised children 20 mg/kg/dose 4×/day for 7–10 days; immunocompromised adolescents 400 mg 3×/day for 5–10 days or until resolution. Significant or disseminated disease in an immunocompromised child needs IV acyclovir (5–10 mg/kg/dose q8h) rather than a prolonged oral course. Shortens fever, oral lesions, and viral shedding only if started within 72 h of symptom onset; not routine for the well child presenting late.
  • Distinguish from herpangina (coxsackievirus — ulcers on the soft palate/tonsillar pillars, gingiva spared) and hand‑foot‑and‑mouth disease. Admit/refer the dehydrated, the immunocompromised, or suspected eczema herpeticum / disseminated HSV.
◣ Oral soft‑tissue injuries
  • Tongue lacerations — most heal without sutures (rich blood supply). Repair if the wound gapes at rest, is large (> ~1–2 cm), bleeds persistently, is through‑and‑through, or splits the free edge/tip (a bisecting flap) — these risk a notched tongue.
  • Lip lacerations — a wound that crosses the vermilion border needs precise realignment of the border first (a 1 mm step is visible); through‑and‑through wounds need layered closure. Palpate and image for an embedded tooth fragment or foreign body after a fall onto the teeth.
  • Buccal & gingival mucosa — most intraoral tears heal spontaneously; suture only large, gaping, or food‑trapping wounds. A deep cheek wound can injure the parotid duct or facial nerve — refer.
  • Embedded foreign bodies — account for every tooth fragment: a missing piece may be buried in the lip/tongue (soft‑tissue radiograph or ultrasound) or aspirated (chest X‑ray if unaccounted for). Remove grit/glass, irrigate, and assess tetanus status.
  • Intruded tooth (driven into the socket) — refer to a pediatric dentist. A primary intruded tooth is usually left to re‑erupt spontaneously (do not reposition — protect the permanent tooth bud); a permanent intruded tooth needs dental assessment for repositioning.,
  • Repair intraoral and lip wounds within ~24 h with analgesia; give antibiotics for through‑and‑through lip wounds, bites, or grossly contaminated wounds.
◣ Dentoalveolar abscess / facial swelling
  • Analgesia and dental source control — incision and drainage, root canal (pulp) treatment, or extraction of the causative tooth — with a mandatory dental referral. For a localized abscess without systemic involvement or spreading, definitive dental treatment is the primary management and systemic antibiotics are generally not required; reserve antibiotics for facial cellulitis, systemic signs, significant spreading, or suspected deep‑space infection (per clinical judgment and MOH protocols). These commonly present directly to dental clinics, where the dentist identifies the source and delivers timely definitive treatment. Watch for spread to the deep neck, floor of mouth, or orbit — a spreading facial‑space infection can progress to Ludwig's angina (next).
⚠ Airway — Ludwig's angina
Firm submandibular swelling — in children often unilateral at onset before becoming bilateral — with a raised (elevated) tongue, drooling, or trismus is a deep‑space infection that can obstruct the airway. Call for airway help early — anesthesia, oral & maxillofacial surgery, ENT, or pediatric surgery (all are equipped to manage these cases), give IV antibiotics, and do not lay the child flat. Time‑critical — urgently call or refer.
✦ Your role — the general pediatrician
  • Most of what reaches you is yours to start.
  • For an avulsed permanent tooth, reimplant or store it in cold milk and send urgently — minutes decide the tooth; never reimplant a primary tooth.
  • Give analgesia, control post‑extraction bleeding with pressure ± tranexamic acid, assess tetanus for contaminated wounds, and suture only the soft‑tissue lacerations that need it — account for every tooth fragment.
  • Treat herpetic gingivostomatitis supportively, watching hydration.
  • Escalate the two true emergencies fast: a spreading facial‑space infection or Ludwig's angina (airway — call/refer anesthesia, oral & maxillofacial surgery, ENT, or pediatric surgery), and refer to dental / maxillofacial for avulsion, pulp exposure, or abscess.
◣ Refer
  • Refer — now — dental / maxillofacial urgently — avulsion, fractures with pulp exposure, facial fractures, or a facial‑space infection; for any airway threat call anesthesia, oral & maxillofacial surgery, ENT, or pediatric surgery — all are equipped to manage these cases.
  • Refer — clinic — an intruded tooth → pediatric dentist.

Dermatologic Emergencies

HOURSCAN'T‑MISS

Fever + rash — find the killers: meningococcemia / purpura fulminans, SJS/TEN, staph scalded skin, and eczema herpeticum.

▸
⚠ Non‑blanching rash + fever
  • Petechiae or purpura that do not blanch in an unwell/febrile child = invasive meningococcal disease / sepsis / purpura fulminans until proven otherwise — take blood cultures, give empiric IV antibiotics immediately, follow the Septic Shock pathway.
  • Do not wait for investigations.
◣ The can't‑miss rashes
  • SJS / TEN — dusky/targetoid macules with skin detachment and erosions of ≥ 2 mucosal sites (eyes, mouth, genitals), 1–3 weeks after a drug (antibiotics, anticonvulsants). Stop the culprit; fluids, skin + eye care, urgent dermatology + ophthalmology, transfer to a burns/PICU unit. Avoid the culprit drug and relevant cross‑reacting agents — broad beta‑lactam avoidance applies mainly when a beta‑lactam is the suspected culprit (see Antibiotic Allergy).
  • Staphylococcal scalded skin syndrome (SSSS) — young child, fever, tender diffuse erythema with superficial peeling (Nikolsky +) and perioral crusting; mucosae spared. Toxin‑mediated: IV anti‑staphylococcal antibiotic (cefazolin first‑line in Kuwait, as flucloxacillin is not available locally) + analgesia + fluids.
  • Eczema herpeticum — clusters of monomorphic punched‑out vesicles/erosions on eczematous skin in an unwell child → start acyclovir urgently; ophthalmology if periocular. (HSV superinfection.)
  • DRESS — fever, widespread morbilliform rash, facial edema, lymphadenopathy, eosinophilia, and organ (liver) involvement 2–8 weeks after a drug → stop the drug, supportive care ± steroids.
  • Necrotizing fasciitis — pain out of proportion, rapidly spreading dusky/edematous skin, systemic toxicity → surgical emergency + broad‑spectrum antibiotics.
◆ SJS / TEN — focused workup & management
  • Confirm the signs — dusky/targetoid macules with skin detachment and erosions of ≥ 2 mucosal sites; Nikolsky + (lateral shearing pressure detaches epidermis on non‑blistered skin), Asboe–Hansen + (a blister extends sideways with slight tangential pressure), and widespread skin tenderness — typically 1–3 weeks after a culprit drug.
  • Prognosis — calculate SCORTEN (best at day 1 and day 3). In children it over‑estimates mortality (pediatric death rates are far lower), so use it for guidance, not as a ceiling.
  • Investigations — CBC with differential, urea & electrolytes, LFTs, glucose, bicarbonate, coagulation profile, CRP/ESR, magnesium, phosphate, lactate, urinalysis. Sepsis is the leading cause of death — infective screen (blood cultures; skin swabs for HSV/VZV and bacteria) and treat superadded infection. Chest X‑ray; Mycoplasma testing guided by the clinical picture (in children, reactive infectious mucocutaneous eruption [RIME] — the current term, which subsumes the former Mycoplasma-induced rash and mucositis [MIRM] — is a distinct, milder mimic with prominent mucositis and little skin loss; RIME can also follow other respiratory pathogens, so test by presentation rather than routinely). Skin biopsy if the diagnosis is unclear.
  • Act now — stop the culprit drug immediately (earlier withdrawal improves survival); transfer to a burns unit or PICU — in children, transfer is required at ≥ 10% body surface detachment (burn center if > 30%) and may be considered below 10%; organ dysfunction needing intensive care is an indication at any extent.
  • Supportive care is the mainstay — IV fluids & electrolytes, thermoregulation, nutrition, analgesia; gentle handling, minimize friction/shear; non‑adherent dressings (petrolatum‑impregnated gauze or silicone/advanced dressings); avoid prophylactic systemic antibiotics — treat proven infection. Early multidisciplinary team: dermatology, ophthalmology (prevent ocular scarring; amniotic‑membrane grafting in severe eye disease), urology/gynecology (prevent genital adhesions), wound care, pain, psychology.
  • Systemic immunomodulation — specialist decision, low‑certainty evidence. Drug withdrawal + supportive care remain the priority. If an agent is used, ciclosporin and corticosteroids showed the most promising (low‑certainty) mortality signals; IVIG showed no benefit as monotherapy. Etanercept (off‑label) may be considered (S3 2024); if IVIG is used at all, give it combined with corticosteroids — the only regimen with a survival signal in network meta‑analysis (SMR 0.53, low certainty). Individualized by the specialist team.,,
  • After recovery — screen for ocular, cutaneous, urogenital and psychological sequelae; document the culprit, give a clear allergy alert (avoid re‑exposure and cross‑reacting agents), and consider HLA‑guided avoidance where relevant (e.g. HLA‑B*15:02 & carbamazepine, HLA‑B*58:01 & allopurinol).
Evidence: BAD children & young people SJS/TEN guideline 2018; German (AWMF/DDG) S3 guideline 2024; RIME term introduced by Ramien et al. (2021), RIME/MIRM terminology per Damari et al., J Hosp Med 2025. Culprit‑drug withdrawal + supportive care have the clearest benefit; all systemic immunomodulators remain low‑certainty.
◆ SSSS (staphylococcal scalded skin) — focused workup & management
  • Recognize — young child, fever, tender diffuse erythema with superficial peeling (Nikolsky +); desquamation of the flexures and radial fissuring/crusting around the eyes, mouth and nose; mucosae are spared. Toxin‑mediated (exfoliative toxin from a distant staphylococcal focus).
  • Cultures — swab the focus, not the blisters. Nasopharynx/nares, conjunctivae, throat, umbilicus, urine, blood, and any suspected primary site; in a neonate include the umbilical stump and circumcision site. Bulla fluid is sterile (unlike bullous impetigo) — do not culture it. Skin biopsy is usually unnecessary — reserve it (or a frozen section) for when SJS/TEN cannot be excluded (SSSS splits high in the granular layer; TEN is full‑thickness).
  • Antibiotics — start an IV anti‑staphylococcal agent: cefazolin is first‑line in Kuwait (the penicillinase‑resistant penicillins — flucloxacillin, nafcillin, oxacillin — are the international first‑line but are not available locally), switching IV → oral once improving; clindamycin only as an anti‑toxin adjunct where susceptible (added benefit uncertain in children, resistance rising); vancomycin if MRSA is suspected/prevalent or first‑line fails. Doses below — de‑escalate once afebrile and per sensitivities.
  • Supportive care — treat like a superficial burn: fluid & electrolyte balance, thermoregulation, nutrition, analgesia, and minimal handling. Wound care with petrolatum/Vaseline‑impregnated gauze (apply to the dressing — do not smear emollient directly onto raw skin); warm compresses to facial crusting. Watch for fluid loss and secondary sepsis.
  • Prognosis — good in children with prompt treatment (low mortality); higher risk in neonates and with extensive involvement.
AntibioticDose (pediatric)Route & notes
Cef­a­zo­lin (first‑line IV)25–33 mg/kg/dose q8h (max 2 g/dose)IV; first‑generation cephalosporin — anti‑staphylococcal first‑line in Kuwait (flucloxacillin not available locally)
Flu­clox­a­cil­lin / naf­cil­lin / oxa­cil­lin (where available)25–50 mg/kg/dose q6h (max 2 g/dose)IV; penicillinase‑resistant anti‑staphylococcal — the international first‑line, not currently available in Kuwait
Clin­da­my­cin (anti‑toxin adjunct)10 mg/kg/dose q8h (max 900 mg/dose)IV/PO; optional — suppresses toxin, only where susceptible; benefit uncertain in children
Van­co­my­cin (if MRSA)15 mg/kg/dose q6h (max 1 g/dose)IV; if MRSA suspected/prevalent or first‑line fails
Oral step‑downCeph­a­lex­in 25 mg/kg/dose q6–8h (max 1 g/dose)PO once afebrile & improving; complete ~7‑day course (di­clox­a­cil­lin/flu­clox­a­cil­lin where available)
Evidence: pediatric SSSS systematic review (Pediatr Dermatol 2025); Merck Manual (professional). Bullae are sterile — culture the primary focus; anti‑staphylococcal therapy + supportive care is the mainstay.
◆ Eczema herpeticum — focused workup & management
  • Recognize — clusters of monomorphic punched‑out vesicles/erosions on eczematous skin in an unwell child; honey‑colored crusting means the lesions are impetiginized (secondary S. aureus).
  • Isolate — contact precautions: gloves and gown until lesions are dry and crusted.
  • Confirm (don't delay treatment) — deroof an intact vesicle with a sterile needle and swab the clear fluid for HSV‑1/2 & VZV PCR (± Tzanck smear as a rapid bedside adjunct); take a bacterial swab (C&S) for secondary infection. Diagnosis is clinical — start antivirals empirically.
  • Baseline labs — CBC and a metabolic/renal panel, and check hydration, before IV acyclovir (renal safety).
  • Antivirals early — they save lives — IV acyclovir 10 mg/kg/dose q8h under 12 years (5–10 mg/kg/dose from 12 years; under 3 months 20 mg/kg/dose q8h as for neonatal HSV), each dose over 1 h (dose by ideal body weight in obesity; ensure hydration) if systemically unwell, severe/disseminated, periocular, or poor oral intake; oral acyclovir per local protocol for milder disease. Continue ~10–14 days / until lesions crust; step IV → oral on improvement.
  • Cover secondary infection — if impetiginized, add an oral anti‑staphylococcal antibiotic for S. aureus.
  • Eyes — facial/periocular involvement warrants urgent ophthalmology to exclude corneal disease (herpetic keratitis); start topical ophthalmic antiviral if corneal lesions are suspected.
  • Skin / eczema care — once antivirals are started (many pause topical steroids for ~48 h, then restart the appropriate‑potency topical corticosteroid as the child improves — steroids must never delay antivirals). Bland ointment emollients (avoid creams — they sting); non‑soap cleansers; lukewarm 5‑min baths, pat (never rub) dry, no soap; warm compresses to crusted areas; loose cotton clothing; avoid friction.
  • Supportive & referral — fluids/electrolytes, analgesia, nutrition; admit if extensive/systemic/dehydrated. Neurology if CNS involvement is suspected; dermatology at discharge for ongoing eczema management.
Evidence: StatPearls (Eczema Herpeticum); pediatric emergency guidance. Early antivirals are the priority; topical steroids treat the underlying eczema but must not delay antivirals.
◆ DRESS / DIHS — focused workup & management
  • Recognize — morbilliform rash with facial edema starting on the face → upper trunk → extremities (can worsen even after the drug is stopped), plus fever, lymphadenopathy, eosinophilia and atypical lymphocytes. Onset is late: 2–8 weeks after starting the culprit — but within ~24 h on re‑challenge. Commonest culprits: anticonvulsants (carbamazepine, phenytoin, lamotrigine, phenobarbital), allopurinol, and antibiotics (sulfonamides, vancomycin, minocycline). First‑degree relatives carry up to ~25% risk with the same drug (HLA‑linked).
  • Organ involvement — liver first (hepatitis), then lung, kidney, heart (myocarditis), spleen, GI and neurologic; HHV‑6/7, EBV, CMV reactivation is characteristic. Late endocrine autoimmunity (hypothyroidism, type 1 diabetes) can appear months afterwards.
  • Diagnose — clinical, scored with the RegiSCAR or J‑SCAR criteria. Labs: CBC + differential (eosinophilia, atypical lymphocytes), LFTs (may stay abnormal for months), renal panel + urinalysis (proteinuria/hematuria), CK, lipase, CRP/ESR/ferritin, baseline TFTs + glucose, viral PCR (HHV‑6/7, EBV, CMV), ECG + troponin + baseline echo, and CXR if respiratory symptoms; extend the work‑up by clinical suspicion. Skin biopsy to exclude mimics.
  • Manage — stop the culprit immediately and label the patient hypersensitive; supportive care; high‑potency topical corticosteroids. For organ involvement, systemic corticosteroids — prednisolone 1–2 mg/kg/day (moderate organ involvement 1–1.5 mg/kg/day; severe / danger signs: IV methylprednisolone 2 mg/kg/day for 3–5 days then oral 2 mg/kg/day, specialist‑led) until resolution, then a slow taper (~10–15% per week) over 6 weeks–3 months (up to 6 months in severe disease) to avoid relapse; adjuncts/alternatives (specialist): ciclosporin, IVIG (limited evidence), JAK inhibitors (anecdotal).
  • Monitor & avoid — screen for autoimmune sequelae (thyroiditis, type 1 diabetes): TSH, free T4 and glucose (with CBC, LFTs, renal function) at regular intervals for at least 6 months and up to 3 years or longer. Strict lifelong avoidance of the culprit and cross‑reacting drugs; document the allergy clearly.
Evidence: EAACI position paper on DRESS in children 2025; RegiSCAR / J‑SCAR criteria. Prompt drug withdrawal + staged (skin‑only vs organ) therapy; steroids taper slowly to prevent relapse.
◆ Necrotizing fasciitis — focused workup & management
  • Recognize — pain out of proportion and edema extending beyond the visible erythema; rapidly spreading dusky skin, fever, crepitus, bullae, necrosis or ecchymosis, and a hard "wooden" feel of the subcutaneous tissue; cutaneous anesthesia is a late sign. Lower > upper extremities. Special forms: perineum (Fournier gangrene), head & neck, and neonatal infection (e.g. from omphalitis).
  • It is a surgical emergency — call the surgeon now. Early aggressive debridement is the single biggest determinant of survival; do not let the LRINEC score or imaging delay surgery.
  • Scoring / labs — the LRINEC score can help distinguish necrotizing fasciitis from other soft‑tissue infection, but a low score does not exclude it (poor sensitivity in children). Send CBC + differential, basic metabolic panel, glucose, CRP, serum lactate, coagulation profile, and blood cultures (2 sets) — then start antibiotics without waiting.
  • Imaging — CT (or MRI) may support the diagnosis but must never delay surgical exploration.
  • Empiric antibiotics (after cultures) — broad‑spectrum covering gram‑positive incl. MRSA + gram‑negative + anaerobes, plus clindamycin for its antitoxin effect: e.g. vancomycin 15 mg/kg/dose q6h (max 1 g/dose) + piperacillin‑tazobactam 100 mg/kg/dose (piperacillin component) q6–8h (max 4 g piperacillin/dose) (or meropenem 20 mg/kg/dose q8h, max 1 g/dose) + clindamycin 10–13 mg/kg/dose q8h (max 900 mg/dose); de‑escalate on sensitivities.
  • Surgery = the gold standard — surgical exploration is both the definitive diagnosis and the treatment (expect repeat looks/debridement); send intra‑operative specimens for Gram stain, culture, and histology — alert microbiology in advance: processing is time‑critical once tissue reaches the lab (expedite the Gram stain and keep direct communication).
  • Who leads — shared surgical responsibility. The operative lead follows the anatomical site: orthopedics (limbs), ENT or maxillofacial (head & neck), plastics (soft‑tissue coverage), urology (perineum / Fournier), general/pediatric surgery (trunk / abdomen). In complex or multi‑region cases, several surgical subspecialties may need to collaborate together in the ED.
  • Support & referral — aggressive hemodynamic resuscitation / PICU; IVIG may be considered by the specialist team as an adjuvant in streptococcal toxic shock (evidence inconclusive — IDSA 2014 makes no recommendation for it). Refer to infectious diseases and plastic/reconstructive surgery (with pediatric/general surgery).
Evidence: IDSA skin & soft‑tissue infection guidelines 2014. Surgery is time‑critical — neither the LRINEC score nor imaging should delay operative exploration.
⚠ Neonate
Vesicles, or an unwell neonate with a rash, may be neonatal HSV — start high‑dose IV acyclovir 20 mg/kg/dose every 8 h and a full sepsis work‑up without delay. Treat for 14 days (skin‑eye‑mouth disease) or 21 days (CNS or disseminated disease); for CNS disease, repeat CSF HSV PCR near the end of therapy and continue until it is negative, then give oral acyclovir suppression — 300 mg/m²/dose 3×/day for 6 months.
✦ Pearl — read the pattern
Non‑blanching + unwell = sepsis; monomorphic vesicles on eczema = eczema herpeticum; widespread peeling with mucosal erosions = SJS/TEN, versus mucosa spared / superficial = SSSS.
◣ Refer
  • Refer — now — dermatology + the relevant team urgently; PICU/burns for extensive TEN; ophthalmology for any mucosal/ocular involvement; urology/gynecology for genital involvement.

Pediatric ENT Emergencies

MINUTESAIRWAY / ENT

The airway threats, bleeds, and batteries that can't wait — stabilize first, then call ENT.

▸
⚠ Button battery in the nose or ear — hours matter
  • A disc battery lodged in the nose or ear causes liquefactive necrosis and septal/ostial perforation within hours; unilateral foul or bloody discharge is the clue.
  • ENT emergency — urgent removal; do not irrigate a nasal battery. (Swallowed batteries → Button Battery Ingestion.)
◣ Recognize & act
  • Acute upper‑airway obstruction — stridor, drooling, tripod posture → epiglottitis / bacterial tracheitis / severe croup: keep the child calm and upright, minimal handling, call anesthesia + ENT, and do not examine the throat (see Croup, Difficult Airway, Retropharyngeal Abscess).
  • Post‑tonsillectomy bleeding — any bleed (classically day 5–10) is an emergency: sit up, suction, IV access + fluids/blood, tranexamic acid, call ENT + anesthesia, prepare for the operating room. Swallowed blood hides the true loss.
  • Deep‑neck / peritonsillar / retropharyngeal abscess — trismus, muffled “hot‑potato” voice, neck stiffness or torticollis → IV antibiotics, imaging, ENT; watch the airway.
  • Acute mastoiditis — post‑auricular swelling/erythema with a protruding pinna after otitis media → IV antibiotics + ENT (risk of intracranial spread / venous sinus thrombosis).
  • Severe epistaxis — sit forward, pinch the soft part 10–15 min, topical vasoconstrictor; if uncontrolled or recurrent, ENT — consider a bleeding disorder, or juvenile angiofibroma in an adolescent boy.
  • Ear/nose foreign body — refer for removal; for a live insect, instill lidocaine or oil first.
⚠ Airway
Do not try to visualize the airway or lay the child flat when epiglottitis or a deep‑neck abscess is suspected — summon anesthesia/ENT, keep the child calm and upright.
✦ Pearl — unilateral discharge = foreign body / battery
Unilateral foul or bloody nasal discharge in a toddler is a foreign body — and a battery until excluded; examine, image if needed, and remove urgently.
✦ Your role — the general pediatrician
  • Secure the child first, not the diagnosis.
  • In suspected epiglottitis or a deep‑neck abscess, keep the child calm and upright, give oxygen, do not examine the throat or lay them flat, and summon anesthesia + ENT.
  • For post‑tonsillectomy bleeding, get IV access, fluids/blood, and tranexamic acid while ENT is called — assume swallowed blood hides the true loss.
  • Recognize the emergencies that can't wait: a nasal/aural button battery and unilateral bloody discharge need same‑hour ENT.
  • Control epistaxis with 10–15 min of firm pressure before escalating.
  • Your job is early recognition, first stabilization, and a timely ENT / anesthesia call.
◣ Refer
  • Refer — now — ENT urgently — nasal/aural battery, post‑tonsillectomy bleed, deep‑neck abscess, mastoiditis, or uncontrolled epistaxis; anesthesia for any airway threat.

Pediatric Neurosurgical Emergencies

MINUTESTIME‑CRITICAL

Shunt failure, rising ICP, and cord compression — recognize early, control the pressure, and call neurosurgery.

▸
⚠ VP shunt malfunction — treat as raised ICP
  • In a child with a shunt, headache, vomiting, drowsiness, irritability, a bulging fontanelle, or any change from baseline = a blocked shunt until proven otherwise.
  • Assess, image (CT or rapid‑sequence MRI + shunt series), call neurosurgery urgently.
  • Shunt infection (fever, redness/swelling along the tract, or a new malfunction) carries the same urgency — manage on a defined pathway: sample CSF from the shunt/reservoir plus blood cultures; start empiric antimicrobials covering staphylococci (including MRSA) and Gram‑negative organisms — e.g. vancomycin + an anti‑pseudomonal beta‑lactam (cefepime, ceftazidime, or meropenem); plan removal or externalization of the infected hardware; and involve neurosurgery and infectious diseases early.
  • Controlling raised ICP is the priority while awaiting neurosurgery.
◣ Recognize & act
  • Raised ICP / impending herniation — falling GCS, an unequal or fixed pupil, Cushing's triad (hypertension, bradycardia, irregular breathing), or abnormal posturing → head up 30°, midline neck, normocapnia, treat seizures, hyperosmolar therapy (hypertonic saline or mannitol), urgent neurosurgery (see Raised ICP).
  • Non‑traumatic intracranial hemorrhage — sudden severe headache, focal deficit, or coma (AVM, aneurysm, tumor) → urgent CT + neurosurgery.
  • Depressed / open skull fracture or penetrating head injury → neurosurgery + antibiotics + tetanus (see Traumatic Brain Injury).
  • Acute spinal cord compression — neck or back pain with arm or leg weakness, a sensory level, or bladder/bowel dysfunction (tumor, abscess, trauma) → urgent MRI, dexamethasone if tumor, and urgent spine‑surgical referral — neurosurgery or pediatric orthopedic spine surgery (either may be consulted for extradural pathology: epidural abscess, vertebral/extradural tumor, or bony trauma) ± oncology — time‑critical for recovery. In traumatic spinal cord injury, also involve PICU for hemodynamic (MAP) support — maintain mean arterial pressure and avoid hypotension to preserve cord perfusion; watch for neurogenic shock (hypotension with bradycardia).
  • CSF leak — clear rhinorrhea/otorrhea or a tense pseudomeningocele after surgery/trauma → neurosurgery (meningitis risk).
⚠ Don't delay imaging
A shunted child who is drowsy or vomiting needs urgent imaging and a neurosurgical call — deterioration can be rapid; do not attribute it to a viral illness.
✦ Pearl — ask the parents
Parents of a shunted or hydrocephalic child usually recognize their own child's “shunt‑failure pattern” — take that history seriously and image.
✦ Pearl — protect the pupil exam
Have ophthalmology look for papilledema, but avoid dilating the pupils in a drowsy or deteriorating child — mydriatic drops abolish the pupillary response, a key sign of herniation.
✦ Your role — the general pediatrician
  • Recognize, control the pressure, and call — you are not expected to operate.
  • In any shunted child, treat headache / vomiting / drowsiness / any change from baseline as a blocked shunt until proven otherwise: image (CT or rapid‑sequence MRI + shunt series) and call neurosurgery.
  • While waiting, deliver the ICP first‑aid that is yours — head up 30°, midline neck, normocapnia, treat seizures and fever, and give hyperosmolar therapy for impending herniation.
  • Take a parent's “this is his shunt‑failure pattern” seriously.
  • Don't anchor on a viral illness, and refer time‑critically for cord compression (urgent MRI) and open / depressed skull fractures.
◣ Refer
  • Refer — now — neurosurgery urgently — shunt malfunction/infection, raised ICP, intracranial hemorrhage, or a depressed/open skull fracture; acute spinal cord compression — neurosurgery or pediatric orthopedic spine surgery (either for extradural pathology); add PICU for traumatic cord injury (MAP support).
08

Gastroenterology & Hepatology

GI bleeding · liver failure · pancreatitis · hepatitis · neonatal cholestasis · ingestion (foreign body / battery) · feeding‑tube problems → Common Acute Conditions

Upper Gastrointestinal Bleeding

MINUTES

Hematemesis or melena — resuscitate first, then find and treat the source.

▸
◣ Recognize & stratify
  • Bleeding proximal to the ligament of Treitz: hematemesis (fresh or coffee‑ground) or melena. Confirm true blood — swallowed maternal or epistaxis blood and red foods mislead.
  • Clinically significant = hemodynamic instability, a hemoglobin fall ≥ 2 g/dL, or a transfusion requirement — most need PICU.
  • Age‑based causes: neonate — swallowed maternal blood, vitamin K deficiency bleeding, stress gastritis; infant/child — reflux esophagitis, gastritis, peptic ulcer, Mallory‑Weiss tear; any age with liver disease — varices. Consider an ingested button battery (urgent chest X‑ray; see Button Battery Ingestion).
◯ Investigate — order → look for → what it means
OrderLook forWhat it tells you
CBC + serial hemoglobinHb fall ≥ 2 g/dL; thrombocytopeniaSeverity & transfusion need
Blood group + crossmatch—Prepare blood early in any significant bleed
Coagulation — PT/INR, aPTT, fibrinogenCoagulopathyNon‑variceal bleed: correct a true coagulopathy before/with endoscopy. Suspected variceal bleed with chronic liver disease: do NOT give FFP just to correct the INR (no hemostatic benefit; the volume load raises portal pressure) — plasma/platelets/cryoprecipitate only case‑by‑case (failure to control bleeding, sepsis/DIC, another bleeding source). A prolonged INR also flags underlying liver disease
LFTs + albuminHigh bilirubin, low albuminChronic liver disease → suspect a variceal source
Urea & creatinineUrea raised out of proportion to creatinineSupports an upper (vs lower) GI source — absorbed blood‑protein load
Venous blood gas + lactateMetabolic acidosis, rising lactateHypoperfusion → the bleed is severe; escalate
① Resuscitate first ABC, two large‑bore IVs, crystalloid; send crossmatch; correct coagulopathy/thrombocytopenia (no routine FFP for the INR in variceal bleeding). Protect the airway in brisk hematemesis.
Hemodynamically unstable?
UNSTABLE / MASSIVE
Resuscitate to hemodynamics and activate the massive transfusion protocol (empiric RBC:plasma:platelet ratios) — not a fixed Hb target. PICU; urgent endoscopy once stabilized.,
STABLE
Restrictive transfusion — transfuse at Hb < 7 g/dL, target 7–9 g/dL (extrapolated from adult data). Over‑transfusion raises portal pressure and can worsen variceal bleeding.,,
Variceal suspected? (known/suspected liver disease, splenomegaly, umbilical‑catheter history)
VARICEAL
Octreotide infusion (start early, after senior/GI discussion). In cirrhotic portal hypertension, add broad‑spectrum IV antibiotic prophylaxis (per local susceptibility) for 5–7 days (e.g., ceftriaxone); role in non‑cirrhotic PH unclear. Endoscopy within 24 h — band ligation preferred (sclerotherapy if ligation is not feasible).
NON‑VARICEAL
High‑dose IV proton pump inhibitor. Endoscopy for hemostasis — injection + cautery/clips (± hemostatic powder for refractory bleeding — adult guidance) — early (≤ 24 h) once resuscitated; emergent/urgent (≤ 6–12 h) endoscopy only if still unstable despite resuscitation (adult guidance).
Uncontrolled bleeding → balloon tamponade (Sengstaken‑Blakemore) as a bridge in massive variceal bleeding; interventional radiology (TIPS) or surgery — keep the massive transfusion protocol running.
DrugDoseRoute & notes
Octreotidebolus 1–2 mcg/kg (max 50 mcg)
then 1–2 mcg/kg/h infusion (max 50 mcg/h); if bleeding continues titrate up to ~5 mcg/kg/h, still not exceeding 50 mcg/h
IV; variceal bleeding. Continue 2–5 days after endoscopy, then wean gradually (rebound risk); monitor glucose
Pantoprazole / omeprazole1–2 mg/kg (max 40 mg — intentional pediatric maximum, gastroenterology review) IV bolus
then 0.1–0.2 mg/kg/h infusion (max 8 mg/h) for severe bleeding
Non‑variceal bleeding. Bolus + infusion is an adult‑derived regimen (80 mg then 8 mg/h for up to 72 h); pediatric evidence is limited and shows no advantage over intermittent dosing. Stress‑ulcer prophylaxis uses standard once‑daily dosing, not this regimen
Ceftriaxone50 mg/kg/dose once daily (max 2 g)Broad‑spectrum IV prophylaxis per local susceptibility, 5–7 days, in cirrhotic portal hypertension with acute variceal bleeding; benefit in non‑cirrhotic portal hypertension unclear
PRBC transfusionrestrictive: transfuse at Hb < 7 g/dL, target 7–9 g/dLEspecially variceal/cirrhosis (threshold extrapolated from adult data); transfuse promptly for hemodynamic instability or ongoing massive bleeding regardless of Hb,,
⚠ At the bedside
Do not routinely place a nasogastric tube — in adults it does not improve outcomes, is complicated in about a third of patients, and endoscopy is the diagnostic and therapeutic tool (adult data)., If varices are suspected (known chronic liver disease or portal hypertension, splenomegaly, prior varices), avoid blind nasogastric tube insertion — it can traumatize varices and provoke bleeding, and gains nothing before endoscopy; leave gastric access to the endoscopy/anesthesia team (expert consensus — not guideline‑stated). Protect the airway in brisk hematemesis; do not over‑transfuse a stable variceal bleed.,
◣ Admit · Discharge · Refer
  • Admit — all significant bleeds → resuscitation and endoscopy.
  • Home from the emergency department — a minor self‑limited bleed after observation, with follow‑up.
  • Refer — now — gastroenterology (endoscopy); surgery/interventional radiology for uncontrolled bleeding.

Lower Gastrointestinal Bleeding

HOURSAGE‑STRATIFIED

Hematochezia — most are benign, but resuscitate first and never miss the surgical causes.

▸
◣ Recognize & stratify
  • Bleeding distal to the ligament of Treitz: hematochezia (fresh or maroon blood/clots per rectum), or melena from a brisk right‑colonic/small‑bowel source. Confirm it is blood — red foods, drugs, and bismuth mislead.
  • Separate the sick from the well first: a pale, tachycardic child, or blood with bilious vomiting or severe pain, points to a surgical emergency (intussusception, malrotation with volvulus, or NEC in a neonate) — see the red lines below.
  • Age‑based commonest causes:
    • Neonate — swallowed maternal blood, anal fissure, cow's‑milk protein allergy, NEC, vitamin K deficiency bleeding, malrotation/volvulus.
    • Infant / toddler — anal fissure, cow's‑milk protein colitis, intussusception, Meckel diverticulum (painless, brisk), infectious colitis.
    • Child / adolescent — infectious colitis, juvenile polyp (painless), anal fissure, inflammatory bowel disease, Henoch‑Schönlein purpura, hemorrhoids.
◯ Investigate — order → look for → what it means
OrderLook forWhat it tells you
CBC + serial hemoglobinAnemia, Hb fall, thrombocytopenia; microcytosisSeverity & chronicity (microcytic = chronic loss)
Coagulation — PT/INR, aPTTCoagulopathyBleeding diathesis; vitamin K deficiency bleeding in a neonate
Blood group + crossmatch—Prepare blood for any significant bleed
Urea & creatinineA raised urea:creatinine ratioSuggests an upper source instead — reconsider
Stool — culture, C. difficile, ova/parasites; fecal calprotectinPathogen; raised calprotectinInfectious colitis vs inflammatory bowel disease
Abdominal ± Doppler ultrasoundTarget / pseudo‑kidney signIntussusception (bowel ultrasound is an adjunct in NEC)
Abdominal X‑ray (supine + left‑lateral decubitus)Pneumatosis, portal venous gas, free air; obstructionNEC / perforation / obstruction — neonate with bloody stools, or any distension/peritonism
99mTc‑pertechnetate (Meckel) scanEctopic gastric mucosaMeckel diverticulum in painless brisk bleeding
① Resuscitate first ABC, IV access, crystalloid, crossmatch; transfuse by the restrictive strategy (Hb < 7 g/dL) unless unstable or massively bleeding.
Sick child, or surgical features?
SURGICAL / UNSTABLE
Bilious vomiting, peritonism, a palpable mass or currant‑jelly stool, or a distended tender neonatal abdomen → urgent surgical review + imaging (ultrasound for intussusception; contrast study for malrotation). Do not delay.
WELL / STABLE
Treat by the likely cause — fissure care and address constipation; trial a cow's‑milk‑protein‑free diet in a well infant with colitis; supportive care for infectious colitis.
Persistent, significant, or unexplained bleeding → endoscopy (colonoscopy ± upper endoscopy) by pediatric gastroenterology; a Meckel scan for painless brisk bleeding.
⚠ Red lines — do not miss
  • Intussusception — colicky pain, drawing up the legs, currant‑jelly stool, a sausage‑shaped mass — ultrasound first, then air/contrast enema reduction.
  • Malrotation with volvulus — bilious vomiting with rectal bleeding is a surgical emergency until excluded.
  • Meckel diverticulum — massive painless rectal bleeding in a young child.
  • NEC in a preterm/neonate — distension, bloody stools, systemic upset (see Necrotizing Enterocolitis).
◣ Admit · Discharge · Refer
  • Admit — any significant bleed, hemodynamic compromise, or a suspected surgical cause.
  • Home from the emergency department — a well child with a minor self‑limited cause (fissure, small polyp bleed) and follow‑up.
  • Refer — now — pediatric surgery for intussusception/volvulus/Meckel/NEC; gastroenterology for endoscopy.
  • Refer — clinic — gastroenterology for suspected IBD or recurrent/unexplained bleeding.

Acute Liver Failure

HOURS

Coagulopathy not corrected by vitamin K — transfer to a transplant center early.

▸
◣ Define (PALF)
  • Biochemical liver injury with a coagulopathy not corrected by vitamin K: INR ≥ 1.5 with hepatic encephalo­pathy, or INR ≥ 2.0 without it — and no known chronic liver disease.
  • Encephalopathy is hard to read in infants (irritability, poor feeding, reversed sleep). Look for hypoglycemia, jaundice, hyperammonemia.
  • Seek a treatable cause: acetaminophen, herpes simplex virus, autoimmune hepatitis, Wilson disease, metabolic (galactosemia, tyrosinemia), gestational alloimmune liver disease.
◯ Investigate — order → look for → what it means (NASPGHAN)
OrderLook forWhat it tells you
PT / INRINR ≥ 1.5 with encephalopathy, or ≥ 2.0 without it — not corrected by vitamin KMeets the PALF diagnostic criterion; the trend is the key prognostic marker
Ammonia, glucose, venous gas/bicarbonate, lactate (± pyruvate)Hyperammonemia, hypoglycemia, metabolic acidosis, high lactateComplications & severity — drive PICU/transplant escalation
Bilirubin, albumin/total protein, AST/ALT/GGTRising bilirubin, low albuminDegree of hepatocellular injury & synthetic failure
CBC, electrolytes, Ca/Mg/phosphateCytopenias, electrolyte derangementSupportive‑care targets; bleeding risk
Etiology panel: acetaminophen level, HSV PCR + viral serology, autoimmune markers, ceruloplasmin/Wilson studies, metabolic screen (galactosemia, tyrosinemia), gestational alloimmune liver disease workupA treatable causeDirects specific therapy — NAC, acyclovir, immunosuppression, chelation, exchange/IVIG
Suspect it → contact a pediatric liver transplant center / PICU immediately
Support
  • Treat hypoglycemia (continuous dextrose, glucose infusion rate 6–8 mg/kg/min, titrated — concentrate the dextrose rather than raising the fluid rate; total IV fluids about 90% of maintenance unless resuscitating)
  • Give one dose of parenteral vitamin K. Do not routinely correct the INR without bleeding or a pre‑invasive procedure — it is the prognostic marker the transplant team needs.
  • Manage hyperammonemia/encephalo­pathy with transplant‑hepatology/PICU guidance (lactulose/ammonia‑lowering, nurse head‑up, avoid sedatives, transfer early); cover empirically for sepsis if unwell.
  • Every neonate/young infant (≤ 90 days) with acute liver failure: send HSV PCR (blood; surface swabs/CSF as feasible) and start IV acyclovir 20 mg/kg/dose every 8 h empirically — do not wait for vesicles or a maternal history; stop only when HSV is excluded. Start N‑acetylcysteine without delay when acetaminophen toxicity is confirmed or suspected (regimen: Poisoning card).
DrugDoseRoute & notes
Dextrose infusion (10%; concentrate to 12.5–20% or more via a central line as needed)start at glucose infusion rate 6–8 mg/kg/min and titrate to glucose 90–120 mg/dL (5–6.7 mmol/L) — up to 10–15 mg/kg/min may be required; keep total IV fluids at about 90% of maintenance unless resuscitatingRaise the dextrose concentration, not the fluid rate; check glucose frequently
Vitamin K1 mg in infants, scaled by age/weight up to 10 mg in older adolescents — one parenteral dose (subcutaneous or slow IV; not oral)To exclude vitamin K–responsive coagulopathy; recheck the INR
N‑acetyl­cysteineper acetaminophen protocolAcetaminophen toxicity (confirmed or highly suspected) only. Not for non‑acetaminophen acute liver failure — the pediatric RCT showed no survival benefit and significantly lower 1‑year transplant‑free survival with N‑acetylcysteine (35% vs 53%), especially under 2 years; any use outside acetaminophen toxicity is a transplant‑center decision
Acyclovir20 mg/kg/dose every 8 hIV; empiric in every neonate/young infant (≤ 90 days) with acute liver failure until HSV PCR is negative — HSV is a treatable cause
⚠ Avoid harm
  • Avoid sedatives/benzodiazepines (not cleared by a failing liver; they mask encephalo­pathy) and hepatotoxic drugs. Do not chase a normal INR with plasma in a non‑bleeding child — it erases the key trend.
  • Watch for cerebral edema (rising intracranial pressure) as encephalo­pathy advances.
◣ Admit · Discharge · Refer
  • Admit — all → PICU/transplant center.
  • Home from the ward — not acutely.
  • Refer — now — hepatology/transplant urgently; PICU for encephalopathy/cerebral edema.

Acute Pancreatitis

HOURSNASPGHAN 2018

Diagnose on two of three — then fluids, analgesia, and early feeding.

▸
◣ Diagnose (≥ 2 of 3)
  • Abdominal pain compatible with acute pancreatitis (epigastric, may radiate to the back).
  • Amylase and/or lipase ≥ 3× the upper limit of normal (lipase is more specific).
  • Imaging consistent with acute pancreatitis (ultrasound first; CT/MRI if needed).
  • Look for a cause in every case: structural/biliary, trauma (including inflicted injury), drugs, infection, metabolic, systemic illness, genetic.
◯ Investigate — order → look for → what it means
OrderLook forWhat it tells you
Lipase (± amylase)≥ 3× the upper limit of normalDiagnostic criterion (lipase more specific than amylase)
CBC, CRP, hematocritLeukocytosis, rising CRP, hemoconcentrationInflammatory burden & early severity
BUN, creatinineRising BUN, acute kidney injuryKey severity predictor — escalate fluids/PICU
Glucose, calciumHyperglycemia, hypocalcemiaSeverity markers
ALT, AST, GGT, ALP, bilirubin + triglycerides + calcium (every first attack)Raised ALT/bilirubin; high triglycerides or calciumBiliary (gallstone) vs metabolic cause — suspected obstruction: MRCP first, then ERCP only when a therapeutic procedure is needed
Abdominal ultrasound first‑line; MRCP for suspected biliary or pancreatic‑duct obstruction/anomaly; CT for suspected complicationsGallstones, necrosis, ductal anomaly, choledocholithiasisEtiology & complications
① Fluids Crystalloid 1.5–2× maintenance first 24–48 h (10–20 mL/kg bolus for hypovolemia). Target urine output > 0.5–1 mL/kg/h; monitor cardiac, pulmonary, and renal status closely for 48 h.
② Analgesia & feeding
  • Adequate analgesia, including opioids when needed. Start enteral nutrition early (within 48–72 h, as tolerated — oral/gastric/jejunal); enteral is preferred over parenteral.
  • Prolonged gut rest is no longer recommended.
No routine prophylactic antibiotics — reserve them for proven infection (e.g., infected necrosis).
TherapyDose / settingNotes
Crystalloid (balanced, or saline + 5% dextrose)1.5–2× maintenance, first 24–48 h
avoid overly aggressive fluids — reassess for pulmonary edema, AKI, and shock, especially in severe disease
Most important early intervention
Morphine0.05–0.1 mg/kg IV, titrateOpioid analgesia when needed
Early enteral nutritionwithin 48–72 hOral/gastric/jejunal; enteral preferred over parenteral
⚠ Watch for severe disease
  • Most complications declare within 48 h.
  • Persistent organ dysfunction (respiratory, cardiovascular, renal) defines severe acute pancreatitis — escalate to PICU.
  • Gallstone pancreatitis: cholangitis or persistent obstructive jaundice → urgent therapeutic ERCP (within 48 h; adult data) — do not delay for MRCP. Obstruction only suspected/unclear → MRCP (or endoscopic ultrasound) first, then ERCP only if a stone/obstruction is confirmed. Involve surgery and GI; cholecystectomy before discharge after mild biliary pancreatitis.
◣ Admit · Discharge · Refer
  • Admit — essentially all confirmed cases — for IV fluids, analgesia, and monitoring; ICU for organ dysfunction or predicted severe disease.
  • Home from the ward — mild disease once pain is controlled, feeding is re‑established, and the cause is being addressed.
  • Refer — now — surgical or gastroenterology review for biliary/structural causes, necrosis, or complications.

Acute Hepatitis

HOURS

Most recover — the job is to catch the few progressing to liver failure.

▸
◣ Assess
  • Raised transaminases ± jaundice, nausea, anorexia, right‑upper‑quadrant pain, dark urine, pale stools.
  • Causes: viral (hepatitis A/B/C/E, EBV, CMV, adenovirus, enterovirus, herpes simplex virus, SARS‑CoV‑2), drug‑induced (including acetaminophen), autoimmune hepatitis, Wilson disease, metabolic, ischemic.
  • Check synthetic function and a coagulation profile (INR) at presentation — it separates uncomplicated hepatitis from evolving liver failure. In a sick or deteriorating child, also send ammonia, lactate, glucose, and a toxicology (acetaminophen) screen.
◯ Investigate — order → look for → what it means
OrderLook forWhat it tells you
AST/ALT, bilirubinMarkedly raised transaminases ± jaundiceConfirms hepatocellular injury
PT/INR, albuminProlonged INR, low albuminSynthetic failure → evolving acute liver failure — separates it from uncomplicated hepatitis
Ammonia, glucose, lactate, venous gasHyperammonemia, hypoglycemia, acidosisComplications & severity in a sick/deteriorating child
Acetaminophen level; viral panel — hepatitis A/B/C/E, EBV, CMV, HSV PCRA treatable/infectious causeDirects specific therapy (NAC, acyclovir) and public‑health notification
Autoimmune markers, ceruloplasmin, ferritinAutoimmune hepatitis, Wilson disease, HLHSpecific etiologies not to miss
Manage
  • Mostly supportive: hydration, antiemetics, avoid hepatotoxins, review every drug.
  • Test for viral hepatitis as indicated; send autoimmune markers, ceruloplasmin, and ferritin. Notify per public‑health requirements for notifiable viral hepatitis.
Red flags → treat as acute liver failure: a rising INR not corrected by vitamin K, hypoglycemia, or any encephalo­pathy. Refer urgently.
⚠ Don't miss the turn
  • A child with hepatitis who develops coagulopathy (INR ≥ 1.5–2.0), hypoglycemia, or altered behavior is no longer “just hepatitis” — escalate to the Acute Liver Failure pathway (see Acute Liver Failure) and contact a transplant center.
  • Consider acetaminophen toxicity and Wilson disease in any severe presentation.
◣ Admit · Discharge · Refer
  • Admit — any coagulopathy, hypoglycemia, encephalopathy, severe vomiting or dehydration, or diagnostic uncertainty.
  • Home — well child with stable or improving enzymes, normal INR, tolerating oral intake, with follow‑up.
  • Refer — now — urgent transplant‑center/hepatology referral if it evolves to acute liver failure (rising INR, encephalopathy).

Neonatal Cholestasis

ASSESSNASPGHAN/ESPGHAN 2017 · FISPGHAN 2025

Conjugated jaundice is never physiological — the biliary‑atresia clock is ticking.

▸
◣ The rule
  • Any infant still jaundiced at 2 weeks, whatever the feeding, needs a fractionated (total and direct) bilirubin — so does any infant with pale or acholic stools or an enlarged liver or spleen at any age; do not assume breast‑milk or physiological jaundice.
  • Cholestasis = conjugated/direct bilirubin > 1.0 mg/dL (> 17 µmol/L), regardless of the total bilirubin — always pathological (NASPGHAN/ESPGHAN 2017; the older “> 20% of total” rule is no longer used).,
  • Pale (acholic) stools and dark urine point to biliary obstruction — use a stool‑color reference card.
  • Prioritize the treatable causes — exclude biliary atresia (time‑critical), sepsis, urinary tract infection, hypothyroidism, hypopituitarism, galactosemia, and tyrosinemia.
◯ Investigate — order → look for → what it means
OrderLook forWhat it tells you
Fractionated (total + direct) bilirubinDirect > 1.0 mg/dL (> 17 µmol/L), regardless of the total= cholestasis — always pathological,
GGT, ALT/AST, albuminPattern of injury (high- vs low‑GGT)Narrows the differential
Coagulation (PT/INR)CoagulopathyFat‑soluble vitamin deficiency → give vitamin K
Abdominal ultrasound (fasting), first‑lineAbsent/small gallbladder, triangular‑cord sign; choledochal cyst — a normal ultrasound does NOT exclude biliary atresiaClue to biliary atresia (time‑critical)
Septic + metabolic screen — glucose, ammonia, lactate, blood gas, urine reducing substances, thyroid, culturesA treatable causeExclude sepsis/UTI, hypothyroidism, galactosemia, tyrosinemia
Neonatal conjugated hyperbilirubinemia = a medical emergency → urgent pediatric gastroenterology consultation
Act now Start the workup above the same day; give vitamin K (cholestasis impairs fat‑soluble vitamin absorption and risks bleeding); do not wait for an outpatient appointment.
⚠ Biliary atresia is time‑critical
  • The earlier the Kasai portoenterostomy, the better the native‑liver survival — a meta‑analysis confirms the benefit of diagnosis and surgery before 30 days of life; by convention results fall off sharply after 60 days.
  • A delayed referral for “prolonged jaundice” can cost the native liver.
  • When in doubt, fractionate the bilirubin and refer the same day.
◣ Admit · Discharge · Refer
  • Admit — for workup and any decompensation — a medical emergency for evaluation.
  • Home from the emergency department — a stable infant with an expedited outpatient workup.
  • Refer — now — pediatric hepatology urgently for the admitted infant (exclude biliary atresia before 6 weeks).
  • Refer — clinic — pediatric hepatology urgently (expedited) for the stable infant sent home (exclude biliary atresia before 6 weeks).

Foreign Body Ingestion

HOURSESPGHAN 2026

X‑ray to locate it first; then the object and where it sits decide the timing.

▸
◣ First step
  • Ask what, when, and how many.
  • Plain radiographs — a chest X‑ray (PA or AP frontal + lateral, including the neck / upper esophagus) and an abdominal X‑ray; together these cover neck‑to‑pelvis. The frontal (AP) film shows the button‑battery double‑ring / halo sign and the lateral film its step‑off (vs a coin), and the lateral also locates an esophageal object; the abdominal film tracks an object that has passed into the stomach or bowel.
  • Radiolucent objects (most plastic, wood, glass, thin aluminum, fish/food bones) may not show — a normal film does not exclude them; consider further imaging or endoscopy if suspicion is high.
  • Keep child fasting (nothing by mouth) until disposition decided.
TimingWhich swallowed objects
Now
endoscopy ≤ 2 h
Button battery in the esophagus; two or more magnets, or a magnet plus a metal object, while still within endoscopic reach (beyond it, involve surgery); sharp or pointed object in the esophagus; esophageal blockage — drooling, unable to swallow saliva; airway distress or signs of perforation; any symptomatic child.
Within 24 h
next day at the latest
Any other object lodged in the esophagus — never leave one there beyond 24 h. Sharp object sitting in the stomach or duodenum (very low threshold to remove).
Elective
planned, > 24 h
Large blunt object in the stomach (> 2.5 cm wide or > 6 cm long; smaller limits in infants/toddlers) — unlikely to pass: plan elective endoscopic removal under optimal conditions if asymptomatic; urgent if symptomatic.
Observe
at home, elective
A single blunt object (e.g., a coin) already past the esophagus into the stomach, < 2.5 cm wide and < 6 cm long, with no battery or magnet. 80–90% pass within 1–2 weeks. No routine serial films; if passage has not been observed, repeat the abdominal X‑ray at ~ 2–4 weeks (earlier if symptoms) and remove electively if the object is still in the stomach.,
Water beads
early: discuss emergency endoscopy; then admit & observe with surgery
Superabsorbent (water) beads are radiolucent — plain films miss them; use abdominal ultrasound. Small ingestions (a few beads) usually pass: admit, serial abdominal examination, watch for bilious vomiting, distension or pain. Early presentation with beads possibly still in the stomach: discuss emergency endoscopy to attempt retrieval (ESPGHAN 2026); if retrieval fails or is incomplete, or the beads are already post‑pyloric, admit for close observation. Involve pediatric surgery early for large ingestions or any sign of obstruction — most symptomatic children need an operation.,
⚠ Red lines
  • Batteries and multiple magnets are never simply observed — an esophageal battery or two or more magnets is an emergency at any level (see Button Battery Ingestion).
  • A confirmed single magnet with no other metallic object may be managed as a blunt object (keep away from other magnets/metal; if any doubt about a second magnet, treat as multiple).
  • An esophageal foreign body left beyond 24 h risks pressure necrosis, perforation, and aorto-/tracheo‑esophageal fistula.
  • Return for pain, vomiting, fever, drooling, bleeding, or black stool.
◈ Who removes it A foreign body lodged in the upper (cervical) esophagus, at the level of the clavicles (T2), typically removed by ENT with a rigid esophagoscope; objects lower (esophagus/stomach) usually managed by GI with flexible endoscopy.
◣ Admit · Discharge · Refer
  • Admit — symptomatic, an esophageal object, or high‑risk (magnets, sharp, long).
  • Home from the emergency department — asymptomatic gastric blunt object with return advice.
  • Refer — now — GI/surgery for endoscopy (esophageal, magnets, sharp objects).

Button (Lithium) Battery Ingestion

MINUTESESPGHAN 2026

An esophageal battery burns within 2 hours — move fast.

▸
Localize Urgent chest X‑ray (PA or AP frontal + lateral) covering neck to upper esophagus (add an abdominal X‑ray if the battery is not seen). A "double‑ring / halo" sign distinguishes battery from coin. Esophageal location = emergency. Do not induce vomiting.
Battery in the esophagus?
YES — ESOPHAGEAL
Endoscopic removal within 2 hours. See mitigation doses below — do not let them delay removal. Delayed presentation (> 12 h since ingestion) or bleeding: CT (angiography) and surgical/cardiothoracic/IR back‑up before removal. At endoscopy, if no perforation, irrigate with 50–150 mL of 0.25% sterile acetic acid (where local protocol allows).
PAST ESOPHAGUS, asymptomatic
Consider endoscopy (inspect the esophagus, remove the battery) if ingestion was unwitnessed or > 12 h earlier and age < 5 years and battery ≥ 20 mm, or with prior GI surgery/anatomical abnormality; in delayed diagnosis also consider CT to exclude vascular injury. Remove urgently if symptomatic or a magnet was co‑ingested. Otherwise outpatient: repeat abdominal X‑ray in 7–14 days (sooner if symptoms) and remove if not passed.
MitigationDoseRoute & notes
Honey10 mL every 10 min, up to 6 dosesOral; only if ingestion was < 12 h ago. Pre‑hospital. Only if ≥ 12 months — never give honey under 12 months.
Sucralfate1 g every 10 min, up to 3 dosesOral; in‑hospital, before removal; not if ingestion was > 12 h ago
⚠ After removal
Injury continues — watch for delayed strictures and tracheo-/aorto‑esophageal fistula; an aorto‑esophageal fistula can present up to ~ 28 days later — give written return advice. If mucosal injury is severe: CT/MRI within 24–48 h, repeated every 48–72 h if the injury is close to major vessels (ESPGHAN 2026).
◣ Admit · Discharge · Refer
  • Admit — all esophageal batteries → emergency.
  • Home from the emergency department — after confirmed passage past the esophagus in an asymptomatic child, per protocol.
  • Refer — now — GI/ENT/surgery IMMEDIATELY for esophageal lodgement — do not delay.

Functional Constipation & Fecal Impaction

ASSESSESPGHAN/NASPGHAN · NICE

Common, benign, and clinical — but disimpact before maintenance and screen for red flags.

▸
◣ Recognize (Rome IV)
  • < 4 years — ≥ 2 of the following for ≥ 1 month; ≥ 4 years — ≥ 2 at least once a week for ≥ 1 month (with insufficient criteria for IBS):
  • ≤ 2 defecations/week
  • painful or hard stools
  • large‑diameter stools
  • a large fecal mass in the rectum
  • excessive stool retention
  • (if toilet‑trained) ≥ 1 episode of fecal incontinence/week or a history of large stools that may obstruct the toilet.
  • Retentive posturing / withholding — often presents as overflow soiling mistaken for diarrhea.
  • Acute presentations: abdominal pain, a palpable fecal mass, urinary symptoms, or a distressed withholding child.
◣ Diagnose — clinical
  • History + examination make the diagnosis. Without a red flag, no routine investigations — no bloods (celiac, thyroid, calcium, lead), imaging, allergy testing, or transit studies.
  • A digital rectal exam is not needed when ≥ 2 Rome IV criteria are met — reserve it for a single criterion, a red flag, or to confirm impaction when the abdominal exam is unclear. A plain abdominal film is not used to diagnose constipation.
⚠ Red flags — think organic disease, do not just treat
  • Onset from birth or delayed meconium > 48 h (Hirschsprung)
  • ribbon stools
  • failure to thrive
  • unintentional weight loss or slow growth
  • bilious vomiting
  • severe distension
  • blood without a fissure
  • abnormal anal position or tone, absent anal/cremasteric reflex, sacral dimple, hair tuft or lower‑limb weakness (spinal)
  • perianal scarring or extreme fear on exam (safeguarding)
  • family history of autoimmune disease or cystic fibrosis.
  • Examine the perineum and back.
Treat
  • Disimpact first if a fecal mass is present — maintenance alone will worsen overflow soiling. Then start maintenance the same day, add behavioral measures, and review at 2 weeks.
  • Goal — one soft, painless stool daily with no withholding or soiling. Continue maintenance at goal for ≥ 2 months and until symptom‑free for ≥ 1 month — in a toilet‑training child, continue until trained — then wean gradually rather than stopping abruptly; do not stop while symptoms persist.
  • Break the pain–withholding cycle — an anal fissure or painful defecation drives retention; keeping stool soft (with topical fissure care) is what lets maintenance work.
Polyethylene glycol (PEG 3350/4000) — first‑line for both steps
StepDoseNotes
DisimpactionPEG 1–1.5 g/kg once daily (oral) for 3–6 consecutive daysOral is as effective as enemas and less invasive; expect a few messy days. A rectal enema is an alternative if oral is refused or fails. Sodium phosphate (pediatric Fleet) enema: not under 2 years; 2 to under 5 years half a bottle (~30 mL), 5–11 years one bottle (59 mL); no more than one in 24 h; ask a doctor first if the child has kidney disease or is on a sodium‑restricted diet (product label).
MaintenancePEG 0.4–0.8 g/kg/day in 1 or divided doses (start ~0.4 g/kg/day; titrate to effect)First‑line and superior to lactulose. Titrate to the goal above; reassess at 2 weeks if inadequate. If not controlled at ~0.8 g/kg/day, re‑check for impaction/adherence and add a stimulant rather than continuing disimpaction‑range doses (ESPGHAN/NASPGHAN 2026).
Add‑on / alternativeStimulant (senna or bisacodyl, age‑appropriate)
lactulose if PEG unavailable
Second‑line adjunct when PEG alone is insufficient — not a substitute for disimpaction.
◆ PEG — with or without electrolytes
  • Same drug (macrogol); the only difference is added balancing salts. With electrolytes for high‑volume disimpaction; without (more palatable) is an equal option for maintenance. The electrolyte‑containing macrogol stocked locally covers both; improve palatability by chilling and mixing it into a flavored drink.,
◆ Side‑effects & precautions
  • PEG (osmotic) — dose‑related loose stools, bloating, flatulence and nausea; over‑titration can cause diarrhea or overflow soiling — reduce the dose, do not stop. Maintain adequate fluid intake. Clinically significant electrolyte disturbance is rare (the electrolyte form guards against it further), and there is no tolerance or dependence with long‑term use.
  • Stimulants (senna, bisacodyl) — abdominal cramps and diarrhea; in diaper‑wearing or incontinent children, prolonged skin contact with senna can cause a blistering perianal (“senna”) dermatitis, so keep the skin clean and barrier‑protected. No good evidence for a “lazy bowel” at therapeutic doses.
  • Lactulose — flatulence, bloating and cramps, with more adverse events than PEG and inferior efficacy; reserve it for where PEG is unavailable, unlicensed, unaffordable or not tolerated.,
  • General — titrate to one soft, painless stool daily; do not stop abruptly (relapse); recheck adherence and dose before escalating.
◈ Infants < 1 year
  • ≥ 6 months: PEG is first‑line; lactulose is the alternative where PEG is unavailable or unlicensed. < 6 months: evidence for PEG is lacking (expert experience only, usually unlicensed) — lactulose is a reasonable first choice; use PEG on specialist advice (ESPGHAN/NASPGHAN 2026).
  • In a refractory infant, consider a 2–4 week trial of a cow's‑milk‑protein‑free diet.
  • Infant dyschezia — straining then passing a soft stool, < 9 months — is not constipation and needs no laxative.
✦ When maintenance isn't working
  • Check adherence and dose first — under‑dosing and stopping too early are the commonest reasons for relapse.
  • Re‑check for a retained impaction; re‑disimpact if present.
  • Add a stimulant (senna or bisacodyl); then reconsider the diagnosis / red flags.
  • Linaclotide (6–17 years, 72 mcg once daily) may be considered by a pediatric gastroenterologist when PEG ± stimulant has failed (ESPGHAN/NASPGHAN 2026); prucalopride and lubiprostone are not established in children.
✦ Diet, behavior & counseling
  • Normal fiber and fluid; fiber supplements and extra fluid beyond the daily requirement are not proven, routine probiotics are not recommended (one specific mixture has low‑certainty evidence), and none replaces a laxative.
  • Demystify and remove blame; scheduled toilet sits ~5 min after meals with foot support; a stool diary and reward system.
  • Long‑term PEG is safe and not habit‑forming — reassure families to keep the dose adequate.
  • Relapse is common and treatment often runs months; about half are off laxatives by 6–12 months — set expectations and follow up.
◣ Admit · Discharge · Refer
  • Admit — rarely — failed disimpaction or severe symptoms.
  • Home from the emergency department — most, with disimpaction, maintenance laxatives, and education.
  • Refer — clinic — pediatric gastroenterology for red flags / suspected organic disease, failure of optimized maintenance after ~3 months, diagnostic uncertainty, or a child needing ongoing second‑line therapy; surgery for suspected Hirschsprung — rectal suction biopsy is the gold standard (contrast enema and anorectal manometry are adjuncts).

Reflux & GERD

ASSESSINFANT‑FOCUSED · 2018

Distinguish the thriving "happy spitter" from true reflux disease.

▸
◣ Reflux vs disease
  • GER (physiological): effortless regurgitation in a comfortable, thriving infant; peaks ~4 months, resolves by 12–18 months. Not a disease — reassurance.
  • GERD: reflux causing troublesome symptoms or complications — feeding refusal, faltering growth, esophagitis, recurrent aspiration.
① Reassure + conservative
  • Parental education; avoid overfeeding; smaller, more frequent feeds; thickened feeds; hold upright after feeds; continue breastfeeding.
  • Do not use prone/side positioning for sleep (SIDS risk).
② Trial if not improving (infant) 2–4 weeks of extensively hydrolyzed (or amino acid) formula, or maternal dairy exclusion if breastfed — overlaps with cow's milk protein allergy.
INFANT · still not responding
Refer to gastroenterology — do not start acid suppression in an infant yourself. The gastroenterologist assesses and decides the next step: a PPI / H2 trial, or upper‑GI endoscopy or a contrast study.
OLDER CHILD · confirmed GERD
Time‑limited 4–8 week trial of acid suppression (proton‑pump inhibitor or H2‑antagonist), then wean and reassess.
⚠ Do not acid‑suppress simple reflux
  • Proton‑pump inhibitors are not recommended for unexplained crying, distress, or visible regurgitation in an otherwise well infant — no benefit and real harms.
  • Avoid acid suppression for isolated cough/wheeze. Red flags (investigate / refer): bilious or projectile vomiting, blood in vomit or stool, onset after 6 months or persisting beyond 12–18 months, faltering growth, fever, lethargy, or a bulging fontanelle.
◣ Admit · Discharge · Refer
  • Admit — rarely — only for complications (apnea, faltering growth, aspiration) or diagnostic uncertainty.
  • Home from the emergency department — uncomplicated reflux with reassurance and feeding advice.
  • Refer — clinic — gastroenterology for red flags, faltering growth, or treatment failure.

Ingestion Injuries — See Also

Corrosive ingestion is covered in the Toxicology section.

▸
◈ Cross‑reference Caustic (Corrosive) Ingestion (Toxicology & Environmental) — acid/alkali esophageal injury; no charcoal, no emesis, airway first, endoscopy at 12–24 h.

Acute IBD Flare & Toxic Megacolon

MINUTESESPGHAN‑ECCO 2025

Bloody diarrhea with systemic upset — and the colon that dilates and can perforate.

▸
◣ Recognize
  • Known or new IBD with frequent bloody stools, abdominal pain, fever, tachycardia and raised inflammatory markers; grade severity (e.g. PUCAIPUCAI in ulcerative colitis).
  • Toxic megacolon — transverse colon ≥ 56 mm on abdominal X‑ray (> 40 mm if under 10 years) with systemic toxicity (fever, tachycardia, tenderness/distension); a surgical emergency.
⚠ What makes it worse
  • Avoid antimotility agents, opioids, anticholinergics and NSAIDs — they can precipitate toxic megacolon or worsen the colitis.
  • Exclude infection (including C. difficile and enteric pathogens) before/while escalating immunosuppression.
  • Rising distension, worsening toxicity, or free air means surgery.
◣ Workup
  • PUCAI at admission and daily (score it below, or use the PUCAI calculator) — acute severe colitis = PUCAI ≥ 65. Day 3 > 45 → plan second‑line therapy (screen, discuss); day 5 ≥ 65 → start second‑line; 35–65 on day 5 → continue IV steroids 2–5 more days with daily scoring; < 35 → responding, continue and transition to oral.
  • CBC, CRP/ESR, albumin, electrolytes, renal and liver function.
  • Stool infection panel including C. difficile (consider CMV on biopsy if steroid‑refractory).
  • Abdominal X‑ray for colonic dilatation / toxic megacolon; limited unprepped sigmoidoscopy where needed.
◈ PUCAI — six clinical items, no labs (0–85)
ItemScore
Abdominal painnone 0 · can be ignored 5 · cannot be ignored 10
Rectal bleedingnone 0 · small amount, in < 50% of stools 10 · small amount with most stools 20 · large amount (> 50% of stool content) 30
Stool consistency (most stools)formed 0 · partially formed 5 · completely unformed 10
Stools per 24 h0–2 0 · 3–5 5 · 6–8 10 · > 8 15
Nocturnal stools (waking the child)no 0 · yes 10
Activity levelno limitation 0 · occasional limitation 5 · severely restricted 10
  • < 10 remission · 10–34 mild · 35–64 moderate · ≥ 65 severe (acute severe colitis — admit for IV steroids).,
StepApproachNotes
ResuscitateIV fluids, correct electrolytes (esp. K⁺), transfuse if neededMonitor for toxic megacolon
Treat the flareIV methylprednisolone 1 mg/kg once daily (max 40 mg); 1.5 mg/kg (max 60 mg) at the gastroenterologist’s discretion; total IV course no longer than 7–10 daysGastroenterology‑directed; escalate by day 5 if inadequate response — infliximab preferred (cyclosporine or tacrolimus as alternatives); consider pharmacologic VTE prophylaxis in every child admitted with acute severe colitis — enoxaparin 1 mg/kg SC once daily (max 40 mg), or 0.5 mg/kg twice daily under 40 kg, continued until discharge
Toxic megacolonBowel rest, decompression, urgent surgical reviewColectomy if deteriorating/perforation
◣ Admit · Refer
  • Admit — all acute severe colitis.
  • Refer — now — pediatric gastroenterology and surgery (early joint care for toxic megacolon).
09

Hematologic & Oncologic

Neutropenia · tumor lysis · sickle cell · bleeding

Chemotherapy‑induced Febrile Neutropenia

MINUTES

Fever in a child on chemotherapy — a medical emergency until proven otherwise.

▸
◈ Not on chemotherapy?
  • This card is for the oncology / chemotherapy (or post‑transplant) patient. For a well, previously healthy, immunocompetent child with an incidental fever + neutropenia, use Febrile Neutropenia — Otherwise Healthy Child instead — empiric antibiotics are usually not required.,
◣ Define
  • Fever — single oral temp ≥ 38.3 °C, or ≥ 38.0 °C sustained over 1 h between checks, without antipyretic use (even if first reported at home) — plus absolute neutrophil count < 500 cells/µL (or expected to fall below 500 within 48 h).
Empiric broad‑spectrum antibiotics immediately — target within 1 hour (NICE: an acute medical emergency; IDSA: within 2 h) — do not wait for the count,
Workup
  • Blood cultures (peripheral + each central line lumen — at least one must be drawn, central preferred; do not delay antibiotics waiting for both), full blood count with differential, renal panel (electrolytes, creatinine, glucose), lactate, urinalysis ± culture, focused exam (skin, mouth, perianal inspection, line site) — no rectal temperatures (oral or axillary only) and avoid rectal manipulation
  • Start antibiotics immediately if unstable — even without labs collected.
DrugDoseRoute & notes
Piperacillin‑​tazobactam75–80 mg/kg/dose (piperacillin component) every 6 h (max 4000 mg/dose)IV; first‑line anti‑pseudomonal monotherapy,
Cefepime50 mg/kg/dose every 8 h (max 2000 mg/dose)IV; alternative monotherapy if piperacillin‑tazobactam is unavailable
Meropenem20 mg/kg/dose every 8 h (max 1 g/dose)
CNS infection (or severe/resistant infection on ID advice): 40 mg/kg/dose every 8 h (max 2 g/dose)
IV; an option in penicillin or cephalosporin allergy (low carbapenem cross‑reactivity) — NOT after SJS/TEN/DRESS to any β‑lactam; with previous anaphylaxis discuss with ID/allergy (non‑β‑lactam alternative: aztreonam + vancomycin, or ciprofloxacin + clindamycin); also for resistant organisms, CNS infection, or instability
Ceftazidime (+ vancomycin)50 mg/kg/dose every 8 h (max 2000 mg/dose)IV; if piperacillin‑tazobactam is unavailable — give with vancomycin for gram‑positive cover
Vancomycin (add only if indicated)15 mg/kg/dose every 6 h if < 12 yr
every 8 h if ≥ 12 yr (max 1 g/dose; level‑guided)
IV; for instability, line/skin infection, known resistant organism — not routine; requires drug‑level monitoring
◈ Local choice
  • Follow your local antibiogram — the empiric agent should match local resistance.
  • Add an aminoglycoside (amikacin or gentamicin) only for hemodynamic instability or known/suspected multidrug‑resistant gram‑negative rods, and until culture results are available.
  • Selected low‑risk (including but not limited to: anticipated neutropenia ≤ 7 days, no comorbidity, stable, tolerating oral intake, reliable caregiver & transport) may be managed as an outpatient as per local protocol: day‑1 IV ceftriaxone (100 mg/kg, max 4 g) + gentamicin, stepping down to oral ciprofloxacin + amoxicillin‑clavulanate; review daily.
  • Do not routinely add vancomycin (other than as the gram‑positive companion to ceftazidime above). Granulocyte colony‑stimulating factor only in consultation with hematology/oncology. Age < 2 months (rare): ampicillin + ceftazidime, in consultation with infectious diseases / pediatric hematology‑oncology (expert practice — not guideline‑stated).
◣ Admit · Discharge · Refer
  • Admit — high‑risk febrile neutropenia (oncology/chemotherapy) → immediate empiric antibiotics.
  • Home from the emergency department — only selected low‑risk oncology patients, after formal risk assessment, the first antibiotic dose and agreement with oncology, within an established outpatient pathway with daily review. (The well non‑oncologic child: see Febrile Neutropenia — Otherwise Healthy Child.)
  • Refer — now — oncology/hematology.

Febrile Neutropenia — Otherwise Healthy Child

ASSESSIMMUNOCOMPETENT CHILD

The well child with fever, commonly a viral illness, found to have an incidental low ANC — usually transient and benign, unlike chemotherapy‑induced neutropenia from myelosuppression. Some malignancies (e.g., a localized brain tumor) do not suppress the marrow and so do not cause neutropenia.

▸
◈ The key question — which came first?
  • Infection → neutropenia (a virus transiently suppresses or consumes neutrophils in a healthy child) behaves very differently from neutropenia → infection (marrow failure, malignancy, post‑transplant).
  • Most well, febrile children with incidental neutropenia are the former and do not need empiric febrile‑neutropenia antibiotics.
◣ Definitions & mechanism
  • Neutropenia = absolute neutrophil count (ANC) < 1500/µL.
  • Mild 1000–1500
  • moderate 500–1000
  • severe < 500; very severe < 200.
  • Normal ANC varies by age and ancestry: Duffy‑null associated neutrophil count (DANC, formerly 'benign ethnic neutropenia') is common in people of Middle Eastern and African ancestry — a lifelong lower ANC (often about 1000–1500/µL, sometimes lower) without added infection risk; in a well child with persistent isolated neutropenia consider a red‑cell Duffy phenotype (Fy a−b−) with hematology (JCO Glob Oncol 2026; CERSI‑PGx guideline 2026).
  • Fever: temperature > 38 °C (CPS). The oncology definition (single oral ≥ 38.3 °C, or ≥ 38.0 °C sustained over 1 h) applies to Chemotherapy‑induced Febrile Neutropenia. Avoid rectal temperatures (mucosal trauma).
  • Common viral triggers: RSV, influenza A/B, parvovirus B19, Epstein‑Barr virus (EBV), cytomegalovirus (CMV), human herpesvirus 6 (HHV‑6), varicella‑zoster. Other unidentified viruses may also cause neutropenia or other transient cytopenias. Mechanisms: transient marrow suppression, peripheral destruction/margination, or an autoimmune process.
◣ What makes it low‑risk (usually presumed viral)
  • Age 6 months–18 years, first episode, well‑appearing, immunocompetent and fully immunized, clear viral context, no features of sepsis or primary immunodeficiency, no central line or chronic disease (e.g., sickle cell disease), no other cytopenia or high MCV, no hepatosplenomegaly or lymphadenopathy. Under 6 months: not covered by this pathway — discuss with hematology (see also Fever in a Well‑Appearing Infant < 2 Months). ANC < 500/µL: review within 24–48 h; at ANC 0–200/µL empiric antibiotics may be considered.
  • Short anticipated duration — viral neutropenia typically resolves within ~2–4 weeks, rarely beyond 6 weeks; risk rises mainly when neutropenia is prolonged (> 30 days).
  • No prior neutropenia, recurrent/severe infections, failure to thrive, or family history of a congenital syndrome; not on a neutropenia‑inducing drug; not immunosuppressed.
Ill‑appearing or any high‑risk feature?
LOW‑RISK · WELL CHILD
Well‑appearing, presumed viral, short‑duration, no clue to an underlying cause. Low risk of serious infection — manage supportively with close follow‑up. A history of a previously normal ANC is reassuring here.
HIGH‑RISK
Ill‑appearing (hypothermia, hypotension, lethargy), or known/suspected severe congenital neutropenia (no prior normal ANC on record; e.g., Kostmann), aplastic anemia, or other marrow‑failure/immunodeficiency → medical emergency.
Most transient neutropenia is viral — it does not require antimicrobial therapy.
Low‑risk — evaluation & disposition
StepWhat to doNotes
CulturesBlood culture stratified by severity: not required in mild (ANC 1000–1500), consider in moderate (500–1000), obtain in severe (< 500)
consider urine culture (esp. young / female)
CPS: ensure a peripheral blood culture in severe neutropenia (ANC < 0.5 ×10⁹/L) and in any ill‑appearing child; consider urinalysis/urine culture in incontinent children (generally < 24 months) or with UTI risk factors. Don’t rely on urinalysis — pyuria is often absent in neutropenia (expert consensus). In a meta‑analysis of well‑appearing febrile neutropenic children, serious bacterial infection was uncommon (pooled 1.9%, range < 0.01–11%), similar to non‑neutropenic children.
Blood filmPeripheral blood film in all newly discovered neutropenia (if not already done)Look for blasts, dysplasia or a left shift — helps exclude malignancy / marrow failure.
Identify the virusConsider a respiratory multiplex PCR (not just influenza/RSV)Confirming a viral cause supports a benign, transient course; may not always identify a specific viral species.
Targeted testsAs indicated: chest radiograph, abdominal imaging, lumbar puncture, stool testingA normal radiograph can mislead — infiltrates may appear only as the ANC recovers.
DispositionDischarge home with close follow‑up if well and follow‑up assuredRecheck CBC to confirm recovery; most normalize within ~2–4 weeks.
High‑risk — management
Empiric therapyAgent / approachNotes
Act promptlyFull infectious work‑up, hospitalize, start empiric antimicrobials without waiting for the ANC trendInvolve hematology ± infectious diseases early.
First‑linePiperacillin-tazobactam (broad‑spectrum, anti‑pseudomonal)Backbone of high‑risk empiric cover, as in chemotherapy‑related FN.
Tailor by riskAdjust for known colonization (MDRO, MRSA), prior prophylaxis, local antibiogramAdd MRSA cover (vancomycin) for hemodynamic instability, line, or skin/soft‑tissue infection.
⚠ Don’t over‑treat — or under‑treat
  • The well child with an incidental low ANC during a viral illness is not chemotherapy‑induced myelosuppression — reflexive broad‑spectrum antibiotics add resistance and harm with little benefit.
  • Conversely, never anchor on “just a virus”: an ill‑appearing child, prolonged neutropenia (> 30 days), recurrent/severe or unusual infections, oral ulcers, or failure to thrive warrant a congenital/marrow‑failure work‑up and prompt treatment.
◣ Admit · Discharge · Refer
  • Admit — only if febrile with concerning features or a suspected/confirmed bacterial infection.
  • Home from the emergency department — well child — expectant management with a scheduled recheck of counts.
  • Refer — clinic — hematology for persistent (> 6 weeks), profound (< 500 consistently), or recurrent neutropenia.

Tumor Lysis Syndrome

MINUTESBSH 2025 · COIFFIER 2008

Massive cell breakdown — after starting chemotherapy, or spontaneously in high‑burden leukemia/lymphoma.

▸
◣ The biochemical quartet
  • High potassium, high phosphate, high uric acid; low calcium → acute kidney injury (see Acute Kidney Injury), arrhythmia, seizures.
① Hydration is the backbone of care
  • Established TLS: IV hyperhydration starting at 3 L/m²/day, up to 4 L/m²/day in children by renal function and fluid status (BSH 2025); adjust to keep urine output ≈ 100 mL/m²/h (80–100 mL/m²/h; 4–6 mL/kg/h if ≤ 10 kg); 200 mL/kg/day if ≤ 10 kg — BSA & hyperhydration calculator.,
  • No potassium in any IV fluid — balanced crystalloids (Hartmann’s, Plasma‑Lyte) contain potassium; avoid potassium and phosphate supplements; loop diuretic only for fluid overload; caution in high‑count leukemia with low hemoglobin (hemodilution).
  • Prophylaxis: oral fluids 2–3 L/m²/day the day before, the day of and the day after starting therapy; IV hydration if high risk or unable to drink.
  • Routine urinary alkalinization not recommended.,
Risk level?
INTERMEDIATE
Allopurinol + hydration.
HIGH / ESTABLISHED
Rasburicase + hydration. Do not give allopurinol on a rasburicase day. High risk (BSH 2025) includes acute leukemia with white cell count ≥ 100 ×10⁹/L (ALL also with bulky disease); Burkitt or lymphoblastic lymphoma at advanced stage, or with LDH ≥ 2× the upper limit of normal or bulky disease; and late‑stage high‑grade lymphoma with LDH ≥ 2× the upper limit or bulk. The older Coiffier 2008 scheme set the AML threshold lower, at ≥ 50 ×10⁹/L. Pre‑existing high uric acid, potassium or phosphate, or renal impairment, raises the risk further.
② Treat the electrolytes
  • Manage hyperkalemia (see Electrolyte Emergencies).
  • Treat symptomatic hypocalcemia with appropriate replacement.
  • For refractory derangement or oliguric kidney injury, escalate urgently to nephrology/PICU — dialysis is a specialist decision (AEIOU indications); the threshold is lower than in other AKI because lysis is ongoing.
  • Monitor potassium, uric acid, phosphate, calcium and creatinine every 6–12 h in established TLS (more often for life‑threatening hyperkalemia); at least twice daily, up to 3–4×/day, in high‑risk prophylaxis; strict fluid balance and urine output.
DrugDoseRoute & notes
Allopurinol10 mg/kg/day PO divided every 8 h (max 800 mg/day)
= 100 mg/m² 8‑hourly (BSH)
PO; start ≥ 12 h before chemotherapy; prevents new urate; reduce the dose by 50% in renal impairment; reduce 6‑mercaptopurine or azathioprine by 50–70% when given together; interactions also with thiazide diuretics, amoxicillin/ampicillin and cyclophosphamide; skin reactions.,
Rasburicase — oncology‑directed0.2 mg/kg IV over 30 min once daily
Repeat doses and duration are decided with the oncology team by uric acid and clinical response (licensed course up to 5 days; 3–5 days is often sufficient; BSH allows up to 7 days for established TLS in adults)
Stop allopurinol while on rasburicase; restart 24 h after the last dose
Breaks down existing urate. Start, repeat doses and duration are the oncology team’s decision — the licensed 0.2 mg/kg/day is the recommended pediatric dose., Samples for uric acid on ice. Do NOT give in known G6PD deficiency; in a very unwell child the consultant may give it without waiting for the result after weighing the risks.
⚠ Rasburicase + G6PD deficiency
  • Rasburicase is contraindicated in glucose‑6‑phosphate dehydrogenase deficiency (causes hemolysis and methemoglobinemia) — screen at‑risk patients before giving — G6PD level if status unknown (e.g., new diagnosis not yet screened); especially relevant here given high prevalence.
  • Send urate samples on ice.
◣ Admit · Discharge · Refer
  • Admit — all at‑risk or established TLS → hyper‑hydration and monitoring (allopurinol for intermediate risk; rasburicase for high risk or rapidly rising uric acid); severe/refractory → PICU with the dialysis team (nephrology).
  • Home from the ward — not acutely; after resolution of TLS and confirmed stability.
  • Refer — now — oncology/nephrology (dialysis for refractory).

Sickle Cell Crises

MINUTES

Pain crisis, acute chest syndrome, splenic sequestration, and stroke — plus every patient is functionally asplenic.

▸
Vaso‑occlusive (pain) crisis
StepActionNotes
Analgesia — fastOpioid within 30–60 min; add NSAID/acetaminophenUse a pain protocol; reassess every 15–30 min. Do not delay analgesia — splinting (shallow, guarded breathing from pain) can progress to acute chest syndrome.,
HydrationOral if able; if unable to drink, IV at no more than maintenance rateAvoid over‑hydration (acute chest risk)
Oxygen + warmthIf SpO₂ < 95% on room air (or below baseline)Keep warm; treat the trigger
⚠ Acute chest syndrome
  • Definition: new pulmonary infiltrate + respiratory symptoms / fever / chest pain — the leading cause of death in patients with sickle cell disease.
  • Treatment: oxygen (keep SpO₂ > 95%), broad‑spectrum antibiotics covering atypicals (cefotaxime + azithromycin/clarithromycin), bronchodilator if wheezing, incentive spirometry while awake.
  • Escalation: early hematology/PICU discussion for simple vs exchange transfusion if severe hypoxia or falling hemoglobin. Severe acute chest syndrome → red cell exchange (automated preferred) over simple transfusion; moderate → simple transfusion or exchange, moving to exchange if it progresses rapidly, fails to respond to simple transfusion, or the hemoglobin is too high for a simple transfusion (ASH 2020 transfusion guideline).
⚠ Splenic sequestration
  • Rapidly enlarging spleen + falling hemoglobin and/or platelet count → hypovolemic shock. Give fluids for shock and consult hematology immediately.
  • Transfuse cautiously to raise the hemoglobin to a stable level, not to normal. Over‑transfusion risks rebound hyperviscosity as the spleen releases trapped cells (expert consensus).
  • Any red‑cell transfusion in sickle cell disease: ABO/RhD plus Rh (C, E) and K‑matched units; an extended red‑cell antigen profile (genotype preferred) before the first transfusion. When transfusing before surgery, do not exceed a post‑transfusion hemoglobin of 11 g/dL (ASH 2020 transfusion guideline).
⚠ Acute stroke
  • Sudden focal deficit, seizure, or new altered consciousness → urgent neuroimaging with immediate hematology and neurology involvement.
  • Ischemic stroke — transfuse urgently, within 2 h of presentation (ASH 2020). Exchange transfusion is preferred (post‑exchange HbS typically 15–20% per ASH — < 30% in other guidance; keep total Hb ≤ 10 g/dL to avoid hyperviscosity), under hematology and neurology. If exchange cannot start within 2 h and Hb is ≤ 8.5 g/dL, give a simple (top‑up) transfusion first — do not raise Hb above ~10 g/dL — and proceed to exchange as soon as it is available.
  • Hemorrhagic stroke is managed case by case, in tandem with neurosurgery.
◈ Fever in sickle cell disease is an emergency All patients functionally asplenic, at risk of overwhelming infection by encapsulated organisms — fever ≥ 38.5 °C: urgent CBC + differential, reticulocyte count and blood culture (urine culture if UTI suspected; chest X‑ray if cough, tachypnea, dyspnea or rales), then prompt empiric parenteral antibiotics — ceftriaxone 50–75 mg/kg IV/IM (max 2 g) is the agent of choice (once‑daily; enables outpatient management of low‑risk cases). Admit if ≥ 39.5 °C and ill‑appearing (NHLBI 2014). Use cefotaxime in infants < 1 month, in whom ceftriaxone is contraindicated (bilirubin displacement); another broad‑spectrum agent covering encapsulated bacteria may be used if allergic., Assess for the crises above. Consider oral antibiotics only if strictly low‑risk (per local protocol): age > 1 year and clinically well with normal vitals (SpO₂ ≥ 95%); no focal source, severe pain, acute chest, or sequestration; reassuring labs (WBC 5–30 ×10⁹/L, reticulocytes > 100 ×10⁹/L, platelets > 100 ×10⁹/L); a first parenteral antibiotic dose given in the ED with 2–4 h observation; and a reliable home situation with guaranteed 24‑h follow‑up.
◣ Admit · Discharge · Refer
  • Admit — severe uncontrolled pain, acute chest syndrome, sequestration, stroke, priapism, or sepsis.
  • Home — pain controlled on oral analgesia, well and hydrated, with follow‑up.
  • Refer — now — hematology; PICU for acute chest/stroke; exchange‑transfusion decisions.

Acute Bleeding in Hemophilia

MINUTES

"Factor First" — replacing clotting factor is always the priority; give factor before imaging or detailed assessment so there is no delay to life/limb‑saving treatment.

▸
◣ Principle
  • In any serious bleed — especially head injury — give factor immediately, before the CT scan or full work‑up. Each unit/kg of factor VIII (factor 8) raises the level by ~2%; each unit/kg of factor IX (factor 9) by ~1%.
Scenario / agentDoseTarget & notes
Hemophilia A — severe / head injuryFactor VIII ~50 units/kgIV; aim factor level 80–100%
Hemophilia A — minor bleedFactor VIII ~25 units/kgIV; aim ~50%
Hemophilia B — severeFactor IX 100–140 units/kg (product‑dependent: the upper end allows for the lower recovery of recombinant factor IX — confirm the product with hematology)IV; aim 80–100% (100% correction for major bleeds; the WFH peak for hemophilia B is 60–80 IU/dL)
Mild hemophilia ADesmopressin (DDAVP)Only if a documented prior response; not for major bleeds
Known inhibitor — life/limb threatrFVIIa 90 mcg/kg (repeat per hematology, no more often than every 2 h), or FEIBA 75–100 units/kg
On emicizumab (or within 6 months of the last dose): rFVIIa only (90–120 mcg/kg)
IV; bypassing agents — call hematology urgently. ⚠ First ask: is the child on emicizumab? If yes, avoid FEIBA (thrombotic microangiopathy / thrombosis); if there is no alternative, ≤ 50 units/kg per dose and ≤ 100 units/kg/24 h with monitoring. Emicizumab without an inhibitor: treat bleeds with factor VIII at the usual doses
Tranexamic acid (mucosal / oral bleeds)25 mg/kg/dose PO (max 1.5 g) every 8 h, or 10 mg/kg/dose IV (max 1 g) every 8 hExcellent adjunct for oral/mucosal bleeds. Avoid with FEIBA (thrombosis risk) and in hematuria (ureteric clot obstruction).
⚠ Head injury
  • Treat to 100% factor level immediately and before the CT — the severe/head‑injury doses in the table above.
  • Contact the on‑call hematologist.
  • Do not hesitate to give factor; use the Broselow (length‑based) tape to estimate weight if unknown.
◣ Admit · Discharge · Refer
  • Admit — major or life‑threatening bleeds (head, neck, gut, compartment).
  • Home from the emergency department — minor bleeds controlled after factor, with a home plan.
  • Refer — now — hematology for all; neurosurgery/surgery as needed — give factor before imaging.

Immune Thrombocytopenia (ITP)

ASSESSASH 2019

Isolated thrombocytopenia in a well child — treat the bleeding, not the number.

▸
◣ Recognize
  • Sudden bruising, petechiae or mucosal bleeding in an otherwise well child (often 1–4 weeks after a viral illness), isolated platelets < 100 ×10⁹/L with normal hemoglobin, white count and film.
  • Grade the bleeding, not just the count: “dry” purpura (skin only) vs “wet” purpura (mucosal — oral blood blisters, epistaxis, GI/urinary) — wet bleeding drives treatment.
⚠ Red flags — this is not simple ITP
  • Hepatosplenomegaly, lymphadenopathy, bone/joint pain, pallor or fatigue, any other cytopenia, or an atypical film → suspect leukemia, aplastic anemia, HUS or NAI and involve hematology before steroids.
  • Steroids can partially treat and mask leukemia — never start empiric steroids without a film reviewed by hematology.
✦ First decision — observe or treat
  • For a child with no or minor (dry) bleeding, observation is preferred regardless of platelet count — most childhood ITP is self‑limiting.
  • Drug therapy is for significant mucosal (wet) bleeding or bleeding that affects daily life, not for a low number alone. Actively bleeding toddlers with counts < 10 ×10⁹/L may need a short oral‑steroid course — decided case by case.
◣ Workup
  • CBC + peripheral blood film — confirm isolated thrombocytopenia and look for blasts, schistocytes or other cytopenias.
  • Blood group, and a direct antiglobulin test (Coombs test) before anti‑D.
  • No routine bone marrow in typical ITP — not needed before corticosteroids, after IVIG failure, or before splenectomy; reserve it for atypical features (other cytopenias, organomegaly, constitutional symptoms).
OptionDoseRoute & notes
Prednisolone / prednisone2–4 mg/kg/day (max 120 mg/day) for 5–7 days, then stopPO; short courses need no taper (taper only if prolonged/recurrent); ideally the film is seen first; cost‑effective with tolerable short‑course side‑effects
IV immunoglobulin (IVIG)0.8–1 g/kg as a single dose (may repeat once)IV; fastest platelet rise — first‑line when a rapid rise is needed; expensive and requires special access
Anti‑D immunoglobulin50–75 µg/kg once (formulary dosing)IV; only if Rh(D)-positive, non‑splenectomized, no autoimmune hemolysis — watch for hemolysis
Tranexamic acidPO 15–25 mg/kg/dose (max 1.5 g) every 8 h
IV 10 mg/kg/dose (max 1 g) every 8 h by slow injection
PO/IV; adjunct for mucosal bleeding. Pediatric doses (4 weeks–18 years: PO 15–25 mg/kg max 1.5 g, IV 10 mg/kg max 1 g, two to three times daily — Perth Children’s Hospital monograph, citing BNF for Children 2024); the same figures are the SmPC adult doses, — avoid in hematuria (upper urinary tract bleeding risks ureteric obstruction)
Platelet transfusionOnly for life‑threatening bleedingGive with IVIG + steroid; consumed rapidly — not for the count alone
◈ Bridge to definitive care
  • For life‑threatening bleeding (intracranial, massive GI): platelets + IVIG 1 g/kg + IV methylprednisolone 30 mg/kg (max 1 g) + tranexamic acid together, and call hematology/critical care (international consensus report: Provan et al., Blood Adv 2019;3:3780–3817).
  • Avoid IM injections, aspirin/NSAIDs and contact sport while counts are low.
◣ Admit · Refer
  • Admit — wet purpura, severe bleeding, or any diagnostic doubt.
  • Refer — now — hematology (call) for all new severe thrombocytopenia; urgently if red flags for malignancy — do not hesitate to reach out for guidance.

New‑Diagnosis Oncologic Emergencies

MINUTESELN 2019 · REVIEW-BASED

The child who arrives before anyone knows they have cancer — new malignancies can present with emergencies that are lethal in hours.

▸
◣ Patterns to recognize
  • Hematologic malignancy (5): febrile neutropenia / sepsis (functionally neutropenic despite a high WBC), hyperleukocytosis, mediastinal mass, tumor lysis syndrome, and severe coagulopathy (a subset of leukemia — APML).
  • Solid tumors (3): tumor lysis syndrome, mediastinal mass (by origin/location), and local effects (spinal cord compression, raised ICP).
◣ Mediastinal mass (SVC compression syndrome)
  • Orthopnea, stridor, facial/neck swelling and plethora, distended neck veins, cough worse when supine — often T‑cell lymphoma/leukemia.
  • Do NOT sedate or lie the child flat and avoid general anesthesia — the airway and great vessels can collapse irreversibly. Keep upright, give oxygen, get an erect chest film / echo, and call oncology + anesthesia/critical care. Always consult hematology‑oncology once a mediastinal mass is identified.
  • Getting tissue safely: obtain the diagnosis by the least‑invasive route that avoids general anesthesia — peripheral node, bone marrow, or pleural/pericardial fluid. If a procedure is unavoidable in a cooperative child, use light sedation with local/regional anesthesia and preserve spontaneous ventilation (avoid muscle relaxants and positive‑pressure ventilation). When general anesthesia, rigid bronchoscopy, or ECMO might be needed, give steroids and — if the child is stable — postpone to let the mass shrink; if general anesthesia is unavoidable in moderate‑to‑high‑risk disease, plan to escalate fast: rigid bronchoscopy, airway stent, and ECMO on standby.
◣ Hyperleukocytosis / leukostasis
  • WBC > 100 ×10⁹/L with headache, hypoxia, confusion, priapism or visual change.
  • Hydrate at about 3 L/m²/day (≈ 2× maintenance; 200 mL/kg/day if ≤ 10 kg) with no potassium, watching fluid balance closely; start tumor‑lysis prophylaxis (see Tumor Lysis Syndrome), and avoid red‑cell transfusion unless critically anemic — it raises viscosity. Keep platelets ≥ 20–30 ×10⁹/L. Urgent oncology ± leukapheresis.
◣ Coagulopathy (suspect APML)
  • Deranged coagulation studies in suspected leukemia are a medical emergency. Inform hematology/oncology and the hematopathologist promptly to identify acute promyelocytic leukemia (APML) on morphology.
  • If APML is suspected (smear + coagulopathy), start All‑Trans Retinoic Acid (ATRA) immediately on hematology/oncology advice — do not wait for cytogenetic/molecular confirmation (it is simply stopped if APML is excluded). At the same time correct the coagulopathy and keep it corrected: platelets > 30–50 ×10⁹/L, fibrinogen > 1–1.5 g/L, INR < 1.5. Avoid central lines, lumbar puncture and leukapheresis until the coagulopathy is controlled.
◣ Malignant spinal cord compression
  • Back pain (esp. night/waking) — or neck pain with arm weakness or numbness when the compression is cervical — leg weakness, a sensory level, urinary retention or constipation — a neurosurgical‑oncological emergency (expert consensus).
  • Give dexamethasone immediately, arrange whole‑spine MRI, and call oncology plus the pediatric spine service — orthopedics or neurosurgery, depending on local coverage — outcome depends on how quickly power is preserved (expert consensus).
◣ Workup
  • All: CBC + differential, peripheral blood smear, electrolytes, renal & liver profile, uric acid, LDH, phosphate, potassium, calcium, and coagulation screen (tumor‑lysis / DIC).
  • Mediastinal mass / SVC: erect (upright) PA + lateral chest X‑ray and echocardiogram; CT chest only if the child can hold the position comfortably without sedation (semi‑upright, lateral or prone if needed; anesthesia informed) — never lay a symptomatic child flat; obtain the least‑invasive diagnostic tissue (peripheral blood, effusion, marrow).
  • Leukostasis: WBC, coagulation, type & crossmatch; neuroimaging if neurological signs.
  • Cord compression: whole‑spine MRI with contrast — do not wait for it to start dexamethasone if the deficit is progressing (expert consensus).
DrugDoseRoute & notes
Dexa­methasone (cord compression)1–2 mg/kg IV once (max 10 mg), then per oncologyIV; do not delay for imaging if deficit is progressing — but confirm no undiagnosed leukemia first where possible. Dose: expert/formulary practice — not given in the cited review.
Methyl­predniso­lone (anterior mediastinal mass)16 mg/m²/dose IV every 12 h
if IV access is difficult, PO prednisone 20 mg/m²/dose every 12 h
IV/PO; obtain a biopsy first if the patient's condition allows — steroids can rapidly shrink lymphoma and obscure the diagnosis. If a malignant effusion is present, it may be aspirated and sent for flow cytometry. Assess airway security before any sedation or positioning. Dose: expert/formulary practice — not given in the cited review.
IV fluids (leukostasis / TLS)About 3 L/m²/day (≈ 2× maintenance; 200 mL/kg/day if ≤ 10 kg), no potassium initiallyIV; with rasburicase/allopurinol per Tumor Lysis Syndrome
⚠ Two traps
  • Sedating a child with an anterior mediastinal mass for a “quick CT” or line has caused fatal airway collapse — imaging is erect and unsedated.
  • And giving steroids before a film in possible hematological malignancy can obscure the diagnosis — coordinate with oncology.
◣ Refer
  • Refer — now — call pediatric oncology urgently for all of the above; involve critical care, anesthesia, neurosurgery and hematopathology as required.
10

Neonatal

NRP 2025 · AAP hyperbilirubinemia 2022

Neonatal Resuscitation

MINUTESNRP 2025

Effective ventilation is the single most important step.

▸
Term? Good tone? Breathing or crying?
YES
Delayed cord clamping ≥ 60 s, dry, skin‑to‑skin, keep warm, monitor.
NO
Warm, dry, stimulate, position airway, clear secretions if needed. SpO₂ (right hand) + ECG. Keep temperature 36.5–37.5 °C.
apnea / gasping / HR < 100
Golden minute Start PPV within 60 s. Starting oxygen (NRP 2025): ≥ 35 wk 21%; 32–34 wk 21–30%; < 32 wk 30–100% — then titrate to the pre‑ductal SpO₂ targets: 2 min 65–70% · 3 min 70–75% · 4 min 75–80% · 5 min 80–85% · 10 min 85–95%. Assess for chest rise after 15 s; if none, perform MR SOPA corrective steps.
HR < 60 after 30 s effective PPV
Compressions Coordinate 3:1 (90 compressions + 30 breaths/min), increase to 100% oxygen, ideally via a secured airway. Reassess after 60 s. Compressions are effective only after establishing good chest rise.
HR still < 60
Give epinephrine; treat hypovolemia; reconsider airway, pneumothorax, dose, technique.
After any major resuscitation (prolonged PPV, compressions, epinephrine, low Apgar at 10 min, severe acidosis): check glucose, avoid hyperthermia (keep ≤ 37.5 °C), and examine for encephalopathy (consciousness, tone, reflexes, seizures). Term/late‑preterm infant with moderate–severe encephalopathy → call the NICU / cooling center immediately — therapeutic hypothermia must start within 6 h of birth.
Drug / fluidDoseRoute & notes
Epinephrine (adrenaline)IV/IO 0.02 mg/kg (0.2 mL/kg)
ET 0.1 mg/kg (1 mL/kg)
0.1 mg/mL (1:10,000). IV/IO preferred; ET only while establishing access. Repeat every 3–5 min.
Volume (saline or blood)10 mL/kgIV/IO, for hypovolemia
◈ Algorithm Full AHA/AAP neonatal resuscitation algorithm — cpr.heart.orgQR.

Critical CHD — Pulse Oximetry Screening

ASSESS≥ 24 H · AAP 2025

Screen every well newborn before discharge — catches duct‑dependent lesions before they collapse.

▸
◣ Who & how to screen
  • Who: asymptomatic infants at ≥ 24 hours of age (or shortly before discharge if earlier), in the well‑baby nursery, not on supplemental oxygen.
  • How: measure SpO₂ in the right hand (pre‑ductal) and either foot (post‑ductal).
Result of the screen?
PASS
SpO₂ ≥ 95% in BOTH limbs and ≤ 3% difference between them. Routine newborn care.
IMMEDIATE FAIL
Any reading < 90% in either limb → straight to echocardiography.
borderline
Retest once 90–94% in either/both limbs, or > 3% hand–foot difference → repeat once after 1 hour (one retest, not two). Still not passing → fail.
any fail
Urgent echocardiography — and rule out sepsis, PPHN, and respiratory causes (4–5× more common than CCHD)
⚠ Screening does not replace examination
  • It can miss left‑sided obstruction, especially coarctation of the aorta.
  • Check femoral pulses and four‑limb saturations/blood pressure on every newborn.
  • Some CCHD is not hypoxemic in the first hours — a normal screen does not exclude it.
  • For the lesions, presentation, and emergency management, see Neonatal & Infant CHD (Cardiac & Shock).
◣ Admit · Discharge · Refer
  • Admit — a failed screen → keep for echo; cyanosis/shock → NICU + alprostadil.
  • Home from the ward — a passed screen with a normal exam (newborn nursery, before discharge).
  • Refer — now — pediatric cardiology for any failed screen (echo before discharge).
◈ See also Lesion recognition & management: Neonatal & Infant CHD and the Hypercyanotic (Tet) Spell (Cardiac & Shock).

Persistent Pulmonary Hypertension (PPHN)

MINUTESTERM / LATE PRETERM

Labile, severe hypoxemia out of proportion to the lung disease — the circulation never made the switch.

▸
◣ Recognize
  • Severe cyanosis/desaturation poorly responsive to oxygen, often labile (large swings with handling).
  • Differential cyanosis: pre‑ductal SpO₂ (right hand) higher than post‑ductal (foot) by > 5–10% — right‑to‑left shunt across the duct.
  • Common settings: meconium aspiration, sepsis/pneumonia, birth asphyxia, congenital diaphragmatic hernia, or idiopathic.
  • Confirm by echocardiography — and exclude duct‑dependent congenital heart disease before committing to therapy.
① Optimize lungs, avoid swings
  • Intubate and ventilate — recruit the lung (gentle ventilation; surfactant if parenchymal disease — meconium aspiration / RDS). Minimal handling, cluster cares, sedation/analgesia.
  • Keep temperature, glucose, calcium, and pH normal.
② Targets Pre‑ductal SpO₂ low‑to‑mid 90s, PaO₂ 55–80 mmHg (7.3–10.6 kPa). Support blood pressure and cardiac output with fluids/inotropes so systemic pressure ≥ pulmonary pressure.
③ Pulmonary vasodilator
  • Suspected PPHN needs urgent neonatology/cardiology/PICU care; iNO, milrinone, norepinephrine, and ECMO referral are specialist‑directed.
  • Start inhaled nitric oxide once the oxygenation index is ≥ 20–25 (after lung recruitment)
  • Response is a clear rise in oxygenation within ~30 min.
No response with OI rising toward ~40, or refractory shock → ECMO — refer to an ECMO center early.
⚠ Echocardiogram — always
  • A neonatal echocardiogram should always be performed when PPHN is suspected — to confirm the diagnosis and exclude underlying congenital heart disease; iNO can be detrimental in some CHDs.
TherapyDose / settingNotes
Inhaled nitric oxidestart 20 ppmAbove 20 ppm rarely adds benefit and raises methemoglobin/NO₂ — monitor. Assess response after 20–30 min. Do not stop abruptly (rebound)
Milrinone / inotropesspecialist‑directedSupport cardiac output; milrinone for left‑ventricular dysfunction, in addition to its pulmonary vasodilator properties
Norepinephrinespecialist‑directedAdd‑on to milrinone when blood pressure drops — raises systemic vascular resistance and further lowers the pulmonary/systemic pressure ratio
◈ Note
  • The approach above is suggested when the cause of pulmonary hypertension is increased pulmonary vascular resistance (PVR) and evidence of an ischemic hit is absent. Other scenarios of pulmonary hypertension are approached differently.
  • A trial of oral sildenafil can be attempted where iNO is not available, after specialist consultation.
⚠ Oxygenation index & a key contraindication
  • OI = (mean airway pressure × FiO₂ × 100) ÷ PaO₂ in mmHg. Do not give inhaled nitric oxide in duct‑dependent congenital heart disease — confirm the heart on echo first.
  • Wean FiO₂ and settings slowly; sudden small drops can trigger prolonged desaturation.
◣ Admit · Discharge · Refer
  • Admit — all → NICU/PICU.
  • Home from the ward — not acutely; after weaning support, with follow‑up.
  • Refer — now — neonatology/cardiology; an ECMO center if refractory.
◈ See also Neonatal & Infant CHD — exclude duct‑dependent CHD before attributing cyanosis to PPHN.

Neonatal Hypoglycemia

HOURSCPS 2019

Often asymptomatic — screen the at‑risk, treat early, find the persistent few.

▸
◢ Recognize & who to screen
  • Signs are non‑specific: jitteriness, poor feeding, lethargy, hypotonia, temperature instability, apnea — and, when severe, seizures. Many affected newborns are asymptomatic, so at‑risk infants must be screened.
  • Screen at‑risk infants from ~2 h of age, pre‑feed: infant of a diabetic mother (IDM), large- or small‑for‑gestational‑age (LGA / SGA‑IUGR), late‑preterm / preterm, perinatal stress or asphyxia, hypothermia or sepsis, maternal beta‑blocker, and congenital syndromes (e.g. Beckwith‑Wiedemann) or midline / microphallus features (suggesting hypopituitarism).
  • Confirm a low point‑of‑care (POC) reading with a laboratory plasma glucose — whole‑blood / POC reads ~15% lower and falls further with processing delay — but treat first; do not wait for the lab.
PhaseThresholdMeaning
Transitional — first 72 h< 2.6 mmol/L (47 mg/dL)The physiologic nadir is normal — catch the at‑risk or persistently low infant, don't over‑treat healthy transitional dips.
Persistent — beyond 72 h< 3.3 mmol/L (60 mg/dL)Also applies to hypoglycemia first presenting after 72 h — below this warrants investigation for a hypoglycemia disorder.,
On IV dextrosefirst 72 h: keep ≥ 2.6 mmol/L (47 mg/dL); after 72 h: ≥ 3.3 mmol/L (60 mg/dL); suspected/confirmed hyperinsulinism: > 3.9 mmol/L (70 mg/dL)Suspect a disorder if the target cannot be held without a GIRGIR above 8–10 mg/kg/min. PES 2015 advises > 3.3 mmol/L for any at‑risk neonate needing IV dextrose.
First 72 h — glucose < 2.6 mmol/L (47 mg/dL): symptomatic or asymptomatic?
SYMPTOMATIC with glucose < 2.6 mmol/L, or any glucose < 1.8 mmol/L (32 mg/dL)
IV D10 mini‑bolus 2 mL/kg, then infusion at 80 mL/kg/day (GIR ≈ 5.5 mg/kg/min). Recheck in 30 min; increase the glucose supply stepwise, rechecking 30 min after each step. No IV access → glucagon IM.
ASYMPTOMATIC 1.8–2.5 mmol/L (32–45 mg/dL)
Feed + buccal 40% dextrose gel 0.5 mL/kg; recheck in 30 min.,
still 1.8–2.5 mmol/L
Repeat once Feed ± a second buccal gel dose; recheck in 30 min.
second repeat, or symptoms appear
Start IV D10 — mini‑bolus 2 mL/kg then GIR 5–8 mg/kg/min; escalate as needed.
DrugDoseRoute & notes
Dextrose 10%2 mL/kg (200 mg/kg) bolusIV/IO; then infusion at GIR 5–8 mg/kg/min, escalate by 2 mg/kg/min as needed. Concentrations > 12.5% need central access.
Dextrose gel 40%0.5 mL/kg (200 mg/kg) buccalFirst‑line for asymptomatic; massage into buccal mucosa, then feed. May repeat once.
Glucagon0.2 mg/kg (200 mcg/kg) — max 1 mgIV bolus (CPS: 0.1–0.3 mg/kg, or infusion 10–30 mcg/kg/h), or IM/SC as a bridge when IV access is not yet available; in hyperinsulinism it typically raises glucose within 10–15 min (PES: 0.5–1 mg usually effective)., Watch for hyponatremia.
Diazoxide1.7–5 mg/kg/dose PO q8hEndocrinology‑led, for confirmed hyperinsulinism; start a thiazide diuretic with it (chlorothiazide). Echocardiogram at baseline where feasible and again ~1 week after starting, and with any respiratory deterioration (fluid retention, pulmonary hypertension); baseline CBC (International Hyperinsulinism Guidelines, De Leon et al. 2024).
⚠ Persistent / refractory — think hyperinsulinism
Persisting beyond 48–72 h, recurring, or needing GIR > 8–10 mg/kg/min to stay euglycemic warrants a critical (hypoglycemia) sample, drawn when plasma glucose is < 2.8 mmol/L (< 50 mg/dL), before correcting: plasma glucose, insulin, C‑peptide, beta‑hydroxybutyrate (ketones), free fatty acids, cortisol, growth hormone — plus ammonia, lactate, and an acylcarnitine profile / urine organic acids. Hyperinsulinism = inappropriately low ketones and free fatty acids with detectable insulin, a glycemic response to glucagon, and a high glucose requirement. Refer to endocrinology / metabolic.
✦ Pearls
  • Glucose is normally lowest in the first 24–72 h (transitional); the goal is to catch the at‑risk or persistently low infant, not to over‑treat healthy transitional dips.
  • Prophylactic dextrose gel given to at‑risk infants before any low glucose is measured is not recommended: at 6–7 years it did not reduce neurocognitive impairment (59% vs 57%) and was associated with more emotional‑behavioral difficulty (24% vs 18%). Gel is for a measured asymptomatic low glucose (table above).
  • Do not discharge an at‑risk infant until persistent hypoglycemia is excluded — i.e. pre‑feed glucose stays above target through a normal feed–fast cycle.
◣ Admit · Discharge · Refer
  • Admit — symptomatic, persistent, or needing IV dextrose/high glucose‑infusion rate.
  • Home from the ward — transient, resolved, feeding well with stable pre‑feed glucose.
  • Refer — now — endocrinology/metabolic for persistent or recurrent hypoglycemia (hyperinsulinism workup).

Neonatal Hyperbilirubinemia

HOURS≥ 35 WK · AAP 2022

Use total serum bilirubin against the hour- and gestation‑specific nomogram.

▸
◣ Assess & decide
  • Any jaundice under 24 h, or visible jaundice → measure bilirubin. Transcutaneous bilirubin (TcB) is a valid screen; confirm with a total serum bilirubin (TSB) when the TcB is within 3 mg/dL (50 µmol/L) of the phototherapy threshold, is ≥ 15 mg/dL (250 µmol/L), or once phototherapy has started. Use the total value against the threshold (do not subtract the direct fraction). Severe hyperbilirubinemia = peak TSB > 425 µmol/L (25 mg/dL) or need for exchange transfusion.
  • Thresholds for phototherapy and exchange depend on gestational age (35–40 wk), age in hours, and neurotoxicity risk factors — read the AAP nomogram or app each time, never a single fixed number.
  • Neurotoxicity risk factors that move the infant to the “WITH risk factor” graphs: albumin < 3.0 g/dL (30 g/L), isoimmune hemolysis (positive DAT), G6PD deficiency or other hemolysis, sepsis, clinical instability in the prior 24 h. Gestation < 38 weeks is also a risk factor but is already built into every curve — if it is the only one, use the “NO risk factor” graphs.
  • Suspect hemolysis when the TSB rises ≥ 5 µmol/L/h (0.3 mg/dL/h) in the first 24 h or ≥ 3.5 µmol/L/h (0.2 mg/dL/h) thereafter, or fails to respond to intensive phototherapy → CBC, reticulocytes, smear, DAT, G6PD/pyruvate‑kinase assay; sepsis screen if clinically indicated.
  • Find the cause when the level is high or rising — hemolytic: ABO/Rh isoimmunization (DAT), G6PD deficiency, hereditary spherocytosis; non‑hemolytic: cephalohematoma or bruising, polycythemia, sepsis, hypothyroidism, and breast‑milk vs inadequate‑breastfeeding jaundice.
  • Conjugated (direct) hyperbilirubinemia is a different problem — for neonatal cholestasis see Neonatal Cholestasis in the GI & Hepatology section.
Treat At/above the phototherapy line → phototherapy + feeding/hydration + find the cause.
within 30 µmol/L of the exchange line (CPS 2026; the AAP margin of 2 mg/dL is ≈ 34 µmol/L) — pre‑exchange zone
Escalation of care Intensive phototherapy + IV fluids without delay; withhold enteral feeds; urgent TSB, direct bilirubin, CBC, albumin, chemistries, type & crossmatch, hemolysis work‑up; repeat TSB every 2–3 h; consult neonatology and prepare transfer to a unit that can perform exchange. IVIG is not routine: give 0.5–1 g/kg over 2 h (may repeat once at 12 h) for isoimmune hemolytic disease at the pre‑exchange threshold when exchange cannot be performed promptly.,
at/above exchange line, or encephalo­pathy
Immediate exchange transfusion for any sign of acute bilirubin encephalo­pathy (high tone, arching, high‑pitched cry, lethargy). NICU.
◈ Nomogram & follow‑up
  • Kuwait laboratories report bilirubin in µmol/L. Plot the hour‑specific total serum bilirubin on the AAP 2022 threshold curves — in µmol/L using the CPS 2026 figures (Figures 2–3 phototherapy, Figures 6–7 exchange transfusion; AAP data reproduced with permission; cps.ca), or the online calculators below, which accept either unit (÷ 17.1 converts µmol/L to mg/dL). Decision values on this card are given in both units.
  • Calculators: peditools.org/bili2022QR or bilitool.orgQR.
  • Before discharge, set the follow‑up interval by the gap between the TSB and the phototherapy threshold: the smaller the gap, the sooner the recheck (often within 24 hours).
Treatment thresholds in µmol/L — AAP 2022 curves, 35 to ≥ 40 weeksRedrawn from the AAP 2022 hour‑specific thresholds as published in µmol/L by the Canadian Paediatric Society (2026), gridlines every 10 µmol/L and 6 h, 0–168 h; beyond 168 h some lines still rise by up to 20 µmol/L (35–38 weeks on the no‑risk‑factor phototherapy chart; 35–36 weeks on the other charts) and the rest are flat — use the calculator for days 8–14. Full text: CPS 2026 guideline (doi:10.1093/pch/pxaf034) · AAP 2022 guideline (doi:10.1542/peds.2022-058859). Neurotoxicity risk factors: albumin < 30 g/L, isoimmune or other hemolytic disease, sepsis, significant clinical instability in the preceding 24 h.,
100 150 200 250 300 350 400 0 12 24 36 48 60 72 84 96 108 120 132 144 156 168 Age (hours) TSB (µmol/L) Phototherapy threshold — NO neurotoxicity risk factor ■ ≥ 40 wk ■ 39 wk ■ 38 wk ■ 37 wk ■ 36 wk ■ 35 wk 50 100 150 200 250 300 350 0 12 24 36 48 60 72 84 96 108 120 132 144 156 168 Age (hours) TSB (µmol/L) Phototherapy threshold — WITH neurotoxicity risk factor(s) ■ ≥ 38 wk ■ 37 wk ■ 36 wk ■ 35 wk 250 300 350 400 450 500 0 12 24 36 48 60 72 84 96 108 120 132 144 156 168 Age (hours) TSB (µmol/L) Exchange transfusion threshold — NO neurotoxicity risk factor ■ ≥ 38 wk ■ 37 wk ■ 36 wk ■ 35 wk 200 250 300 350 400 450 0 12 24 36 48 60 72 84 96 108 120 132 144 156 168 Age (hours) TSB (µmol/L) Exchange transfusion threshold — WITH neurotoxicity risk factor(s) ■ ≥ 38 wk ■ 37 wk ■ 36 wk ■ 35 wk
◈ ΔTSB — the “rules of 30” (CPS 2026)
  • ΔTSB = hour‑specific phototherapy threshold − measured TSB or TcB (screen at ≥ 12 h of age, before discharge; TcB valid only if not on phototherapy).
  • ΔTSB ≤ 30 µmol/L → delay discharge: < 24 h old, consider starting phototherapy; ≥ 24 h old, repeat TSB in 4–12 h and start phototherapy if rising. 31–60 → repeat TSB in 12–24 h. 61–90 → repeat in 24–48 h. > 90 → routine follow‑up with the primary provider.
  • With neurotoxicity risk factors, phototherapy may be started when the TSB is within 30 µmol/L of the threshold.
  • Stop phototherapy once the TSB is > 30 µmol/L below the threshold (≥ 38 wk) or > 60 µmol/L below (35–37 wk). Re‑check TSB 12–24 h after stopping for rebound (re‑crossing the threshold within 72–96 h); with hemolytic disease re‑check at 6–12 h, then every 24 h until the TSB is falling and ΔTSB > 60. TcB may be used ≥ 18 h after phototherapy stops.
⚠ Don't rely on a single value
  • Plot against time.
  • A rapidly rising level, early jaundice, or hemolysis can cross thresholds fast — recheck on the interval the nomogram specifies.
  • TcB should not be used for follow‑up when the baby is on phototherapy — use serum bilirubin.
◣ Admit · Discharge · Refer
  • Admit — levels at/above phototherapy or exchange thresholds, or a rapid rise.
  • Home — below threshold, feeding well, with a bilirubin‑recheck plan.
  • Refer — now — hematology for hemolysis; an exchange‑capable unit near exchange thresholds.
  • Refer — clinic — audiology (formal hearing assessment) if peak TSB > 400 µmol/L, the pre‑exchange threshold was reached, or exchange was performed; neurodevelopmental follow‑up if the pre‑exchange threshold was reached, exchange was performed, or neurological signs occurred; after immune hemolytic disease, check hemoglobin at 4–10 weeks for late anemia.

Neonatal Sepsis — Early‑Onset (rapid approach)

MINUTES

Non‑specific: temperature instability, poor feeding, lethargy, apnea, distress.

▸
◣ Act on suspicion
  • Septic screen (blood culture ≥ 1 mL ± CSF; blood count, CRP), check glucose. Urine culture is not part of the early‑onset (< 72 h) screen — add it for late‑onset sepsis. Start empiric antibiotics promptly — do not wait for results. Support airway/breathing/circulation; NICU.
◈ Early‑ vs late‑onset
Early‑onset (≤ 72 h) is vertically acquired — group B Streptococcus, E. coli, Listeria; empiric ampicillin + gentamicin (below). Late‑onset (> 72 h) is often hospital‑acquired, especially in preterm infants with prolonged stays and invasive procedures (coagulase‑negative staphylococci, S. aureus, Gram‑negatives) and needs different empiric cover per your unit protocol.
DrugDoseRoute & notes
Ampicillin50 mg/kg/dose q8h (0–7 days), q6h (8–28 days)
Meningitis (term): 100 mg/kg/dose q8h (0–7 days), 75 mg/kg/dose q6h (8–28 days)
IV; term intervals as shown (Lexicomp); preterm ≤ 34 weeks: every 12 h in the first week (Red Book). Use the meningitic dose if CSF not obtained or CNS involvement.,
Gentamicin4–5 mg/kg/doseIV, extended‑interval dosing by gestational/postnatal age (e.g. NICE NG195: 5 mg/kg every 36 h) — never 8–12‑hourly.
Cefotaxime50 mg/kg/doseIV, add if meningitis suspected; every 12 h in the first week of life, every 8 h at 1–4 weeks (for meningitis use the intervals on the Fever in the Young Infant card).
Acyclovir20 mg/kg every 8 hIV, add if herpes simplex suspected
⚠ Bilious vomiting in a neonate
Green vomiting is malrotation with volvulus until proven otherwise — see Surgical.
◣ Admit · Discharge · Refer
  • Admit — any neonate with clinical signs of sepsis → cultures, then empiric antibiotics without delay. Well‑appearing infants ≥ 35 weeks with risk factors only → risk‑stratify (categorical risk factors, Neonatal Early‑Onset Sepsis Calculator, or structured serial examination, e.g. every 4–6 h through 48 h of age) rather than treating all.
  • Home from the ward — not until sepsis is excluded/treated; a reassuring 36–48 h course with negative cultures may stop antibiotics.
  • Refer — now — neonatology/PICU for instability.
◈ See also The neonate (≤ 28 days) is always high‑risk in the febrile‑infant pathway — use Fever in the Young Infant for the full age‑stratified workup; this card is the neonatal‑specific rapid approach.

Omphalitis & Delayed Umbilical Separation

HOURSNEONATE

Red or discharging umbilical stump — treat as neonatal sepsis; watch for necrotizing fasciitis.

▸
◣ Recognize
  • Periumbilical erythema, induration, tenderness; purulent or malodorous discharge from the stump.
  • Spreading abdominal‑wall cellulitis, or systemic signs (poor feeding, lethargy, temperature instability, tachycardia) = invasive infection / sepsis.
  • Uncommon with dry cord care in high‑resource settings (~1 in 1000, AAP 2016) but can progress rapidly — treat as a neonatal emergency.
  • Risk factors: low birth weight or prematurity, prolonged rupture of membranes or maternal infection, non‑sterile or home delivery, umbilical catheterization, and unclean cord practices (e.g., cow‑dung application — also a tetanus risk). Onset is typically around day 3.
⚠ Red flags → necrotizing fasciitis / myonecrosis (surgical emergency)
  • Pain or tenderness out of proportion, rapidly spreading or dusky / bullous skin, crepitus, peau‑d'orange edema, systemic toxicity.
  • It can deteriorate fast despite mild initial findings — reassess often and mark the margins.
  • Any of these → urgent pediatric surgery for debridement; do not delay for imaging.
  • Debridement resects the umbilical vein, both arteries, and any urachal remnant (even if they look normal); reported mortality is high (~60–85%), so err toward early surgical exploration in the critically ill infant.
Investigate & treat
  • Blood culture (+ discharge swab), CBC, CRP; full neonatal sepsis workup.
  • Start IV antibiotics immediately — cover staphylococci (incl. MRSA), group A Streptococcus, Gram‑negatives (E. coli, Klebsiella, Proteus) and anaerobes (Bacteroides, Clostridium); the exact regimen follows the local antibiogram and neonatal formulary.
  • If systemic: keep nil by mouth (septic ileus), IV fluids / parenteral nutrition; manage as neonatal sepsis.
Empiric IV antibiotics — neonatal doses, term neonate (per dose · interval); preterm infants: by postmenstrual age per the unit formulary; adjust for hepatic/renal impairment; confirm against the local formulary and antibiogram
DrugDose (per dose · interval)Role
Cefotaxime50 mg/kg/dose q12h (0–7 days); q8h (8–28 days)Gram‑negative cover
+ Cefazolinper neonatal formularyGram‑positive (MSSA) — use vancomycin where MRSA is prevalent
± Metronidazole7.5 mg/kg/dose q12h (< 8 weeks of age)Add for anaerobes — foul discharge or maternal chorioamnionitis; accumulates if < 40 weeks' gestation
Meropenem20 mg/kg/dose q8h (q12h if GA < 32 wk and age < 14 days); 30 mg/kg/dose q8h if GA ≥ 32 wk and age ≥ 14 daysOR (severe cases) — alternative for necrotizing fasciitis (with vancomycin + clindamycin); 40 mg/kg q8h is the meningitis dose — specialist advice
± Vancomycin15 mg/kg load, then 10 mg/kg/dose q12h (first week of life); q8h thereafter to 1 monthWhere MRSA is prevalent; level‑guided; longer intervals in preterm infants
± Clindamycin5 mg/kg/dose q8h (term, > 7 days; q12h in the first week)Necrotizing fasciitis (antitoxin effect)
Infant > 28 daysgeneral pediatric doses: cefotaxime 50 mg/kg q6h; vancomycin 15 mg/kg q6h (max 1 g/dose); metronidazole 7.5–10 mg/kg q6–8h; meropenem 40 mg/kg q8h (severe)Not for neonates
◈ Duration
  • About 7 days for uncomplicated periumbilical cellulitis; 10–14 days IV with bacteremia or sepsis; 14–21 days if meningitis; prolonged and surgically‑guided in necrotizing fasciitis (local practice — not guideline‑stated).
  • Tailor to cultures, susceptibilities, and clinical response — older infants may step down to oral once clearly improving.
◈ Delayed umbilical separation
  • Normal separation is by ~2 weeks (range 3–45 days, mean ~10 days); antiseptic cord care delays it versus dry care, so a well infant is usually benign.
  • Not off by 3–4 weeks = delayed (up to ~10% of newborns). ⚠ Suspect leukocyte adhesion deficiency (LAD) if delayed separation + omphalitis or soft‑tissue infection that forms no pus + persistent marked leukocytosis without infection (often 40–60 ×10⁹/L) + poor wound healing → consult immunology whenever LAD is suspected. There is a growing group of LAD syndromes with variable defects; normal expression of CD18 alone is not sufficient to exclude LAD‑1 — functional assays must be performed if clinical suspicion is high.
  • Most isolated delay in a well infant with a normal white count is not LAD.
  • Other causes: a patent urachus or omphalomesenteric duct (see below), factor XIII deficiency (stump bleeding).
Umbilical granuloma
  • Moist pink granulation after separation → silver‑nitrate cautery (protect surrounding skin) or topical salt.
  • Refer if persistent discharge or a polyp suggests a duct remnant.
⚠ Don't miss — patent duct remnants
  • Patent omphalomesenteric (vitelline) duct = persistent ileum‑to‑umbilicus connection; patent urachus = bladder‑to‑umbilicus. Both present after cord separation with intermittent umbilical drainage: small‑bowel contents (omphalomesenteric duct) or clear urine‑like fluid, more with crying or voiding (urachus).,
  • A sinus or small opening may be visible at the umbilical base; ultrasound may show a tubular structure extending deep to the umbilicus. If an opening is present it can be cannulated for a sinogram/fistulogram to demonstrate communication with the ileum or bladder.,
  • Other remnants that mimic granuloma: umbilical polyp (bright‑red, mucosa‑covered, does not respond to silver nitrate — ectopic ileal/gastric mucosa) and urachal or omphalomesenteric cyst/sinus (persistent wetness, infected periumbilical mass).
  • ▸ Refer all to pediatric surgery — prolapsed bowel through a patent omphalomesenteric duct is a surgical emergency; small urachal remnants often close spontaneously in infancy, so excision is decided by the surgeon.,
◣ Admit · Discharge · Refer
  • Admit — all → IV antibiotics (neonatal‑sepsis pathway).
  • Home from the ward — not acutely; complete the IV course — older infants may step down to oral.
  • Refer — now — pediatric surgery for necrotizing fasciitis.
  • Refer — clinic — pediatric surgery for a suspected duct remnant; immunology for suspected leukocyte adhesion deficiency.

Necrotizing Enterocolitis

HOURSModified Bell

Preterm or stressed neonate: feeding intolerance, distension, bloody stools.

▸
◢ Recognize
  • Feeding intolerance, bilious or rising gastric residuals, abdominal distension and tenderness, bloody stools.
  • Systemic: lethargy, apnea, temperature instability, shock. Mostly preterm (onset often the 2nd–4th week, later at lower gestation); term infants with congenital heart disease or asphyxia are also at risk.
  • Risk rises with prematurity and formula feeding; human (breast) milk and standardized feeding protocols are protective.
Confirm
  • Abdominal X‑ray (supine + left‑lateral decubitus): pneumatosis intestinalis (intramural gas — the radiologic hallmark), portal venous gas, a persistent fixed dilated loop, or free air.
  • Bloods: CBC, CRP, blood gas, lactate, blood culture, coagulation, electrolytes.
  • Bowel ultrasound (wall thickness/perfusion, free fluid) is a useful adjunct.
  • Repeat X‑ray every 6 h while acute.
Modified Bell stageFindingsBowel rest + antibiotics
I — SuspectedNonspecific signs (apnea, temperature instability), distension, occult or gross blood
X‑ray normal or ileus
NPO + NG drainage ~3 days; stop antibiotics if NEC is excluded
II — Definite (proven)Above + absent bowel sounds ± tenderness
pneumatosis ± portal venous gas (IIB: metabolic acidosis, thrombocytopenia)
IIA: NPO + NG and antibiotics 7–10 days; IIB: 14 days
III — AdvancedCritically ill: shock, acidosis, DIC, peritonitis. IIIA bowel intact
IIIB perforated (pneumoperitoneum)
As IIB (14 days) plus fluid resuscitation, inotropes and ventilation; IIIB: surgery
Treat
  • Stop enteral feeds (NPO), nasogastric tube on free drainage, IV fluids and parenteral nutrition.
  • Broad‑spectrum IV antibiotics covering Gram‑negatives and anaerobes — e.g. ampicillin + gentamicin + metronidazole (or piperacillin‑tazobactam); add vancomycin if a central line or a resistant organism is suspected (regimen per local practice).
  • Correct acidosis, thrombocytopenia, and coagulopathy; support blood pressure.
  • Serial exams and X‑rays.
  • Surgical consultation if no improvement or signs of perforation are present.
⚠ Surgery now
Pneumoperitoneum (perforation) is an absolute indication. Also: deterioration despite maximal medical therapy, a fixed dilated loop, abdominal‑wall erythema, a palpable mass, or a positive paracentesis (stool / bile / pus). Options: laparotomy with resection, or a primary peritoneal drain in the unstable extremely‑low‑birth‑weight infant — in the NEST trial laparotomy was favored when the preoperative diagnosis was NEC rather than isolated perforation.
✦ Pearls
  • Pneumatosis intestinalis is the radiologic hallmark; portal venous gas signals more extensive disease and a worse prognosis.
  • Spontaneous intestinal perforation (SIP) is a distinct entity — earlier onset (first week), often after indomethacin or steroids, a focal perforation with no pneumatosis; treat with broad‑spectrum antibiotics including anaerobic cover plus peritoneal drainage or laparotomy.
◣ Admit · Discharge · Refer
  • Admit — all → NICU, nil by mouth, gut decompression, antibiotics.
  • Home from the ward — not acutely; after recovery, with feeding advice.
  • Refer — now — pediatric surgery (perforation or deterioration).

Neonatal Seizures

MINUTESILAE 2023

Often subtle — and often a treatable cause behind them.

▸
◢ Recognize & confirm
  • Subtle signs: lip‑smacking, cycling or pedaling, eye deviation, apnea, focal clonic or tonic movements.
  • Only focal clonic and focal tonic seizures can be diagnosed clinically — all other types need EEG or amplitude‑integrated EEG (aEEG) to confirm. Electrographic‑only seizures are common, especially after the first drug (electroclinical dissociation), so monitor with EEG and treat electrographic seizures.
  • Common causes: hypoxic‑ischemic encephalo­pathy (most common), stroke, intracranial hemorrhage, infection / meningitis, metabolic (low glucose, calcium, sodium, magnesium), inborn errors, and genetic or structural epilepsies.
  • ⚠ Seizures or encephalopathy after perinatal asphyxia in a term or late‑preterm baby < 6 h old → time‑critical: call the NICU / cooling center now to assess for therapeutic hypothermia (must start within 6 h of birth); avoid hyperthermia; do not delay referral for imaging. Therapeutic hypothermia also lowers seizure burden in HIE.
Find the cause
  • Glucose, calcium, magnesium, sodium; blood gas, lactate, ammonia.
  • Sepsis screen including lumbar puncture, with CSF HSV PCR (start empiric IV acyclovir if neonatal HSV is possible)
  • Cranial ultrasound, then MRI. If unexplained: metabolic work‑up (plasma amino acids, urine organic acids, CSF glucose / lactate / glycine) and genetic testing for early‑onset epilepsy (e.g. KCNQ2, SCN2A). Correct reversible causes first — refractory hypocalcemia is often driven by low magnesium.
DrugDoseRoute & notes
Phenobarbital20 mg/kg IV load (further 10–20 mg/kg to ~40 mg/kg total)First‑line regardless of etiology (superior to levetiracetam, NEOLEV2) — except when a channelopathy is likely (e.g. family history of neonatal seizures, KCNQ2/KCNQ3): start a sodium‑channel blocker (phenytoin or carbamazepine) first. Use the shortest course; discontinue before discharge once acute provoked seizures have stopped and there is no evidence of neonatal‑onset epilepsy.
Levetiracetam40 mg/kg IV load; a further 20 mg/kg if required (maintenance 40–60 mg/kg/day in 3 doses)IV; second‑line — preferred when there is cardiac disease.
Phenytoin / fosphenytoin20 mg/kg (PE) over 30 minIV; second‑line; first‑line for a likely channelopathy (e.g. KCNQ2/KCNQ3 self‑limited familial neonatal epilepsy) — carbamazepine 10 mg/kg/day PO in 2 doses is the alternative.
Midazolam infusionload 0.05–0.15 mg/kg, then 0.06 mg/kg/h (1 mcg/kg/min); increase in steps of 0.06 mg/kg/h to a maximum of 0.3 mg/kg/h (5 mcg/kg/min)IV; second‑line/refractory; respiratory depression and hypotension — ventilatory support available.
Lidocaine (lignocaine)specialist infusion (load, then taper)IV; refractory. Avoid with phenytoin and in cardiac disease (proarrhythmic).
Pyridoxine100 mg IVTrial under EEG + cardiorespiratory monitoring (apnea / cerebral depression); for vitamin B6‑dependent epilepsy or unexplained refractory seizures.
Pyridoxal‑5‑phosphate (PLP)30 mg/kg/day PO/NG ÷ 3 doses for 3–5 daysIf pyridoxine fails and PNPO deficiency is suspected.
Folinic acid3–5 mg/kg/dayAdd‑on for pyridoxine‑dependent epilepsy with incomplete response.
Dextrose 10% / calcium gluconate 10% / magnesium sulfate2 mL/kg / 0.5–1 mL/kg slow / 0.1–0.2 mmol/kgIV; correct hypoglycemia, hypocalcemia, hypomagnesemia.
✦ Pearls
  • Phenobarbital remains first‑line (superior to levetiracetam for electrographic control, NEOLEV2 RCT), but use the shortest course: after acute provoked seizures have stopped and with no evidence of neonatal‑onset epilepsy, discontinue before discharge home regardless of MRI or EEG findings.
  • Refractory with no cause found: trial pyridoxine, then pyridoxal‑5‑phosphate if PNPO is suspected, then add folinic acid — these treat vitamin‑responsive epilepsies that anticonvulsants miss.
⚠ Jittery is not seizing
  • Jitteriness stops with gentle holding and has no eye or autonomic features; true seizures do not stop with restraint.
  • Don't miss glucose, calcium, magnesium, or infection.
◣ Admit · Discharge · Refer
  • Admit — all → NICU with monitoring/aEEG.
  • Home from the ward — not acutely; under neurology with a plan.
  • Refer — now — neurology and metabolic/genetics for the cause.

Vitamin K Deficiency Bleeding (VKDB)

MINUTESAAP 2022

Preventable with one injection at birth — the late form presents as catastrophic intracranial hemorrhage.

▸
◣ Recognize (three windows)
  • Early (0–24 h) — usually maternal drugs that interfere with vitamin K: enzyme‑inducing anticonvulsants, antituberculosis drugs (rifampicin, isoniazid), some antibiotics, and vitamin K antagonists (warfarin).
  • Classic (day 2–7) — bruising, GI or umbilical bleeding in a baby who missed prophylaxis.
  • Late (about 2 weeks to 6 months; peak 2–8 weeks) — exclusively breastfed, no/oral‑only prophylaxis, or malabsorption/cholestasis; up to half present with intracranial hemorrhage (bulging fontanelle, seizures, pallor, poor feeding).
⚠ Any bleeding neonate
  • Check a coagulation screen (prolonged PT/aPTT with normal platelets and fibrinogen suggests VKDB), give vitamin K without waiting for confirmation, and image the brain if any neurological sign.
  • Investigate for cholestasis/malabsorption in late VKDB.
◣ Workup
  • Coagulation screen — prolonged PT (most sensitive) and aPTT with normal platelets and fibrinogen (distinguishes from DIC); rapid correction after vitamin K confirms.
  • CBC / film.
  • Neuroimaging (cranial ultrasound / CT) if any neurological sign — late VKDB commonly presents as intracranial hemorrhage.
SettingDoseRoute & notes
Prophylaxis at birthPhytonadione (vitamin K₁) 1 mg if > 1500 g; 0.3–0.5 mg/kg if ≤ 1500 g (AAP 2022; the CPS alternative is a flat 0.5 mg)IM — single dose within 6 h of birth; the reliable route
Active bleedingVitamin K₁ 1–2 mg slow IV (formulary dosing)Plus FFP or prothrombin complex concentrate for serious/intracranial bleeding (expert practice — not addressed by the AAP prophylaxis statement)
◈ Counseling
  • IM prophylaxis at birth prevents both classic and late VKDB; purely oral regimens are less protective, especially in breastfed infants and cholestasis.
  • Reinforce with families who decline the injection.
◣ Admit · Refer
  • Admit — any bleeding neonate; PICU/neurosurgery for intracranial hemorrhage.
  • Refer — now — gastroenterology if underlying cholestasis/malabsorption.

Neonatal Abstinence Syndrome

ASSESSESC‑NOW · NEJM 2023

The jittery, inconsolable, poorly feeding newborn after in‑utero drug exposure.

▸
◣ Recognize
  • Tremors/jitteriness, irritability and a high‑pitched cry, hypertonia, poor feeding/uncoordinated suck, vomiting/loose stools, sweating, sneezing, and disturbed sleep — typically within the first days after opioid exposure (later for long‑acting agents).
⚠ Exclude mimics; watch for seizures
Hypoglycemia, sepsis, hypocalcemia, hyperthyroidism and hypoxic‑ischemic encephalo­pathy can look similar — check them. Seizures occur in severe withdrawal and warrant pharmacological treatment and escalation. ⚠ Do not give naloxone to a newborn with known or suspected chronic in‑utero opioid exposure — it can precipitate acute withdrawal and seizures; support ventilation instead.
✦ Non‑pharmacological care first
  • The Eat‑Sleep‑Console approach — rooming‑in, breastfeeding where appropriate, swaddling, low stimulation, skin‑to‑skin — reduces the need for medication and shortens stay.
  • Reserve opioids (morphine or methadone) for infants who cannot feed, sleep or be consoled despite optimal supportive care.
◣ Workup
  • Primarily clinical — the Eat‑Sleep‑Console assessment (feeds ≥ 1 oz / breastfeeds · sleeps ≥ 1 h · consoled ≤ 10 min).
  • Confirm exposure with maternal history + maternal/infant toxicology (urine, meconium, or umbilical cord).
  • Exclude mimics: glucose, calcium, sepsis screen and thyroid studies as indicated.
◣ Admit · Refer
  • Admit — admit/observe for scoring (AAP 2020): 3 days after immediate‑release opioids, 4–7 days after buprenorphine or sustained‑release opioids, 5–7 days after methadone; escalate if seizures or failure of supportive care. If a second drug is needed, the AAP favors clonidine over phenobarbital.
  • Refer — now — neonatology, social work and safeguarding as indicated.

Neonatal Dosing by Postmenstrual Age (PMA)

DOSINGLexicomp · confirm against unit formulary

The dose per kg barely changes — postmenstrual and postnatal age change the interval.

▸
◣ The one idea
  • Postmenstrual age (PMA) = gestational age at birth + weeks since birth. Immature kidneys clear renally‑eliminated drugs slowly, so the more premature the baby and the younger the postnatal age, the longer the interval between doses.,
  • For aminoglycosides and vancomycin, the dose stays roughly the same per kg while the gap between doses stretches.
⚠ Levels govern, not a fixed schedule
  • Any published regimen is a starting point only.,
  • After the first doses, the drug level sets the interval for gentamicin, amikacin and vancomycin — take a trough immediately before the next dose (gentamicin: before the 2nd dose, then before every 3rd dose). Do not withhold the dose while waiting for the result unless there is evidence of impaired renal function (raised urea/creatinine, oliguria/anuria) or a previous high trough. If the trough is high (gentamicin ≥ 2 mg/L; aim < 1 mg/L if the course exceeds 3 doses), extend the interval. Extend the interval (do not cut the dose) for renal impairment / oliguria, perinatal asphyxia or therapeutic cooling, and concurrent indomethacin / ibuprofen or vancomycin.
  • Confirm every value against your unit's formulary and a live NeoFax / BNF for Children.,
◣ Doses — use a neonatal reference
  • Neonatal and premature dosing is PMA‑ and postnatal‑age‑dependent, and aminoglycoside/vancomycin regimens are titrated to drug levels — so specific doses and intervals are not reproduced here.,,
  • Use a maintained neonatal dosing reference — NeoFax, Lexicomp, or the BNF for Children — for gentamicin, amikacin, vancomycin and β‑lactam dosing by PMA and postnatal age, and confirm every value against your unit protocol / NICU formulary.,,
◈ Empiric early‑onset sepsis — ampicillin + gentamicin (ampicillin covers group B Streptococcus and Listeria; gentamicin adds Gram‑negative cover and synergy). Avoid ceftriaxone in neonates (bilirubin displacement, calcium precipitation)., AAP 2018 · FDA label
✦ Caffeine citrate — the quintessential neonatal drug
  • Apnea of prematurity: load 20 mg/kg, then 5 mg/kg once daily maintenance (up to 10 mg/kg/day for refractory apnea).
  • Always prescribe as citrate — caffeine base is half the number (20 mg citrate = 10 mg base). Caffeine · CAP trial
11

Neurologic

AES / ESETT · febrile seizure

Convulsive Status Epilepticus (> 1 month of age)

MINUTES

Seizure ≥ 5 minutes or repeated without recovery — treat by the clock.

▸
0–5 min · stabilize (clock starts at seizure onset)
  • Time is counted from the start of the seizure, not from arrival. A child who reaches you already seizing ≥ 5 min gets the benzodiazepine immediately — airway, oxygen and IV/IO access proceed in parallel, never before the drug.,
  • Airway + oxygen 10–15 L/min via non‑rebreather mask · IV/IO · monitor.
  • Check glucose (treat if low); send sodium, calcium, magnesium, glucose.
5 min from onset · 1st line
Benzodiazepine — may repeat once after 5 min (maximum 2 doses in total, counting any pre‑hospital dose) Lorazepam IV/IO, or diazepam IV/IO; no IV access → do not wait for one: intramuscular midazolam (preferred), buccal/intranasal midazolam, or rectal diazepam.,
~15–20 min · 2nd line
ESETT: the three are equally effective Levetiracetam (often preferred — quick and simple to give, few interactions; in ESETT efficacy and safety did not differ between the three), valproate, or fosphenytoin/phenytoin (phenobarbital is an alternative).
~40 min · refractory
3RD LINE · PICU Refractory status epilepticus: urgent PICU/anesthesia/neurology (anesthetic infusion, continuous EEG, find the cause). Intubation is a team decision whenever needed — not reserved for this step.
First line — benzodiazepines
DrugDoseRoute & notes
Lorazepam0.1 mg/kg (max 4 mg)IV/IO
Diazepam0.2–0.3 mg/kg (max 10 mg) IV/IO · rectal 0.5 mg/kg (max 20 mg)IV/IO; rectal when there is no IV access — an accepted first‑line route
Midazolam0.1 mg/kg IV (max 4 mg)
0.2 mg/kg IM or intranasal (max 10 mg)
Buccal 0.2–0.5 mg/kg (max 10 mg) — in practice by age: 3 mo–< 1 y 2.5 mg · 1–< 5 y 5 mg · 5–< 10 y 7.5 mg · ≥ 10 y 10 mg
IM/buccal/intranasal preferred when no IV access
Second line — choose one
DrugDoseRoute & notes
Levetiracetam40–60 mg/kg (max 4.5 g)IV; often preferred — quick and simple to give, few interactions (efficacy and safety did not differ between the three in ESETT)
Valproate40 mg/kg (max 3 g)IV (given over 10 min in ESETT). Avoid in known/suspected mitochondrial (POLG) or metabolic disease including urea‑cycle disorders, liver disease, thrombocytopenia/coagulopathy; under 2 years use only on neurology advice (boxed warning — fatal hepatotoxicity; ESETT enrolled ≥ 2 y only). Carbapenems (e.g., meropenem) sharply lower valproate levels.
Fosphenytoin20 mg PE/kg (max 1,500 mg PE)IV at ≤ 2 mg PE/kg/min (max 150 mg PE/min); continuous ECG, BP and respiratory monitoring (PE = phenytoin sodium equivalents — prescribe in mg PE)
Phenytoin20 mg/kg (max 1.5 g)IV over ≥ 20 min: ≤ 1 mg/kg/min, never > 50 mg/min; dilute in 0.9% saline only, in‑line filter, large vein; continuous ECG + BP — use if fosphenytoin unstocked
Phenobarbital15–20 mg/kg IVAlternative second‑line; monitor for respiratory depression and hypotension
◈ Dravet syndrome
  • Known/suspected Dravet syndrome (prolonged febrile hemiclonic seizures in infancy): prefer levetiracetam or valproate; sodium‑channel blockers (phenytoin/fosphenytoin) are avoided as maintenance but are not contraindicated for acute status epilepticus.
  • Phenobarbital is an alternative.
Third line — refractory (PICU)
DrugDoseRoute & notes
Midazolam infusion0.2 mg/kg load → 0.05–0.4 mg/kg/h to start; PICU may titrate higher (up to 2 mg/kg/h) to EEG seizure suppressionIV; titrate to EEG
Ketamine / thiopental / propofolspecialist dosingIV infusion titrated to EEG; propofol short‑term only (propofol infusion syndrome — monitor labs)
Pyridoxine100 mg IVTrial in refractory seizures in infants < 2 yr.
Dextrose 10% (if low glucose)2 mL/kgIV/IO
◣ Admit · Discharge · Refer
  • Admit — all → monitored bed; refractory or needing infusions → PICU.
  • Home from the ward — not from the acute episode; a first seizure that stops may go home after workup, neurology follow‑up.
  • Refer — now — neurology (EEG, cause); PICU for refractory status, or airway/hemodynamic compromise.
Convulsive status epilepticus — treat by the clockStabilize → benzodiazepine at 5 min → second‑line at ~20 min → refractory (PICU) at ~40 min.
!SEIZURE ≥ 5 MIN = STATUS EPILEPTICUSTwo benzodiazepine doses maximum (count pre‑hospital doses), then move to second‑line.STABILIZEAirway + O₂ 10–15 L/min · IV/IO · monitor. Check glucose(treat if low); send Na, Ca, Mg.10–5 minBENZODIAZEPINE (1st line)Lorazepam 0.1 mg/kg IV (max 4) — may repeat once. No IV →IM/intranasal midazolam 0.2 mg/kg (buccal 0.2–0.5 mg/kg).25 minSECOND‑LINE AGENTLevetiracetam 40–60 mg/kg, valproate 40 mg/kg, orfosphenytoin 20 mg PE/kg — ESETT: equally effective.3~15–20 minREFRACTORY — PICUAnesthetic infusion, continuous EEG, find the cause.Involve PICU, anesthesia and neurology.4~40 min

Febrile Seizure

HOURS6 MO–5 YR

Seizure with fever, no CNS infection or prior afebrile seizure, and no pre‑existing neurologic abnormality.

▸
◣ Simple vs complex
  • Simple: generalized, under 15 minutes, once in 24 hours — benign; reassure, treat the fever source, antipyretics for comfort; no routine EEG, imaging, or LP.
  • Complex: focal, over 15 minutes, or recurs within 24 hours — evaluate more carefully.
✦ Pearl — not a simple febrile seizure
  • Not a simple febrile seizure if any are present: focal features, duration > 15 min or recurrence within 24 h (complex), age < 6 months or > 5 years (60 months), incomplete recovery, or a child unwell between events.
  • A febrile seizure is, by definition, a seizure with fever in a child without CNS infection, metabolic disturbance, or prior afebrile seizures. When any of the features above is present, exclude those first — meningitis/encephalitis (see Bacterial Meningitis & Encephalitis), hypoglycemia, electrolyte disturbance, and an underlying (non‑febrile) epilepsy — before labeling it a complex febrile seizure.
⚠ Lower the threshold for lumbar puncture
  • Consider meningitis with any meningism or history/exam suggesting CNS infection; in an infant 6–12 months under‑immunized against Hib or pneumococcus (or of unknown immunization status); or in a child pretreated with antibiotics (may mask meningitis).
  • Age < 12 months alone is no longer an indication — AAP 2011 replaced the 1996 advice to “strongly consider” LP in every infant under 12 months; LP is now an option only for the under‑immunized 6–12‑month‑old or the antibiotic‑pretreated child.
  • A seizure lasting ≥ 5 minutes is status epilepticus (see Convulsive Status Epilepticus) — treat as above.
◣ Admit · Discharge · Refer
  • Admit — complex features, prolonged/focal, incomplete recovery, or a source needing admission.
  • Home from the emergency department — simple febrile seizure, well child, normal exam, reliable carers with safety‑net advice.
  • Refer — now — neurology only for complex, recurrent, or atypical seizures — not routine for simple febrile seizures.

Bacterial Meningitis & Encephalitis

MINUTES> 2 MO

Fever plus altered consciousness, neck stiffness, or a bulging fontanelle — do the LP first, but never delay antibiotics for it.

▸
◣ Recognize & act
  • Infants (non‑specific): fever, poor feeding, lethargy or decreased interaction, vomiting, irritability, ± rash; inconsolable or worsening irritability with progressive lethargy are red flags. Nuchal rigidity is uncommon in infants.
  • Older children: headache, neck pain/stiffness, photophobia, vomiting, impaired consciousness, seizures, non‑blanching rash.
  • Take blood cultures (weight‑based volumes), then give empiric IV antibiotics immediately — do not delay if LP is deferred.
  • Add acyclovir if encephalitis features (behavior change, focal neurology, seizures). Encephalitis criteria: altered mental status ≥ 24 h plus ≥ 2 of — fever, new seizures, focal neurology, CSF pleocytosis, abnormal neuroimaging, or abnormal EEG.
  • Watch for SIADH and raised ICP (see Raised ICP).
◈ Bacterial Meningitis Score — CSF pleocytosis in a well child
  • Use only if age ≥ 2 months, previously healthy, CSF white cells ≥ 10 cells/µL, and no antibiotics in the 72 h before the LP.
  • Do not use if critically ill (severely altered consciousness, signs of herniation, needs respiratory or blood‑pressure support), purpura, ventricular shunt or recent neurosurgery, immunosuppression, or another bacterial infection that needs inpatient antibiotics.
CriterionPoints
CSF Gram stain positive2
CSF neutrophils ≥ 1,000 cells/µL1
CSF protein ≥ 80 mg/dL (≥ 0.8 g/L)1
Blood neutrophils ≥ 10,000 cells/µL (≥ 10 × 10⁹/L)1
Seizure before or at presentation1
  • Score 0 → very low risk: bacterial meningitis in 0.1% (sensitivity 98.3%, negative predictive value 99.9%; 3,295 children); pooled sensitivity 99.3% across 8 validation studies. Outpatient care may be considered.,,
  • Score ≥ 1 → not low risk: manage as bacterial meningitis — admit and give empiric antibiotics until cultures are back.
  • Not for infants < 2 months: both bacterial cases missed in the validation study were younger than 2 months; in infants ≤ 60 days the score’s specificity is 1.6%.,
Empiric & targeted therapy — meningitic doses
DrugDoseRoute & notes
Ceftriaxone50 mg/kg/dose q12h (or 100 mg/kg/dose once daily; max 4 g/day (2 g/dose if q12h))IV (IM if IV not immediate); first‑line empiric. Covers S. pneumoniae, N. meningitidis, H. influenzae.
Cefotaxime50–75 mg/kg/dose q6h (max 3 g/dose)IV; alternative to ceftriaxone — preferred in neonates.
Vancomycin15–20 mg/kg/dose q6h
target trough 15–20 mg/L for CNS infection; current consensus prefers AUC‑guided dosing (AUC/MIC 400–600) (max 1 g/dose)
IV; add empirically for possible cephalosporin‑resistant pneumococcus.
Ampicillin75 mg/kg/dose q6h (or 50 mg/kg/dose q4h; max 12 g/day)
Term neonates: 100 mg/kg/dose q8h (0–7 days), then 75 mg/kg/dose q6h
IV; add for Listeria in neonates / immunocompromised / at risk.,
Meropenem40 mg/kg/dose q8h (max 2 g/dose)IV; alternative if a 3rd‑gen cephalosporin is contraindicated — get ID advice.
Dexa­methasone0.15 mg/kg/dose q6h (max 10 mg/dose)IV; just before or with the first antibiotic dose (may still be started up to 4 h after it) — see steroid note. Not in neonates.
Acyclovir≤ 4 mo: use neonatal HSV dosing (20 mg/kg/dose every 8 h). > 4 mo–< 12 y: 10–15 mg/kg/dose every 8 h (AAP Red Book); up to 20 mg/kg/dose every 8 h is the FDA‑label dose and absolute maximum but carries more nephro‑/neurotoxicity — use only on ID advice with hydration and daily creatinine. ≥ 12 y: 10 mg/kg/dose every 8 h. Duration 21 days (CNS)IV, infuse over 1 h with adequate hydration + renal monitoring; add if HSV encephalitis suspected. Beyond the neonatal period the higher 20 mg/kg dose is not routine — increased neurotoxicity / nephrotoxicity (Lexicomp).
◈ Duration by pathogen
  • N. meningitidis 5–7 days; H. influenzae type b 7–10 days; S. pneumoniae 10–14 days; group B Streptococcus 14–21 days; Listeria ≥ 21 days; aerobic Gram‑negative bacilli 21 days (or ≥ 2 weeks after the first sterile CSF in neonates) — confirm the final duration with infectious diseases.,
  • Confirm the pathogen and tailor to response.
◈ Steroids — dexamethasone
  • Give 0.15 mg/kg/dose q6h just before, with, or within 4 h of the first antibiotic (earlier is better). Continue 4 days if Hib or S. pneumoniae is confirmed.
  • Reduces hearing loss, especially in Hib.
Duration, targeted therapy & follow‑up
  • When susceptibilities return, narrow therapy (penicillin‑susceptible pneumococcus or meningococcus → penicillin G or ampicillin; GBS → penicillin/ampicillin + gentamicin).
  • IV duration: by organism — see the duration list in this card (GBS longer if cerebritis/ventriculitis). Formal audiology before discharge for every child.
  • Repeat LP is not routine — reserve it for failure to improve, resistant pneumococcus, or selected neonates/complex cases after ID advice; also repeat the LP near the end of therapy for confirmed HSV CNS disease in young infants (to document a negative CSF HSV PCR).
  • Arrange chemoprophylaxis for close contacts of meningococcal (and Hib per criteria) via public health.,
⚠ Defer the LP (but never the antibiotics) if
  • Image first (contrast‑enhanced CT and/or MRI) if: reduced or fluctuating consciousness/coma, focal neurological deficit, papilledema or other signs of raised ICP, or new‑onset seizures.
  • Do not LP — imaging does not help — if: coagulopathy, skin infection over the site, signs of herniation, or cardiorespiratory instability/shock (stabilize first).
  • A purpuric / non‑blanching rash with fever is meningococcal sepsis until proven otherwise (see The Rash, Septic Shock).
◣ Admit · Discharge · Refer
  • Admit — all → hospital; reduced consciousness, shock, seizures, or raised ICP → PICU.
  • Home from the ward — not from the acute illness; complete the course with audiology and neurodevelopmental follow‑up.
  • Refer — now — infectious diseases/neurology; PICU for complications; public health for notification and contact prophylaxis.

Brain Tumor — New Presentation

HOURSHeadSmart / RCPCH

Persistent morning headache and vomiting with a visual, coordination, or behavioral sign — image the whole neuraxis, don't LP, and call neurosurgery.

▸
◣ Recognize — HeadSmart red flags
  • Raised ICP: recurrent headache worse on waking or lying down, persistent vomiting (classically early‑morning), and papilledema or a falling conscious level.
  • Visual / eye signs: new squint or double vision, nystagmus, reduced acuity, an abnormal head tilt, or abnormal eye movements.
  • Motor / coordination: ataxia or unsteady gait, new focal weakness or facial droop, and in a young child regression / loss of milestones.
  • Age‑specific: infants — enlarging head, bulging fontanelle, “sunsetting” eyes, developmental regression; older children / teens — behavior or school change, fatigue, delayed or arrested puberty, polyuria/polydipsia (diabetes insipidus), and precocious puberty — associated with intracranial (pineal / suprasellar) germ‑cell tumors.
  • A new focal seizure, or any of the above that is persistent or progressive.
⚠ Do not LP
With a mass or obstructive hydrocephalus, an LP can precipitate herniation — image first. Don't dismiss persistent morning vomiting as gastroenteritis.
◈ Diagnose
  • MRI is the imaging of choice, with contrast CT if MRI is not immediately available or to exclude acute hydrocephalus / hemorrhage. Image the whole spine with contrast as well to stage leptomeningeal / “drop” metastases.
  • Look actively for obstructive hydrocephalus — it is a neurosurgical emergency.
◣ Acute management
  • Position first: head of bed up 30°, neck midline (no venous obstruction), avoid hypotonic fluids and hyperthermia; treat seizures — the same first‑line measures as for raised ICP (see Raised ICP).
  • Dexa­methasone for symptomatic peritumoral (vasogenic) edema / raised ICP — specialist‑directed; commonly 0.25–0.5 mg/kg/day in 2–4 divided doses (max 16 mg/day; many centers use ≈ 0.2 mg/kg/day, max 8 mg/day), and for severe edema or impending herniation a 1–2 mg/kg IV load (max 10–20 mg) then 1–1.5 mg/kg/day divided q6h (max 16 mg/day) — formulary dosing.
  • Call neurosurgery urgently; treat hydrocephalus (EVD / CSF diversion) as directed.
  • Transfer to PICU if drowsy or dropping conscious level, and manage as Raised ICP in the interim.
◣ Admit · Discharge · Refer
  • Admit — any suspected tumor with raised ICP, hydrocephalus, a focal deficit, or a reduced conscious level.
  • Home — not during the acute presentation; expedite imaging and specialist review.
  • Refer — now — pediatric neurosurgery / neuro‑oncology at a specialist center for resection and hydrocephalus management; involve oncology.

Brain Abscess

HOURSNEUROSURGICAL

Fever, headache, focal deficit, or new seizures — image with contrast MRI, treat by source, don't LP.

▸
◣ Recognize
  • Subacute: headache (most common), fever, focal neurological deficit, new‑onset seizures, and features of raised ICP (vomiting, altered consciousness, papilledema). The classic triad (fever + headache + focal deficit) occurs in a minority.
  • The source predicts the organisms: contiguous — otitis/mastoiditis, sinusitis, dental, meningitis; hematogenous — cyanotic congenital heart disease (right‑to‑left shunt), endocarditis, pulmonary; direct — penetrating trauma or neurosurgery; immunocompromise (add fungi, Nocardia, Toxoplasma).
◈ Diagnose
  • Contrast MRI with diffusion‑weighting is the test of choice — abscess shows restricted diffusion (a tumor usually does not); contrast CT if MRI unavailable.
  • Take blood cultures. LP only after neurosurgical evaluation — low yield, herniation risk with a focal mass; abscess drainage and culture is best.
  • Contrast MRI + neurosurgery + IV antibiotics by source.
  • Urgent neurosurgery + ID; empiric therapy follows source and local resistance.
Decision — what is the likely source?
Otogenic / sinus / dental / hematogenous Ceftriaxone (or cefotaxime) + metronidazole — covers the Streptococcus anginosus (milleri) group and anaerobes; add vancomycin only if S. aureus/MRSA is plausible (hematogenous spread/endocarditis, penetrating trauma, known MRSA) or the child is critically ill.
Post‑trauma / post‑neurosurgical Vancomycin + an antipseudomonal beta‑lactam (cefepime, ceftazidime, or meropenem) — covers S. aureus (incl. MRSA), Gram‑negatives and Pseudomonas.
Empiric agents — pediatric doses
DrugDoseRoute & notes
Ceftriaxone50 mg/kg/dose q12h (or 100 mg/kg/dose once daily; max 4 g/day (2 g/dose if q12h))IV; streptococci + Gram‑negatives. Cefotaxime is an alternative.
+ Metronidazole7.5 mg/kg/dose q6h (max 500 mg)IV; anaerobic cover for otogenic / sinus / dental sources.
+ Vancomycin15 mg/kg/dose q6h; trough 15–20 mg/L (max 1 g/dose)IV; add for S. aureus / MRSA or severe disease.
Meropenem (OR — alternative)40 mg/kg/dose q8h (max 2 g)IV; cephalosporin allergy, resistant Gram‑negatives, or suspected Nocardia.
± Vancomycin15 mg/kg/dose q6h (max 1 g/dose)Add to meropenem where S. aureus / MRSA is likely.
Surgery, duration & adjuncts
  • Neurosurgical aspiration or excision for diagnosis and for potential abscess drainage, or if not responding — send pus for aerobic, anaerobic, fungal and mycobacterial studies. IV antibiotics 6–8 weeks (any shorter course only on infectious‑diseases/neurosurgical advice), guided by clinical response and serial imaging; involve infectious diseases. Treat the source (mastoid, sinus, dental). Urgent PICU consult for ICP management; give anticonvulsants for seizures.
  • Reserve steroids for significant edema / mass effect — they can reduce antibiotic penetration.
⚠ Don't LP right away — watch for herniation
  • With a focal mass, an LP can precipitate herniation and rarely changes management — image first.
  • Rapid deterioration, a large abscess with midline shift, or impending herniation → emergency neurosurgery & PICU consult (see Raised ICP / The Comatose Child).
◣ Admit · Discharge · Refer
  • Admit — all → for treatment and monitoring; potential abscess drainage.
  • Home from the ward — after prolonged IV therapy and imaging response, with follow‑up.
  • Refer — now — neurosurgery (drainage) and infectious diseases; find the source (ENT/dental/cardiac).

Raised ICP / The Comatose Child

MINUTES

Protect the brain: airway, glucose, and reverse herniation fast.

▸
◣ Recognize herniation
  • Falling conscious level (GCS / AVPU), unequal or fixed pupils, abnormal posturing, and the Cushing triad (hypertension + bradycardia + irregular breathing) = impending herniation.
  • Coma work‑up — DEFG: "Don't Ever Forget Glucose." Sort causes with AEIOU‑TIPS: alcohol/toxins, epilepsy, insulin/glucose, opioids, uremia/metabolic, trauma, infection, psychiatric, stroke/shock.
Stabilize
  • Airway (add C‑spine control if trauma; use an appropriately sized collar), oxygen, ventilation.
  • Check glucose; treat seizures.
  • Position the head midline and elevate the head of the bed to 30°.
  • Keep normothermic and normoglycemic; avoid hyponatremia — keep sodium in the normal‑to‑high range.
  • Call PICU.
Lower ICP Maintain oxygenation and normocapnia (avoid routine hyperventilation); give hyperosmolar therapy; urgent CT + neurosurgery (measures extrapolated from pediatric severe‑TBI guidance).
DrugDoseRoute & notes
Hypertonic saline 3%2–5 mL/kg over 10–20 minIV; for raised ICP / herniation
Mannitol0.5–1 g/kg over 10–15 minIV; alternative (caution if hypovolemic/hypotensive) — formulary dosing
Dextrose 10% — hypoglycemia only2–5 mL/kg (0.2–0.5 g/kg); recheck glucoseIV/IO only to correct documented hypoglycemia (“don't ever forget glucose”); use the smallest effective dose.
⚠ Fluids — avoid free water
In suspected raised ICP, avoid dextrose‑containing and hypotonic fluids as a bolus or maintenance — once the glucose is metabolized the leftover free water worsens cerebral edema. Maintain with isotonic 0.9% saline (expert consensus — not guideline‑stated). The one exception is documented hypoglycemia, which injures the brain and must be corrected.
⚠ Do not delay transfer
Do not delay transfer to PICU/neurosurgery; repeat hyperosmolar therapy is specialist‑guided.
⚠ Hyperventilation
Brief hyperventilation only as a bridge for impending herniation; sustained hypocapnia causes cerebral ischemia.
◣ Admit · Discharge · Refer
  • Admit — all → PICU.
  • Home from the ward — not from the acute episode.
  • Refer — now — neurosurgery/neurology and the primary‑cause specialty (tumor, infection, metabolic, trauma).

Guillain–Barré Syndrome / Acute Flaccid Paralysis

MINUTESEAN/PNS 2023

Ascending weakness that can reach the diaphragm — the emergency is respiratory failure and autonomic instability.

▸
◣ Recognize
  • Progressive, fairly symmetric ascending weakness with reduced/absent reflexes, often after a GI or respiratory infection; a refusal to walk in a young child.
  • CSF (if done) shows high protein with normal cell count (albuminocytologic dissociation) — may be normal in the first week; MRI may show nerve‑root enhancement.
⚠ The two things that kill
  • Respiratory failure — track vital capacity/effort; rising CO₂ and a falling forced vital capacity (roughly < 15–20 mL/kg) mean elective intubation, not a trial of NIV — avoid succinylcholine (denervation → hyperkalemic arrest; use rocuronium) and expect hemodynamic lability at induction. Autonomic instability — labile blood pressure, arrhythmia, ileus; put the child on a cardiac monitor.
  • Rapid progression or bulbar weakness (choking, weak cough) = ICU.
✦ Don’t be reassured by a normal early tap
  • Weakness can outrun the CSF and the reflexes early on.
  • If the picture fits, admit and monitor breathing serially rather than discharging on a single normal test.
  • Always exclude a compressive cord lesion (a sensory level, back pain or sphincter loss points to the cord, not GBS).
◣ Workup
  • Lumbar puncture — albuminocytologic dissociation (high protein, normal cells); may be normal in the first week.
  • Nerve conduction studies / EMG (subtype; may be normal early — repeat).
  • Serial bedside spirometry — FVC 3–6 times a day depending on severity, and every 4 h while FVC is falling, plus single‑breath count and bulbar assessment. Act on FVC ≤ 20 mL/kg, a > 30% fall from baseline, single‑breath count < 20, or MIP < 40 / MEP < 30 cmH₂O (EAN/PNS 2023). The older “20/30/40” rule (FVC < 20 mL/kg, MIP < 30, MEP < 40 cmH₂O) comes from a mainly adult ICU cohort.
  • Spirometry is unreliable under ~5–6 years or with facial/bulbar weakness (poor mouth seal) — there, rely on serial clinical assessment: single‑breath count, cough strength, paradoxical breathing, ability to lie flat, and the blood‑gas/CO₂ trend (expert practice — not guideline‑stated).
  • Continuous ECG/BP for dysautonomia.
  • Spinal MRI with contrast (nerve‑root enhancement; excludes a compressive cord lesion).
  • Anti‑ganglioside antibodies (GQ1b for Miller‑Fisher). Stool for poliovirus/enterovirus in acute flaccid paralysis — two specimens ≥ 24 h apart within 14 days of onset.
TreatmentDoseNotes
IV immunoglobulin2 g/kg total — preferably 0.4 g/kg/day × 5 days (a 2‑day course, 1 g/kg/day, gives more early relapses in children); for a child unable to walk unaided or with rapid progression, bulbar or respiratory involvementFirst‑line; equivalent to plasma exchange — a second course is not recommended in non‑responders (SID‑GBS)
Plasma exchangePer center protocolAlternative — not combined with IVIG
Cortico­steroidsNot recommendedNo benefit in GBS
◣ Admit · Refer
  • Admit all suspected cases for respiratory and cardiac monitoring.
  • Call neurology; critical care early if bulbar/respiratory involvement or rapid progression. Acute flaccid paralysis is notifiable (polio surveillance) — send stool.

The Child with Neuromuscular Disease

MINUTESDMD Care 2018 · CHEST 2023

A known neuromuscular disease rewrites every emergency — the weak cough, the anesthetic that can kill, the heart, and the steroids.

▸
◣ Respiratory — the usual killer
  • It is the weak cough, not the lungs: a “simple” chest infection tips into hypercapnic respiratory failure. Support ventilation with NIV (bilevel) and clear secretions with mechanical insufflation–exsufflation (cough assist) — not oxygen alone.,
  • The oxygen saturation lies — it can be normal while CO₂ climbs. Track capnography / blood‑gas pCO₂, not SpO₂.
⚠ Anesthetic / RSI hazard — flag before any sedation
  • Succinylcholine is contraindicated in dystrophinopathies and many myopathies (hyperkalemic cardiac arrest), and volatile agents (sevoflurane, isoflurane, desflurane) risk anesthesia‑induced rhabdomyolysis / hyperkalemia (see Rhabdomyolysis). Safe approach: total IV anesthesia (propofol, opioid, benzodiazepine) + a non‑depolarizing blocker (rocuronium) reversible with sugammadex.
  • Obtain a baseline CK and an ECG before any procedure, and recheck K⁺ and CK if perioperative rhabdomyolysis is suspected.
⚠ Do not give uncontrolled oxygen
  • High‑flow O₂ masks a rising CO₂ and can abolish respiratory drive → CO₂ narcosis and arrest.
  • Titrate O₂ only with ventilatory support and CO₂ monitoring — correct the hypoventilation, not the number.
◣ Cardiac
  • Duchenne / Becker → dilated cardiomyopathy and arrhythmia (may be silent — reduced mobility hides symptoms). Emery‑Dreifuss / LGMD1B → progressive AV / conduction block and sudden death (may need pacing).,
  • Any acute deterioration: 12‑lead ECG + echocardiogram; troponin and BNP/NT‑proBNP if acute myocardial injury or heart failure is suspected.
◣ Adrenal — stress‑dose steroids
  • A child on chronic daily steroids (prednisone/deflazacort for Duchenne) cannot mount a stress response. Acute illness, vomiting, trauma, surgery or shock needs stress‑dose steroids to prevent adrenal crisis — never stop steroids abruptly (see Adrenal Crisis).
◣ Fracture / fall
  • A Duchenne boy with a long‑bone fracture or leg trauma (even a minor fall) who becomes confused, breathless/hypoxemic or tachycardic has fat embolism syndrome until proven otherwise → respiratory support, PICU, orthopedics, and stress‑dose steroids.
◣ Myasthenic crisis
  • Worsening bulbar/respiratory weakness → treat with IVIG or plasma exchange and support the airway. Follow FVC and NIF, not SpO₂.
  • Avoid drugs that worsen myasthenia: aminoglycosides, macrolides, fluoroquinolones, IV magnesium, beta‑blockers, and procainamide.
✦ Two numbers that mislead, one that doesn’t
  • In neuromuscular weakness a normal SpO₂ and a normal respiratory rate are falsely reassuring — the child fails from CO₂ retention and a failing cough.
  • The honest bedside numbers are pCO₂ (capnography/gas) and FVC / NIF.
  • A metabolic/mitochondrial myopathy adds a fourth: start IV dextrose (D10) early — fasting and catabolic stress precipitate metabolic decompensation (limit or avoid dextrose in pyruvate-metabolism disorders or on a ketogenic diet).
◣ Workup
  • VBG/ABG with pCO₂ + continuous capnography — the key respiratory measure; FVC and NIF where the child can cooperate.
  • Electrolytes incl. potassium, magnesium, calcium; creatine kinase; renal function; glucose; lactate.
  • 12‑lead ECG; troponin + BNP/NT‑proBNP; echocardiogram if cardiac concern.
  • Chest X‑ray ± sputum culture if infective; swallow/bulbar assessment.
SituationDoseRoute & notes
Stress steroids — tolerating oral (moderate illness/injury)Never omit the usual daily steroid. Add oral hydrocortisone ≈ 30–50 mg/m²/day in 3–4 divided doses (≈ 3 × physiologic replacement — not 3 × the Duchenne treatment dose)PO; per the child's written stress plan / PJ Nicholoff protocol. If on prednisone/prednisolone the usual daily dose may instead be split twice daily; do not rely on extra deflazacort and never use vamorolone for stress cover. Vomiting, cannot take oral, severe illness, major trauma or surgery → IM/IV hydrocortisone (next row)
Stress steroids — unwell / vomiting / shockHydro­corti­sone ≈ 2 mg/kg (or 50 mg/m²) IV, then continuedIV/IM; treat as adrenal crisis — do not wait. DMD care considerations: emergency IM hydrocortisone 50 mg (< 2 yr) or 100 mg (≥ 2 yr); stress dosing 50–100 mg/m²/day in severe illness, major trauma or surgery.
Myasthenic crisisIVIG 2 g/kg over 2–5 days or plasma exchangePlus airway support; treat the trigger/infection
Metabolic myopathy — catabolic stressIV dextrose (D10) earlyPrevents fasting‑driven decompensation / rhabdomyolysis
◈ Local & anticipatory
  • Ask for the child’s emergency / anesthesia alert card and neuromuscular care plan on arrival, and involve the neuromuscular team early.
  • Keep succinylcholine and volatile agents off the plan for dystrophinopathies, and flag the diagnosis to anesthesia/critical care before any transfer, sedation or intubation.
◣ Admit · Refer
  • Admit — any respiratory decompensation, myasthenic/adrenal crisis, new cardiac signs, or a child who needs assisted airway clearance.
  • Refer — now — call neuromuscular/neurology, cardiology and critical care/anesthesia; new acute flaccid weakness without a known diagnosis → see Guillain–Barré / Acute Flaccid Paralysis.
12

Orthopedic & Musculoskeletal

The limping child · fractures & NAI · SCFE · compartment syndrome · bone & joint infection

Orthopedic Emergencies — Call Now

MINUTES

Immediate orthopedic (± vascular/spinal) consultation — do not wait for imaging.

▸
⚠ Immediate orthopedic consultation
  • Septic arthritis
  • Compartment syndrome
  • Open fracture
  • SCFE
  • Joint dislocation
  • Fracture with pulseless limb
  • Unstable pelvic injury
  • Spine injury with neurological deficit

Osteoarticular Infections

HOURSRECOGNIZE

Acute hematogenous osteomyelitis (AHO) and septic arthritis (SA) — consider in any limp, refusal to use a limb, or pseudoparalysis.

▸
◣ Clinical presentation
  • Pseudoparalysis / limp / refusal to weight‑bear, or focal limb pain — often the only symptom. Fever supports diagnosis but may be absent.
  • Osteomyelitis: point tenderness over the metaphysis of a long bone ± localized swelling/erythema; fluctuance suggests a periosteal abscess.
  • Septic arthritis: joint effusion, swelling, and pain on any movement of the isolated joint; the limb is held in a position of comfort.
  • S. aureus → acute, rapidly progressive, higher CRP (MRSA more severe). Kingella kingae (young children) → milder, indolent, lower markers.
  • Chronic recurrent multifocal osteomyelitis (CRMO/CNO) — consider with recurrent bone pain, multifocal lesions, sterile cultures, and poor response to antibiotics.
◣ Most common sites & pathogens
  • Bone: metaphysis of long bones — femur, tibia, humerus. Pelvic bones are easily missed (vague pain, mimics abdomen).
  • Joint: hip and knee most common, then ankle, elbow, shoulder. SA + adjacent osteomyelitis is common (≈ 32% of SA), especially with S. aureus and longer symptom duration.
  • Pathogens: S. aureus overall most common; K. kingae dominates under ~4 yr (inoculate fluid into blood‑culture bottles). Add Salmonella in sickle cell disease; H. influenzae type b if under‑immunized.
◈ Kocher criteria — hip SA vs transient synovitis
  • Four predictors, one point each: non‑weight‑bearing; history of fever (> 38.5 °C); ESR ≥ 40 mm/h; white‑cell count > 12,000/µL.
  • Many add CRP > 20 mg/L as a strong independent predictor.
  • A risk‑stratification aid for the hip, not a rule‑out.
  • More positive criteria substantially raise septic‑arthritis probability, but always interpret alongside CRP, ultrasound, and clinical judgment.
Kocher — probability of septic arthritis
Predictors presentApprox. probability of SA
0 of 4< 0.2 %
1 of 4~ 3 %
2 of 4~ 40 %
3 of 4~ 93 %
4 of 4~ 99 %
⚠ Work‑up
  • Blood cultures before antibiotics. CRP at baseline (sensitive, falls fast — best for monitoring; ESR less useful).
  • Plain films to exclude mimics; ultrasound for hip/shoulder effusion; MRI is the imaging modality of choice (add contrast if abscess or soft‑tissue extension is suspected); MRI with gadolinium is the most sensitive/specific test, defining abscess, adjacent osteomyelitis, and soft‑tissue extent.
◣ Admit · Discharge · Refer
  • Admit — all suspected septic arthritis/osteomyelitis → IV antibiotics after cultures/aspiration. Ill‑appearing child or rapidly progressive infection: start empiric IV antibiotics immediately after blood cultures — do not wait for joint aspiration. Child who is not clinically ill: antibiotics may be withheld under close observation until the joint aspirate is obtained, provided aspiration is prompt (PIDS/IDSA 2023).
  • Home from the ward — not acutely; step down to oral with monitoring and orthopedic follow‑up.
  • Refer — now — orthopedics (aspiration/washout) and infectious diseases.

Osteoarticular Infections — Management

HOURSCULTURES FIRST

Cultures first, then empiric IV cefazolin; involve orthopedics early for any septic joint or bony abscess.

▸
Osteomyelitis or septic arthritis?
OSTEOMYELITIS (AHO)
Most respond to antibiotics alone. Surgery (drainage/debridement) for a subperiosteal/intraosseous abscess, or if not improving in the first few days — repeat imaging and reconsider debridement.
SEPTIC ARTHRITIS
Orthopedic emergency — urgent aspiration ± arthroscopic/open drainage & irrigation; send synovial fluid for cell count/differential, Gram stain and culture, with molecular (PCR) testing if no pathogen is identified, especially in preschool children (K. kingae). Hip and shoulder are especially time‑critical (avascular‑necrosis risk; expert consensus).
Empiric therapy after cultures: IV cefazolin — covers MSSA and K. kingae.
Antibiotic therapy
ScenarioDrug & doseNotes
Empiric — first‑line IVCefazolin 33–50 mg/kg/dose IV q8h (100–150 mg/kg/day; max 2 g/dose; upper end for serious invasive infection)Covers MSSA and K. kingae — the two commonest pathogens. Start after blood cultures.
Under 4 yr / unimmunizedCefuroxime 50 mg/kg/dose IV q8h (max 1.5 g/dose)Broadens to cover H. influenzae in unimmunized young children.
MSSA — confirmedContinue cefazolin, or cloxacillin 37.5–50 mg/kg/dose IV q6h (cloxacillin max 2 g/dose)Cloxacillin narrows further but irritates veins.
MRSA — suspected/confirmedAdd/use vancomycin 15 mg/kg/dose IV q6h (max 1 g/dose; level‑guided)Where MRSA prevalent or known carrier. Note: K. kingae is resistant to vancomycin and clindamycin but typically susceptible to cephalosporins.
Oral step‑down — MSSA / culture‑negCephalexin 25–33 mg/kg/dose PO TID (75–100 mg/kg/day; max 4 g/day — some experts give up to 6 g/day in 4 doses)First‑line oral. Cloxacillin 25 mg/kg/dose QID is an alternative (poor taste). Formulary dosing.
Oral step‑down — MRSAClindamycin, TMP‑SMX, or linezolidPer susceptibilities, with infectious‑diseases input; MRSA usually needs longer before switching (expert practice).
◈ IV → oral switch & duration
  • Switch to oral when clinically improved (afebrile, using the limb) and CRP falling, with an active, well‑tolerated oral option and assured adherence., Duration (CRP‑guided): AHO 3–4 weeks
  • uncomplicated SA as short as 10–14 days total (IV + oral) when improving rapidly with a progressively falling CRP by the end of week 1
  • SA with adjacent osteomyelitis, a slow response, or the hip/shoulder: longer, individualized course with infectious‑diseases input.
  • Randomized data (Peltola) support short courses once response is good and CRP normalizes early.
⚠ Follow‑up
  • Confirm clinical resolution and a normal/normalizing CRP before stopping.
  • End‑of‑therapy radiographs mainly if the growth plate was involved or a large lytic lesion present — these and any physeal involvement need orthopedic follow‑up.
  • Routine follow‑up MRI/CT is not needed — reserve for complications or non‑improvement.
◈ Difficult IV access? Reassess for an early IV→oral switch at every line failure rather than re‑sticking — see IV → Oral Switch & the DIVA Patient (Quick Reference).

The Limping Child

ASSESSAPPROACH

A limp is a symptom — use age and red flags to separate the benign from septic joint, SCFE, malignancy, and abuse.

▸
◣ Define
  • A limp is any deviation from normal age‑appropriate gait; pain present in ~80%. Broad differential — separate benign causes from the can't‑miss ones: septic joint, osteomyelitis, SCFE, malignancy, and inflicted injury.
◣ Approach — age narrows the differential
  • Toddler (1–3 y): toddler's fracture, transient synovitis, developmental dysplasia of the hip, inflicted injury.
  • Child (4–10 y): transient synovitis, Legg‑Calvé-Perthes, septic arthritis, reactive/juvenile idiopathic arthritis.
  • Adolescent (> 10 y): SCFE, apophysitis/overuse, sports injury.
  • Spinal: consider discitis, vertebral osteomyelitis, or a spinal tumor in a child refusing to walk with a normal hip exam — especially with back pain or spinal tenderness.
  • Malignancy: persistent night pain, pain out of proportion to the exam, constitutional symptoms, or failure to improve → urgent investigation.
  • History: pain, trauma, fever, systemic or night symptoms. Examine gait (antalgic vs Trendelenburg), hip, knee, spine, neurology — knee pain often means hip disease.
  • Any age — look beyond the hip: consider a first presentation of juvenile idiopathic arthritis (JIA), which occurs across all age groups, and examine every joint — not only the painful one (a commonly missed step that reveals oligo- or polyarticular disease).
⚠ Work‑up
Plain radiographs of the involved site — both hips (add a frog‑leg view for SCFE) if the exam does not localize. FBC, CRP/ESR, blood culture if febrile or systemically unwell; ultrasound for a hip effusion; MRI if osteomyelitis or malignancy is suspected.
◣ Red flags
  • Fever + refusal to weight‑bear + raised inflammatory markers → septic joint/osteomyelitis. Normal early CRP/ESR/white count do not exclude osteoarticular infection — reassess if symptoms persist or worsen.
  • Night pain, weight loss, pallor, bruising, or hepatosplenomegaly → malignancy/leukemia.
  • Multiple or unexplained fractures, or a fracture in a non‑ambulatory infant → inflicted injury.
  • Adolescent hip or knee pain with a limp → SCFE until excluded.
✦ Pearl — point to the hip
Isolated knee or thigh pain in a child is hip pathology until proven otherwise — SCFE and Perthes both refer pain to the knee.
◣ Admit · Discharge · Refer
  • Admit — septic arthritis, osteomyelitis, fracture, or systemic illness; unable to weight‑bear with red flags.
  • Home from the emergency department — transient synovitis in a well child with safety‑net advice and review.
  • Refer — now — orthopedics for red flags.
  • Refer — clinic — oncology/rheumatology as indicated.

Transient Synovitis vs Septic Arthritis

HOURSKOCHER

The commonest atraumatic limp — but rule out the septic joint first; fever + non‑weight‑bearing + high CRP means aspirate.

▸
◣ Define
  • Transient synovitis — a benign, self‑limited, often post‑viral hip inflammation and the commonest cause of an atraumatic limp. Typically 3–8 years; symptoms usually resolve within 7–10 days (expert consensus). Must be separated from septic arthritis, a surgical emergency.
◣ Approach — read the child
  • Transient synovitis: a well child, low‑grade or no fever, weight‑bears with discomfort, mildly raised markers, often a recent upper‑respiratory infection.
  • Septic arthritis: an unwell/febrile child who refuses to move the joint, severe pain on any movement, the limb held in flexion/abduction/external rotation.
◈ Kocher criteria — hip: septic arthritis vs transient synovitis
  • One point each: non‑weight‑bearing; history of fever (> 38.5 °C); ESR ≥ 40 mm/h; WBC > 12,000/µL.
  • Many add CRP > 20 mg/L as a strong independent predictor.
  • Probability of septic arthritis: 0/4 < 0.2%
  • 1/4 ≈ 3%
  • 2/4 ≈ 40%
  • 3/4 ≈ 93%
  • 4/4 ≈ 99%.
  • A risk aid, not a rule‑out.
⚠ Work‑up
  • FBC, CRP, ESR, blood culture; hip ultrasound (an effusion is seen in both and does not distinguish).
  • If septic arthritis is suspected → urgent ultrasound‑guided aspiration (cell count, Gram stain, culture into a blood‑culture bottle).
◣ Management
  • Septic arthritis — orthopedic emergency: urgent joint drainage plus IV antibiotics after cultures (see Osteoarticular Infections).
  • Transient synovitis — rest, NSAIDs, review in 24–48 h; settles over days. Re‑evaluate promptly if it does not improve or markers rise (expert consensus — not guideline‑stated).
✦ Pearl — when in doubt, aspirate
Fever + refusal to weight‑bear + a raised CRP is a septic joint until an aspirate proves otherwise — do not label it transient synovitis by default.
◣ Admit · Discharge · Refer
  • Admit — any suspicion of septic arthritis (Kocher criteria, raised markers) → aspiration.
  • Home from the emergency department — transient synovitis, afebrile, mobilizing, with review.
  • Refer — now — orthopedics for aspiration/washout if septic.

Nursemaid's Elbow

ASSESS1–4 YR

A pulled, pronated arm the child will not use — reduce by hyperpronation; no film needed if the story is classic.

▸
◣ Define
  • Nursemaid's elbow (radial head subluxation, 'pulled elbow') — the annular ligament slips over the radial head after axial traction on an extended, pronated arm. Commonest elbow injury in children aged 1–4 years.
◣ Approach & work‑up
  • Typical story: sudden pull or lift on the arm. Child holds the arm slightly flexed and pronated, refuses to use it, with no swelling, bruising, or deformity and minimal tenderness.
  • No imaging needed with a classic history and a normal‑looking arm. Image if the story is atypical, or there is swelling, focal bony tenderness, or deformity.
⚠ Red flags
  • Swelling, bruising, point bony tenderness, or deformity → suspect a fracture and radiograph.
  • An inconsistent or implausible history should prompt consideration of inflicted injury.
◣ Management — reduce it
  • Hyperpronation (support the elbow, firmly pronate the forearm) — a Cochrane review and a meta‑analysis show fewer first‑attempt failures than supination‑flexion (≈ 9% vs 26%; low‑certainty evidence); it may also be less painful, but the pain evidence is very uncertain — do it first.
  • Alternative: supination‑flexion (supinate the forearm, then fully flex the elbow). A palpable click often signals success.
  • Child usually resumes normal use within 5–30 minutes. If reduction fails, try the other maneuver; if still unsuccessful, immobilize, image, reassess.
✦ Pearl — no film needed if it works
  • With a classic pull mechanism and no swelling, reduce without imaging — if the child uses the arm normally afterwards, diagnosis is confirmed and no radiograph is required.
  • Do not attempt repeated reductions if there is swelling, bruising, focal tenderness, or an atypical history — image and consider safeguarding.
◣ Admit · Discharge · Refer
  • Admit — not required.
  • Home from the emergency department — after successful reduction and return of normal arm use.
  • Refer — now — orthopedics only if reduction fails, or for swelling/deformity suggesting fracture (image first).

Slipped Capital Femoral Epiphysis (SCFE)

HOURSCAN'T MISS

Peri‑pubertal limp with hip or knee pain — stop weight‑bearing and get frog‑leg views of both hips.

▸
◣ Define
  • Slipped capital femoral epiphysis (SCFE) — the proximal femoral epiphysis slips through the physis. Peri‑pubertal; obesity is the strongest risk factor; up to ⅓ bilateral. Consider endocrinopathy if the child is young (< 10 years), underweight, or atypical.
◣ Approach & work‑up
  • Limp with hip, groin, thigh, or knee pain; the leg lies externally rotated with limited internal rotation and obligate external rotation on hip flexion (Drehmann sign).
  • Stable (able to weight‑bear, with or without walking aids) vs unstable (cannot bear weight — high avascular‑necrosis risk).
  • AP + frog‑leg lateral radiographs of BOTH hips. For an unstable slip avoid forced frog‑leg positioning and use AP + cross‑table lateral to prevent further displacement; Klein's line may fail to intersect the epiphysis on the affected side but is insensitive on the AP view alone (expert practice).
⚠ Red flags
  • An unstable slip (non‑weight‑bearing) carries high avascular‑necrosis risk.
  • Missed or delayed diagnosis → progression and permanent deformity.
  • Assess both hips.
◣ Management
  • Make the child non‑weight‑bearing immediately and refer urgently to orthopedics for in‑situ screw fixation.
  • Do not attempt reduction — forceful manipulation increases avascular‑necrosis risk (expert consensus — not guideline‑stated).
  • Consider prophylactic contralateral fixation in high‑risk patients (young age, obesity, endocrinopathy) — a specialist decision (expert consensus).
✦ Pearl — frog‑leg both hips
Any obese adolescent with a limp or knee pain gets frog‑leg views of both hips and is kept off the leg until SCFE is excluded — knee pain is the classic decoy.,
◣ Admit · Discharge · Refer
  • Admit — all → non‑weight‑bearing, urgent surgery.
  • Home from the ward — post‑operative.
  • Refer — now — orthopedics urgently (surgical fixation).
  • Refer — clinic — endocrinology if bilateral or atypical.

Fractures — Patterns & Non‑Accidental Red Flags

ASSESSSAFEGUARDING

Know the common breaks — and the fractures that mandate a child‑protection assessment.

▸
◣ Define
  • Common pediatric fracture patterns and — critically — the fractures that trigger a child‑protection assessment. Children's growing bone breaks differently from adults'.
◣ Approach — common accidental patterns
  • Buckle/torus (distal radius, stable) and greenstick fractures, and the toddler's fracture (spiral distal tibia in an ambulant toddler).
  • Physeal (Salter‑Harris) fractures cross the growth plate and risk growth arrest — always classify and follow up.
  • Radiograph the joint above and below; obtain comparison views when needed (standard radiographic practice).
  • Supracondylar humeral fractures need careful neurovascular assessment — document radial pulse, capillary refill, and median (including anterior interosseous), radial, and ulnar nerve function before and after splinting/reduction. A pulseless or poorly perfused hand needs immediate orthopedic consultation.
⚠ Red flags — inflicted injury
  • Escalate to safeguarding when the injury is inconsistent with the stated mechanism or the child's development — especially a long‑bone (femur/tibia) fracture in a non‑ambulatory infant, delayed presentation, multiple fractures of different ages, or rib, metaphyseal 'corner', scapular, or spinous‑process fractures.
  • In children < 2 years with a suspicious fracture, obtain a skeletal survey.
  • Associated bruising, patterned burns, retinal hemorrhage, or other unexplained injuries further raise suspicion of abuse.
◣ Management
  • Immobilize, provide analgesia, and refer to orthopedics for displaced, physeal, or unstable fractures.
  • Where abuse is suspected, follow the mandatory child‑protection pathway — evaluation and reporting are not optional.
◈ Kuwait — reporting is mandatory
  • Under the Child Rights Law No. 21 of 2015, children are protected from all forms of violence, abuse, exploitation, and neglect, and physicians are legally obliged to report suspected child maltreatment.
  • Refer through the Kuwait National Child Protection Program (KNCPP), Ministry of Health, via the national Child Protection Hotline 147.
  • Ensure the child's immediate safety, document findings objectively, and involve the hospital child‑protection team.
✦ Pearl — if they can't walk, be suspicious
A fracture in a child who is not yet walking is highly suspicious for abuse until proven otherwise — do the skeletal survey and involve safeguarding.
✦ Pearl — document the neurovascular exam
Every supracondylar fracture needs documented radial pulse, capillary refill, and median (including anterior interosseous), radial, and ulnar nerve function before and after splinting or reduction. A pulseless hand is an orthopedic emergency, even if it remains pink.

Compartment Syndrome

MINUTESLIMB‑THREATENING

Rising compartment pressure starves muscle and nerve — in children the 3 A's beat the 5 P's; fasciotomy is the fix.

▸
◣ Define
  • Acute compartment syndrome — rising pressure in a fascial compartment cuts perfusion → muscle/nerve ischemia. Limb‑threatening; clinical diagnosis. Most follow fractures (tibia, forearm), tight casts, crush, or reperfusion.
⚠ Red flags — the 3 A's in children
  • The adult '5 Ps' (pain out of proportion, pain on passive stretch, paresthesia, pallor, pulselessness) are unreliable in children.
  • Suspect from the 3 A's — rising Analgesia requirement, Anxiety, and Agitation — in the one series that measured it, a rising analgesic need preceded neurovascular change by more than 7 hours (Bae 2001; Lin & Samora 2020 meta-analysis).,,
  • Tensely swollen compartment = most consistent sign. Pulselessness and paralysis are late.
⚠ Work‑up
  • Clinical diagnosis.
  • Reserve compartment‑pressure measurement for the obtunded or equivocal patient (ΔP < 30 mmHg from diastolic is concerning). Do not delay fasciotomy to obtain pressures.
◣ Management
  • Remove or split all constricting casts and dressings down to skin; keep the limb at heart level (do not elevate).
  • Analgesia, oxygen, correct hypotension. Dense regional/nerve blocks can mask ischemic pain — in high‑risk limb injuries prefer low‑concentration blocks and stay vigilant (breakthrough or escalating pain, rising analgesic needs).
  • Emergency surgical fasciotomy without delay — the definitive treatment.
✦ Pearl — escalating pain = call surgery
A child with a limb injury whose analgesia needs keep climbing has compartment syndrome until proven otherwise — split the cast and call surgery.
◣ Admit · Discharge · Refer
  • Admit — all suspected → emergency.
  • Home from the ward — post‑operative.
  • Refer — now — orthopedic (lower limb) / plastic surgery (upper limb) IMMEDIATELY (fasciotomy); do not delay for pressure measurement in a clear case.

Open Fracture

HOURSANTIBIOTICS EARLY

Skin breach over bone — early IV antibiotics, tetanus cover, saline dressing, and urgent orthopedics.

▸
◣ Define
  • Open (compound) fracture — fracture with an overlying skin breach communicating with bone; high infection risk. Graded Gustilo‑Anderson I–III by wound size, contamination, and soft‑tissue injury.
◣ Approach & work‑up
  • Visible wound/bleeding over the fracture, exposed bone, or gross deformity. Assess neurovascular status distal to the injury.
  • Remove gross contamination, photograph the wound once, then cover with a saline‑soaked sterile dressing; radiograph; check tetanus status.
⚠ Red flags
  • A pulseless, pale, cold limb needs urgent reduction/vascular assessment.
  • Gross contamination, type‑III wounds, and evolving compartment syndrome raise the stakes.
Management
DrugDoseRoute & notes
Antibiotics — timingFirst IV dose as soon as possible (ideally < 1 h, at latest < 3 h)The clock starts at injury, not arrival.
Type I–IICefazolin 30 mg/kg/dose IV (max 2 g) every 8 hFirst‑generation cephalosporin — gram‑positive cover (regimen adult‑derived; pediatric weight‑based dose per formulary).,
Type IIIAdd gentamicin 5–7 mg/kg/dose IV once daily
add benzylpenicillin for farm/soil contamination (anti‑clostridial cover)
Add gram‑negative cover for high‑grade/contaminated wounds (adult‑derived; pediatric dose per formulary).,
Farm / soil contaminationAdd penicillinAnti‑clostridial cover.
◣ Then
  • Tetanus prophylaxis per immunization status; analgesia; realign and splint the limb.
  • Urgent orthopedic referral for formal debridement, irrigation, and stabilization in the operating room.
✦ Pearl — antibiotics on the clock
Give the first cephalosporin within an hour of injury, update tetanus, cover with a saline dressing, call orthopedics — early antibiotics drive the infection rate down.
◣ Admit · Discharge · Refer
  • Admit — all open fractures and significant limb injuries.
  • Home from the ward — not acutely; post‑operative/reduction.
  • Refer — now — orthopedics (early antibiotics, tetanus, debridement); vascular surgery if perfusion is threatened.

Fracture with Pulseless Limb

MINUTESLIMB‑THREATENING

An absent pulse needs urgent assessment; a pale, cool, poorly perfused limb needs emergent restoration of circulation.

▸
◣ Define
  • A fracture with an absent distal pulse may indicate arterial compression, entrapment, or injury.,
◣ Approach
  • Obtain urgent radiographs.
  • Record injury time, pulses, capillary refill, skin temperature and color, and individual peripheral‑nerve function; compare with the opposite limb.
  • Reassess and document after realignment, splinting, reduction, and surgery.
  • Persistent suspected arterial injury requires consultant‑directed vascular imaging, usually CT angiography, coordinated so that emergency revascularization is not delayed.
⚠ Red flags
  • Pallor, coolness, delayed refill, worsening pain, progressive sensory or motor deficit, or deteriorating perfusion → immediate orthopedic and vascular escalation.
  • Increasing pain or swelling also warrants reassessment for compartment syndrome.
◣ Management
  • Pulseless deformed limb (any fracture/dislocation other than a supracondylar humeral fracture): urgently realign with gentle in‑line traction under analgesia, splint, then re‑check and document pulses and perfusion; if still pulseless → immediate orthopedic + vascular escalation (CT angiography must not delay revascularization). Supracondylar humeral fracture: do not manipulate repeatedly in the emergency room — splint in a position of comfort (elbow ~20–40° flexion, never forced flexion) and proceed to emergent reduction and pinning in the operating room.
  • Emergent reduction and pinning in the operating room.
  • Reassess circulation immediately post‑reduction; vascular exploration if the limb remains cold and pulseless.
  • Supracondylar fracture with a pink, warm hand — arrange urgent reduction and fixation. If the hand remains well perfused afterwards, an absent radial pulse alone does not mandate brachial‑artery exploration; the orthopedic consultant documents the decision and arranges close inpatient neurovascular observation.
✦ Pearl — the pink hand is still an emergency
A pink pulseless hand remains an orthopedic emergency; its perfusion after reduction determines the need for immediate vascular exploration.
◣ Admit · Discharge · Refer
  • Admit — all fractures presenting with a pulseless limb.
  • Home from the ward — only after definitive management and consultant confirmation that perfusion is restored.
  • Refer — now — orthopedics immediately; vascular surgery immediately for ischemia or suspected persistent arterial injury.

Joint Dislocation

MINUTESLIMB‑THREATENING

Reduce traumatic dislocations promptly; compromised perfusion or threatened skin needs immediate intervention.

▸
◣ Define
  • Traumatic loss of joint alignment, with or without an associated fracture.
◣ Approach
  • Assess the mechanism, associated injuries, deformity, skin condition, and distal neurovascular function; document findings before and after reduction.
  • Obtain joint radiographs to identify associated fractures — unless imaging would delay treatment of vascular compromise or threatened skin.
  • Obtain post‑reduction imaging and repeat the neurovascular examination.
⚠ Red flags
  • Absent or diminished pulses, impaired perfusion, neurological deficit, an open injury, or threatened skin → immediate orthopedic assessment.
◣ Management
  • Analgesia, then prompt reduction by an orthopedic surgeon under appropriate sedation or anesthesia with monitoring — emergency room or operating room depending on hospital capability.
  • Immobilize after reduction and obtain post‑reduction radiographs.
  • Definitive management depends on the joint, injury pattern, and any associated fracture.
✦ Pearl — the hip clock
A delay in reduction > 6 hours greatly increases the risk of avascular necrosis in traumatic hip dislocation.
◣ Admit · Discharge · Refer
  • Admit — hip or true knee (not patellar) dislocations; open, irreducible, unstable, or neurovascularly compromised injuries; associated fractures needing inpatient treatment.
  • Home from the emergency department — selected uncomplicated injuries after stable reduction, satisfactory imaging, normal neurovascular findings, and arranged follow‑up; advise return for increasing pain, swelling, or numbness.
  • Refer — now — orthopedics immediately; vascular surgery immediately for ischemia or suspected persistent arterial injury.

Unstable Pelvic Injury

MINUTESLIFE‑THREATENING

Treat a suspected unstable pelvic injury as major trauma — stabilization and hemorrhage control begin before radiological confirmation.

▸
◣ Define
  • A pelvic‑ring injury with mechanical instability, usually anterior and posterior ring disruption. Mechanical and hemodynamic instability are distinct: a child may initially maintain circulation despite an unstable fracture.
◣ Approach
  • Pediatric trauma primary survey (see Major Trauma — Primary Survey).
  • Look for pelvic pain, deformity, limb‑length asymmetry, and shock.
  • Avoid pelvic springing and repeated stability testing; minimize unnecessary movement.
  • Apply a pelvic binder as soon as possible; arrange targeted CT once sufficiently stable, with the trauma team — imaging must not delay stabilization or hemorrhage control.
⚠ Red flags
  • Persistent tachycardia, poor perfusion, hypotension, altered consciousness, or deterioration despite resuscitation → major hemorrhage.
  • Open injury, blood at the urethral meatus, or lower‑limb neurological abnormality → immediate specialist assessment.
◣ Management
  • Activate the pediatric trauma and major‑hemorrhage pathways; resuscitate while arranging urgent orthopedic, pediatric‑surgical, anesthetic, and intensive‑care support.
  • A sheet applied over the greater trochanters serves as a pelvic binder when an unstable pelvic fracture is suspected — do not delay application for imaging.
  • Ongoing hemodynamic instability despite resuscitation and binding needs immediate hemorrhage control — operative intervention or angioembolization; orthopedics determines temporary and definitive pelvic stabilization.
  • Seek urological or pediatric‑surgical advice before urethral catheterization if urethral injury is suspected.
  • Open injuries require antibiotics and tetanus assessment.
✦ Pearls
  • An apparently reduced pelvis on imaging obtained with a binder on does not establish fracture stability.
  • A negative FAST (Focused Assessment with Sonography for Trauma) examination does not exclude pelvic bleeding.
◣ Admit · Discharge · Refer
  • Admit — all suspected or confirmed unstable pelvic injuries; may need intensive care.
  • Home from the ward — only after definitive stabilization, mobility, and a follow‑up plan.
  • Refer — now — triage to a pediatric‑capable major trauma service; coordinate transfer and hemorrhage control with orthopedics and pediatric surgery.

Spine Fracture with Neurological Deficit

MINUTES

Protect spinal alignment, support oxygenation and circulation, and obtain immediate spinal‑surgical advice.

▸
◣ Define
  • Traumatic cervical, thoracic, or lumbar fracture or dislocation with new motor, sensory, or sphincter dysfunction suggesting spinal cord, conus medullaris, or cauda equina injury. The same emergency pathway applies when neurological findings occur without a visible fracture (SCIWORA — spinal cord injury without radiographic abnormality).
◣ Approach
  • Pediatric trauma primary survey with strict cervical‑spine immobilization and log‑roll precautions (see Major Trauma — Primary Survey).
  • Document the time and evolution of weakness, sensory loss, and bladder or bowel symptoms; repeat the neurological assessment after transfers and any deterioration.
  • Urgent radiographs and/or CT for injury characterization; urgent MRI for suspected cord or ligamentous injury.
  • Do not delay referral to pediatric orthopedic spine or neurosurgery in order to complete imaging.
⚠ Red flags
  • Progressive weakness, a sensory level, saddle sensory loss, new urinary retention or incontinence, or respiratory compromise → immediate escalation.
  • Hypotension with bradycardia may be neurogenic shock — but hemorrhage must also be excluded.
◣ Management
  • Maintain age‑appropriate spine immobilization and minimize unnecessary movement.
  • Analgesia and monitored resuscitation; correct hypoxemia and hypotension promptly.
  • Involve intensive care early for mean arterial pressure support — in older children a lower limit of 75–80 mmHg and upper limit of 90–95 mmHg, maintained for 3–7 days according to injury severity and neurological recovery; there is no established MAP target for young children.
  • The spine surgeon urgently determines the role of surgical decompression and stabilization, aiming for intervention within 24 hours of injury when clinically feasible to optimize neurological recovery (adult‑derived: STASCIS enrolled ages 16–80).
  • Do not give high‑dose methylprednisolone routinely for traumatic spinal cord injury; adult AOSpine guidance offers a 24‑h infusion only as an option when started within 8 h of injury (not after 8 h, and never a 48‑h infusion) — a specialist decision.
◣ Admit · Discharge · Refer
  • Admit — all; PICU for cord injury, neurogenic shock, or respiratory compromise.
  • Home from the ward — not acutely.
  • Refer — now — pediatric orthopedic spine or neurosurgery immediately; pediatric‑capable major trauma service.
13

Pediatric Trauma & TBI

Primary survey & resuscitation · secondary survey & decisions · traumatic brain injury

Trauma Team & Roles

MINUTES

Know who leads before the patient arrives — role confusion costs the golden hour.

▸
◣ Who leads — set locally
  • Trauma team leader (TTL) — identified by each hospital's own trauma pathway; the designation differs between hospitals and this guide does not prescribe it. Whoever leads runs the primary survey and resuscitation and keeps the overview; the airway is managed by the most skilled airway operator present.
  • Pediatric surgery (where available; otherwise general surgery) — the surgical survey, hemorrhage source control, and performance of any operation. The decision to operate, to image first, or to transfer is a team decision, based on shared situational awareness of the child's physiology and trajectory — not a single‑specialty call.,
  • No trauma team on site (private hospital, peripheral facility): stabilize with the primary survey (cABCDE), control hemorrhage, secure oxygenation and access, keep the child warm, and transfer to the nearest trauma‑capable center while resuscitating — call the receiving team early. Do not delay transfer for imaging or specialist review that cannot change management locally.,
⚠ Agree the pathway in advance
Confirm the trauma call, role allocation, and transfer route locally before the patient arrives — front‑door role confusion costs time in the golden hour.

Major Trauma — Primary Survey & Resuscitation

MINUTES

Stop the bleeding, protect the brain, keep them warm — and read the physiology, because children compensate then crash.

▸
◢ How children differ — anticipate it
  • Large head, thin scalp: head injury is common; scalp‑wound blood loss can be significant in a small child.
  • Compliant chest wall: serious lung injury (pulmonary contusion) occurs without rib fractures — a normal‑looking chest wall does not exclude it.
  • Less‑protected solid organs: liver and spleen injure easily in blunt abdominal trauma.
  • Great reserve, then sudden collapse: children hold blood pressure by tachycardia and vasoconstriction, so hypotension is a late, pre‑terminal sign — act on tachycardia, cool peripheries, and prolonged capillary refill long before the BP falls.
  • High surface‑area‑to‑mass: they cool fast — hypothermia drives coagulopathy. In traumatic arrest treat the reversible causes at once: hemorrhage, tension pneumothorax and pericardial tamponade.
<C> Catastrophic hemorrhage Control visible bleeding first: direct pressure, wound packing, a limb tourniquet (record the exact time applied) for uncontrolled extremity bleeding, and a pelvic binder for a suspected pelvic fracture.
A — Airway + C‑spine
  • Manual in‑line stabilization; open (using a jaw‑thrust maneuver) and clear the airway.
  • Anticipate a difficult airway (large occiput flexes the neck; large tongue). In younger children — especially < 2 yr — a shoulder roll helps: maintain C‑spine precautions and avoid over‑extension or flexion.
  • Secure the airway if GCS ≤ 8 or it is not protected.
B — Breathing
  • Oxygen 10–15 L/min via non‑rebreather mask. Tension pneumothorax is a clinical diagnosis — treat before imaging. Needle decompression at the 5th intercostal space, mid‑axillary line, or the 2nd intercostal space (over the top of the 3rd rib), mid‑clavicular line. Then finger thoracostomy/chest drain — see Pneumothorax.
  • Seal an open pneumothorax; suspect massive hemothorax and pulmonary contusion.
C — Circulation
  • Two large‑bore IV lines; go early to intraosseous if access fails.
  • Find the bleeding — chest, abdomen, pelvis, long bones, and the floor. Resuscitate with blood, not repeated crystalloid; give tranexamic acid as early as possible, within 3 h of injury — do not start it more than 3 h after injury., Activate the massive transfusion protocol when required.
D — Disability GCS or AVPU (alert / voice / pain / unresponsive), pupils, and a glucose (do not miss hypoglycemia). Manage raised ICP with urgent neurosurgery consult — see the Traumatic Brain Injury card.
E — Exposure / Environment Fully undress to examine and log‑roll, then cover and actively warm — every degree of cooling worsens clotting.
Resuscitation — blood, not crystalloid
Drug / productDoseNotes
Packed red cells10 mL/kg boluses, reassess after each,First‑line for hemorrhagic shock; balanced 1:1:1 (RBC:plasma:platelets) in massive hemorrhage; activate the hospital massive transfusion protocol (pre‑agreed with the blood bank); 1:1:1 ratio evidence is adult‑derived (PROPPR)
Crystalloid (warmed)≤ one 20 mL/kg bolus, only if blood not yet availableEach further crystalloid bolus → more coagulopathy, ventilator and ICU days
Tranexamic acid (TXA)15 mg/kg (max 1 g) IV over 10 min, then 2 mg/kg/h for at least 8 h or until bleeding stops (not above the adult rate of 125 mg/h)
≥ 12 years / adult‑sized: 1 g over 10 min, then 1 g over 8 h
Within 3 h of injury; weight‑based pediatric regimen per BSH 2016; ≥ 12 y adult regimen per RCPCH 2012; CRASH‑2 was an adult trial; pediatric evidence is observational (PED‑TRAX)
◈ Resuscitation reasoning
  • Estimated blood volume ~70–80 mL/kg in a child (up to ~90 mL/kg in a term infant), so small losses matter.
  • Move early to blood products and minimize crystalloid. During active hemorrhage, transfuse according to hemorrhagic‑shock and hemostatic‑resuscitation needs — not to a fixed hemoglobin target. Once bleeding is controlled and the child is hemodynamically stable, use a restrictive red‑cell strategy, generally around Hb 7 g/dL; with acute brain injury (TBI) a higher threshold may be appropriate — TAXI: consider transfusion at Hb 7–10 g/dL., Target a systolic BP no less than 70 + 2 × age (yr) mmHg (1–10 yr band; use the age‑specific systolic thresholds in the Shock card for other ages). Address ongoing losses. Avoid hypotension.,
⚠ The lethal triad — and reassess
  • Hypothermia, acidosis, and coagulopathy feed each other: keep the child warm, give blood early, correct coagulopathy.
  • If the patient deteriorates at any point, go back to A and work through again.,

Major Trauma — Secondary Survey & Decisions

MINUTES

Once the primary survey is controlled — find the injuries and make the calls.

▸
◢ Secondary survey — head‑to‑toe + AMPLE history (allergies, medications, past history, last meal, events)
  • Start only after <C>ABCDE is controlled and resuscitation underway. Examine front and back (log‑roll): scalp and face, neck, chest, abdomen, pelvis and perineum, back, limbs, and a focused neurological exam.
  • AMPLE history: Allergies, Medications, Past history, Last meal, Events/mechanism. Mechanism predicts the injuries — ask for it explicitly.
Abdomen — does this child need a CT?
PECARN (Pediatric Emergency Care Applied Research Network) intra‑abdominal injury rule — 7 features:
abdominal wall trauma / seatbelt sign
GCS < 14 (i.e. 13 or less)
abdominal tenderness
chest‑wall trauma
abdominal pain
decreased breath sounds
vomiting.
NONE present
Very low risk for injury needing intervention — CT can usually be safely avoided; observe with serial examination.
ANY present / unstable
ANY present → not very‑low‑risk; CT is not automatic. Decide with the surgical team by the number and type of predictors (strongest first: abdominal‑wall trauma/seat‑belt sign, GCS < 14, abdominal tenderness): CT if hemodynamically stable and the risk is appreciable; a stable child with an isolated lower‑risk predictor (e.g. vomiting or abdominal pain alone) can usually be observed with serial examination ± laboratory tests/ultrasound. Unstable → resuscitate and urgent surgical decision, not CT. A negative FAST does not exclude intra‑abdominal injury in children (FAST = Focused Assessment with Sonography for Trauma — bedside ultrasound for free fluid in the abdomen and pericardium).
Chest CXR for hemo/pneumothorax and pulmonary contusion; place a chest drain for a hemothorax or significant pneumothorax. (Tension pneumothorax is already decompressed in the primary survey.)
Pelvis Confirm the binder is correctly positioned and image (pelvic X‑ray ± CT); do not distract or repeatedly spring the pelvis — it can increase bleeding. (The binder is applied in the primary survey.)
C‑spine
  • PECARN C‑spine rule (blunt trauma, < 18 y) — 3 tiers:
    CT if ANY high‑risk factor — GCS 3–8 or unresponsive (AVPU = U); abnormal airway, breathing or circulation; focal neurological deficit (paresthesia, numbness or weakness).
    Plain radiographs if none of these but ANY of — neck pain; altered mental status (GCS 9–14, AVPU = V or P, or other signs); substantial head injury; substantial torso injury; posterior midline neck tenderness (“substantial” = needing inpatient observation or surgery).
    None of the nine → clinical clearance without imaging (NPV 99.9%). Derived and validated in pediatric trauma centers; not yet validated in community EDs.
  • SCIWORA (spinal cord injury without radiographic abnormality) is commoner in children — a normal X‑ray does not exclude cord injury; keep the spine immobilized and call neurosurgery/spine urgently if there is any neurological deficit (weakness, sensory change, or bladder/bowel dysfunction), even with normal imaging.
Limbs & analgesia Splint long‑bone fractures and check distal pulses. Give timely analgesia (intranasal or IV opioid) — pain is routinely undertreated in injured children.,
⚠ Always consider inflicted injury
  • Be alert when the history is inconsistent with the injury or the child’s development, presentation is delayed, or the pattern is suspicious (bruising or fracture in a non‑mobile infant, torn frenulum, multiple injuries of different ages).
  • Document carefully and escalate through local safeguarding.
◦ Escalate & transfer early
  • With no in‑house pediatric surgery, involve the trauma team, anesthesia, intensive care and the receiving trauma center early — do not wait for the patient to deteriorate.,
  • Package for transfer: airway secured, hemorrhage controlled, the child warm, and blood en route.
  • Do not delay transfer for a CT that will not change what you do before the child leaves.,

Traumatic Brain Injury

MINUTES

Decide who needs a CT; in severe injury, stop the second insult.

▸
◢ Imaging decision — PECARN
  • Use the PECARN rule to select children for CT after blunt head trauma and safely avoid imaging in the very‑low‑risk group. It is age‑stratified — use the correct age column below. PECARN was not derived or validated for suspected abusive (inflicted) head trauma — keep a low threshold to image regardless of the rule when abuse is suspected.
PECARN head‑CT — by age group
Risk tier< 2 years≥ 2 years
CT recommended
(high risk)
Any of: GCS ≤ 14, altered mental status / agitation / slow response, or a palpable skull fracture.Any of: GCS ≤ 14, altered mental status, or signs of a basilar skull fracture.
CT vs observe
(intermediate)
Any of: occipital / parietal / temporal scalp hematoma, LOC (loss of consciousness) ≥ 5 s, severe mechanism, or not acting normally per the parent — shared decision‑making + observation.Any of: LOC, vomiting, severe mechanism, or severe headache — shared decision‑making + observation.
No CT
(low risk)
None of the above.None of the above.
◈ Decision tools
  • PECARN pediatric head‑CT rule — mdcalc.comQR.
  • Severe‑TBI management — Brain Trauma Foundation pediatric guideline, 3rd ed — doi.orgQR.
Severe TBI (GCS ≤ 8)
  • Secure the airway.
  • Keep SpO₂ ≥ 94% and normocapnia (PaCO₂ 35–40 mmHg).
  • Avoid hypotension — target SBP no less than 70 + 2 × age mmHg (1–10 yr band; age‑specific thresholds otherwise; PALS hypotension definition)., Higher blood‑pressure targets may be beneficial in isolated severe TBI, but the threshold, and whether to target SBP or MAP, are not established — set targets with neurosurgery and the receiving intensive care unit (PICU or ICU, per hospital policy).
  • Head midline, elevate the head of the bed 30°; treat pain, agitation, glucose, and temperature.
Impending herniation — bridge to definitive care
  • Recognize: new pupil asymmetry or a fixed dilated pupil, Cushing response (bradycardia + hypertension + irregular breathing), extensor posturing, or a falling GCS.
  • Bridge: head up 30° and midline; secure oxygenation and normocapnia; avoid hypotension; give one hyperosmolar bolus (3% saline 2–5 mL/kg, or mannitol 0.5–1 g/kg if not hypovolemic); brief hyperventilation only for signs of herniation, as a temporizing measure.
  • Hand over for urgent CT and neurosurgical review; ongoing intracranial‑pressure and perfusion management is intensive‑care therapy (PICU or ICU, per hospital policy) and is beyond the scope of this guide.
AgentDoseNotes
Hypertonic saline 3%2–5 mL/kg IV over 10–20 min (impending herniation)First‑line hyperosmolar bridge; infusion regimens are intensive‑care therapy
Mannitol0.5–1 g/kg over 10–15 minAlternative; caution if hypovolemic or hypotensive — formulary dosing (the Brain Trauma Foundation guideline gives no evidence‑based mannitol dose)
Levetiracetam20–55 mg/kg IV (max 4.5 g), then 10 mg/kg BID (local formulary dosing — not guideline‑stated)Prophylaxis to reduce early post‑traumatic seizures in severe TBI — a short course (~7 days); phenytoin / fosphenytoin an alternative
⚠ Prevent the second insult
  • Hypoxia and hypotension each independently worsen outcome — avoid both.
  • Do not routinely hyperventilate (vasoconstriction lowers cerebral blood flow).
  • Avoid hyperthermia and treat seizures promptly.
◣ Admit · Discharge · Refer
  • Admit — all moderate/severe TBI and any abnormal CT to intensive care (PICU or ICU, according to each hospital's internal policy) with neurosurgical review. Until the child leaves the department, care is led by the consultant responsible at the patient's location — in the emergency department, the trauma team leader.
  • Home from the emergency department — minor head injury meeting a validated low‑risk rule, observed, with head‑injury advice.
  • Refer — now — neurosurgery for surgical lesions or deterioration; safeguarding if abuse is suspected.

Child Protection & Safeguarding

ASSESSAAP · ACR 2025

The injury that doesn’t fit the history — recognizing it once may prevent a fatal second event.

▸
◣ Recognize (red‑flag patterns)
  • Any bruise in a not‑yet‑mobile infant is a sentinel injury until proven otherwise. Use TEN‑4‑FACESp (children < 4 years): bruising of the Torso, Ear or Neck; ANY bruise in an infant 4 months or younger (up to 4.99 months); bruising of the Frenulum, Angle of jaw, Cheek (fleshy) or Eyelid, or Subconjunctival hemorrhage; or patterned bruising.
  • History that is absent, inconsistent, or doesn’t match the developmental stage or the injury; delayed presentation; injuries of different ages.
⚠ Abusive head trauma
  • An infant with unexplained irritability, vomiting, apnea, seizures or reduced consciousness may have abusive head trauma. Typical findings include subdural hemorrhage, complex retinal hemorrhages, encephalopathy and other intracranial or spinal injury, often with rib and other fractures — but no single finding or “triad” makes or excludes the diagnosis, which is reached by multidisciplinary evaluation of the history, examination, imaging and laboratory results.,
  • Image the brain and arrange a dilated fundoscopy; it is easily mistaken for sepsis or a feeding problem.,
✦ Examine, document, escalate
  • Fully undress and examine; document injuries factually with sizes and a body map (photograph per policy).
  • In children < 2 years with suspected physical abuse, arrange a skeletal survey and consider coagulation studies to exclude mimics.
  • Care for the child first; you do not need to be certain to refer.
◈ Local & legal Follow Kuwait MOH child‑protection procedures — involve the hospital child‑protection team/social work and make the mandatory report; ensure the child is in a safe place and that siblings are considered.
◣ Workup
  • Skeletal survey — all children < 24 months; 2–5 years selectively (radiographs of areas of concern; full survey if multiple or occult injuries are suspected); not useful > 5 years. Repeat limited survey at ~2 weeks when the first is negative or equivocal — it reveals healing rib and metaphyseal fractures.,
  • Neuroimaging — immediate non‑contrast head CT for any neurological symptom or sign, scalp swelling, or a low hemoglobin (the strongest predictors of an abnormal CT: head swelling OR 46.7, neurological impairment OR 20.6, low hemoglobin OR 11.8). Neurologically normal: CT head is still usually appropriate < 24 months — occult head injury (skull fracture and/or intracranial injury) is found in up to 37% of high‑risk children < 2 years (rib or multiple fractures, facial injury, age < 6 months).,, Where rapid non‑sedated MRI is available and expertly reported, MRI may replace CT as first‑line in a stable infant whose injuries are unrelated to the head. MRI brain ± whole spine at day 2–5 whenever CT shows hemorrhage, parenchymal injury or skull fracture, or neurology persists.,
  • Dilated indirect ophthalmoscopy by ophthalmology — within 24 h, no later than 72 h (hemorrhages fade): for intracranial hemorrhage or injury on imaging, unexplained coma, seizures or altered consciousness in a child < 5 years, visible eye injury, or coagulopathy. Not a screening test in the neurologically normal infant — image the brain first.
  • Bleeding‑disorder evaluation when bruising or intracranial hemorrhage is what raises the concern. Bruising: PT, aPTT, CBC with platelets, von Willebrand antigen and activity, factor VIII and IX activity. Intracranial hemorrhage: PT, aPTT, CBC with platelets; add factor VIII and IX activity if there is a history of trauma, and d‑dimer and fibrinogen if there is neurologic compromise. Any abnormal result → pediatric hematology. Unnecessary when injuries are patterned (hand marks; ear, neck or genital bruising) or clearly non‑hemorrhagic (fractures, burns). After transfusion, delay testing until transfused products have cleared; viscoelastic tests (TEG/ROTEM) are not acceptable for this purpose.
  • Occult abdominal injury — screen every child < 5 years: AST, ALT, lipase, urinalysis. Contrast‑enhanced abdominal CT if AST or ALT > 80 IU/L or abdominal bruising, tenderness or distension — a quarter of injuries with raised transaminases have no abdominal signs.,
◣ Admit · Refer
  • Admit — for safety and investigation whenever abuse is a realistic concern.
  • Refer — now — child‑protection team, social work, and safeguarding lead; police per local law.

Massive Transfusion & Blood Products

MINUTESEur. trauma guideline 2023

Balanced‑ratio resuscitation with the per‑kg doses — and the two silent killers, ionized hypocalcemia and the cold, acidotic child.

▸
◣ Activate early — on clinical grounds
  • Activate on clinical grounds — uncontrolled hemorrhage with shock/instability, an elevated SIPA, or ongoing bleeding despite initial red cells; do not wait for a volume threshold.
  • Definitions (recognition/audit): blood loss of 40 mL/kg in 3 h or 2–3 mL/kg/min, or 80 mL/kg (≈ 1 blood volume) in 24 h; ≥ 40 mL/kg of all blood products in 24 h (Neff 2015).
  • Uncontrolled hemorrhage with instability, a high pediatric age‑adjusted shock index (SIPA)pediatric age‑adjusted shock index (SIPA), or clinical judgment — activate the protocol early, not late.
Component (aim 1:1:1)DoseNotes
Packed red cells20 mL/kg (max 4 adult units)BSH major‑hemorrhage aliquot. Emergency (blood group unknown): group O red cells — RhD‑negative for girls — and group AB plasma, until type‑specific and crossmatched products are ready
Fresh frozen plasma20 mL/kg (max 4 adult units)Give in a 1:1:1 ratio with red cells & platelets (pediatric consensus; adult RCT evidence),; BSH major‑hemorrhage aliquot (ATLS gives 10–20 mL/kg)
Platelets15–20 mL/kg (max 1 adult therapeutic dose)BSH major‑hemorrhage aliquot (ATLS gives 10–20 mL/kg)
Cryo­precipitate10 mL/kg (max 2 pools)BSH major‑hemorrhage aliquot. For fibrinogen < 1.5 g/L (or give fibrinogen concentrate),
⚠ The two silent killers
Ionized hypocalcemia — citrate in stored products chelates calcium, worsening coagulopathy and cardiac contractility; keep ionized Ca ≥ ~1.1 mmol/L and recheck it with every blood gas during transfusion., The lethal triad — hypothermia + acidosis + coagulopathy: warm every product and the child, correct acidosis, and treat coagulopathy early.
AdjunctDoseNotes
Tranexamic acid (TXA)15 mg/kg (max 1 g) IV over 10 min, then 2 mg/kg/h for at least 8 h or until bleeding stops (not above the adult rate of 125 mg/h)
≥ 12 years / adult‑sized: 1 g over 10 min, then 1 g over 8 h
Give as early as possible, within 3 h of injury — do not start it more than 3 h after injury (treatment started after 3 h increased death from bleeding in CRASH‑2),,; consider in TBI with GCS ≤ 12 or intracranial bleeding on CT (adult trial, CRASH‑3)
Calcium gluconate50–100 mg/kg IV (max 2–3 g) — local practice
US label initial bolus: 29–60 mg/kg (> 1 mo to < 17 yr); 100–200 mg/kg (neonate); 1–2 g (≥ 17 yr)
Slow IV via a secure IV line; extravasation can cause calcinosis cutis and tissue necrosis
◣ Targets
  • Fibrinogen > 1.5 g/L,, · platelets > 75 ×10⁹/L during major hemorrhage (BSH pediatric) — > 100 ×10⁹/L with TBI (adult European guideline) · PT ratio < 1.5.,
✦ Don’t drop the pressure
  • In children, and especially with TBI or threatened perfusion, maintain age‑appropriate blood pressure throughout resuscitation — target SBP no less than 70 + 2 × age (yr) mmHg, address ongoing losses, avoid hypotension.,
  • Use viscoelastic testing (TEG — thromboelastography / ROTEM — rotational thromboelastometry; bedside whole‑blood clotting tests) to guide which component to give, where available,, and watch for hyperkalemia with large‑volume or irradiated red cells.
◣ Workup — send at activation, repeat every 30–60 min
  • CBC (hemoglobin, platelets), fibrinogen, PT/INR ± aPTT, ionized calcium, blood gas with lactate / base deficit, type & crossmatch; point‑of‑care viscoelastic coagulation testing (thromboelastography, TEG/ROTEM) if available; monitor temperature and potassium.
◈ Local & evidence
  • Activate your hospital massive‑hemorrhage protocol and follow its ratios and dosing.,,
  • Pediatric ratios and thresholds are largely extrapolated from adult RCTs (PROPPR, CRASH‑2/CRASH‑3); the pediatric TXA signal (PED‑TRAX) is observational.,,,
  • Verify every dose against local protocol.
14

Renal & Urology

AKI · HUS · hypertensive emergency · acute scrotum · foreskin emergencies · priapism · hematuria

Acute Kidney Injury

HOURS

Abrupt fall in kidney function — rising creatinine and/or falling urine output.

▸
◣ Recognize & define
  • Suspect in any child with oliguria/anuria, rising creatinine, edema or fluid overload, or unexplained electrolyte disturbance.
  • KDIGO (Kidney Disease: Improving Global Outcomes) stages AKI 1–3 — Stage 1 is the threshold that diagnoses AKI (see the table below).
KDIGO staging — grade by the worse of creatinine or urine output
StageSerum creatinineUrine output
11.5–1.9× baseline (within the prior 7 days), or a rise ≥ 26.5 µmol/L (≥ 0.3 mg/dL) within 48 h< 0.5 mL/kg/h for 6–12 h
22.0–2.9× baseline< 0.5 mL/kg/h for ≥ 12 h
3≥ 3.0× baseline, or ≥ 353.6 µmol/L (≥ 4.0 mg/dL), or dialysis started, or — if age < 18 y — eGFR < 35 mL/min/1.73 m²< 0.3 mL/kg/h for ≥ 24 h, or anuria ≥ 12 h
Find the category — it drives treatment
PRE‑RENAL · impaired perfusion (commonest)
Hypovolemia, shock, sepsis — poor perfusion. → Restore perfusion: if volume loss, give fluid; if another cause, treat that cause. Reversible if treated early.
RENAL · intrinsic
HUS (see Hemolytic Uremic Syndrome), glomerulonephritis, acute tubular necrosis, nephrotoxins. → Supportive care; treat the cause.
POST‑RENAL · obstruction
Posterior urethral valves, stones, neurogenic bladder. → Insert a urinary catheter first, then image. After relief, watch for post‑obstructive diuresis (urine > 3.5–5 mL/kg/h — local practice threshold, not guideline‑stated) — replace fluid/electrolytes with nephrology.
⚑ Manage — volume status drives fluid therapy
Assess volume status first, then treat by category:
  • Hypovolemic / intravascularly deplete (cool peripheries, tachycardia, prolonged capillary refill, low BP, weight loss) — resuscitate with isotonic crystalloid.
  • Euvolemic (well‑perfused, no edema, no fluid‑overload signs) — match intake to insensible losses (300–400 mL/m² per 24 h) plus measured urine output; do not apply routine 4‑2‑1 (Holliday–Segar) maintenance during established AKI (expert consensus — not guideline‑stated).
  • Hypervolemic / overloaded (edema, hypertension, raised JVP, pulmonary crackles or a gallop, weight gain) — restrict fluids; diuretics do not aid recovery but may be used for established hypervolemia.
Stop nephrotoxins (NSAIDs, aminoglycosides, contrast) and adjust drug doses. Watch potassium, sodium, acid–base; avoid potassium in maintenance fluids unless treating hypokalemia. Involve nephrology for KDIGO stage 2–3 or worsening AKI; arrange structured follow‑up (stage 2–3, AKI ≥ 7 days, incomplete recovery, pre‑existing CKD, or recurrent AKI).
⚑ When to call nephrology / PICU for dialysis — the "AEIOU" triggers

Refer urgently for dialysis / CRRT when any of these will not correct with medical treatment:

  • A — Acidosis: severe metabolic acidosis (pH < 7.1) despite bicarbonate / ventilation.
  • E — Electrolytes: hyperkalemia that keeps rising or recurs despite full medical therapy.
  • I — Intoxication: a dialyzable poison / drug (salicylate, methanol, ethylene glycol, lithium, theophylline).
  • O — Overload: fluid overload / pulmonary edema — or severe hypertension driven by volume overload — not responding to fluid restriction + diuretics (especially if it limits feeding or ventilation).
  • U — Uremia: symptomatic — encephalo­pathy, pericarditis, or bleeding.

The clinical picture — not the creatinine or urea number — decides. Recognize early and call; the specialist chooses the modality (hemodialysis, CRRT, or peritoneal dialysis).

⚠ Cross‑reference
Treat life‑threatening hyperkalemia immediately — see Acute Electrolyte Emergencies (Endocrine & Metabolic).
◣ Admit · Discharge · Refer
  • Admit — all but mild pre‑renal AKI; oliguria, hyperkalemia, fluid overload, or acidosis → high‑dependency.
  • Home — resolving pre‑renal AKI with normalizing function and follow‑up.
  • Refer — now — nephrology for KDIGO stage 2–3, no clear cause, or need for dialysis.

Hemolytic Uremic Syndrome

HOURS

Triad: microangiopathic hemolytic anemia + thrombocytopenia + acute kidney injury.

▸
◣ Recognize
  • Typical (STEC): preceded by bloody diarrhea; pallor, reduced urine, edema, petechiae, irritability.
  • Blood film: fragmented red cells (schistocytes), low platelets, negative direct antiglobulin test, high lactate dehydrogenase.
  • Atypical (non‑diarrheal) HUS: STEC‑negative; any age. Primary — inherited or antibody‑mediated complement dysregulation (low C3, family history, relapsing course). Secondary — invasive S. pneumoniae (pneumonia/empyema, meningitis, bacteremia; direct antiglobulin test positive; avoid plasma‑containing products — use washed red cells and platelets; treat the infection), HIV, drugs (chemotherapy, calcineurin inhibitors, ionizing radiation), systemic disease (lupus, antiphospholipid syndrome, scleroderma), and cobalamin C defect (methylmalonic aciduria with homocystinuria — check homocysteine and methylmalonic acid in infants). The underlying condition is usually already known; this guide details the complement‑mediated form.
◣ Workup
  • CBC + film, U&E/creatinine, LDH, haptoglobin, direct Coombs (negative).
  • Send C3, C4, CH50 and ADAMTS13 (ADAMTS13 = the von Willebrand factor–cleaving enzyme; severely low confirms TTP (thrombotic thrombocytopenic purpura), normal points to HUS) before any plasma therapy or eculizumab. If available, also send anti–factor‑H antibodies and complement‑gene screening (CFH, CD46/MCP, CFI, C3, CFB, THBD and DGKE) to confirm complement dysregulation, guide prognosis and estimate recurrence risk, including after transplantation — results take weeks and must not delay treatment. Not currently available in Kuwait: store samples and send out.,
  • Stool culture for E. coli O157 and Shiga‑toxin PCR/antigen when diarrhea is present.
Supportive care is the mainstay
  • Careful fluid and electrolyte management — in suspected STEC‑HUS, early isotonic volume expansion before oligo‑anuria may reduce kidney injury; once oliguric or fluid‑overloaded, restrict fluids and involve nephrology.
  • Manage the acute kidney injury (see Acute Kidney Injury); transfuse packed red cells for symptomatic anemia or Hb < 6–7 g/dL (platelets only for active bleeding or a procedure); dialysis as needed — dialysis does not change STEC‑HUS prognosis.
  • Monitor closely through the 5–14‑day peak period: daily CBC, creatinine, electrolytes and LDH, plus urine output, blood pressure and weight.
Typical (STEC) or atypical (complement‑mediated)?
TYPICAL · STEC
Supportive care only. Benefit of eculizumab in STEC‑HUS is unproven — not routine. The only placebo‑controlled RCT (100 children) showed no improvement in the acute course, dialysis or extrarenal disease; use, if any, is a nephrology decision in severe neurological involvement.,
ATYPICAL · aHUS
Complement inhibition (eculizumab/ravulizumab) — nephrology directed. Meningococcal risk is > 1,000‑fold and vaccination alone does not prevent it: give MenACWY + MenB ≥ 2 weeks before the first dose; if treatment cannot wait, vaccinate and start antibiotic prophylaxis (e.g., penicillin V) for the duration of therapy. Boosters: MenACWY every 5 years (if the primary series was given before age 7, the first booster at 3 years, then every 5 years); MenB 1 year after the series, then every 2–3 years while on treatment. Any fever = emergency blood cultures and IV ceftriaxone — 14 of 16 US cases occurred in vaccinated patients, most from non‑groupable strains.,
⚠ Avoid
  • Antibiotics in STEC (may increase toxin release — generally avoided), antimotility agents (loperamide), and NSAIDs.
  • Do not transfuse platelets unless active bleeding or a procedure is planned.
◣ Admit · Discharge · Refer
  • Admit — all → monitoring and supportive care; anuria/severe → high‑dependency. PICU for neurologic symptoms or hemodynamic instability; involve nephrology early for atypical HUS.
  • Home from the ward — not acutely; after hematologic and renal recovery.
  • Refer — now — nephrology (dialysis); atypical HUS → a nephrology specialist for complement inhibition / eculizumab.

Hypertensive Emergency

MINUTES

Severe hypertension with new or progressing end‑organ damage (encephalo­pathy, seizures, facial palsy, severe headache; heart failure or chest pain; acute kidney injury; retinopathy or blurred vision).

▸
◣ Assess for end‑organ damage
  • Brain: headache, vomiting, altered mental status, seizures, visual symptoms, focal deficits.
  • Heart: tachycardia, gallop, pulmonary edema, heart failure, chest pain (older children).
  • Kidney: AKI, oliguria, hematuria, proteinuria.
  • Eyes: blurred vision, retinal hemorrhages, papilledema.
◣ Workup
  • CBC, electrolytes, urea, creatinine.
  • Urinalysis ± urine protein.
  • ECG.
  • Chest radiograph if heart failure suspected.
  • Echocardiography if LV dysfunction suspected.
  • Fundoscopy if available.
  • Renal ultrasound ± Doppler when a renal cause is suspected.
  • CT/MRI brain only if neurological symptoms or concern for intracranial pathology.
✦ Pearl
In children, severe hypertension is secondary until proven otherwise — renal disease is the commonest cause.
Lower gradually — controlled descent
  • A true hypertensive emergency needs PICU/high‑dependency monitoring with a titratable IV infusion under specialist guidance.
  • Reduce blood pressure by no more than 25% of the planned reduction (presenting BP minus target, ≈ 95th percentile) in the first 8 hours, then the remainder gradually over the next 12–24 hours (AAP 2017).
  • Abrupt drops risk cerebral, renal, and retinal ischemia.
Treat complications Seizures → benzodiazepine. Fluid overload (e.g., acute glomerulonephritis) → furosemide. Monitor in PICU.
Medications — titratable IV agents preferred
DrugDoseRoute & notes
Labetalolbolus 0.2–1 mg/kg (max 40 mg); infusion 0.25–3 mg/kg/hIV; preferred first‑line (best option) in Kuwait; avoid in asthma, heart failure
Hydralazine0.1–0.2 mg/kg/dose, up to 0.4 mg/kg/dose (usual adult max 20 mg)IV/IM every 4 h; second‑line; may cause reflex tachycardia
Sodium nitroprussidestart 0–3 mcg/kg/min; max 10 mcg/kg/minIV; reserve — cyanide risk with prolonged use/renal impairment
Esmolol100–500 mcg/kg/min infusionIV; short‑acting, constant infusion preferred; may cause profound bradycardia or bronchospasm
Nicardipinebolus 30 mcg/kg (max 2 mg); infusion 0.5–4 mcg/kg/minIV; where available (titratable alternative); reflex tachycardia; raises cyclosporine and tacrolimus levels
Furosemide1–2 mg/kg (max 40–80 mg)IV; if fluid overloaded (e.g., post‑streptococcal glomerulonephritis)
◈ Note Oral or sublingual nifedipine can cause a precipitous, uncontrolled fall and is not recommended for a true hypertensive emergency.
◣ Admit · Discharge · Refer
  • Admit — all true emergencies → PICU with a titratable infusion.
  • Home from the ward — not from the emergency; controlled blood pressure with a plan.
  • Refer — now — nephrology/cardiology for cause.
  • Refer — clinic — nephrology/cardiology for long‑term control.

Nephrotic Syndrome

HOURSIPNA 2023

Heavy proteinuria, low albumin, and edema — usually steroid‑responsive, but watch the complications. Doses follow the International Pediatric Nephrology Association (IPNA) 2023 guideline.

▸
◣ Recognize
  • The triad: nephrotic‑range proteinuria (urine protein/creatinine > 200 mg/mmol, or ≥ 3+ on dipstick), hypoalbuminemia < 30 g/L (< 3.0 g/dL), and edema (periorbital → generalized, ascites, scrotal/labial); usually with hyperlipidemia.
  • In a child 1–10 years without the atypical features below, it is almost always steroid‑responsive minimal‑change disease — treat without a biopsy.
Confirm & assess
  • Confirm proteinuria (first‑morning‑void protein/creatinine ratio preferred over a 24‑hour collection); send albumin, renal function and electrolytes, lipids; weigh, record blood pressure, assess volume status.
  • Assess clinically for active infection before commencing high‑dose corticosteroids; investigate according to symptoms and risk factors rather than performing routine infection screening in an otherwise well child.
First presentation
  • Oral prednisolone 60 mg/m²/dose (≈ 2 mg/kg/dose, max 60 mg) once daily for 4–6 weeks, then 40 mg/m² (max 40 mg) on alternate days for a further 4–6 weeks (total 8–12 weeks)
  • Add a no‑added‑salt diet (no fluid or protein restriction) and ensure pneumococcal vaccination; routine antibiotic prophylaxis is not recommended — instead treat suspected infection promptly, including spontaneous bacterial peritonitis.
⚠ Complications to pre‑empt
  • Hypovolemia can hide behind gross edema — abdominal pain, cool peripheries, tachycardia, prolonged capillary refill, oliguria; needs urgent senior/nephrology input. Withhold diuretics (and ACE inhibitors/ARBs) while hypovolemic. Shock or hypotension: 4–5% albumin (or isotonic crystalloid if unavailable) without furosemide. Hypovolemia without shock: 20–25% albumin 0.5–1 g/kg IV over 4–6 h; add furosemide 1–2 mg/kg IV mid‑ or end‑infusion only once volume is restored and urine output remains poor. Monitor closely during albumin (pulmonary edema, hypertension). Hypervolemia presents differently — edema with strong peripheral pulses and warm peripheries; treat with diuretics and close reassessment.
  • Watch for spontaneous bacterial peritonitis (pneumococcal) and other sepsis, venous or arterial thromboembolism (these children are hypercoagulable), and acute kidney injury (AKI).
◣ Admit · Discharge · Refer
  • Admit — first presentation, hypovolemia, peritonitis or sepsis, thromboembolism, severe edema with respiratory compromise, AKI, or a relapse not responding to oral steroid.
  • Home — steroid responsiveness is not required before discharge, provided close OPD follow‑up is arranged: a well child with no complications, able to tolerate oral steroids, with the family able to monitor first‑morning urine and act on a written plan.
  • Refer — now — Nephrology for any atypical feature (age < 1 or > 12 years, persistent hypertension, gross hematuria, low complement (C3), renal impairment) — these may need a biopsy or second‑line therapy.
  • Refer — clinic — Nephrology for steroid resistance or frequent relapse — these may need a biopsy or second‑line therapy.

Circumcision — Kuwait Practice

ASSESS≥ 1 WK · Ped SURGERY

Near‑universal in Kuwait — screen first, always give analgesia, and know the complications.

▸
◣ Before you circumcise — checklist
  • Examine the genitalia first. Do NOT circumcise if hypospadias, epispadias, chordee, ambiguous genitalia / suspected DSD, micropenis, or buried / webbed penis — the foreskin may be needed for repair → refer to pediatric surgery / urology.
  • Contraindicated in an unstable or sick infant — confirm normal feeding, elimination and thermoregulation; ensure vitamin K given.
  • Family history of a bleeding disorder → coagulation studies / defer.
  • Informed parental consent. In Kuwait usually performed by pediatric (or general) surgery from ~1 week of age (and later in infancy / childhood).
◈ Analgesia — never omit
  • Dorsal penile nerve block or subcutaneous ring block (lidocaine 1% without epinephrine: nerve block 0.4 mL each side, or ring block 0.8 mL in total — AAP 2012; stay within 3–4 mg/kg) — the most effective analgesia studied for newborn circumcision; minor bleeding, swelling or hematoma can occur.,
  • Add topical EMLA, oral sucrose, non‑nutritive sucking and acetaminophen.
  • Sucrose or EMLA alone are not enough; combination analgesia is best.
Methods
Gomco clamp, Mogen clamp, or Plastibell (ring) device — each with its own technique and complication profile.
Wound care
  • Clean gently with warm water at each diaper change; avoid soap and wipes (they sting).
  • Gomco / Mogen: apply petroleum jelly (or antibiotic ointment) to the glans and on the diaper for ~5–7 days to stop the wound sticking. A moist yellow coating (granulation) on the glans is normal healing, not infection.
  • Plastibell: the ring falls off by itself in ~5–10 days — do not pull it; sponge‑bathe until it separates; seek review if it slips onto the shaft or has not fallen by 10–14 days.
  • Heals in ~7–10 days. After healing, gently retract the skin at the groove to prevent adhesions / skin bridges.
⚠ Complications — when to seek urgent review
  • Bleeding more than a few drops (commonest — direct pressure and a compressive dressing around the penis, then pediatric surgery review + coagulation workup)
  • spreading redness up the shaft, pus or fever = wound infection
  • no urine for ~8 h = retention
  • Plastibell ring migrated with a dusky glans = constriction (emergency)
  • trapped / concealed penis, adhesions, skin bridges, or late meatal stenosis (deflected stream) → pediatric surgery / urology.

Acute Scrotum

MINUTES6‑HOUR WINDOW

Sudden scrotal pain is testicular torsion until proven otherwise — a clinical diagnosis; do not wait for imaging.

▸
◣ Define
  • Acute scrotum = sudden scrotal pain/swelling. Testicular torsion until proven otherwise — a time‑critical surgical emergency. Bimodal peaks: the neonate and the peri‑pubertal boy.
  • Differential: torsion of the appendix testis (blue‑dot sign, gradual, milder), epididymo‑orchitis (dysuria, gradual, older/sexually active), trauma, idiopathic scrotal edema, incarcerated inguinal hernia.
◣ Approach — favors torsion
  • Sudden severe pain ± nausea/vomiting, high‑riding testis, horizontal lie, absent cremasteric reflex, diffuse tenderness.
  • The TWIST score (hard testis, swelling, nausea/vomiting, absent cremasteric reflex, high‑riding testis) risk‑stratifies but does not replace surgical judgment.
⚠ Work‑up
  • Torsion is a clinical diagnosis — do not delay surgical exploration for imaging. Color Doppler ultrasound (absent intratesticular flow) is useful only when the diagnosis is equivocal and will not delay surgery.
  • Urinalysis: pyuria or bacteriuria supports bacterial epididymitis — but a normal urinalysis does not exclude epididymitis, and an abnormal one does not exclude torsion; send a culture.
⚠ Red flags — the clock
  • Testicular salvage is time‑dependent: near‑universal (≈ 97%) if detorsion occurs within ~6 hours of onset, falling progressively thereafter (≈ 79% at 7–12 h, ≈ 42% at 19–24 h).
  • Neonatal torsion and any delayed presentation need urgent senior/urology input.
◣ Management
  • Immediate urology/surgical referral for scrotal exploration, detorsion, and bilateral orchidopexy.
  • If surgery is delayed, a trained clinician may attempt manual detorsion (usually 'opening a book' — medial‑to‑lateral) only if experienced as a temporizing measure while immediate exploration is arranged, guided by pain relief; success does not remove the need for surgery and orchidopexy.
  • Consult surgery/urology at once and confirm the diagnosis. Torsion → surgery. Once torsion is excluded: appendix‑testis torsion → NSAID analgesia and rest; epididymo‑orchitis → NSAIDs, rest and scrotal support. Prepubertal boys: antibiotics only if urinalysis or urine culture shows bacterial infection (send the culture before treating — prepubertal epididymitis is usually non‑bacterial). Sexually active adolescents: send urine NAAT for chlamydia/gonorrhea and treat presumptively at the visit (e.g., ceftriaxone 500 mg IM once [1 g if ≥ 150 kg] + doxycycline 100 mg PO twice daily for 10 days; CDC).
✦ Pearl — abdominal pain can be a torsion
Examine the testes in every boy with acute lower‑abdominal or groin pain — torsion frequently refers pain to the abdomen and is missed when the scrotum is not examined.
◣ Admit · Discharge · Refer
  • Admit — torsion (confirmed or not excluded) → emergency exploration; incarcerated hernia; epididymo‑orchitis only if systemically unwell, an infant, or unable to take oral analgesia.
  • Home from the emergency department — once the surgical/urology team has excluded torsion: appendix‑testis torsion and epididymo‑orchitis go home on NSAIDs ± antibiotics per urine results, review in 48–72 h.
  • Refer — now — surgery/urology IMMEDIATELY to confirm the diagnosis (torsion → exploration within 6 h).
  • Refer — clinic — consider outpatient renal‑tract ultrasound after prepubertal epididymitis, particularly if recurrent, culture‑positive or in an infant (underlying urogenital anomaly reported in ~25–30%; routine full urological evaluation of every case is debated).
◈ See also Testicular Torsion — the time‑critical diagnosis to exclude first.

Testicular Torsion

MINUTESADOLESCENT & NEONATE

Salvage window ~6 hours. A boy's abdominal pain → examine the scrotum.

▸
◣ Recognize
  • Sudden severe scrotal/lower‑abdominal pain, nausea/vomiting, swelling. High‑riding/horizontal testis, absent cremasteric reflex, negative Prehn sign.
Clinical suspicion = urgent exploration. Don't delay for imaging.
Act
  • Immediate urology / pediatric surgery → exploration, detorsion + bilateral orchidopexy.
  • Color Doppler ultrasound only if it will not delay surgery.
  • Manual detorsion may temporize only in experienced hands — do not attempt if untrained (can worsen the torsion), and never let it delay surgical exploration.
◣ Admit · Discharge · Refer
  • Admit — all → emergency exploration.
  • Home from the ward — post‑operative.
  • Refer — now — pediatric surgery/urology IMMEDIATELY (explore within 6 h); do not delay for imaging.
◈ See also Acute Scrotum for the full differential.

Paraphimosis

HOURSREDUCE PROMPTLY

A retracted foreskin trapped behind the glans — edema then ischemia; reduce promptly.

▸
◣ Define
  • Paraphimosis — a retracted foreskin trapped behind the glans, cannot be reduced. The constricting band causes progressive glans and distal‑foreskin edema, then venous → arterial compromise. A urological emergency.
  • Commonly iatrogenic — the foreskin is left retracted after catheterization, cleaning, or examination.
◣ Approach & work‑up
  • Painful, swollen glans with an edematous 'collar' of foreskin proximal to it. Diagnosis is clinical.
  • Distinguish from balanoposthitis (foreskin/glans inflammation without a trapped retracted ring).
⚠ Red flags
Increasing edema, dusky glans, or pain out of proportion signal arterial compromise and impending necrosis — reduce promptly; escalate to urology if reduction fails.
Management
◣ Reduce it
  • Analgesia first — penile block with plain lidocaine 1% (no epinephrine; see Maximum Local Anesthetic Doses) or procedural analgesia (expert practice).
  • Reduce edema — sustained manual compression of the glans (± a wrap such as saline‑soaked gauze squeezed gently but firmly for 5–10 min, ice, or an osmotic agent such as granulated sugar); multiple punctures of the edematous foreskin or hyaluronidase under the constricting band are described for difficult cases.
  • Reduce the foreskin — push the glans back with the thumbs while drawing the foreskin forward over it with the fingers.
  • If manual reduction fails — urology for a dorsal‑slit or emergency reduction.
✦ Pearl — prevention is the cure
Always return the foreskin to its natural forward position after any catheterization, cleaning, or examination, and teach carers never to force‑retract a child's foreskin.
◣ Admit · Discharge · Refer
  • Admit — if reduction fails or there is tissue compromise.
  • Home from the emergency department — after successful reduction with follow‑up.
  • Refer — now — urology for failed reduction.
  • Refer — clinic — urology for recurrent episodes.

Balanitis / Balanoposthitis & Phimosis

ASSESSCOMMON

Glans/foreskin inflammation and non‑retractile foreskin; physiologic phimosis is normal, needs no treatment.

▸
◣ Define
  • Balanitis = inflammation of the glans; balanoposthitis = glans + foreskin. Phimosis = non‑retractile foreskin — physiologic (normal in young boys) or pathologic (scarred).
  • Physiologic phimosis is normal: non‑retractile in most infants, becomes retractile with age (≈ 99% by 17 years). Needs no treatment.
◣ Approach & work‑up
  • Balanitis: red, swollen, tender glans/foreskin ± discharge, dysuria. Usually hygiene‑related or candidal; consider sexually transmitted causes in adolescents.
  • Distinguish physiologic phimosis (soft, healthy, pink opening) from pathologic (scarred white fibrotic ring — balanitis xerotica obliterans/lichen sclerosus).
  • Clinical diagnosis; swab if recurrent/purulent; urinalysis if voiding symptoms.
⚠ Red flags
Pathologic phimosis (white scarred ring / BXO), recurrent balanoposthitis, ballooning or difficulty voiding, or urinary retention — refer to urology.
Management
DrugDoseRoute & notes
Balanitis — generalHygiene, warm saline soaksRetract gently only as far as comfortable; avoid irritants.
Balanitis — bacterial/candidalTopical/oral antibiotic or topical antifungalGuided by likely organism; treat/screen for STI in adolescents.
Physiologic phimosisNo treatment; do not force‑retractReassure; resolves with age.
Symptomatic / early pathologic phimosisTopical betamethasone 0.05% applied twice daily for 4–8 weeks (expert practice; the review gives no regimen)Success 67–95% with betamethasone (about 80% overall); avoids or defers circumcision.
Pathologic phimosis / BXO / recurrentRefer for circumcisionDefinitive for scarred foreskin or lichen sclerosus.
✦ Pearl — hands off the young foreskin
Never forcibly retract a young boy's foreskin — it tears, bleeds, and scars, converting harmless physiologic phimosis into pathologic phimosis.
◣ Admit · Discharge · Refer
  • Admit — rarely — severe infection or urinary retention.
  • Home from the emergency department — most, with hygiene and topical treatment.
  • Refer — clinic — urology for pathological phimosis, recurrent balanitis, or balanitis xerotica obliterans.

Priapism

MINUTES> 4 H = EMERGENCY

Painful rigid erection > 4 hours; ischemic priapism is a penile compartment syndrome — relieve fast.

▸
◣ Define
  • Priapism — persistent erection > 4 hours unrelated to stimulation. Ischemic (low‑flow, painful, rigid corpora — penile compartment syndrome, a true emergency) versus non‑ischemic (high‑flow, usually post‑traumatic, not urgent).
  • Most pediatric priapism is ischemic and associated with sickle cell disease (the cause in about two‑thirds of childhood cases); short self‑limiting 'stuttering' episodes are common in SCD and can progress to a prolonged ischemic event.
◣ Approach & work‑up
  • Rigid, painful corpora cavernosa with a soft glans and corpus spongiosum → ischemic. Ask about sickle cell disease and drugs.
  • Cavernosal blood gas distinguishes: ischemic = dark, hypoxic, acidotic blood. Color Doppler ultrasound also separates the two (ischemic = absent/low cavernosal flow; non‑ischemic = normal/high flow). Do not delay treatment for imaging.
⚠ Red flags — the clock
  • Smooth‑muscle edema and atrophy begin as early as ~6 hours; risk of permanent erectile dysfunction rises with duration.
  • Ischemic priapism > 4 hours is a time‑sensitive emergency needing immediate urology (and hematology in sickle cell disease) — do not delay urologic intervention for sickle‑cell measures.
Management
◣ Relieve the erection first
  • In sickle cell disease, do not delay penile intervention for exchange transfusion — urologic relief comes first; sickle measures (hydration, oxygen, analgesia) run concurrently.
  • Corporal aspiration ± saline irrigation plus intracavernosal phenylephrine (urology‑directed), repeated as needed, with blood‑pressure and heart‑rate monitoring.
  • Surgical shunting only after aspiration + sympathomimetic have failed.
DrugDoseNotes
Phenylephrine (intracavernosal)Adult/post‑pubertal: 100–200 mcg per injection every 3–5 min, diluted in 0.9% saline to 100–500 mcg/mL; maximum cumulative dose 1 mg within the first hourUrology‑directed. Children and patients with cardiovascular disease: lower doses/lower concentration in smaller volumes. Monitor BP and HR (e.g., every 15 min for 1 h after injection).,
✦ Pearl — call urology now
Acute ischemic priapism is an emergency; in sickle cell disease relieve the erection first and give sickle‑specific care alongside — not instead.
◣ Admit · Discharge · Refer
  • Admit — ischemic priapism → urgent intervention.
  • Home — after detumescence with follow‑up.
  • Refer — now — urology (aspiration/irrigation) and hematology in sickle cell disease; do not delay urology.

Gross Hematuria

ASSESSAPPROACH

Confirm true hematuria, then sort glomerular from non‑glomerular — that split directs the entire work‑up.

▸
◣ Define
  • Gross hematuria — visibly bloody or tea/cola‑colored urine. Confirm true hematuria (dipstick positive and ≥ 5 RBC/high‑power field on microscopy) — exclude mimics: foods (beetroot), drugs (rifampin), myoglobin, urate, menstrual contamination.
◣ Approach — glomerular vs non‑glomerular
  • Glomerular — brown/cola‑colored, dysmorphic RBCs or RBC casts, proteinuria, hypertension, edema → glomerulonephritis (post‑infectious, IgA nephropathy, Alport). Recurrent painless gross hematuria with a fever, viral illness or exercise → most likely IgA nephropathy; hematuria with hearing impairment (or a family history of kidney failure) → Alport syndrome — send genetics first.
  • Non‑glomerular — bright red ± clots → urologic: UTI, hypercalciuria/stones, trauma, benign urethrorrhagia, rarely tumor. Timing helps: blood at the start of the stream → urethra; at the end → bladder. Benign urethrorrhagia — prepubertal boys, spots of blood at the end of or between voids, resolves spontaneously.
  • Commonest causes overall: UTI and hypercalciuria; gross hematuria without glomerular features is usually benign.
⚠ Work‑up
  • Urinalysis with microscopy (casts, dysmorphic RBCs), urine culture, blood pressure; urine protein:creatinine and calcium:creatinine ratios; serum creatinine/electrolytes; C3/C4 and anti‑DNase B if glomerulonephritis is suspected; renal‑bladder ultrasound — stones, polycystic kidney disease, trauma.
  • Image for trauma or obstructing clot as indicated.
◣ Red flags
  • Hypertension, edema, oliguria, or rising creatinine → glomerulonephritis with acute kidney injury.
  • Flank pain with clots (stones), significant trauma, a palpable mass, or systemic symptoms.
◣ Management
  • Treat the underlying cause. Nephrology referral for glomerular features (hypertension, proteinuria, casts, reduced GFR); urology for structural/urologic causes.
  • Isolated gross hematuria with normal blood pressure, no proteinuria, and normal ultrasound can usually be observed.
✦ Pearl — dipstick + microscopy + blood pressure
Those three bedside steps triage most children — color and RBC morphology sort glomerular from non‑glomerular and direct the whole work‑up.
◣ Admit · Discharge · Refer
  • Admit — clot retention, significant bleeding, hypertension, or acute nephritis with impairment.
  • Home from the emergency department — well child with a benign cause and outpatient workup.
  • Refer — clinic — nephrology (glomerular) or urology (structural, stones, or mass).

Acute Post‑infectious Glomerulonephritis (PIGN)

ASSESS2–12 YR

The commonest acute nephritis in children — cola urine, puffy eyes and a high blood pressure 1–6 weeks after an infection, classically streptococcal.

▸
◣ Recognize
  • Acute nephritic syndrome — cola/tea‑colored urine, periorbital/leg edema, hypertension, oliguria; onset 1–3 weeks after pharyngitis or 3–6 weeks after impetigo (skin infection is the commoner trigger in hot climates). Group A streptococcus is the classic cause, but other bacteria, viruses, fungi and parasites cause the same immune‑mediated nephritis — hence post‑infectious (infection‑related) GN.,
  • Ask about recent sore throat, skin sores or scabies; examine the skin, blood pressure and volume status.
◣ Work‑up
  • Urinalysis and microscopy — dysmorphic RBCs, RBC casts, proteinuria (usually sub‑nephrotic); urine protein:creatinine ratio.
  • Creatinine, urea, electrolytes (potassium), albumin, CBC.
  • Low C3 with normal C4 supports the diagnosis; anti‑DNase B confirms recent streptococcal infection (positive in nearly all; ASO titer adds little); throat or skin swab if there is a current infection.,
  • Chest X‑ray if breathless or overloaded; renal ultrasound only if the picture is atypical.
Manage — supportive care
  • Manage fluid balance (strict input/output, daily weight, fluid restriction if oliguric or overloaded) and a no‑added‑salt diet.
  • Treat hypertension — furosemide 1–2 mg/kg IV/oral for edema, overload or hypertension is usually enough; add a calcium‑channel blocker if still hypertensive. Severe hypertension with headache, seizures or visual change → Hypertensive Emergency.
  • Penicillin for every patient (benzathine penicillin G preferred; amoxicillin, or a macrolide if allergic) to eradicate any remaining group A streptococci and limit spread to household contacts (CDC) — it does not alter the course of the nephritis.
  • No corticosteroids or immunosuppression for uncomplicated disease.
⚠ Red flags
  • Hypertensive encephalopathy (headache, vomiting, seizures, altered consciousness) — about 1 in 10 admissions.
  • Pulmonary edema, hyperkalemia, or a rapidly rising creatinine → possible crescentic glomerulonephritis — nephrology the same day (see Acute Kidney Injury).,
✦ Expected course
Diuresis and normal blood pressure within 1–2 weeks; C3 normalizes by 8 weeks; microscopic hematuria may persist up to a year; recurrence is rare (course timelines: expert consensus — not guideline‑stated). Long‑term prognosis is good.
◣ Admit · Discharge · Refer
  • Admit — hypertension, oliguria, edema/overload, raised creatinine or hyperkalemia.
  • Home — normal blood pressure and urine output; check blood pressure and urinalysis at 1–2 weeks, C3 at 6–8 weeks.
  • Refer — now — nephrology if creatinine keeps rising or nephrotic‑range proteinuria — these may need a biopsy.
  • Refer — clinic — nephrology if C3 still low at 12 weeks (consider C3 glomerulopathy), or hematuria/proteinuria beyond 1 year — these may need a biopsy.

Rhabdomyolysis

MINUTESDASAIM/DSIT 2019 · Mannix 2006

Muscle breakdown → tea‑colored urine, a very high CK, and the twin threats of hyperkalemia and AKI.

▸
◣ Recognize
  • Myalgia, weakness and dark (tea-/cola‑colored) urine that is dipstick‑positive for blood but shows few red cells (myoglobin), with creatine kinase > 5× the upper limit. Triggers: viral myositis (influenza), trauma/crush, extreme exertion or heat, seizures, toxins/drugs, and metabolic myopathies.
⚠ Two immediate dangers
  • Hyperkalemia — get an ECG and treat at once (see Acute Electrolyte Emergencies). Acute kidney injury — start early, generous IV fluids to maintain a good urine output.
  • Also watch calcium/phosphate and for compartment syndrome in a swollen, painful limb. Routine urinary alkalinization and mannitol are not recommended (adult guidance).
✦ Chase the cause
Recurrent or exertion‑out‑of‑proportion rhabdomyolysis, or a family history, suggests an underlying metabolic myopathy — refer for metabolic work‑up once the acute episode is controlled.
◣ Workup
  • Creatine kinase (diagnostic > 5× the upper limit of normal (ULN); serial to track the trend); AKI risk climbs > 5000 U/L (adult trauma data).
  • Potassium + ECG, calcium, phosphate.
  • Renal function, venous blood gas/bicarbonate; urinalysis (heme‑positive with few RBCs = myoglobinuria) + urine myoglobin.
  • Uric acid, LDH, AST; metabolic/genetic screen if recurrent or exertion‑disproportionate.
◣ Admit · Refer
  • Admit — significant CK elevation, any renal impairment or hyperkalemia.
  • Refer — now — nephrology if AKI; surgery for compartment syndrome.
15

Respiratory, Allergy & Immunology

Airway, breathing, anaphylaxis, allergy & immunology

Anaphylaxis

MINUTES

Acute multisystem allergic reaction — epinephrine first, always.

▸
◣ Recognize & diagnose
  • Diagnose anaphylaxis (GA²LEN 2024 criteria) when any one applies:
    1 · No known allergen — acute skin/mucosal signs plus respiratory or cardiovascular involvement.
    2 · Likely or known allergen exposure — any two of: skin/mucosa · respiratory · cardiovascular · severe GI symptoms (severe crampy pain, repeated vomiting).
    3 · Known allergen exposure — respiratory involvement alone (non‑inhaled allergen) or cardiovascular involvement alone (hypotension, poor perfusion, collapse) — skin signs may be absent.
  • If in doubt, give epinephrine. Epinephrine is given immediately for suspected anaphylaxis and may be given on clinical judgment before the criteria are fully met — the risk of a missed dose exceeds the risk of an unnecessary one.,
  • Skin: urticaria, flushing, angioedema, pruritus (absent in up to 20%).
  • Breathing: stridor, wheeze, hoarseness, falling SpO₂, cyanosis, increased work of breathing, signs of respiratory distress, persistent cough.
  • Circulation: poor perfusion, hypotension, collapse — reduced BP = low systolic for age or > 30% drop from baseline. Infants: floppiness, drooling, pallor, sudden behavior change.
  • GI: severe crampy abdominal pain or repeated vomiting — counts toward the diagnosis, especially after a likely allergen.
  • Not anaphylaxis: repeated vomiting 1–4 h after a food without skin, respiratory or cardiovascular signs → think food protein‑induced enterocolitis syndrome (FPIES) — fluids and ondansetron, not epinephrine (see Acute FPIES). If the infant is lethargic or hypotensive, treat shock immediately (20 mL/kg bolus) and give epinephrine if anaphylaxis cannot be excluded.
1ST LINE · IM EPINEPHRINE IM epinephrine now — 0.01 mg/kg of 1 mg/mL (max 0.3 mg before puberty, 0.5 mg in adolescents) into the anterolateral thigh; there is no contraindication,
Then
  • Remove the allergen if possible — stop the infusion or drug, remove the stinger.
  • Lay supine, legs up (sit if breathing is hard; never stand suddenly).
  • Oxygen 10–15 L/min via non‑rebreather mask.
  • Stridor, voice change, or tongue/uvula swelling = impending airway obstruction → call anesthesia/ENT now for early, controlled intubation (see Difficult Airway).
  • Fluid bolus for hypotension.
  • Repeat epinephrine every 5–15 min if needed.
refractory after ≥2 IM doses
2ND–3RD LINE Refractory after repeated IM epinephrine → urgent PICU/anesthesia support; IV epinephrine infusion only by an experienced team with monitoring · IV fluids · glucagon if on a beta‑blocker.,
Medications — each given separately
DrugDoseRoute & notes
Epinephrine (adrenaline) — 1st line0.01 mg/kg (max 0.3 mg before puberty; 0.5 mg in adolescents)IM, 1 mg/mL (1:1000), anterolateral thigh; repeat every 5–15 min,
Epinephrine autoinjector (limited availability)0.1 / 0.15 / 0.3 mgDispensed from the emergency department or the general pediatric clinic to cover the child until the allergy clinic review. 0.1 mg (7.5 to < 15 kg) · 0.15 mg (15 to < 25 kg) · 0.3 mg (≥ 25 kg; US label ≥ 30 kg). If the 0.1 mg device is unavailable, the 0.15 mg device may be used down to 7.5 kg.
Epinephrine infusion (refractory)0.1–1 mcg/kg/min (max 10 mcg/min — local practice)IV infusion via an infusion pump; titrate to effect under PICU supervision with continuous cardiac monitoring; dose range = PALS epinephrine‑infusion range
Balanced crystalloid20 mL/kgIV bolus for hypotension, repeat
Salbutamol (for wheeze)2.5–5 mg nebulizedAdjunct only — does not replace epinephrine
Diphen­hydramine (for skin symptoms)1 mg/kg/dose (max 50 mg/dose)IV/IM; adjunct only, not first‑line. A second‑generation antihistamine (e.g., cetirizine, age‑appropriate dose) avoids sedation
Glucagon20–30 mcg/kg (max 1 mg)IV over 5 min, only if on a beta‑blocker and refractory
CorticosteroidsNot routineConsider only for persistent bronchospasm, or severe reactions needing more than 2 IM epinephrine doses or an IV epinephrine infusion; never delay epinephrine
⚠ Observe every child before any discharge decision — no early discharge from the emergency department
  • Admit — usually, for the 12‑h tier: minimum 12 h if more than two doses were needed, history of severe asthma, anaphylaxis with severe respiratory compromise, possible continuing allergen absorption, presentation at night/out of hours, difficult access to emergency care, or the family cannot recognize and respond to deterioration.
  • Home from the emergency department — 2‑h tier: minimum 2 h after full resolution, only when every criterion is met — good response within 5–10 min to a single IM dose given within 30 min of symptom onset, symptoms completely resolved, the child leaves with two in‑date autoinjectors dispensed and demonstrated, and a trained adult supervising.,
  • Home from the emergency department — longer tiers: observe 4–6 h whenever possible, and always when any criterion is unmet or the department cannot dispense autoinjectors; minimum 6 h if two IM doses were needed or there is a history of a biphasic reaction.,
◣ Admit · Observe · Discharge · Refer
  • Admit — more than two epinephrine doses or an epinephrine infusion; ongoing or biphasic symptoms; moderate–severe respiratory distress or hypotension at any point; airway involvement; history of severe asthma; any child in the 12‑h observation tier.,
  • Home from the emergency department — after observation (emergency department / short stay): resolution after one or two IM doses, the observation tier above completed, no respiratory distress at review.
  • Home from the emergency department — checklist (Kuwait pathway) — Home epinephrine: dispense an epinephrine autoinjector from the emergency department or the general pediatric clinic, with hands‑on training, to cover the child until the allergy clinic review. If none can be dispensed, give clear written instructions: strict avoidance of the suspected trigger, the warning signs, and to come straight to the emergency department (call emergency services) at the first sign. Written action plan; allergen‑avoidance advice; non‑sedating antihistamine for residual urticaria only; no routine steroid.,
  • Refer — now — PICU for refractory anaphylactic shock despite repeated IM epinephrine requiring an epinephrine infusion, or airway compromise requiring definitive airway management.
  • Refer — clinic — Allergy/Immunology for every case.
Anaphylaxis — epinephrine firstRecognize (GA²LEN criteria) → IM epinephrine immediately → fluids & repeat → refractory (PICU).
!IM EPINEPHRINE FIRST, ALWAYSThere is no contraindication — give it before antihistamine or steroid.RECOGNIZE — GA²LEN CRITERIA1 No known allergen: skin/mucosa + respiratory or cardiovascular2 Likely allergen: any 2 of skin/mucosa · respiratory · cardiovascular · severe GI3 Known allergen: respiratory alone or cardiovascular aloneIf in doubt, give epinephrine.1recognizeIM EPINEPHRINE0.01 mg/kg (max 0.3 mg; teen 0.5 mg) of 1:1000 IM,anterolateral thigh. Supine, legs up; O₂ 10–15 L/min.2nowFLUIDS · REPEATFluid bolus for hypotension. Repeat IM epinephrine every5–15 min as needed.35–15 minREFRACTORY — PICUUrgent PICU/anesthesia. IV epinephrine infusion by expertsonly; glucagon if on a beta‑blocker.4≥ 2 doses!IM EPINEPHRINE FIRST, ALWAYSThere is no contraindication — give it beforeantihistamine or steroid.RECOGNIZE — GA²LEN CRITERIArecognize1 No known allergen: skin/mucosa + respiratory or cardiovascular2 Likely allergen: any 2 of skin/mucosa · respiratory · cardiovascular · severe GI3 Known allergen: respiratory alone or cardiovascular aloneIf in doubt, give epinephrine.IM EPINEPHRINEnow0.01 mg/kg (max 0.3 mg; teen 0.5 mg) of 1:1000 IM,anterolateral thigh. Supine, legs up; O₂ 10–15 L/min.FLUIDS · REPEAT5–15 minFluid bolus for hypotension. Repeat IM epinephrineevery 5–15 min as needed.REFRACTORY — PICU≥ 2 dosesUrgent PICU/anesthesia. IV epinephrine infusion byexperts only; glucagon if on a beta‑blocker.1234

Acute Asthma

MINUTESGINA 2026

Grade severity continuously: speech, work of breathing, SpO₂, silent chest. Doses follow the Global Initiative for Asthma (GINA) 2026 strategy; PICU‑level therapies are beyond GINA's scope and follow critical‑care practice.

▸
◣ Grade severity first
  • Use a validated score — the PRAM (Pediatric Respiratory Assessment Measure)QR (validated 2–17 yr) or PASS (Pediatric Asthma Severity Score) — with SpO₂ on room air, work of breathing, and ability to speak or feed; reassess and re‑score after each step.,
  • PRAM bands: 0–3 mild · 4–7 moderate · 8–12 severe (Canadian Paediatric Society); re‑score after each step. Life‑threatening = drowsy/confused or silent chest (GINA 2026).
✦ Pearl — when it isn't asthma
  • Doubt the diagnosis and look for a mimicker when wheeze is present from the first weeks of life, is monophonic or focal, fails to respond to adequate bronchodilator and steroid, or comes with faltering growth, clubbing, or chronic wet cough.
  • Think: inhaled foreign body, tracheo-/bronchomalacia or a vascular ring, cystic fibrosis or primary ciliary dyskinesia, bronchiolitis in the infant, a cardiac cause (heart failure), aspiration/gastroesophageal reflux disease (GERD), and — in adolescents — inducible laryngeal obstruction (vocal cord dysfunction).
1ST LINE
  • Oxygen — start it when SpO₂ is below 92%. Then titrate: children 6 years and older — keep SpO₂ 92 to 95%; children under 6 years — keep SpO₂ at or above 92%. Do not push saturations higher (avoid over‑oxygenation).
  • Inhaled salbutamol by spacer every 20 min × 3 in the first hour, reassessing before each repeat, then titrate to response (dose by age in the table).
  • Systemic corticosteroid for a moderate–severe exacerbation or inadequate response to salbutamol (oral — prednisolone or dexamethasone — as effective as IV). Not routine for mild; avoid routine oral steroids for mild viral wheeze in preschoolers.
2ND LINE moderate–severe
  • Add ipratropium × 3.
  • Severe or poor response → IV magnesium sulfate.
  • Call PICU.
life‑threatening / not responding
3RD LINE · PICU Not responding / life‑threatening → call PICU urgently. Continuous nebulized salbutamol, IV salbutamol, non‑invasive ventilation and intubation are PICU‑directed (see “Beyond GINA” below).
Bronchodilators
DrugDoseRoute & notes
Salbutamol (inhaler + spacer)< 6 yr: mild 2–4 · moderate 4 · severe 6 puffs
≥ 6 yr: mild 4 · moderate 4–6 · severe 6–10 puffs
100 mcg/puff; shake before each puff, one puff at a time (4–5 breaths each); every 20 min × 3 in the first hour, then titrate to response (hourly → every 1–4 h). GINA sets no fixed cap
Salbutamol (nebulized)< 6 yr: 2.5 mg (any severity)
≥ 6 yr: mild 2.5 mg · moderate 2.5–5 mg · severe 5 mg
Every 20 min × 3, then titrate to response; spacer is preferred when the child can use it. Not responding → PICU: continuous nebulized or IV salbutamol — see Beyond GINA.
Ipratropium bromide< 6 yr: 80 mcg by spacer (4 puffs of 20 mcg) or 250 mcg nebulized
≥ 6 yr: 4–8 puffs (80–160 mcg) or 250–500 mcg nebulized
Moderate–severe: give with each salbutamol dose, every 20 min × 3 in the first hour only
Magnesium sulfate40–50 mg/kg (max 2 g)IV over 20 min, age ≥ 2 yr
Beyond GINA — critical‑care therapies (PICU‑directed)
TherapyDoseNotes
Salbutamol — continuous nebulization0.5 mg/kg/h, maximum 20 mg/h (many units use 10–15 mg/h)NAEPP dose. GINA accepts continuous nebulized salbutamol for severe exacerbations in the emergency department; the mg/kg/h regimen and the high‑output nebulizer are critical‑care practice. Cardiac + K⁺ monitoring
Salbutamol IVbolus then infusionNot routine (no GINA recommendation); PICU only, cardiac monitoring; watch for hypokalemia and lactic acidosis
Aminophylline5 mg/kg load, then infusionNot recommended (GINA 2026) — poor efficacy, narrow safety margin, potentially fatal toxicity (especially with prior oral theophylline); no reduction in symptoms or length of stay in children. PICU rescue only, after IV salbutamol and magnesium; monitor levels,
Heliox (helium–oxygen ≥ 70:30)driving / breathing gasNo proven benefit in routine exacerbations (Cochrane); may be considered in severe exacerbations in an ICU setting. Needs ≥ 70% helium, so unsuitable when a high FiO₂ is required,,
Corticosteroids — choose one; oral before IV (IV doses are not GINA doses)
DrugDoseRoute & notes
Prednisolone< 2 yr: 1–2 mg/kg (max 20 mg)
2–5 yr: 1–2 mg/kg (max 30 mg)
6–11 yr: 1–2 mg/kg (max 40 mg)
≥ 12 yr: 1–2 mg/kg (max 50 mg)
once daily
PO; 3–5 days (≤ 11 yr) · 5–7 days (≥ 12 yr — GINA adult/adolescent regimen 40–50 mg/day); age‑specific maxima per GINA
Dexa­methasone0.3–0.6 mg/kg once daily (max 12–16 mg)PO/IV, 1–2 days.
Methyl­predniso­lone1–2 mg/kg/day IV in 2 divided doses (max 60 mg/day)IV drug of choice when oral is not tolerated. Not a GINA dose — NAEPP EPR‑3; confirm with clinical pharmacy.
Hydro­corti­sone4 mg/kg/dose every 6 h on day 1 (max 100 mg/dose), then every 12 h on day 2 and once daily on day 3 — or switch to oral prednisoloneOnly if methylprednisolone is unavailable. Not a GINA dose — Australian Asthma Handbook. Not equivalent to the row above: about 3 mg/kg/day of methylprednisolone on day 1; higher steroid doses add no benefit.
◈ Steroid choice & availability
  • Oral prednisolone and oral dexamethasone are equally effective, and oral steroid is as effective as IV; reserve IV steroid for the child who cannot take oral.
  • When IV is needed, methylprednisolone is the drug of choice; use hydrocortisone only if it is unavailable.
  • Note that hydrocortisone's mineralocorticoid effect can add to the hypokalemia caused by high‑dose salbutamol, and all systemic steroids can raise blood pressure and glucose.
  • All four are widely stocked.
⚠ Clinical pearls & red flags
A silent chest, a falling respiratory rate with rising drowsiness, or a normal/rising PaCO₂ in a tiring child is pre‑arrest — not improvement. Call PICU urgently: decisions on sedation (e.g., ketamine), non‑invasive ventilation, imaging, and intubation are made by the critical‑care team, aiming to maximize urgent treatment before any intubation decision.
◣ Admit · Discharge · Refer
  • Admit — ongoing oxygen requirement, incomplete response after first‑hour therapy, salbutamol needed more often than every 3–4 h, or prior PICU admission/intubation.
  • Home — when all are met:
    • SpO₂ ≥ 92% on room air.
    • Salbutamol needed no more often than every 4 h.
    • Feeding and talking.
    • Inhaler and spacer technique checked.
  • Discharge prescription
    • Salbutamol by inhaler and spacer (face mask under 3 years): 2–6 puffs every 4 h, weaning over days.
    • Nebulized salbutamol only for a child who cannot use an inhaler and spacer with face mask — e.g. too young or too weak to breathe effectively through the spacer (dose as in the table above, every 4 h, weaning)., A home nebulizer must not delay care: if salbutamol is needed more often than every 4 h, return at once. GINA links home nebulized salbutamol with a higher risk of asthma death; nebulizers can also spread respiratory viruses.,
    • Oral steroid course (table above).
    • Inhaled corticosteroid (ICS):
      • ≥ 6 years — start or step up ICS‑containing maintenance treatment; no child leaves on salbutamol alone.
      • Under 6 years with asthma or recurrent wheeze — a 2–3‑month trial of daily low‑dose ICS when this episode needed oral steroids or urgent care, or symptoms occur between episodes more than twice a week; review the response at 2–3 months.,
    • Written action plan; review within 1 week.
  • Refer — now — PICU for impending respiratory failure.
  • Refer — clinic — Pulmonology for any PICU‑level escalation, ≥ 2 admissions per year, or diagnostic doubt; Allergy/Immunology for difficult‑to‑control atopic disease.
✦ Before discharge — screen for what keeps asthma uncontrolled (GINA 2026)
An exacerbation is the moment to look for the drivers. Ask and act on: allergic rhinitis / rhinosinusitis (intranasal corticosteroid — improves asthma control); obesity (harder to control; weight management in the plan — even 5–10% loss helps); obstructive sleep apnea (habitual snoring, witnessed apnea → sleep referral; see OSA); gastro‑esophageal reflux (treat only if symptomatic — anti‑reflux therapy does not improve asthma without reflux symptoms); food allergy (confirmed food allergy is a risk factor for asthma death → allergy testing and an epinephrine plan); anxiety or depression in adolescents; inducible laryngeal obstruction when cough or “wheeze” does not respond to bronchodilator; and exposures — tobacco, vaping or shisha smoke at home or in the car (parents must never smoke or vape in rooms or cars the child uses), pets, mold, school triggers. Check adherence and inhaler technique last — they explain more exacerbations than any comorbidity. Refer to pulmonology/allergy when asthma stays uncontrolled despite treating these.

Croup

HOURSMINUTES if severe / impending failure6 MO–6 YR

Barking cough, hoarse voice, inspiratory stridor; worse at night. Grade severity clinically — stridor at rest, indrawing, sustained agitation, lethargy or cyanosis (mild · moderate · severe · impending failure) — or with the Westley score (0–17: ≤ 2 mild · 3–5 moderate · 6–11 severe · ≥ 12 impending respiratory failure), summing level of consciousness, cyanosis, stridor, air entry, and retractions.

▸
Keep calm Agitation worsens obstruction — examine on a parent's lap, minimal handling.
Stridor at rest / respiratory distress?
MILD
Single steroid dose; discharge with clear return‑precaution advice (safety‑netting).,
MODERATE–SEVERE
Steroid + nebulized L‑epinephrine; observe ≥ 2–4 hours for rebound; oxygen if hypoxic.
DrugDoseRoute & notes
Dexa­methasoneMild: 0.15 mg/kg
Moderate–severe: 0.6 mg/kg
(max 16 mg)
PO/IM/IV, single dose. 0.15 mg/kg may be as effective as 0.6 mg/kg in mild–moderate croup (Cochrane 2023; 0.6 scored better at 24 h). Dexamethasone probably reduces return visits compared with prednisolone (RR 0.55, 95% CI 0.28–1.11 — not statistically significant); prednisolone 1 mg/kg is an acceptable alternative when dexamethasone is unavailable (non‑inferior in the largest RCT)
Budesonide (nebulized)2 mgIf oral steroid not tolerated (nebulized budesonide 2 mg performed similarly to oral dexamethasone),
Epinephrine (nebulized)L‑epinephrine (adrenaline) 1:1000 (1 mg/mL) 0.5 mL/kg nebulized (max 5 mL)Moderate–severe; observe for rebound
◈ Concentration check
Do not confuse 1:1000 (1 mg/mL) with 1:10 000 (0.1 mg/mL) epinephrine — different concentrations.
◈ Heliox in severe croup
  • In severe croup with significant distress not settling after dexamethasone and nebulized L‑epinephrine, heliox (helium–oxygen) may temporize while the steroid takes effect or transfer/airway support is arranged — in small trials its effect was comparable to oxygen plus epinephrine.
  • It is a bridge, not a substitute, and the evidence is very limited (low certainty).
  • Needs ≥ 70% helium, so it is unsuitable when a high oxygen requirement is present. Involve ICU/anesthesia early.
⚠ Differentials
  • Drooling + toxic + no cough → epiglottitis (do not examine the throat).
  • Sudden choking → inhaled foreign body.
◣ Admit · Discharge · Refer
  • Admit — stridor at rest persisting after a steroid ± nebulized L‑epinephrine, any oxygen requirement, or a repeat epinephrine dose needed.
  • Home from the emergency department — mild croup (no stridor at rest, no distress) after a single steroid dose, feeding well, with reliable carers and safety‑netting; if epinephrine was given, observe ≥ 2–4 h after the dose for rebound before the child goes home.
  • Refer — now — early ICU / anesthesia consult for impending obstruction or failure to respond; ENT if an alternative airway diagnosis is suspected. If intubation is considered, do it in a controlled setting (PICU or operating room) with anesthesia and ENT present and difficult‑airway equipment ready — see Difficult Airway.
◈ See also Pediatric ENT Emergencies (epiglottitis, bacterial tracheitis) in Section 07.

Retropharyngeal Abscess

HOURS1–5 YR

Deep neck‑space infection after recent upper‑respiratory illness — fever, neck pain, refusal to move the neck, drooling; guard the airway.

▸
◣ Recognize
  • Peak age 1–5 yr (median ~3 yr), usually after upper‑respiratory infection.
  • Symptoms: fever, sore throat, odynophagia/dysphagia, neck pain and swelling, muffled (“hot‑potato”) voice, trismus, and drooling.
  • Signs: neck tenderness, limited neck extension or torticollis, and cervical lymphadenopathy. Neck pain and refusal to move or extend the neck are the most useful clues.
⚠ Guard the airway
  • Stridor, respiratory distress, tripod posture, or pooling of secretions signal an airway threat (it mimics epiglottitis).
  • Keep the child calm and sitting upright, give oxygen, do not examine the throat or lie the child flat, and involve ENT + anesthesia for a controlled airway before any manipulation.
◈ Imaging
  • Lateral neck radiograph is a screening test when the diagnosis is equivocal and there is no airway obstruction (widened prevertebral soft tissue — > 7 mm at C2 or > 14 mm at C6). Contrast‑enhanced CT of the neck is the preferred, confirmatory test — it separates a drainable abscess (rim‑enhancing hypodensity) from retropharyngeal cellulitis/phlegmon and maps the extent.
  • No specific laboratory test is usually required.
Airway compromise, or a large / loculated abscess? (large = CT cross‑sectional area > 2 cm² or diameter > 2.5 cm; rim enhancement is the strongest predictor of pus at surgery),
YES
Secure the airway with ENT / anesthesia, then surgical incision & drainage; send pus for culture.
NO — cellulitis / small abscess
A 48‑hour trial of IV antibiotics first — many children resolve without surgery. Re‑image and drain if not improving.
DrugDoseRoute & notes
Ceftriaxone + clindamycin — first lineCeftriaxone 50 mg/kg once daily (max 2 g)
clindamycin 10 mg/kg/dose every 8 h (max 900 mg/dose)
IV; together cover group A streptococcus, oral anaerobes, Gram‑negatives and MRSA (methicillin‑resistant Staphylococcus aureus) — Kuwait Pediatric Council antibiotic policy.,
Amoxicillin‑​clavulanate — second line30 mg/kg/dose of co‑amoxiclav (= amoxicillin 25 mg/kg + clavulanate 5 mg/kg) every 8 h IV (max 1.2 g/dose = amoxicillin 1 g + clavulanate 200 mg)IV alternative when the first line is unsuitable. No oral amoxicillin‑clavulanate step‑down at standard dose — it does not cover S. pneumoniae adequately; choose the oral step‑down agent with infectious diseases/ENT per the Council policy.
◣ Admit · Discharge · Refer
  • Admit — all suspected retropharyngeal abscess for IV antibiotics and observation; a monitored bed if there is any airway concern.
  • Home from the ward — not from the acute phase; step to an oral agent chosen with infectious diseases/ENT (per the Council policy) once afebrile, improving and swallowing, with ENT follow‑up.
  • Refer — now — ENT for drainage and anesthesia for airway control; a screening lateral neck film only if it will not delay a needed CT or airway management.

Difficult Airway

MINUTES

Oxygenate first, then work the three zones — optimize (yellow) → intubate (green) → front‑of‑neck (red); change one thing with every attempt.

▸
◣ Anticipate & prepare
  • Predictors: craniofacial anomaly / syndrome (Pierre Robin, Treacher Collins, Goldenhar, Down), limited mouth opening or neck movement, deep‑neck infection or airway swelling (retropharyngeal abscess, epiglottitis, angioedema, burns), stridor, a large tongue, or a previously documented difficult airway.
  • Anticipated — manage in a controlled setting (PICU / OR) with ENT + anesthesia back‑up available. Unanticipated (ineffective bag‑mask ventilation, or a failed first direct / video laryngoscopy (DL / VL) attempt) — call for help now.,
  • Muscle relaxants at the discretion of anesthesia / PICU. Keep spontaneous breathing (minimal sedation or inhalational anesthesia) where muscle tone is holding the airway open — anterior mediastinal mass, epiglottitis, large tongue, deep‑neck abscess, or known impossible mask ventilation.,
  • Prepare: assign the team (1st + 2nd airway managers, assistant, respiratory therapist, drug nurse, circulating nurse); a time‑out to agree Plan A + B + C (1st / 2nd intubator and technique, and the surgical‑airway option, with personnel and equipment ready); check equipment and drugs; full monitoring; assess the airway (history + exam).
⚠ Oxygenation is the goal — not the tube
  • Pre‑oxygenate fully and keep apneic oxygenation (nasal cannula / high‑flow nasal cannula (HFNC)) running through every attempt.
  • Change one variable with each attempt — operator, device, blade, position, or adjunct — rather than repeating the same one. If in doubt, take it out and oxygenate.,
The Three‑Zones approach (Kuwait algorithm)
✦ For the general pediatrician
Recognize the predictors, keep the child oxygenated (yellow zone) and call anesthesia/ENT early. The green and red zones below are the airway team's work — shown so you can anticipate and assist, not to lead.
● YELLOW ZONE · OPTIMIZE — make bag‑mask ventilation effective: position (head tilt / chin lift, jaw thrust; shoulder roll if < 2 yr), suction, 100% FiO2, change mask size / adjust the seal, two‑person bag‑mask ventilation (BMV), insert a nasogastric tube (NGT). Add an oropharyngeal / nasopharyngeal airway (OPA / NPA). Add a supraglottic airway (laryngeal mask airway, LMA) if ventilation is still ineffective.,
saturated & stable
● GREEN ZONE · INTUBATE — intubate when this is the best saturation you can get and the child is as stable as possible. Videolaryngoscopy with an age‑adapted standard blade is the first choice (use a stylet with a hyperangulated blade);, max 4 attempts total (DL + VL). Between attempts change operator or blade (straight / curved / hyperangulated), add a bougie or a flexible intubation scope (FIS) — through a supraglottic airway, via the nasal route, or by a hybrid technique (FIS guided by the videolaryngoscope view) — or try a smaller endotracheal tube (ETT). Keep apneic O2 (NC / HFNC) running and treat laryngospasm. If oxygenation falls or the patient deteriorates → go back to the yellow zone and re‑optimize.,
can't intubate, can't ventilate
● RED ZONE · CAN'T INTUBATE, CAN'T VENTILATE (CICV) — declare it early. ENT available: rigid bronchoscopy ventilation or tracheostomy. ENT not available: child ≥ 1 yr — needle (cannula) cricothyrotomy / cricotracheal puncture with pressure‑limited oxygen; percutaneous cricothyrotomy, or a surgical “slash” cricothyrotomy (scalpel technique), in the older child (usually from about 12 years, when the cricothyroid membrane is easily felt) by trained hands. Neonate or infant < 1 yr — needle and surgical cricothyrotomy are unreliable (ESAIC/BJA 2024): the most competent operator available performs an emergency surgical tracheostomy; consider ECMO where it exists. Call for help if it has not arrived.,
✦ Confirm placement
On successful intubation, confirm the tube primarily with continuous waveform capnography (EtCO2); support with equal chest rise, rising SpO2, bilateral air entry on auscultation, misting of the tube, and a chest X‑ray with the tip in the mid‑trachea — midway between the inferior clavicular border and the carina (too shallow above the clavicle, too deep at or below the carina; malposition is found in about one in five children despite normal clinical signs); in extremely preterm infants keep the tip at T1–T2.,,,
◣ Have ready (difficult‑airway cart)
Videolaryngoscope (standard + hyperangulated blades), a range of tubes, bougie and stylets, supraglottic airways (LMA) in graded sizes, a flexible intubation scope (FIS), and a front‑of‑neck‑access / cricothyrotomy kit — checked and immediately available before induction.

Bronchiolitis

HOURS< 2 YR

Viral (e.g., RSV): coryza → cough, fast breathing, wheeze/crackles, feeding difficulty.

▸
◣ Supportive care is the treatment
  • Superficial nasal suction when secretions impair breathing or feeding (avoid routine deep suction); small frequent feeds; NG or IV fluids if intake under 50–75% or dehydrated.
  • Give oxygen for persistent SpO₂ < 90% (consider < 92% in young infants, prematurity, cardiac/lung disease, or severe work of breathing).,
SeverityClinical featuresSupport and setting
MildNormal behavior; normal or mildly fast breathing; no or mild chest recession; no apnea; feeding normallyNo oxygen; emergency department or primary care
ModerateIntermittent irritability; fast breathing; moderate chest recession, tracheal tug or nasal flaring; may have brief apneas; reduced or difficult feedingFluid support (NG or IV) and/or oxygen — low‑flow nasal cannula first, high‑flow only after low‑flow fails; ward (or PICU per local pathway),,
SevereIncreasing irritability, lethargy or fatigue; marked increase or decrease in breathing rate; marked recession, tracheal tug or nasal flaring; frequent or prolonged apneas; hypoxemia that may not correct with oxygen; reluctant or unable to feedHigh‑flow before CPAP; HDU/PICU
  • Oxygen follows the SpO₂ threshold above, not the severity grade.
✦ Pearl — first wheeze vs the mimickers
A first episode of wheeze with coryza in a child under 12 months in the bronchiolitis season is bronchiolitis. Recurrent or episodic wheeze, a strong atopic or family history, or wheeze that responds well to a bronchodilator points instead to viral‑induced wheeze or pre‑school asthma; persistent focal signs raise a retained foreign body or a structural airway lesion; and an infant who is failing to feed with hepatomegaly or a murmur may have heart failure, not bronchiolitis.
✕ Not routinely recommended
Bronchodilators (salbutamol, epinephrine), corticosteroids, nebulized hypertonic saline, antibiotics, chest physiotherapy, routine chest X‑ray or viral testing., Red flags: apnea, grunting, severe recession, SpO₂ < 90%, dehydration, age < 3 months (highest risk < 10 weeks), comorbidity.
◈ RSV immunoprophylaxis — who qualifies (AAP 2026)
  • First season, all infants < 8 months born during or entering the RSV season: one dose of a long‑acting monoclonal antibody (nirsevimab or clesrovimab), unless the birthing parent received the RSV vaccine (RSVpreF) ≥ 14 days before delivery. Infants born in season: give within the first week of life, ideally before discharge from the birth hospital.
  • Second season, 8–19 months, high‑risk only: born < 32 weeks; chronic lung disease of prematurity (or other significant neonatal lung disease) needing steroids, diuretics or oxygen in the previous 6 months; hemodynamically significant congenital heart disease; anatomic pulmonary abnormality or neuromuscular disorder; severe immunocompromise; Down syndrome or other chromosomal difference raising RSV risk; cystic fibrosis with severe lung disease or weight‑for‑length < 10th centile.
  • Doses per label: nirsevimab 50 mg (< 5 kg) or 100 mg (≥ 5 kg) IM in the first season, 200 mg in the second; clesrovimab 105 mg IM in the first season — a single 210 mg dose before the second season was well tolerated in high‑risk children (RSV lower respiratory infection 7.3% through day 180).,
◣ Admit · Discharge · Refer
  • Admit — SpO₂ persistently < 90% (< 92% in high-risk infants), apnea, intake under 50–75% or dehydration, marked work of breathing — especially if high-risk (age < 3 months — risk highest in the youngest; the Australasian guideline flags < 10 weeks — prematurity, or cardiopulmonary disease).
  • Home — (NICE NG9, 2021) clinically stable; taking adequate oral fluids; SpO₂ in room air maintained for 4 hours including a period of sleep: > 90% if ≥ 6 weeks old, > 92% if < 6 weeks or any underlying health condition; work of breathing settling; carers confident, with written safety‑netting (worsening work of breathing, intake 50–75% of normal or no wet diaper for 12 h, apnea or cyanosis, exhaustion) and a clear route back.,,
  • Refer — now — PICU (for escalation to high‑flow nasal cannula or continuous positive airway pressure (CPAP)) for rising work of breathing, recurrent apnea, or hypoxia despite oxygen.

Community‑Acquired Pneumonia

HOURSCPS 2024

The healthy, immunized child with fever, cough, and tachypnea — treat S. pneumoniae, mostly orally, and keep it short.

▸
◣ Recognize & assess severity
  • Acute fever + cough + tachypnea (the most useful sign; respiratory rate for age — see Normal Vital Signs by Age) ± increased work of breathing, chest or abdominal pain, poor feeding. Wheeze + hypoxia points to bronchiolitis or asthma, not bacterial CAP.
  • Check SpO₂ in everyone — hypoxemia may not be clinically obvious; give oxygen for sustained SpO₂ < 90% (PIDS/IDSA).
  • Likely cause by age: infants/preschool — mostly viral (RSV, influenza, human metapneumovirus); Streptococcus pneumoniae is the leading bacterial cause at all ages; school‑age — add atypicals (Mycoplasma, Chlamydophila).
◈ Keep investigations targeted
  • A chest radiograph is not essential for a non‑severe outpatient with a typical picture; obtain posteroanterior + lateral when the diagnosis is uncertain or the child is admitted (extent, effusion, abscess).
  • Do not image typical bronchiolitis or asthma.
  • In hospitalized children: complete blood count (CBC)/C‑reactive protein (CRP) + blood culture before antibiotics; consider respiratory viral testing in influenza season. If influenza is suspected or confirmed in moderate–severe or hospitalized CAP, start oseltamivir at once — do not wait for the result (most benefit within 48 h; still treat later if severe): age ≥ 1 yr — ≤ 15 kg 30 mg, > 15–23 kg 45 mg, > 23–40 kg 60 mg, > 40 kg 75 mg; infant 2 wk to < 1 yr — 3 mg/kg/dose; all PO twice daily for 5 days.,
Outpatient or admit?
OUTPATIENT · NON‑SEVERE
Well‑hydrated, tolerating oral intake, no respiratory compromise. Oral amoxicillin is the mainstay — high‑dose covers S. pneumoniae. Most do not need a chest radiograph.
ADMIT
Inadequate oral intake or intolerance, hypoxemia / grunting / nasal flaring / apnea, severe or complicated pneumonia, or age < 6 months. Start IV ampicillin.
Amoxicillin (oral) or ampicillin (IV) is first‑line — cover S. pneumoniae.
Empiric therapy
Setting / drugDoseNotes
Amoxicillin — outpatient, first‑line25–30 mg/kg/dose PO q8h (max 4 g/day)Drug of choice for non‑severe CAP. TID dosing (not BID). 5 days is enough if responding.
Ampicillin — admitted, first‑line50 mg/kg/dose IV q6h (max 12 g/day)IV first‑line for hospitalized, non–life‑threatening CAP. Step down to oral amoxicillin on improvement.
Ceftriaxone — severe / respiratory failure50 mg/kg/dose IV q12–24h (max 2 g/dose)For respiratory failure or septic shock (or cefotaxime 50 mg/kg/dose q6–8h). Broader cover incl. β-lactamase H. influenzae.
+ Vancomycin — if MRSA suspected15 mg/kg/dose IV q6hAdd for rapidly progressing multilobar disease or pneumatoceles until cultures return; send nasal MRSA screen first; stop if MRSA excluded.
Azithromycin — atypical (Mycoplasma)10 mg/kg (max 500 mg) on day 1, then 5 mg/kg (max 250 mg) once daily on days 2–5School‑age with atypical features. Macrolide resistance rising; doxycycline is an alternative from 8 years (CPS).
⚠ Duration, course & follow‑up
  • 5 days for non‑severe CAP (ambulatory, or admitted and responding within 24–36 h); 7–10 days for more significant disease.
  • Expect improvement (appetite, fever, tachypnea, O₂ need) within 48 h.
  • If not improving by 48–72 h → re‑image (radiograph/ultrasound) for empyema or abscess and reconsider the diagnosis (foreign body, tuberculosis, atypical).
  • Routine end‑of‑therapy radiograph is not needed — radiographic clearance lags 4–6 weeks.
◣ Admit · Discharge · Refer
  • Admit — hypoxia (sustained SpO₂ < 90%), respiratory distress, dehydration or feeding failure, a moderate‑to‑large effusion or empyema (a small effusion in a well child may be treated as CAP with early review — see Complicated Pneumonia), or failure of outpatient therapy.
  • Home — well child maintaining saturations in air, feeding, on oral antibiotics with follow‑up arranged.
  • Refer — now — PICU for respiratory failure or sepsis; surgical or respiratory review for empyema or non‑resolving disease.
◈ Difficult IV access? Reassess for an early IV→oral switch at every line failure rather than re‑sticking — see IV → Oral Switch & the DIVA Patient (Quick Reference).

Complicated Pneumonia — Empyema

HOURSIDSA/PIDS 2026 · CPS 2024

Pneumonia + pus or a moderate‑to‑large pleural effusion — antibiotics plus, when needed, drainage with a fibrinolytic.

▸
◈ Definition & stages
  • Empyema = intrapleural pus, or a moderate‑to‑large exudative parapneumonic effusion.
  • It evolves: stage 1 exudative (free‑flowing) → stage 2 fibrinopurulent (loculated) → stage 3 organized (thick fibrinous peel).
  • Small parapneumonic effusions are common in uncomplicated pneumonia and do not need drainage.
  • Lung abscess and necrotizing pneumonia are separate complications.
◣ Recognize & diagnose
  • Suspect it when an initially uncomplicated pneumonia is poorly responsive — persistent fever after 48–72 h, worsening distress or hypoxia, or new effusion signs (decreased breath sounds, dullness, reduced expansion).
  • Imaging: chest radiograph first, then chest ultrasound (confirms effusion, estimates size, distinguishes free‑flowing from loculated). Computed tomography (CT) is not routine — reserve for a suspected alternative diagnosis (e.g., malignancy).
  • Pathogens: S. pneumoniae (most common), S. aureus (incl. MRSA), S. pyogenes (group A streptococcus). Send drained fluid for culture and Gram stain (± pneumococcal PCR where available); blood cultures positive in only ~10%. Labs often show high white‑cell count/ESR/CRP, thrombocytosis, hypoalbuminemia — these normalize with recovery.
How big is the effusion, and how sick is the child?
SMALL / MILD — ANTIBIOTICS ALONE
Small effusion, mild distress, no mediastinal shift → a trial of antibiotics alone is reasonable with close monitoring.
MODERATE–LARGE / COMPROMISE — DRAIN
Moderate‑to‑large effusion, significant respiratory distress, or mediastinal shift → drainage plus antibiotics, early. Consult thoracic surgery / interventional radiology promptly.
◣ Drain when
Moderate‑to‑large effusion or empyema causing respiratory compromise, or occupying much of the hemithorax ± mediastinal shift; loculated (stage 2) or organized collection on ultrasound, or frank pus on aspiration; or failure of antibiotics alone (not improving, or progressing, after an adequate trial).
◈ Fibrinolytic (alteplase / tPA)
  • First‑line, most cost‑effective drainage = small‑bore (≤ 12 Fr) percutaneous chest tube + intrapleural fibrinolytic, preferred over surgical debridement (VATS) in most cases — reserve VATS for refractory disease or extensive loculation. Alteplase 4 mg in 30–50 mL of 0.9% saline (40 mL in the trials; use a smaller volume in small infants per local protocol) instilled via the chest tube, clamp/dwell 1 hour, then drain — once daily for up to 3 doses. tPA alone is now preferred over tPA + DNase (no added benefit, higher cost).,
  • Prescribe and label as ALTEPLASE.
Antibiotics for empyema
AgentDoseNotes
Cefotaxime / ceftriaxone — first‑lineCefotaxime 50 mg/kg/dose q6–8h; ceftriaxone 50 mg/kg/dose q12–24hEmpiric IV cover for the usual pathogens; choose per local antibiogram.,
+ Vancomycin — MRSA15 mg/kg/dose IV q6hReserve for culture‑proven or strongly suspected MRSA / severe disease.
Oral step‑down — culture‑negativeAmoxicillin (high‑dose) or amoxicillin-clavulanateSwitch once drainage complete, improving, and off oxygen.
⚠ Duration, course & follow‑up
  • Total 3–4 weeks is reasonable with adequate drainage and no further complication; transition to oral at or just before discharge once drained, improving, and off oxygen. Persistent fever > 72 h is common and — if the child is otherwise improving — usually not treatment failure; serial CRP can confirm improvement.
  • Outcome is excellent: lung function and radiograph normalize over weeks–months (a repeat film at 2–3 months is reasonable).
  • Watch necrotizing pneumonia for bronchopleural fistula → involve surgery / respirology / infectious diseases.
◣ Admit · Discharge · Refer
  • Admit — every child with a parapneumonic effusion or empyema (BTS 2005), for IV antibiotics ± drainage.
  • Home from the emergency department — not for a parapneumonic effusion or empyema: BTS 2005 advises admission for all. A small effusion in a well child usually needs antibiotics only, no drainage.
  • Home from the ward — not acutely; complete therapy with follow‑up imaging.
  • Refer — now — respiratory/surgery for drainage (chest drain ± fibrinolytics or VATS).

Choking (Foreign‑Body Obstruction)

MINUTES

Sudden cough/stridor/one‑sided wheeze with a choking history.

▸
Mild or severe obstruction?
MILD — effective cough
Coughing effectively, can speak/cry, adequate air movement → encourage coughing, stay, monitor closely; no back blows or thrusts.
SEVERE — responsive
Weak or silent cough, cannot speak or cry, cyanosis or color change, altered consciousness, apnea → start maneuvers now. Infant < 1 yr: 5 back blows → 5 chest thrusts, repeat (no abdominal thrusts). Back blows: infant face down along your forearm, resting on your thigh, head lower than the chest; 5 sharp blows between the shoulder blades. Chest thrusts: turn the infant face up, head still low; 5 thrusts on the lower half of the sternum — like compressions but sharper — with the heel of one hand (AHA/AAP 2025) or two thumbs encircling (ERC 2025)., Child ≥ 1 yr: 5 back blows → 5 abdominal thrusts, repeat (AHA/AAP 2025 and ERC sequence).,
becomes unconscious
Start CPR. Check the mouth before breaths; remove the object only if visible. No blind finger sweeps.
⚠ Remove now
  • Foreign body in the larynx or trachea (central airway), stridor at rest, severe distress or cyanosis, or complete obstruction.
  • Call anesthesia/ENT/PICU early and keep managing the child until they arrive: oxygenate, continue the maneuvers above, prepare laryngoscope and Magill forceps, and bring the front‑of‑neck‑access kit to the bedside (local airway practice).
⚠ Airway team — complete obstruction not relieved by maneuvers
  • Recognize: cannot speak, cry or cough; clutching the neck; silent chest; paradoxical chest/abdominal movement; loss of consciousness. Act after two cycles of maneuvers fail or as soon as the child becomes unresponsive.
  • 1 · Laryngoscopy — remove a visible object with Magill forceps (experienced clinician).
  • 2 · Not removable and rigid bronchoscopy available → operating room now: removal by ENT/thoracic surgery with anesthesia.
  • 3 · Unstable, no immediate rigid bronchoscopy — act by level. At or above the cords: remove under direct laryngoscopy (step 1); if that fails and the child cannot be oxygenated → front‑of‑neck access as the last resort — follow the red zone of the Difficult Airway card (ENT: tracheostomy). Below the cords: push the object distally into one main bronchus (tube or rigid bronchoscope) to ventilate the other lung.
  • Anesthetic principle: prefer spontaneous breathing while the obstruction is partial (positive pressure can complete it); neither technique has been shown superior.
◣ Stable child — suspected inhaled foreign body
  • A convincing choking history mandates bronchoscopy even when the chest X‑ray is normal — only about 11% of inhaled objects are radio‑opaque and the film is normal in about 17% of children.
  • Chest X‑ray (add a lateral view if an object is seen). Look for a radio‑opaque object, unilateral air trapping, atelectasis, mediastinal shift or infiltrate; a normal film does not exclude an inhaled foreign body. CT (virtual bronchoscopy) has a role only in a stable, cooperative child with low suspicion; with a convincing history, go to bronchoscopy.
  • Removal is by rigid bronchoscopy (the gold standard), by ENT or thoracic surgery with an experienced anesthesia team, promptly — a stable child may wait for daytime or transfer to a specialist unit. Flexible bronchoscopy can diagnose and, in experienced centers, retrieve; the flexible scopes in our hospitals are not retrieval instruments.,
◣ Admit · Discharge · Refer
  • Admit — after removal, observe for airway injury/aspiration; any hypoxia, stridor, or incomplete relief → ED/PICU.
  • Home — only when a retained foreign body has been excluded (by bronchoscopy, or by ENT/respiratory review with follow‑up arranged); a child can be fully recovered with an effective cough, normal examination and normal SpO₂ and still have a retained object.
  • Refer — now — ENT/anesthesia for suspected retained foreign body → rigid bronchoscopy.

Obstructive Sleep Apnea

ASSESSAAP · ERS

Flagged here for its acute peri‑operative airway risk (post‑adenotonsillectomy compromise, opioid/sedation sensitivity). Habitual snoring and witnessed apnea; by day, hyperactivity in young children, sleepiness and falling school performance in older ones.

▸
◣ Recognize
  • Obstructive sleep apnea (OSA) — habitual snoring (≥ 3 nights/week), witnessed apnea or gasping, restless sleep, mouth breathing, enuresis; by day — hyperactivity and inattention in toddlers and preschoolers; daytime sleepiness (in the car or class), poor concentration and declining school performance in older children. Peak 2–8 years (adenotonsillar hypertrophy).
  • High‑risk groups: obesity, Down syndrome, craniofacial anomalies, neuromuscular disease, Prader‑Willi, achondroplasia, mucopolysaccharidoses, sickle cell disease.,
  • Work‑up is elective, not an emergency task: refer to ENT and to pediatric pulmonology for a sleep study., Chronic treatment is decided in clinic.,
◣ Red flags
  • Severe OSA — AHI ≥ 10 obstructive events/h and/or nadir SpO₂ < 80% (the AAO‑HNS definition used for peri‑operative risk); nocturnal desaturations or hypoventilation.
  • Cor pulmonale / pulmonary hypertension, failure to thrive — complex, high‑risk: refer to a specialist.
  • Cardiorespiratory failure cannot await elective evaluation — treat urgently.
⚠ Peri‑operative & acute care — the bedside priority
  • Post‑adenotonsillectomy respiratory compromise: anesthesia to assess, and consult PICU for any need for respiratory support.
  • Admit overnight after tonsillectomy if < 3 years, severe OSA (AHI ≥ 10/h and/or SpO₂ nadir < 80%), or a comorbidity: obesity, craniofacial anomaly, neuromuscular disorder, cardiac complications of OSA, current respiratory infection, failure to thrive., Opioids: no codeine or tramadol after tonsillectomy/adenoidectomy under 18 years (FDA); ibuprofen and/or acetaminophen are the first‑line analgesics.,
  • In moderate‑to‑severe OSA, minimize opioids and monitor closely — children with recurrent nocturnal hypoxemia (nadir SpO₂ < 85%) needed about half the morphine dose of children with a nadir ≥ 85% for the same analgesia in a small prospective blinded study (n = 22), so start low and titrate with monitoring.,
  • Position ramped, keep airway adjuncts and CPAP ready.
✦ Pearl — snoring and behavior
A snoring toddler or preschooler who is hyperactive and inattentive may have OSA, not just a behavior problem; in an older child, look for daytime sleepiness and falling grades. Ask about snoring and witnessed apnea at every visit.
◣ Admit · Discharge · Refer
  • Admit — from the emergency department: cardiorespiratory compromise, cor pulmonale or severe hypoventilation. After adenotonsillectomy: admit overnight if < 3 years, severe OSA or a comorbidity (above).,
  • Home from the emergency department — all others, with an urgent outpatient sleep study and ENT referral (severe OSA alone is an urgent outpatient, not an admission).
  • Home from the ward — after adenotonsillectomy, when overnight admission is not indicated: discharge per anesthesia/ENT.,
  • Refer — clinic — ENT (adenotonsillectomy) and pediatric pulmonology (sleep study); cardiology if pulmonary hypertension. OSA persists after adenotonsillectomy in up to 40% — re‑refer to pediatric pulmonology/ENT if snoring or symptoms continue (options include CPAP, weight management, sleep endoscopy‑guided surgery and rapid maxillary expansion).

Cow's Milk Protein Allergy

ASSESSINFANT · ESPGHAN 2024 · WAO DRACMA 2023–24 · CPS 2024

The commonest infant food allergy — IgE‑mediated (immediate) or non‑IgE (delayed, cell‑mediated). Over‑diagnosis is common.

▸
◈ See also Acute FPIES (vomiting 1–4 h after a food — criteria and emergency treatment).
◣ Recognize the two patterns
  • IgE‑mediated (minutes–2 h): urticaria, angioedema, vomiting, wheeze, anaphylaxis. Testing: skin‑prick test or specific IgE to cow's milk when the history suggests an immediate reaction — a positive result may indicate sensitization only; allergy referral is indicated.
  • Non‑IgE (hours–days): blood or mucus in the stool, eczema flare, faltering growth, chronic diarrhea; reflux, colic, loose stools or constipation — these four are, on their own, common in healthy infants. Distinct from lactose intolerance (an enzymatic, non‑immune condition).
  • Confirming non‑IgE disease: a 2–4‑week diagnostic elimination (maternal cow's‑milk‑free diet if breastfed; extensively hydrolyzed formula if formula‑fed) followed by planned reintroduction — improvement alone is not enough, because up to 20% of breastfed infants with blood in the stool settle with no change at all. FPIES is the exception: a typical history with resolution on withdrawal is sufficient; a supervised challenge, in a medical facility and according to protocol, only if the history is unclear.
⚠ When to start an elimination — observe first
  • Start a 2–4‑week diagnostic elimination for: severe or persistent bleeding; faltering growth; moderate–severe eczema not responding to treatment; or a strong overall picture of CMPA.
  • Unneeded maternal elimination shortens breastfeeding, and therapeutic formulas taste different and may shape later food preferences — both are reasons to hold the threshold.
◣ Non‑IgE subtypes — recognize the pattern
  • Food protein‑induced allergic proctocolitis (FPIAP) — a well‑appearing infant with blood/mucus streaks in the stool, onset 2–8 weeks; the most common subtype; up to 50% of affected infants are breastfed; mostly benign and self‑limiting.,
  • Food protein‑induced enteropathy (FPE) — chronic diarrhea with faltering growth and malabsorption (steatorrhea, hypoalbuminemia, anemia); emesis and distension may accompany. A thriving infant with loose stools alone does not have FPE. Uncommon. If the picture fits and CMPA is likely, start the elimination and expect improvement within 1–4 weeks; refer to pediatric GI — endoscopy with biopsy (villous atrophy, crypt hyperplasia) confirms the diagnosis and is prioritized when response is poor, features are severe or another cause is suspected. Exclude infection with stool studies and cystic fibrosis with a sweat test; celiac testing applies only once gluten is in the diet.,,
  • Food protein‑induced enterocolitis syndrome (FPIES) — profuse repetitive vomiting 1–4 h after the food, pallor, lethargy ± diarrhea; ~15% develop hypovolemic shock. Rare; mimics sepsis. Criteria and acute treatment: Acute FPIES.
Management — by feeding & subtype (every elimination is a 2–4‑week diagnostic trial, then reintroduce to confirm)
SituationFirst choiceNotes
IgE‑mediated — anaphylaxisAmino acid formula (AAF)DRACMA XVI advises AAF for severe cow's milk allergy; this guide applies that to anaphylaxis and starts AAF from the outset.
IgE‑mediated — milder immediate reactionExtensively hydrolyzed formula (EHF)Step up to AAF only per the rule in the Avoid box below.
IgE‑mediated, breastfedContinue breastfeedingIf the infant is symptom‑free on breast milk, no maternal elimination; eliminate maternal cow's milk only if the infant reacts while exclusively breastfed.
Mixed‑fed (breast + formula)Change the formula; keep breastfeedingIf symptoms occur only with formula and the infant is well on breast milk, use EHF (or AAF per the rows above) and do not restrict the mother's diet — IgE‑CMPA and FPIES., For FPIAP/FPE the same approach is reasonable; add maternal elimination only if symptoms persist on breast milk alone.
FPIAP, breastfed — threshold metMaternal cow's‑milk‑free dietCow's milk (and other mammalian milks) first; remove soy from the maternal diet only if no response after 2–4 weeks (CPS removes both from the start; ESPGHAN cow's milk only)., Continue breastfeeding; dietitian for calcium and vitamin D.
FPIAP, formula‑fed — threshold metExtensively hydrolyzed formula (EHF); amino acid formula (AAF) if no responseWhether to eliminate at all in formula‑fed FPIAP is debated (a cohort linked it to later IgE‑CMPA); if started, reintroduce afterwards. Soy formula is an option > 6 months if tolerated.
FPE, breastfedMaternal cow's‑milk‑free diet, 2–4 wksRemove soy from the maternal diet if no response; monitor growth and nutrition — resolution takes weeks. No improvement → AAF and pediatric GI.,
FPE, formula‑fedAmino acid formula (AAF)First‑line (not EHF) given the malabsorption; pediatric GI.
FPIES, breastfedContinue breastfeedingRare in this group. If reacting to breast milk or faltering: maternal elimination of the trigger with allergy input; if unresolved, consider stopping breastfeeding → EHF/AAF.
FPIES, formula‑fedEHF first; AAF if no improvement in 2 wks10–20% need AAF from the start; AAF preferred if faltering. Strictly avoid all forms (incl. heated/baked) of the trigger.
⚠ Avoid & who decides
  • Avoid: goat's / sheep's milk (high cross‑reactivity) and partially hydrolyzed / “comfort” or “HA” formulas.
  • Step up: EHF → AAF only after 2–4 weeks without response and after checking the diet for hidden milk and reconsidering the diagnosis; AAF is first‑line only for anaphylaxis, FPIES with faltering growth, or FPE.,
  • Who decides: the treating pediatrician may start EHF or a maternal trial; the step to AAF and any prolonged maternal elimination are confirmed with allergy/GI, with a dietitian monitoring calcium and growth.
✦ Re‑challenge
After a confirmed diagnosis, the timing and setting of re‑challenge are planned by the specialist (allergy or pediatric GI). FPIES: supervised challenge — see Acute FPIES.
◣ Admit · Discharge · Refer
  • Admit — from the emergency department: IgE‑mediated reaction with anaphylaxis (manage, observe and admit per Anaphylaxis); acute FPIES with lethargy, dehydration or shock (see Acute FPIES).
  • Home from the emergency department — after assessment: the well infant with blood‑streaked stool, mild immediate symptoms that have resolved, or chronic symptoms — with the observe‑first advice above, written warning signs, and clinic follow‑up within 2–4 weeks; start a diagnostic elimination only if the threshold is met.
  • Home from the ward — once feeding and growing, with the dietary plan, dietitian review and the reintroduction date written down.
  • Refer — now — allergy for anaphylaxis (urgent).
  • Refer — clinic — allergy: IgE‑mediated disease for testing and challenge, FPIES, multiple food allergies; pediatric GI: FPE, faltering growth, no response to EHF, diagnostic doubt; dietitian for every infant on an elimination diet.
◈ Basis ESPGHAN 2024 position paper; WAO DRACMA VII (2023, elimination and reintroduction), X (2023, breastfeeding) and XVI (2024, nutritional management); Canadian Paediatric Society 2024 (non‑IgE subtypes); international FPIES consensus 2017. Where CPS and ESPGHAN differ (maternal soy; observation before elimination) the card follows ESPGHAN and says so.

Acute FPIES (Food Protein‑Induced Enterocolitis Syndrome)

HOURSINFANT · FPIES CONSENSUS 2017

Repetitive vomiting 1–4 h after a food, with pallor and lethargy — a non‑IgE reaction that mimics sepsis; fluids and ondansetron, not epinephrine.

▸
◣ Recognize — 2017 international criteria
  • Major criterion (required): vomiting 1–4 h after ingestion of the suspect food and no classic IgE‑mediated skin or respiratory symptoms.
  • Plus ≥ 3 minor criteria: a second episode after the same food · repetitive vomiting 1–4 h after a different food · extreme lethargy · marked pallor · emergency‑department visit · need for IV fluids · diarrhea within 24 h (usually 5–10 h) · hypotension · hypothermia.
  • Triggers: cow's milk and soy in infants; rice and oat are the commonest solids; also egg, fish, poultry, vegetables. Onset is usually with the first exposures to formula or solids, typically at 2–7 months.,
  • Looks like: sepsis, surgical abdomen, gastroenteritis, metabolic crisis. Clues: the timing after a new food, a well child an hour earlier, rapid recovery with fluids. Blood tests may show neutrophilia, thrombocytosis, acidosis and methemoglobinemia.,
Acute management by severity (FPIES consensus 2017)
SeverityFeaturesTreatment
Mild1–2 vomits, no lethargyOral rehydration — breastfeeding or clear fluids; if ≥ 6 months, ondansetron IM 0.15 mg/kg (FPIES consensus max 16 mg; this guide caps a single pediatric dose at 8 mg — see Gastroenteritis) may be considered. Can resolve at home.
Moderate≥ 3 vomits, mild lethargyOndansetron IM/IV 0.15 mg/kg (FPIES consensus max 16 mg; this guide caps a single pediatric dose at 8 mg — see Gastroenteritis); consider IV access and 0.9% saline 20 mL/kg, repeated as needed; monitor vital signs and observe for at least 4–6 h from onset, until tolerating fluids.
Severe≥ 3 vomits with severe lethargy, hypotonia, ashen or cyanotic appearance, hypotensionIV access; 0.9% saline 20 mL/kg rapidly, repeat as needed; ondansetron IV 0.15 mg/kg (FPIES consensus max 16 mg; this guide caps a single pediatric dose at 8 mg — see Gastroenteritis); consider methylprednisolone IV 1 mg/kg (max 60–80 mg); blood gas, electrolytes, glucose, CBC; correct acid–base and electrolyte abnormalities and methemoglobinemia; manage as shock (see Shock).
⚠ Pitfalls
  • Epinephrine does not treat FPIES (not IgE‑mediated); give it only if anaphylaxis cannot be excluded — see Anaphylaxis.
  • Do not label a sepsis‑like infant as FPIES until the timing fits and infection has been considered; when in doubt treat for both.
  • Ondansetron ≥ 6 months only; monitor the QT interval if repeated (QTcQTc).
◣ Admit · Discharge · Refer
  • Admit — severe reaction, hypotension, ongoing vomiting or lethargy, or dehydration.
  • Home from the emergency department — mild reaction: tolerating oral fluids and well after about 4–6 h of observation from the onset of the reaction. Moderate reaction: observe in the emergency department for at least 4–6 h from onset, until drinking and lethargy has resolved, then home. Both with a written plan to avoid the trigger in all forms and to return for repetitive vomiting after any new food.
  • Refer — clinic — allergy for every new diagnosis (trigger confirmation, written emergency plan, supervised re‑challenge usually 12–18 months after the last reaction); dietitian when a staple food is removed. Chronic feeding choices: see Cow's Milk Protein Allergy.,,
◈ Basis International consensus guidelines for FPIES (Nowak‑Węgrzyn 2017); ESPGHAN 2024 for the diagnostic approach.

Antibiotic Allergy Assessment & Pretesting

ASSESS

Most allergy labels are false. Take a history, don't routinely skin‑test, and de‑label when you can.

▸
◣ The label is usually wrong
  • About 10% of people carry a penicillin/beta‑lactam allergy label, but ~90% are not truly allergic: only 5–10% of children with a “penicillin allergy label” have a true penicillin allergy.
  • Most labels accumulate from non‑allergic events — GI upset, headache, family history, or a viral rash during treatment.
  • In children, a maculopapular rash is more often viral than allergic.
  • Routine pre‑dose intradermal "test dosing" is not standard of care, not validated, and should be abandoned — it delays therapy and misleads (a positive skin test over‑diagnoses allergy — its positive predictive value is below 100%; it misses dose‑independent and enteral reactions).
◈ Why mislabeling harms
A beta‑lactam label drives second‑line agents (vancomycin, clindamycin, fluoroquinolones) that are less effective, broader, and costlier — linked to more C. difficile (+23%), MRSA (+14%) and vancomycin‑resistant enterococci (VRE) (+30%) infections and longer hospital stays (Macy & Contreras, J Allergy Clin Immunol 2014), and to more surgical‑site infections. No reaction history — or a beta‑lactam tolerated since — give the drug. No skin test required.
◣ Risk‑stratify the history — severity, timing, drug class, and any beta‑lactam tolerated since
◈ Reading the tiers
  • Assign the highest tier any feature reaches — one high‑risk feature makes the patient high‑risk.
  • Risk rises with reaction severity (intolerance → hives → anaphylaxis / severe delayed), immediacy (delayed benign → immediate IgE), and recency (remote → recent). None / Low → give the drug or refer for an allergist‑supervised oral challenge; Medium → skin test ± challenge, pick a non‑cross‑reacting oral beta‑lactam meanwhile; High → avoid the culprit, refer, do not challenge.
  • The pediatric category method is preferred; adult scores (e.g., the PEN‑FAST penicillin‑allergy score) are not robustly validated in children. The table below applies to a child with a reported penicillin allergy (cephalosporin allergy excluded).
RiskHistory (any of)Action
History not consistent with allergyNo previous allergic reaction; side effects / intolerance only (GI upset, headache); a reaction history but tolerated the antibiotic since the index event; family history only.De‑label the record. Give penicillin if indicated.
LowBenign, non‑severe delayed reaction — e.g., maculopapular rash starting ≥ 3 days into the course, with no mucosal, blistering, systemic or organ involvement.Oral amoxicillin challenge under allergist supervision (skin testing not required). Tolerated → de‑label the record; give penicillin when indicated.
MediumUrticaria (hives) or other immediate, IgE‑type reaction without anaphylaxis; a "rash" where hives cannot be excluded.Refer to an allergist. Avoid penicillin. See the side‑chain chart below for prescribing oral cephalosporins — oral use only, not IV/IM.
HighAnaphylaxis; recurrent reactions or reactions to multiple beta‑lactams; prior positive skin test; any severe delayed reaction — Stevens‑Johnson syndrome / toxic epidermal necrolysis (SJS/TEN), drug reaction with eosinophilia and systemic symptoms (DRESS), serum sickness, hemolytic anemia, nephritis, hepatitis.Do not test or challenge. Refer to an allergist. Anaphylaxis / immediate reactions: avoid penicillins and cephalosporins. Severe delayed reactions (SJS/TEN, DRESS, serum sickness, organ involvement): avoid all penicillins and cephalosporins.
⚠ When to involve an allergist
Any type‑1 (immediate / IgE‑mediated) reaction — urticaria, angioedema, wheeze, or anaphylaxis — prompts allergist referral; more nuanced than the table alone, which is a triage aid, not a substitute for specialist assessment.
Beta‑lactam cross‑allergy — by side‑chain structure
◈ How to use this chart
  • For oral use only — not IV/IM. Prescribing an oral cephalosporin for a penicillin‑allergic child: choose one that does not share a similar side‑chain structure with penicillins (a “✓” against the penicillin columns below).
  • Cross‑reactivity follows side‑chain similarity — not the shared beta‑lactam ring. Use only for immediate / IgE histories (non‑anaphylactic) — never after anaphylaxis and never for SJS/TEN/DRESS, where all beta‑lactams are avoided.
Beta‑lactam cross‑reactivity by side‑chain structure
Beta‑lactamsAmoxicillinAmpicillinCloxacillinPenicillinPiperacillinCefadroxilCefazolinCephalexinCefoxitinCefprozilCefuroximeCefiximeCefotaximeCeftazidimeCeftriaxoneCefepimeErtapenemImipenemMeropenem
AmoxicillinX1X5X4X3X1✓X1✓X2✓✓✓✓✓✓✓✓✓
AmpicillinX1X5X4X3X2✓X2✓X2✓✓✓✓✓✓✓✓✓
CloxacillinX5X5X5X5✓✓✓✓✓✓✓✓✓✓✓✓✓✓
PenicillinX4X4X5X5✓✓✓X3✓✓✓✓✓✓✓✓✓✓
PiperacillinX3X3X5X5X3✓X3✓X3✓✓✓✓✓✓✓✓✓
CefadroxilX1X2✓✓X3✓X1✓X2✓✓✓✓✓✓✓✓✓
Cefazolin✓✓✓✓✓✓✓✓✓✓✓✓✓✓✓✓✓✓
CephalexinX1X2✓✓X3X1✓✓X2✓✓✓✓✓✓✓✓✓
Cefoxitin✓✓✓X3✓✓✓✓✓X2✓✓✓✓✓✓✓✓
CefprozilX2X2✓✓X3X2✓X2✓✓✓✓✓✓✓✓✓✓
Cefuroxime✓✓✓✓✓✓✓✓X2✓X3X1X3X1X2✓✓✓
Cefixime✓✓✓✓✓✓✓✓✓✓X3X3X3X3X3✓✓✓
Cefotaxime✓✓✓✓✓✓✓✓✓✓X1X3X3X1X1✓✓✓
Ceftazidime✓✓✓✓✓✓✓✓✓✓X3X3X3X3X3✓✓✓
Ceftriaxone✓✓✓✓✓✓✓✓✓✓X1X3X1X3X1✓✓✓
Cefepime✓✓✓✓✓✓✓✓✓✓X2X3X1X3X1✓✓✓
Ertapenem✓✓✓✓✓✓✓✓✓✓✓✓✓✓✓✓X5X5
Imipenem✓✓✓✓✓✓✓✓✓✓✓✓✓✓✓✓X5X5
Meropenem✓✓✓✓✓✓✓✓✓✓✓✓✓✓✓✓X5X5
Penicillin1st‑gen cephalosporin2nd‑gen cephalosporin3rd‑gen cephalosporin4th‑gen cephalosporinCarbapenem
✓Different structure — considered safe
X1Same side chain — clinical evidence of reaction
X2Same side chain — theoretical risk of cross‑reaction
X3Similar side chain — potential risk of cross‑reaction
X4Beta‑lactam ring — clinical evidence of reaction
X5Beta‑lactam ring — theoretical risk of reaction

Read row drug against column drug. ✓ = considered safe; X¹–X⁵ grade the cross‑reactivity risk (see key). Diagonal (same drug) shown solid.

◣ Children with a cephalosporin allergy
  • Immediate hypersensitivity to a cephalosporin — avoid the culprit and cephalosporins sharing its side chain (see chart) and refer to allergy. Non‑anaphylactic reaction (e.g., urticaria): a penicillin, or a cephalosporin with a dissimilar side chain, may be used. Anaphylaxis: use a carbapenem or non‑beta‑lactam alternative until allergist testing; penicillins/dissimilar cephalosporins only after allergist assessment.
  • Inpatient / ICU — avoid all cephalosporins and penicillins and use alternatives; consult Allergy / ID if a penicillin or cephalosporin is the recommended first‑line treatment.
  • Severe cutaneous reaction (SJS/TEN/DRESS) — avoid all penicillins, cephalosporins, and carbapenems; use an alternative and consult allergy or ID.
◈ Basis Kuwait Pediatric Council practice point on skin testing before antibiotic administration; risk table adapted from the Canadian Paediatric Society and Devchand & Trubiano; pathway aligned with the CHOP Penicillin Allergy Clinical Pathway and the AAAAI/ACAAI 2022 drug‑allergy practice parameter. Apply to the local antibiogram; verify doses before use.
⚠ Never test these
Anaphylaxis, SJS/TEN, DRESS, acute generalized exanthematous pustulosis (AGEP), serum sickness, cytopenias, interstitial nephritis, or hepatitis — no skin test, no challenge; refer to an allergist.

Hereditary Angioedema — Acute Attack

MINUTES

Bradykinin‑mediated swelling that does not respond to epinephrine, antihistamine, or steroid.

▸
◣ Recognize
  • Recurrent angioedema without urticaria or itch; laryngeal swelling, abdominal attacks; family history; known C1‑esterase inhibitor deficiency.
  • If anaphylaxis cannot be excluded, give intramuscular epinephrine first (see Anaphylaxis) — failure to respond supports the diagnosis.
Airway is the danger — early anesthetics/ENT for any laryngeal involvement
Specific therapy Give a hereditary angioedema (HAE)‑specific agent early; earlier treatment means a milder, shorter attack. Every child with HAE should have on‑demand therapy available at all times.,
DrugDoseRoute & notes
C1‑esterase inhibitor concentrate20 units/kgIV; best safety evidence in children — first‑line
IcatibantWeight‑based (max 30 mg):
10 mg (12–25 kg)
15 mg (26–40 kg)
20 mg (41–50 kg)
25 mg (51–65 kg)
30 mg (>65 kg)
SC (subcutaneous); bradykinin B2‑receptor antagonist; ready‑to‑use prefilled syringe. Not recommended < 2 years or < 12 kg — no dose established (EMA label, licensed from 2 years; the US FDA label covers adults ≥ 18 years only)
Sebetralstat (oral; ≥ 12 years — availability in Kuwait to confirm)600 mg (two 300 mg tablets) at the first sign
repeat once after ≥ 3 h if inadequate
max 1,200 mg/24 h
with a moderate CYP3A4 inhibitor (e.g., erythromycin, fluconazole): 300 mg, repeat once after ≥ 3 h
Oral plasma kallikrein inhibitor; first‑line on‑demand option from 12 years in the 2026 international pediatric guideline; not approved < 12 years. Avoid with strong CYP3A4 inhibitors (e.g., clarithromycin, itraconazole) — use a parenteral agent. Severe laryngeal attacks were not studied — use a parenteral agent
Fresh frozen plasma10 mL/kgIV; only if specific agents unavailable
◣ Admit · Discharge · Refer
  • Admit — laryngeal or severe attacks → a monitored bed.
  • Home — after resolution with on‑demand therapy and a written plan.
  • Refer — clinic — immunology/allergy (diagnosis, prophylaxis).

When to Suspect Primary Immunodeficiency (IEI)

ASSESS

Inborn errors of immunity — think of it before the next live vaccine or transfusion.

▸
◣ When to suspect — the SPUR pattern
  • Severe, Persistent, Unusual (opportunistic organism or unusually severe course), or Recurrent infection.
  • Family history of immunodeficiency or unexplained early infant death, parental consanguinity, failure to thrive, infections needing intravenous antibiotics or admission.
  • Classic thresholds: ≥ 2 pneumonias or ≥ 4 new ear infections in a year, ≥ 2 deep‑seated infections (abscess, osteomyelitis), persistent oral/skin thrush after age 1, or little response to ≥ 2 months of antibiotics.,
  • Non‑infectious red flags (increasingly recognized): autoimmune cytopenias — especially chronic, refractory, or multi‑lineage — early or treatment‑resistant inflammatory bowel disease (< 2 years), granulomas, lymphoproliferation, severe eczema.
Overview — infection pattern → likely defect
Infection patternThinkTypical clues
Recurrent sino­pulmonary (encap­sulated bacteria), onset mostly after 6 monthsAntibody deficiencyAgammaglobulinemia, common variable immunodeficiency (CVID), IgA deficiency; low immunoglobulins
Early severe viral/​fungal/​oppor­tunistic infection, chronic diarrhea, failure to thriveCombined / T‑cellSevere combined immunodeficiency (SCID): lymphopenia, may have absent thymic shadow — a pediatric emergency (below)
Deep abscesses, unusual organisms (Serratia, Burkholderia, Aspergillus), poor wound healingPhagocyte defectChronic granulomatous disease; leukocyte adhesion deficiency (delayed cord separation)
Recurrent Neisseria (meningo­coccal) or encap­sulated‑​organism infection, or lupus‑like diseaseComplement deficiencyEarly‑onset, recurrent or familial meningococcal disease; lupus‑like autoimmunity (early classical‑pathway defects)
⚠ Suspected SCID is a pediatric emergency
  • Infant in the first months of life with severe or persistent infection, chronic diarrhea, failure to thrive, oral thrush, or an absolute lymphocyte count < 2.5–3 ×10⁹/L (or a positive newborn T‑cell receptor excision circle (TREC) screen) may have severe combined immunodeficiency.
  • Diagnose before live vaccines, non‑irradiated blood, or overwhelming infection — allows a life‑saving transplant.
  • Phone pediatric immunology the same day.
✦ First‑line screen
  • Full blood count with differential (absolute lymphocyte and neutrophil counts), immunoglobulins (IgG, IgA, IgM, IgE), lymphocyte subsets (T/B/NK by flow cytometry), complement (CH50/AH50 — total classical / alternative‑pathway complement activity), and specific antibody responses (vaccine titers, isohemagglutinins); HIV test — exclude secondary immunodeficiency before labeling an inborn error.
  • Add a neutrophil oxidative‑burst test (dihydrorhodamine) if a phagocyte defect is suspected. Save a pre‑treatment serum sample before giving intravenous immunoglobulin (IVIG).
  • To diagnose infections do not rely on serology — antibody production is impaired and IVIG transfers donor antibody; use culture, PCR or antigen detection.
⚠ Acute do / don't when IEI is suspected
  • Do not give live vaccines (BCG, oral polio, rotavirus, MMR, varicella, yellow fever) — they can cause fatal vaccine‑strain disease.
  • If blood products are needed, use only irradiated, CMV‑negative, leukoreduced products (prevents transfusion‑associated graft‑versus‑host disease).
  • Do not delay empiric antibiotics for fever — treat any infection promptly and aggressively; avoid non‑essential steroids/immunosuppression before a diagnosis.
⚠ Suspected SCID — emergency management, under pediatric immunology direction
  • A medical emergency: immunology the same day; confirmatory testing (lymphocyte subsets ± TREC) at a center able to interpret it.,
  • Strict protective isolation from the moment of suspicion — at home or in hospital, at the treating immunologist's discretion (centers differ; infection rates were similar at home and in hospital). At home: caregivers are counselled on safe isolation — no public outings, primary‑care visits deferred, and clinic visits planned so the infant goes straight into a cleaned room, not a waiting room. In hospital: a single positive‑pressure room (HEPA‑filtered or laminar‑flow where available); hand washing, then mask, gown and gloves for everyone entering; non‑essential staff stay out and visitors are kept to a minimum.,,
  • Treat any infection promptly and aggressively — diagnose with cultures, antigen detection and PCR; do not rely on serology. Pneumocystis jirovecii pneumonia (PJP) is frequent — chest X‑ray and bronchoalveolar lavage; if suspected or proven, co‑trimoxazole (trimethoprim‑sulfamethoxazole) 20 mg/kg/day of trimethoprim IV in divided doses.
  • Prophylaxis from 4 weeks of age: co‑trimoxazole 5 mg/kg/day of trimethoprim once daily and fluconazole 5 mg/kg/day once daily — younger infants: consult immunology / infectious diseases (sulfonamides displace bilirubin); RSV prophylaxis (nirsevimab, clesrovimab or palivizumab) in the RSV season,; CMV prophylaxis at the treating immunologist's discretion.,
  • IVIG replacement 400–600 mg/kg every 3–4 weeks.,
  • Only irradiated, CMV‑negative, leukoreduced blood products; all live vaccines are contraindicated for the child with SCID or suspected SCID. Healthy household contacts: oral polio vaccine is contraindicated — use the inactivated (injectable) polio vaccine instead (live intranasal influenza and smallpox vaccines are also contraindicated; they are not given in Kuwait); all other vaccines are permitted. If a household contact develops a rash after varicella vaccine, isolate the child with SCID from that contact and contact health care for varicella‑zoster immunoglobulin (VZIG). Suspend breastfeeding until maternal CMV serology is known — the mother can express and store milk; resume if she is CMV‑seronegative. Contact with chickenpox or shingles: seek immediate medical attention for varicella‑zoster immunoglobulin (VZIG), as early as possible after exposure.,
  • Growth failure → parenteral nutrition, and involve a dietitian early.
  • Involve the transplant (HSCT) team immediately and plan early hematopoietic cell transplantation (or gene therapy) once the diagnosis is confirmed.,
Refer
  • Pediatric immunology for all suspected inborn errors of immunity — the same day for suspected SCID, any opportunistic infection, or profound lymphopenia.
  • IVIG replacement and HLA‑typing proceed under specialist direction.
◣ Admit · Discharge · Refer
  • Admit — as dictated by the presenting infection.
  • Home — per the acute problem (from the emergency department or the ward, as that card dictates), with the workup arranged.
  • Refer — clinic — immunology; avoid live vaccines and use irradiated blood products until cleared.

Pneumothorax — Tension, Traumatic & Spontaneous

MINUTESATLS · NAEMSP 2024 · BTS 2023

Tension: decompress on clinical grounds before any X‑ray. All others: decide who goes home, who is observed, and who needs a drain.

▸
◣ Recognize
  • Tension — rapidly worsening distress and hypoxia with hypotension, unilateral absent/reduced breath sounds, hyper‑resonance, distended neck veins and (late) tracheal deviation — after trauma, in asthma, or in a ventilated child who suddenly desaturates and drops their pressure.,
  • Simple traumatic — blunt or penetrating chest injury, rib fractures, or after a central line or positive‑pressure ventilation. Primary spontaneous — typically a tall, thin adolescent with sudden pleuritic pain ± breathlessness. Secondary spontaneous — asthma, cystic fibrosis, connective‑tissue disease (Marfan, Ehlers–Danlos), congenital lung lesion, necrotizing pneumonia, or ventilation.,,
⚠ Tension pneumothorax — decompress now
  • Tension pneumothorax is a clinical diagnosis — if tension pneumothorax is suspected in an unstable child, do not wait for a chest X‑ray.,
  • Perform immediate needle decompression, or finger thoracostomy where appropriate for the child's size and available expertise, followed by chest‑drain insertion.
  • Not for newborns — neonatal pneumothorax (transillumination, needle/butterfly aspiration) follows the NRP / neonatal unit protocol; see Neonatal Resuscitation.
StepLandmarkNotes
Needle decompression5th intercostal space at the mid‑axillary line, or 2nd intercostal space (over the top of the 3rd rib) at the mid‑clavicular lineOver the top of the rib; aspirate while advancing; ultrasound before puncture whenever time allows.,
Cannula size (suggestions)Infant: 22–20 G × 25–32 mm
Child (≈ 5 y): 20–18 G × 32 mm
Older child (≈ 10 y): 18 G × 45 mm
Adolescent: 16 G × 45 mm (adult‑sized adolescent: adult device)
ATLS range for children: 16–22 gauge, 2.5–4.5 cm, chosen by age and body habitus. These sizes are suggestions. Select an appropriate device for the child's body habitus. The listed length is not the insertion depth. Aspirate continuously during insertion. Once air is aspirated, stop advancing the sharp needle; advance the plastic catheter off the needle and withdraw the needle. Use ultrasound if time allows. Avoid large‑bore cannulas in infants. Chest‑wall thickness varies widely and cannot be predicted from age or weight — choose by body habitus.,,
Finger thoracostomy5th intercostal space, just anterior to the mid‑axillary line (the chest‑drain site)When needle decompression fails, or the child is large enough and expertise is at hand; converts to a drain.
DefinitiveChest drain, 5th intercostal space, just anterior to the mid‑axillary line (same site as in adults)Follows decompression — do not delay for imaging; size by age and indication (hemothorax needs a larger tube); X‑ray afterwards for position.,
◣ Workup (non‑tension)
  • Upright chest X‑ray. Lung ultrasound by a trained operator (absent lung sliding, lung point) is faster and more sensitive than a supine film (meta‑analysis of mostly adult studies) — in trauma as part of eFAST. CT is not needed for a first spontaneous pneumothorax.
◣ Admit · Discharge · Refer — by situation
SituationActionFollow‑up
Tension — any causeDecompress now (needle or finger thoracostomy), then chest drain; PICU.,Inpatient
Drain needed nowHemodynamic compromise, significant hypoxia, bilateral, hemopneumothorax, or a ventilated child with a pneumothorax on X‑ray → chest drain; admit (PICU if ventilated).,Inpatient; pediatric surgery
Traumatic — small, or seen on CT only, child stableAdmit; observe with repeat chest X‑ray. An occult pneumothorax (< 2.7 cm on CT) needs no intervention unless it enlarges or causes symptoms. Drain if it enlarges or the child deteriorates. Observation stays safe if ventilation or an anesthetic is needed, provided a drain can be placed at once; no routine drain before road transfer.,, Before air transfer, discuss a drain with the receiving team.Trauma / pediatric surgery
Primary spontaneous (adolescent) — minimal symptomsNo significant pain or breathlessness, no physiological compromise: observe in the emergency department, no intervention, regardless of size; home if stable on reassessment, with a reliable family and written advice to return at once if breathless.,,Chest X‑ray and respiratory/surgical review in 2–4 weeks; recurrence ≈ 30% after non‑surgical management; no smoking/vaping.,,
Primary spontaneous — symptomaticAdmit; needle aspiration or a small‑bore chest drain.,Surgery if the air leak persists 24–48 h
Secondary spontaneousAsthma, connective‑tissue disease, congenital lung lesion, necrotizing pneumonia: admit; low threshold for a chest drain; respiratory team.Respiratory clinic
Cystic fibrosisLarge (≥ 3 cm apex to cupola): admit, chest drain. Small and stable: close observation. Withhold BiPAP while the pneumothorax is present.Pleurodesis only after a recurrence, never for a first episode; no flying for 2 weeks after resolution
Infants and young childrenAdmit; adult pathways do not apply — decide with pediatric surgery and respiratory.Inpatient
Surgical referral — any groupAir leak beyond 24–48 h; second same‑side or first opposite‑side episode; tension at the first episode; bilateral.,,Pediatric surgery
  • Size: there is no validated pediatric definition. Size alone no longer decides intervention; a rim of ≥ 2 cm laterally or apically is the usual minimum for safe aspiration or drain insertion (adult guidance). Most evidence is adult‑derived (trials enrolled from age 14).
✦ Flying and diving
No flying with an unresolved pneumothorax; fly only ≥ 7 days after X‑ray resolution (2 weeks in CF). Scuba diving is discouraged permanently unless definitive surgery (pleurectomy) has been performed. Adult guidance applied to adolescents.,,
16

Rheumatologic

Cytokine storm (HLH/MAS) & Kawasaki vasculitis

Cytokine Storm — HLH / MAS (Systemic Hyperinflammation)

HOURSEULAR/ACR 2022 · EULAR/PReS 2024

One process, many names: hematology calls it HLH, rheumatology calls it MAS — the joint EULAR/ACR consensus (rheumatology, hematology, immunology, infectious diseases and intensive care) is the common ground this card follows.

▸
◣ Recognize — a pattern that evolves, not a single value
  • Persistent fever that looks like sepsis but does not respond, hepatosplenomegaly, falling counts (≥ 2 lines), very high or rising ferritin, rising triglycerides, falling fibrinogen, rising transaminases and LDH, coagulopathy/DIC, and CNS signs (irritability, seizures, altered consciousness). Individual findings are non‑specific — read them together and over time.
  • Examine perfusion first — tachycardia with cool extremities, prolonged capillary refill or reduced urine output at a normal blood pressure is compensated shock; myocardial dysfunction is common in hyperinflammation, so get an early echocardiogram,.
  • In sJIA / Still’s disease: a falling ESR with rising CRP and ferritin, a falling platelet or white count from a high baseline, and hypofibrinogenemia are early clues (consumption). On canakinumab or tocilizumab the fever and the ferritin rise may be blunted or delayed; the risk also rises when steroids or biologics are tapered,.
  • Ferritin: send it in every child with new or heightened suspicion, even if a previous value was normal, and repeat daily. > 500 ng/mL is 84% sensitive in children (the Histiocyte Society cut‑off) but not specific; pediatric studies use 500–2,000; a rapidly rising or very high (> 10,000) ferritin is highly suggestive.
  • The same process complicates infection (EBV, CMV, dengue, leishmaniasis, tuberculosis, typhoid, brucellosis), malignancy (leukemia, lymphoma), rheumatic disease (sJIA, lupus, Kawasaki), MIS‑C, immunotherapy, and inborn errors (familial HLH, XLP, Chédiak–Higashi, Griscelli).
Criteria — useful in the setting they were built for; none is sufficient everywhere
ToolBuilt forRule
HLH criteria — HLH‑2004, revised 2024HLH (hematology pathway): primary/familial HLH and secondary HLH outside rheumatic disease — not for MAS in sJIA (use MAS‑2016 below)5 of 7: fever ≥ 38.5 °C · splenomegaly · cytopenias in ≥ 2 lines (Hb < 90 g/L, < 100 g/L under 4 weeks; platelets < 100 × 10⁹/L; neutrophils < 1.0 × 10⁹/L) · fibrinogen ≤ 1.5 g/L and/or triglycerides ≥ 3.0 mmol/L (265 mg/dL) · ferritin ≥ 500 µg/L · hemophagocytosis in marrow or other tissue · sCD25 ≥ 2,400 U/mL. NK‑cell activity is no longer a criterion (Histiocyte Society 2024): low perforin or defective degranulation is a separate cellular pathway that supports familial HLH, as do biallelic pathogenic variants or an affected sibling.,
MAS‑2016Febrile child with known or suspected sJIAFerritin > 684 ng/mL and any 2 of: platelets ≤ 181 × 10⁹/L · AST > 48 U/L · triglycerides > 156 mg/dL · fibrinogen ≤ 360 mg/dL
MS scoreMS scoreSeparating MAS from an sJIA flare7 items (CNS dysfunction, bleeding, active arthritis, platelets, fibrinogen, LDH, ferritin); score ≥ −2.1 → MAS (sensitivity 0.85, specificity 0.95)
HScoreAdults; infection- or malignancy‑associated HLHProbability from < 1% (≤ 90) to > 99% (≥ 250); online calculator
⚠ Do not wait to satisfy a set of criteria before treating a deteriorating child
  • In a child with high‑risk features or progression, start empiric immunomodulation during the initial evaluation — diagnostic work‑up, treatment of the trigger and prevention of complications run in parallel,.
◣ Work‑up — starts on suspicion, in parallel with treatment
  • First tier (any hospital, same day): CBC + film, ferritin, CRP, ESR, fibrinogen, D‑dimer, PT/APTT, triglycerides, AST/ALT/GGT/bilirubin/albumin, LDH, creatinine, sodium; blood cultures; EBV and CMV PCR, HIV; other infections by exposure (dengue or malaria after travel, tuberculosis, leishmaniasis, typhoid, brucellosis) — hyperinflammation can be the presentation of an infection. Send serology before IVIG.
  • Second tier (with the specialist teams): sCD25 (soluble IL‑2 receptor‑α) — the most useful confirmatory test where available; bone marrow (also for malignancy — obtain before steroids when malignancy is plausible and it will not delay treatment; hemophagocytosis is neither required nor specific); IL‑18 and CXCL9 where available; NK‑cell function, CD107a degranulation, perforin/SAP/XIAP flow cytometry.
  • Genetics early in every child (multigene panel or exome), and in anyone with consanguinity, family history, recurrence, albinism or prominent CNS disease — consanguinity makes this especially relevant in Kuwait; a genetic diagnosis changes treatment, prognosis and family counseling.
  • CNS: assess every child < 1 year, any suspected familial disease and any neurological sign — CSF (cells, protein, glucose, cytology) and contrast MRI — without delaying treatment.
Treat — empiric immunomodulation early; treat the trigger at the same time (antimicrobials by exposure; an active infection does not delay MAS treatment),
StepDrug & doseNotes
1 · Methyl­predniso­lone — MAS pathway and undiffer­entiated hyper­inflammationMethyl­predniso­lone pulse 15–30 mg/kg/day IV (max 1 g) × 3 days
then 2 mg/kg/day divided
Strongest evidence across all forms of HLH/MAS; shorter‑acting agents are preferred while the diagnosis is still evolving,
1 · Dexa­methasone — HLH pathway (hematology leads) or CNS involvement10 mg/m²/day IV or PO
(≈ 2–4 mg/kg/day methyl­prednisolone)

HLH‑94/2004 8‑week taper:
Wk 1–2 · 10 mg/m²/day
Wk 3–4 · 5 mg/m²/day
Wk 5–6 · 2.5 mg/m²/day
Wk 7 · 1.25 mg/m²/day
Wk 8 · taper to zero
Preferred when HLH is the leading diagnosis because it crosses the blood–brain barrier (better CNS penetration). Long half‑life — a shorter‑acting steroid is preferable while the diagnosis is still evolving.,,
2 · Add early — MAS / sJIA, Kawasaki or MIS‑C overlap, undiffer­entiated hyper­inflammationAnakinra (IL‑1 receptor antagonist)
2–4 mg/kg/day (above the standard 1–2 mg/kg/day)
Critically ill: escalate to 10 mg/kg/day, divided q6–12 h or repeated IV doses
(EULAR/ACR 2022 table: 5–10 mg/kg/day, IV preferred, or SC)
Immunomodulation without immunosuppression; short half‑life; does not obscure a malignancy work‑up,,
2 · IVIG1–2 g/kgEndorsed for empiric use, especially with Kawasaki/MIS‑C overlap; a large colloid load — caution with cardiac dysfunction
3 · Inadequate response at 24–72 h, or severe / rapidly worsening — with the reference teamCiclosporin oral or IV, level‑guided
or tacrolimus 0.1 mg/kg/day PO divided q12h, trough 8–20 ng/mL (EULAR/ACR alternative)
For MAS; not for primary HLH (proven ineffective). Combination therapy on a background of high‑dose glucocorticoid is often needed and may be initial therapy in severe MAS,
3 · Emapalumab (anti‑IFN‑γ)Primary HLH: 1 mg/kg IV twice weekly (with dexamethasone)

Still’s / sJIA‑MAS: 6 mg/kg once, then 3 mg/kg every 3 days to day 16, then twice weekly

If response unsatisfactory — Primary HLH: increase to 3 mg/kg (from day 4), 6 mg/kg (from day 7), max 10 mg/kg/dose (from day 10). Still’s / sJIA‑MAS: increase to a maximum cumulative 10 mg/kg over 3 days (interval may be shortened to every 2 days or daily); reduce once improved
FDA‑approved for primary HLH that is refractory, recurrent or progressive on (or intolerant of) conventional therapy, and for HLH/MAS in known or suspected Still’s disease with inadequate response or intolerance to glucocorticoids or recurrent MAS; test for latent TB before starting and consider zoster, Pneumocystis and antifungal prophylaxis; monitor for TB, adenovirus, EBV and CMV,
3 · RuxolitinibSpecialist, off‑labelJAK inhibition; promising in refractory HLH/MAS,
3 · Etoposide‑­based (HLH‑94)Hematology‑directed

Primary/familial HLH, severe EBV‑HLH:
HLH‑94 induction — etoposide 150 mg/m² IV twice weekly wk 1–2, then weekly to wk 8, with the dexamethasone taper above

Secondary HLH — severe, or no response to steroids ± IVIG at 72 h:
start etoposide promptly — children 150 mg/m² once weekly; older teenagers 50–100 mg/m²
Dose per m² also under 10 kg (some centers use 5 mg/kg). Renal: reduce 25% if creatinine clearance 20–40, 50% if < 20 mL/min/1.73 m² (75% if bilirubin also > 3 mg/dL) — do not withhold.
Life‑saving in primary HLH and severe EBV‑HLH; not first‑line for MAS (low‑dose only if refractory); not for most non‑EBV infections. Ciclosporin is no longer given in the first weeks (HLH‑2004 upfront ciclosporin showed no benefit).,,,
3 · RituximabHematology‑directedEBV‑driven HLH (B‑cell depletion)
✦ Supportive care and monitoring
  • Sepsis‑style resuscitation and broad antimicrobials pending cultures; consider Pneumocystis and antifungal prophylaxis early (part of HLH‑94); no live vaccines; irradiated blood products if transplant is possible.
  • Daily ferritin, CRP, CBC, fibrinogen and ALT (± triglycerides); more often if critical. A ferritin that fails to fall predicts a poor outcome — escalate and re‑examine the diagnosis (lymphoma, unrecognized infection, genetic HLH).
◈ Kuwait joint pathway — rheumatology · hematology/oncology · PICU
  • Same first hour, whichever team is called first: ferritin + first‑tier panel, cultures, methylprednisolone pulse ± anakinra. No team delays glucocorticoids waiting for the other.
  • Rheumatology leads when there is a known or strongly suspected rheumatic context (sJIA/Still’s, lupus, Kawasaki, MIS‑C): MAS pathway — glucocorticoid + anakinra ± ciclosporin → emapalumab.
  • Hematology/oncology leads when: age < 2 years, consanguinity or family history, EBV‑driven disease, cytopenias or organomegaly dominant, possible malignancy, or no rheumatic context: HLH pathway — genetics and marrow first where safe; dexamethasone with the HLH‑94 taper; etoposide when severe or no response at 72 h; emapalumab for refractory, recurrent or progressive primary HLH,.
  • Both are consulted within hours in every case; PICU for organ dysfunction; infectious diseases for the trigger and prophylaxis; immunology for inborn‑error evaluation. A multidisciplinary HLH/MAS team improves recognition and reduces over‑ and under‑treatment. Transfer of care is by agreement, not by admission ward.
◣ Admit · Discharge · Refer
  • Admit — all → high‑dependency/PICU.
  • Home from the ward — not acutely; under the leading team with a written taper and monitoring plan.
  • Refer — now — hematology and rheumatology within hours; PICU.
  • Refer — clinic — genetic counseling for every family tested.

Kawasaki Disease

HOURS

Medium‑vessel vasculitis; leading cause of acquired heart disease in children.

▸
◣ Recognize
  • Fever ≥ 4 days (day 1 = first day of fever) + ≥ 4 of: bilateral non‑exudative conjunctivitis, oral mucosal changes (cracked/red lips, strawberry tongue, diffuse oropharyngeal erythema), polymorphous rash, extremity changes (swelling/peeling), cervical lymphadenopathy ≥ 1.5 cm (usually unilateral). Features need not be present together; with ≥ 4 features the diagnosis can be made on day 4 of fever (day 3 by an experienced clinician).
  • Incomplete Kawasaki is common in infants < 6 months and older children — fewer features but high coronary risk; use inflammatory markers and echocardiography.
✦ Pearl — think incomplete Kawasaki
  • Suspect incomplete Kawasaki in any infant (above all < 6 months) with ≥ 7 days of unexplained fever even without the full clinical criteria — this is the group most often missed and at the highest risk of coronary aneurysms.
  • Check inflammatory markers and arrange echocardiography; treat on a compatible picture rather than waiting for every feature. AHA 2024 pathway: prolonged unexplained fever + 2–3 clinical criteria (or an infant with ≥ 7 days of unexplained fever) → check CRP/ESR; if CRP ≥ 3 mg/dL and/or ESR ≥ 40 mm/h, look for ≥ 3 supplementary lab findings (anemia, platelets ≥ 450 ×10⁹/L, albumin ≤ 3 g/dL, raised ALT, WBC ≥ 15 ×10⁹/L, urine WBC ≥ 10/hpf) or a positive echocardiogram (LAD or RCA Z ≥ 2.5, or ≥ 3 other suggestive features), → treat.
Treat within 10 days of fever onset to protect the coronaries
First‑line
  • IVIG 2 g/kg as a single infusion + low‑dose (antiplatelet) aspirin 3–5 mg/kg/day; baseline echocardiogram.
  • Discuss adjunct corticosteroids with cardiology/rheumatology for high‑risk patients (infants < 1 year, coronary changes, high inflammatory markers, or Kawasaki disease shock syndrome) — AHA 2024 defines high risk as age < 6 months or baseline LAD/RCA z‑score ≥ 2.5 (CRP ≥ 13 mg/dL and Asian ancestry also predict aneurysms) and supports intensified initial therapy for this group.
DrugDoseRoute & notes
IVIG2 g/kg single infusion over 10–12 hIV. IVIG‑resistant fever ≥ 36 h after the end of the infusion → second IVIG 2 g/kg, or corticosteroids, or a biologic (infliximab, now dosed 10 mg/kg IV over 2 h), Echo: baseline at diagnosis (do not delay IVIG for it); if any coronary Z score ≥ 2.5, repeat at least twice weekly in hospital until dimensions stop progressing; repeat before discharge if IVIG‑resistant or high‑risk.,
Aspirin3–5 mg/kg/day PO once daily from diagnosis
continue until 6–8 weeks after illness onset and the follow‑up echocardiogram is normal; continue long term (cardiology‑directed, potentially indefinitely) if any coronary aneurysm
Antiplatelet dose only, from the outset. Anti‑inflammatory doses (30–100 mg/kg/day) are not recommended — no coronary benefit, more adverse effects,. See the aspirin note below
Methyl­predniso­lone → prednisolone (high‑risk)Prednisolone 2 mg/kg/day (max 60 mg/day) IV in 3 divided doses (if IV prednisolone is unavailable, IV methylprednisolone 1.6–2 mg/kg/day as a substitute), switching to oral prednisolone when afebrile
once CRP is normal taper over 15 days (RAISE‑based regimen)
Adjunct to IVIG in high‑risk patients or Kawasaki disease shock syndrome,
⚠ Note
  • Single‑dose methylprednisolone with IVIG is not recommended as routine primary therapy.
  • Avoid ibuprofen with aspirin (antagonizes antiplatelet effect).
  • Aspirin and varicella/influenza: withhold aspirin during active varicella or influenza (Reye syndrome) and use an alternative antiplatelet agent (clopidogrel) meanwhile; give the annual influenza vaccine to every child on aspirin.
◈ Why the antiplatelet dose
  • Anti‑inflammatory dosing has never been shown to reduce coronary aneurysms: a randomized trial found IVIG alone non‑inferior to IVIG + high‑dose aspirin; a network meta‑analysis of 1,944 patients found no difference in coronary lesions, IVIG resistance or hospital stay between no aspirin, 3–5, 30–50 and 80–100 mg/kg/day; meta‑analyses and cohorts show equal coronary outcomes with low‑dose from the outset and fewer adverse effects (GI bleeding, transaminase rise, Reye syndrome),,,.
  • One Japanese database study found more coronary abnormalities at 5 than at 30 mg/kg/day (OR 1.40) — observational and contradicted by the randomized data; a randomized noninferiority trial of moderate‑ vs low‑dose aspirin with IVIG (DAPI) is under way,.
  • AHA 2024 still describes moderate‑ (30–50 mg/kg/day) or high‑dose (80–100 mg/kg/day) aspirin until afebrile 48–72 h as traditional practice, but now states that medium‑ or high‑dose aspirin in the acute phase "is likely not associated with improved CA outcomes" and gives no dose recommendation pending the ongoing randomized trial,; this guide recommends the antiplatelet dose (3–5 mg/kg/day) from diagnosis on the strength of the randomized and pooled evidence above.
Coronary artery involvement — AHA Z‑score classification & cardiology‑directed thromboprophylaxis
CategoryZ score (LAD or RCA)Echo frequency & antithrombotic plan
No involvement< 2Repeat echo 1–2 weeks after discharge and at 4–6 weeks; AHA 2024: if normal at diagnosis and at 1–2 weeks, further imaging only if new concerns arise. Low‑dose aspirin until the follow‑up echo is normal.,
Dilation only2 to < 2.5As above; the AHA also counts a fall in Z score of ≥ 1 during follow‑up as dilation.
Small aneurysm≥ 2.5 to < 5Echo at least twice weekly in hospital until dimensions stop progressing; echo at discharge and again within 1 week. Low‑dose aspirin.,
Medium aneurysm≥ 5 to < 10 and < 8 mmAs for small aneurysm; low‑dose aspirin, clopidogrel may be added; anticoagulation not routinely indicated — except consider continuing anticoagulation (cardiology decision) when a previously large/giant aneurysm has regressed to medium size, especially if regression involved thrombus (AHA 2024).
Large or giant aneurysm≥ 10 or ≥ 8 mmTwice‑weekly echo while expanding, then at least weekly for the first 45 days. Low‑dose aspirin plus anticoagulation (warfarin INR 2–3 or LMWH anti‑Xa 0.5–1.0 U/mL; DOACs emerging); clopidogrel added for very extensive/distal aneurysms or prior thrombosis. Lifelong cardiology follow‑up.,
Kawasaki disease — algorithm A: diagnosis and initial treatmentAdapted from the AHA Kawasaki disease scientific statement, 2024 update,. Aspirin 3–5 mg/kg/day from diagnosis is this guide's policy (see "Why the antiplatelet dose").
1 DIAGNOSE 2 TREAT — RISK-STRATIFY (AHA 2024) Kawasaki disease — A. Diagnosis and initial treatment Adapted from the AHA Kawasaki disease scientific statement, 2024 update · Z = coronary artery Z score (LAD or RCA, adjusted for body surface area) Fever ≥ 4 days without another explanation — think Kawasaki disease. Complete Kawasaki disease ≥ 4 of 5 principal features: • bilateral non-exudative conjunctivitis • oral changes (cracked red lips, strawberry tongue) • polymorphous rash • extremity changes (swelling, erythema, peeling) • cervical node ≥ 1.5 cm Suspected incomplete Kawasaki disease • 2–3 principal features, or • an infant with ≥ 7 days of unexplained fever → check CRP and ESR CRP ≥ 3 mg/dL and/or ESR ≥ 40 mm/h? ≥ 3 supplementary labs* or positive echo? No — re-evaluate daily while fever lasts and repeat CRP/ESR (return to this check); echocardiogram if typical peeling develops. No — echocardiogram now; if negative and fever persists, repeat the echo and consult a Kawasaki expert; treat if it becomes positive. No Yes No TREAT Baseline echocardiogram when the diagnosis is considered — unavailability or technical limits must not delay IVIG. Treat within 10 days of fever onset; after day 10 still treat if CRP > 3 mg/dL with persistent fever or coronary aneurysms. Yes echo positive High risk? Age < 6 months or baseline Z ≥ 2.5 CRP > 13 mg/dL, Asian ancestry, Kawasaki shock syndrome or MAS add to the risk (AHA 2024) Standard risk → IVIG + aspirin • IVIG 2 g/kg, single infusion over 10–12 h • Aspirin 3–5 mg/kg/day (antiplatelet dose) from diagnosis High risk → IVIG + adjunctive therapy • IVIG 2 g/kg, single infusion over 10–12 h • plus ONE adjunct: • Prednisolone IV 2 mg/kg/day (max 60 mg; or IV methylprednisolone 1.6–2), oral when afebrile, taper over 15 days once CRP normal (RAISE-based) • or infliximab 10 mg/kg IV over 2 h No Yes Continue in panel B — reassess at 36 h *Supplementary laboratory findings: anemia for age · platelets ≥ 450 ×10⁹/L after the 7th day of fever · albumin ≤ 3 g/dL · raised ALT · WBC ≥ 15 ×10⁹/L · urine ≥ 10 WBC/hpf. Aspirin 3–5 mg/kg/day from diagnosis is this guide's policy (see card); AHA still lists moderate/high dose until afebrile as an option.
Kawasaki disease — algorithm B: reassessment at 36 h and echocardiogram follow‑up by Z scoreIVIG resistance = persistent or recrudescent fever ≥ 36 h after the end of the infusion; echo at least twice weekly for Z ≥ 2.5 and before discharge when IVIG‑resistant or high‑risk,.
3 REASSESS AT 36 HOURS 4 ECHO FOLLOW-UP BY MAXIMAL Z SCORE Kawasaki disease — B. Reassessment and echocardiogram follow-up Adapted from the AHA Kawasaki disease scientific statement, 2024 update · Z = coronary artery Z score (LAD or RCA, adjusted for body surface area) From panel A — IVIG given (standard or high-risk regimen) Afebrile 36 h after the END of the IVIG infusion? Responder • Continue aspirin • Echo follow-up by Z score (band 4) • Repeat the echo before discharge if high-risk features or any coronary change IVIG resistance (fever persists or recurs) Give ONE of: • Second IVIG 2 g/kg over 8–12 h • Infliximab 10 mg/kg IV over 2 h • Methylprednisolone IV 2 mg/kg/day × 5 days, then oral taper over 2–4 weeks once CRP < 1 mg/dL Still febrile → cyclosporine or anakinra (rheumatology/cardiology) Repeat the echo in hospital and before discharge Yes No Echocardiogram follow-up for every patient — frequency and antithrombotic plan set by the maximal coronary Z score all patients Z < 2 none · 2 to < 2.5 dilation • Echo 1–2 weeks after discharge, then at 4–6 weeks (AHA) • AHA 2024: if normal at diagnosis and at 1–2 weeks, further imaging only for new concerns • Low-dose aspirin until the follow-up echo is normal Z ≥ 2.5 small / medium aneurysm • Echo ≥ twice weekly in hospital until dimensions stop progressing • Echo at discharge and again within 1 week • Small (Z 2.5 to < 5): low-dose aspirin • Medium (Z 5 to < 10, < 8 mm): low-dose aspirin, clopidogrel may be added; anticoagulation not routine (see table) Z ≥ 10 or ≥ 8 mm large / giant • Echo twice weekly while expanding, then ≥ weekly for the first 45 days • Low-dose aspirin + anticoagulation: warfarin (INR 2–3) or LMWH (anti-Xa 0.5–1.0 U/mL) • Clopidogrel added for very extensive/distal aneurysms or prior thrombosis • Cardiology-directed, lifelong follow-up AHA Z-score classification of coronary artery involvement (2024 update) No involvement Z < 2 · Dilation only Z 2 to < 2.5 · Small aneurysm Z ≥ 2.5 to < 5 · Medium aneurysm Z ≥ 5 to < 10 and absolute diameter < 8 mm · Large or giant aneurysm Z ≥ 10 or absolute diameter ≥ 8 mm Source: Jone PN et al. Update on diagnosis and management of Kawasaki disease: a scientific statement from the AHA. Circulation 2024;150:e481–e500 (retains the diagnostic algorithm and Z-score classification of the earlier AHA statement). IVIG resistance = persistent or recrudescent fever ≥ 36 h after the end of the infusion (AHA 2024).
⚠ Watch for
Macrophage activation syndrome (cytokine storm — see HLH / MAS) and Kawasaki disease shock syndrome (hypotension / poor perfusion) — both signal severe, high‑risk disease; escalate, add adjunctive steroids, and involve rheumatology/cardiology + PICU,.
◣ Admit · Discharge · Refer
  • Admit — all → for IVIG and monitoring; PICU for Kawasaki disease shock syndrome or MAS.
  • Home from the ward — afebrile ≥ 36 h after the end of IVIG, with an echocardiogram repeated before discharge if fever persisted or recurred (IVIG resistance), high‑risk features, or any coronary dilation/aneurysm; repeat echo 1–2 weeks after discharge (within 1 week if Z ≥ 2.5) and at 4–6 weeks (AHA 2024: may be omitted when the first two are normal); aspirin plan written down; defer live vaccines (MMR, varicella) for 11 months after IVIG.,
  • Refer — now — cardiology (echo, Z scores) and rheumatology for every case; IVIG‑resistant cases urgently.
  • Refer — clinic — cardiology follow‑up per the Z‑score table; lifelong if an aneurysm ever formed.

IgA Vasculitis (Henoch–Schönlein Purpura)

ASSESSSHARE 2019

Palpable purpura on the legs and buttocks — the commonest childhood vasculitis; the kidney is the long game.

▸
◣ Recognize (purpura + ≥ 1)
  • Palpable purpura (mandatory), lower‑limb/buttock predominant, with normal platelets and coagulation, plus at least one of: diffuse abdominal pain · arthritis/arthralgia · biopsy showing IgA deposition · renal involvement (hematuria/proteinuria).
⚠ Two things that turn it into an emergency
  • Intussusception — usually ileo‑ileal (easily missed on routine imaging — use ultrasound) in a child with severe/colicky abdominal pain or GI bleeding.
  • And testicular pain/swelling can mimic torsion.
  • Severe abdominal pain, GI bleeding, scrotal pain or a rapidly rising creatinine/BP all need admission.
✦ The kidney can declare itself late
  • Nephritis may appear weeks to months after the rash.
  • Check blood pressure and urinalysis at every visit and continue surveillance for 6 months (schedule below) even after the rash resolves,,.
  • Persistent proteinuria → nephrology.
◣ Workup
  • Urinalysis + urine protein:creatinine ratio and blood pressure at every visit — nephritis screen (monitor for 6–12 months even if initially normal).
  • Serum creatinine / eGFR.
  • CBC + coagulation — platelets are normal/high in IgA vasculitis (excludes ITP/HUS).
  • Renal biopsy only for significant or persistent proteinuria or impaired function.
ProblemApproachNotes
Joint / mild painAcetaminophen; NSAIDs if no renal involvement or GI bleedingMost cases are supportive only
Severe abdominal pain / orchitisPrednisolone 1–2 mg/kg/day (max 60 mg), short course with taperEases pain; does not prevent nephritis
Nephritis (significant)Nephrology‑directed (steroids ± immunosuppression)Do not manage severe nephritis alone
◈ Where to manage — most children go home
  • Uncomplicated IgA vasculitis (rash ± joint pain, mild abdominal pain, normal blood pressure, normal or trace urinalysis, eating and walking) is outpatient care: analgesia, counseling, and teaching the family to check the urine for protein at home over the next 3–6 months, with a written follow‑up plan. No guideline recommends routine admission — most children need only supportive treatment,,.
  • Return at once if: severe or worsening abdominal pain, vomiting, blood in the stool, swollen or painful testicle, blood in the urine or foamy urine, swelling of the face/legs, headache or reduced urine output.
  • Admit only for: severe abdominal pain (needs parenteral analgesia), GI bleeding or suspected intussusception, unable to walk or drink, scrotal/testicular involvement until torsion is excluded, hypertension, acute kidney injury or a nephrotic/nephritic presentation, CNS or pulmonary involvement, or an unsafe discharge,.
✦ Follow‑up plan for the nephritis screen — give it in writing at the first visit
  • What: blood pressure + early‑morning urine dipstick at every visit; protein ≥ 1+ → urine protein:creatinine ratio; creatinine/eGFR at diagnosis and whenever the urine is abnormal,.
  • When: diagnosis · day 7 (a normal day‑7 urinalysis predicts a normal renal outcome with 97% negative predictive value) · day 14 · day 28 · months 2, 3 and 6 — at least monthly for 6 months even if normal,. Most nephritis appears within 4 weeks of the rash (about 85%) and nearly all within 6 months (Narchi 2005 systematic review), so early normal results do not shorten the schedule; SHARE advises monitoring for at least 6–12 months.
  • Discharge from surveillance at 6 months if blood pressure and urine have stayed normal; extend to 12 months if any abnormality occurred,; biopsy‑proven nephritis is followed for years by nephrology,.
  • Nephrology now: urine protein:creatinine > 250 mg/mmol at any time (biopsy if it persists 4 weeks); 100–250 mg/mmol persisting (biopsy if 3 months); eGFR < 90 mL/min/1.73 m² (biopsy if < 80); hypertension; nephrotic or nephritic syndrome; acute kidney injury,,. ACE inhibitor/ARB for proteinuria lasting > 3 months.
  • Steroids do not prevent nephritis — no prednisolone for the rash; reserve it for severe abdominal pain/GI bleeding once intussusception is excluded, orchitis, or other severe organ involvement,.
◣ Admit · Discharge · Refer
  • Admit — only for the indications above.
  • Home — outpatient follow‑up per the schedule, with the return precautions explained.
  • Refer — now — surgery if intussusception; urology if the scrotum is involved.
  • Refer — clinic — nephrology per the thresholds above.

MIS‑C (Multisystem Inflammatory Syndrome)

MINUTESCDC/CSTE 2023 · ACR 2022

Post‑COVID hyperinflammation that overlaps Kawasaki and toxic shock — and can crash the heart.

▸
◣ Recognize (criteria)
  • CDC/CSTE 2023 case definition — age < 21 y with fever ≥ 38.0 °C (subjective or documented; no minimum duration), illness severe enough to need admission, CRP ≥ 3.0 mg/dL (30 mg/L), and new involvement of ≥ 2 of 5 systems: cardiac (LVEF < 55 %, coronary dilation/aneurysm/ectasia, or raised troponin) · mucocutaneous (rash, oral mucosal inflammation, conjunctival injection, or extremity erythema/edema) · shock · gastrointestinal (abdominal pain, vomiting, diarrhea) · hematologic (platelets < 150 ×10⁹/L or lymphocytes < 1.0 ×10⁹/L) — with no more likely alternative diagnosis.
  • SARS‑CoV‑2 link: confirmed when PCR or antigen is positive within the 60 days before or during admission, or antibodies are detected during the illness; probable when there was close contact with COVID‑19 in the preceding 60 days.
⚠ It looks like several killers at once
  • Overlaps Kawasaki disease, toxic shock syndrome and sepsis — treat the shock, take cultures and cover for sepsis until excluded.
  • Prominent abdominal pain can mimic appendicitis. Cardiac: myocardial dysfunction, arrhythmia and coronary artery aneurysms — get an early echocardiogram and troponin/BNP.
  • Shock is often compensated at first. Tachycardia, cool or mottled extremities, prolonged capillary refill, weak pulses, reduced urine output or drowsiness with a normal blood pressure is shock until proven otherwise — hypotension is a late sign. Myocardial dysfunction can be insidious and children can decompensate rapidly: examine perfusion at every review, get the echocardiogram early (left‑ventricular function, coronary z‑scores), and repeat troponin/BNP. Fluid cautiously (5–10 mL/kg, reassess) and start epinephrine early if the heart is the problem.
◣ Workup
  • Inflammatory: CRP, ESR, ferritin, procalcitonin, CBC (lymphopenia), fibrinogen, D‑dimer.
  • Cardiac: troponin, BNP/NT‑proBNP, ECG and echocardiogram (coronary arteries + function).
  • SARS‑CoV‑2 PCR and serology; blood cultures to exclude sepsis.
  • CMP, LDH, triglycerides, coagulation.
  • Tiered approach when the child is stable: tier 1 (any facility) CBC with differential, metabolic panel, ESR, CRP, SARS‑CoV‑2 testing → proceed to tier 2 (cardiac markers, ECG, echocardiogram, ferritin, D‑dimer, procalcitonin, cytokine panel if available) when ESR/CRP is raised plus one of: lymphocytes < 1.0 ×10⁹/L, platelets < 150 ×10⁹/L, sodium < 135 mmol/L, neutrophilia or hypoalbuminemia (ACR 2022). A child with shock is treated while the work‑up is completed.
  • Admit for observation while under investigation if any of: abnormal vital signs, respiratory distress, altered mental status, renal or hepatic injury, marked inflammatory markers, abnormal ECG, or raised troponin/BNP. ECG at least every 48 h in hospital; telemetry if conduction is abnormal.
Treatment pathway — ACR 2022 (stepwise; dual therapy first‑line for most admitted children)
StepDrug & doseNotes
1 · First‑line — IVIG (after the first glucocorticoid dose)2 g/kg (ideal body weight, max 100 g)Start IVIG after the first glucocorticoid dose has been given and once cardiac function and fluid status have been assessed; with cardiac dysfunction give 1 g/kg/day over 2 days, slow the rate and/or add a diuretic to avoid volume overload
1 · First‑line — methyl­predniso­lone, given first1–2 mg/kg/day IV
Give the first dose at once — before the IVIG infusion is set up
Dual therapy with IVIG for most hospitalized patients (ACR 2022); giving IV methylprednisolone before the IVIG reduces cardiac inflammation and improves cardiac function before the heart is loaded with the IVIG volume (CPS 2021); furosemide halfway through the infusion may be considered when cardiac function is impaired; IVIG alone only in mild disease or when steroids are contraindicated, with intensification at the first sign of worsening. Glucocorticoid monotherapy is not recommended
2 · Refractory (no response within 24 h: persistent fever or ongoing organ involvement) or shock on inotropesMethylprednisolone pulse 10–30 mg/kg/dayDo not repeat IVIG (hemolysis, volume overload). Children in shock on multiple inotropes/vasopressors respond best to high‑dose glucocorticoid
2 · AlternativesAnakinra > 4 mg/kg/day (often 5–10 mg/kg/day) IV/subcut · or infliximab 5–10 mg/kg IV onceNo infliximab if there are features of macrophage activation syndrome; anakinra also as a steroid‑sparing agent
Aspirin3–5 mg/kg/day PO (max 81 mg)All patients unless active bleeding, significant bleeding risk or platelets ≤ 80 ×10⁹/L; continue until platelets are normal and coronaries are confirmed normal at ≥ 4 weeks; add gastric protection with steroids
Anti­coagulationEnoxaparin (anti‑Xa 0.5–1.0) + low‑dose aspirinCoronary z‑score ≥ 10: enoxaparin for ≥ 2 weeks, then warfarin (INR 2–3) or DOAC for as long as z ≥ 10 · Ejection fraction < 35%: therapeutic anticoagulation until EF > 35% · Documented thrombosis: therapeutic anticoagulation for 3 months, re‑image at 4–6 weeks · Otherwise individualized to thrombosis risk (central line, age > 12 y, PICU, D‑dimer > 5 × ULN)
Taper2–3 weeks or longerGuided by serial CRP/ferritin and cardiac reassessment to avoid rebound
◈ Cardiac follow‑up
  • Repeat echocardiogram at 7–14 days and at 4–6 weeks in every child (more often with LV dysfunction or aneurysms); consider one at 1 year if the heart was involved; cardiac MRI at 2–6 months after moderate–severe LV dysfunction.
◣ Admit · Refer
  • Admit — all confirmed cases; PICU for shock, cardiac dysfunction or conduction abnormality.
  • Refer — now — call pediatric rheumatology/infectious diseases and cardiology from the start (multidisciplinary team).
  • Refer — clinic — follow up coronary imaging.
17

Surgical Emergencies

Recognize early · resuscitate · refer fast

Malrotation / Midgut Volvulus

MINUTESOFTEN < 1 MO

Bilious (green) vomiting in a well infant — the "drop‑everything" abdomen.

▸
Recognize Bilious vomiting ± distension/pain; bloody stool and shock are late (ischemia).
Resuscitate & confirm
  • Nil by mouth, NG decompression, IV fluids, bloods.
  • Urgent upper‑GI contrast (abnormal duodeno‑jejunal junction, "corkscrew") ± Doppler ultrasound.
Consult first
  • Consult pediatric surgery immediately — for definitive care and safe transport.
  • Do not image at a center that will not operate; if surgery is unavailable on‑site, transfer without delaying for contrast studies.
Immediate surgery — Ladd procedure. Peritonitis or shock → straight to the operating room, do not delay for imaging.
◣ Admit · Discharge · Refer
  • Admit — all suspected → emergency, nil by mouth, fluids.
  • Home from the ward — not acutely; post‑operative.
  • Refer — now — pediatric surgery IMMEDIATELY (bilious vomiting = volvulus until excluded); urgent upper‑GI contrast.

Intussusception

HOURS6 MO–3 YR

Telescoping bowel; the classic triad is usually incomplete.

▸
◣ Recognize
  • Intermittent colicky pain (drawing up the legs), vomiting, lethargy between episodes.
  • Sausage‑shaped mass; "redcurrant jelly" stool is late. Unexplained lethargy may be the only clue.
Confirm Ultrasound — "target/doughnut" sign (highly sensitive and specific in experienced hands). Resuscitate with IV fluids first.
Stable, no peritonitis/perforation?
YES
Non‑operative air or contrast enema reduction — perform only at a center with pediatric surgical backup where the child will be definitively treated (perforation needs immediate surgery).
NO / failed
Operative reduction; resect non‑viable bowel.
◣ Admit · Discharge · Refer
  • Admit — all → for reduction and observation.
  • Home from the ward — after successful reduction and an observation period without recurrence.
  • Refer — now — pediatric surgery and interventional radiology (air/contrast enema); surgery if reduction fails or peritonitis.

Hypertrophic Pyloric Stenosis

HOURS3–6 WK

Progressive non‑bilious projectile vomiting in a hungry infant.

▸
◣ Recognize & confirm
  • "Olive" mass, visible gastric peristalsis, dehydration. Labs: hypochloremic hypokalemic metabolic alkalosis. Ultrasound: muscle ≥ 3–4 mm, channel ≥ 14–16 mm.
① Correct first Rehydrate and normalize chloride, potassium and bicarbonate before surgery. NG if vomiting.
② Pyloromyotomy once biochemically stable. The electrolytes are the emergency, not the surgery.
◣ Admit · Discharge · Refer
  • Admit — all → correct fluids/electrolytes before surgery.
  • Home from the ward — post‑operative, feeding established.
  • Refer — now — pediatric surgery (pyloromyotomy) after biochemical correction — it is not a surgical emergency until corrected.

Acute Appendicitis

HOURS

Most common surgical abdomen; young children atypical, high perforation risk.

▸
◣ Recognize
  • Periumbilical pain migrating to the right lower quadrant, anorexia, fever, vomiting; guarding/rebound, pain on movement.
  • Clinical scores (Alvarado / Pediatric Appendicitis ScorePediatric Appendicitis Score) + ultrasound first‑line; CT or MRI selectively.
Manage Nil by mouth · IV fluids · analgesia for pain · urgent surgical evaluation → laparoscopic appendectomy within 24 h of admission. For uncomplicated appendicitis, antibiotics alone are an accepted alternative in children (WSES 2025, conditional) with close monitoring and shared decision‑making — a surgical‑team decision. With an appendiceal abscess, early laparoscopic appendectomy is suggested; non‑operative treatment is the alternative where expertise is lacking, without routine interval appendectomy.
⚠ Mimics
Examine the testes (torsion), consider DKA (see Diabetic Ketoacidosis), lower‑lobe pneumonia, UTI, ovarian torsion (clinical practice point).
⚠ Do not bypass surgical evaluation
  • Antibiotics — not for suspected appendicitis before surgical assessment; started before diagnosis is confirmed, they can partially treat and mask it (blunted WBC/neutrophils, softer signs) — expert practice point, not guideline‑stated.
  • Start once diagnosis is confirmed and surgical plan agreed — or immediately if the child is septic or perforated. Analgesia — never leave a child in pain, but stay opioid‑sparing while awaiting surgical review: give non‑opioid analgesia first (IV or oral acetaminophen).
  • Never give parenteral opioids then discharge an undifferentiated abdomen.
  • Analgesia does not reduce diagnostic accuracy — never a reason to delay evaluation.
Antibiotics — once diagnosis confirmed and surgical plan agreed (or now, if septic/perforated)
DrugDoseRoute & notes
Piperacillin‑​tazobactam100 mg/kg/dose (piperacillin component) IV every 8 h
2–9 months: 80 mg/kg/dose IV every 8 h
> 40 kg (adult dose): 3.375 g (piperacillin 3 g + tazobactam 0.375 g) IV every 6 h
Single‑agent cover including anaerobes; common first choice,.
Ceftriaxone + metronidazoleCeftriaxone 50–75 mg/kg/dose IV once daily (max 2 g) + metronidazole 10 mg/kg/dose IV every 8 h (max 500 mg/dose)Alternative combination; give the first dose promptly once diagnosed,.
◈ Duration
  • Uncomplicated appendicitis: perioperative prophylaxis only — a single pre‑operative dose; WSES 2025 makes no recommendation on postoperative antibiotics in children (very low certainty).
  • Complicated or perforated: continue ~4–5 days after adequate source control, or until afebrile with a normalizing white count and returning bowel function (STOP‑IT — a predominantly adult trial; pediatric use is extrapolated).
◣ Admit · Discharge · Refer
  • Admit — all → under the surgical team (appendectomy, or antibiotics alone in selected uncomplicated cases).
  • Home from the ward — post‑operative per pathway.
  • Refer — now — pediatric surgery; interventional radiology for an abscess (drainage) when non‑operative.

Incarcerated Inguinal Hernia

HOURS

Irreducible tender groin or scrotal lump — reduce it or operate.

▸
◢ Recognize
  • Firm, tender, irreducible swelling in the groin extending to the scrotum or labia; irritability and vomiting (may mimic bowel obstruction).
  • Common in infancy, especially preterm. Overlying skin erythema or a toxic child suggests strangulation.
Reduce
  • If no signs of strangulation: analgesia or sedation, head‑down (Trendelenburg) position, gentle sustained manual reduction (taxis) by experienced hands.
  • If it does not reduce on the first attempt, stop and consult pediatric surgery — repeated attempts worsen edema and make later reduction harder.
  • Once reduced, admit for repair on the same admission — re‑incarceration risk is high,.
⚠ Do not reduce — straight to surgery
Skin erythema, systemic toxicity, peritonitis, bloody stools, or prolonged incarceration — signal ischemic bowel or gonad → emergency exploration.
◣ Admit · Discharge · Refer
  • Admit — all → for reduction/observation or surgery.
  • Home from the ward — after repair on the same admission (usually 24–48 h after reduction, once edema settles); discharge before repair only by explicit pediatric‑surgical decision with a booked early date and clear return advice.
  • Refer — now — pediatric surgery urgently; emergency if irreducible or strangulated.
18

Toxicology & Environmental

Poisoning · burns · heat & drowning

Poisoning & Toxic Ingestion

HOURS

Resuscitate, identify the agent, call for advice, give the antidote.

▸
☎ Kuwait Poison Control Center (KPCC): 1804774 — 24/7. Call early for any exposure: agent‑specific advice, decontamination, antidotes, and disposition.
◣ General approach (ABCDE first)
  • Stabilize airway, breathing, circulation; give oxygen; check glucose and a 12‑lead ECG (QRS width, QT interval).
  • Identify the agent, amount, time, and intent; in any deliberate ingestion send acetaminophen and salicylate levels.,
  • Decontamination: decide in the first hour, with KPCC — single‑dose activated charcoal, whole bowel irrigation, or neither (box below).,,
  • Call KPCC 1804774; give the specific antidote below; observe for delayed toxicity.
◣ Decontamination — decide in the first hour
  • Stabilize first. Gut decontamination is never routine: neither activated charcoal nor whole bowel irrigation (WBI) has been shown to improve outcome — use it only after a potentially toxic ingestion, and decide with KPCC 1804774.,,,
  • Swallowed a poison that charcoal binds, and the airway is safe (awake with intact airway reflexes, or already intubated) → single‑dose activated charcoal, as early as possible: most benefit within 1 h; for many poisons still worthwhile up to 6 h, and later when absorption continues (modified‑release products, tablet masses, very large ingestions).,
  • Carbamazepine, cardiac glycosides, colchicine, dapsone, phenobarbital, phenytoin, thallium or theophylline → multiple‑dose activated charcoal to speed elimination, on toxicology advice.,
  • Substantial iron, lithium or potassium, a sustained‑release or enteric‑coated drug (especially > 2 h after ingestion), or swallowed drug packets (body packing) → consider WBI: charcoal has no role for iron or lithium, and there are few other ways to empty the gut.,,
  • Charcoal and the airway. Not intubated → give charcoal by mouth only; do not pass a nasogastric tube just to give it. Already intubated for another reason (unprotected airway, respiratory failure, low conscious level, refractory seizures, shock) → a nasogastric or orogastric tube for charcoal is reasonable. Do not intubate just to give charcoal, unless life‑threatening toxicity is expected; decide with a toxicologist.
  • Not recommended: routine gastric lavage: should not be used routinely, if ever; if ever considered, only by experienced staff with a protected airway. Ipecac: no benefit; delays charcoal, oral antidotes and WBI.
MethodDose / rateUse for · do not use
Activated charcoal — single dose1 g/kg once
max 50 g
by mouth; by nasogastric/orogastric tube only if intubated (confirm tube position on X‑ray)
additional (second) dose, if advised: same dose,
Use for a potentially toxic amount of a poison that charcoal binds (most drugs), with a safe airway. An additional dose may be advised after carbamazepine, acetaminophen, paraquat, phenobarbital, salicylates, thallium, theophylline, valproic acid or verapamil, modified‑release products, or a dose too large for one charcoal dose. No role (do not give): iron, lithium, alcohols (ethanol, methanol, ethylene glycol), lead, arsenic, copper, caesium, metformin. Do not use if airway reflexes are absent or may be lost (unless intubated), with a risk of bowel perforation, absent peristalsis, likely upper endoscopy (caustics — see Caustic (Corrosive) Ingestion), or a hydrocarbon with high aspiration risk,,
Activated charcoal — multiple dosefirst dose 1 g/kg (max 50 g)
then 1 g/kg (max 50 g) every 4 h
or 0.5 g/kg (max 25 g) every 2 h
continue until the child’s condition and drug levels are improving
IV antiemetic often needed,
Use for poisoning with carbamazepine, cardiac glycosides, colchicine, dapsone, phenobarbital, phenytoin, thallium or theophylline — to speed elimination, on toxicology advice. Do not use without an intact or protected airway, or with bowel obstruction,
Whole bowel irrigation (WBI)polyethylene glycol electrolyte solution (PEG‑ES) by small‑bore nasogastric tube (tip in mid‑stomach on X‑ray)
9 months–6 years: 500 mL/h
6–12 years: 1000 mL/h
adolescents: 1500–2000 mL/h
sitting up, or head of bed ≥ 45°
continue at least until the rectal effluent is clear (many hours); longer if X‑ray or ongoing passage shows toxin still in the gut
vomiting: parenteral non‑sedating antiemetic (metoclopramide also speeds gastric emptying); if it persists, halve the rate for 30–60 min, then resume
Consider for substantial iron, lithium or potassium ingestion; sustained‑release or enteric‑coated drugs, especially > 2 h after ingestion; swallowed packets of illicit drugs (body packing) — no proven outcome benefit. Do not use with bowel obstruction, perforation or ileus, clinically significant gastrointestinal bleeding, an unprotected or compromised airway, hemodynamic instability, or uncontrollable vomiting; caution in debilitated children. Charcoal given during WBI may bind less,
◣ Recognize the toxidrome — the pattern names the poison before the history does

↑ increased · ↓ decreased · ± can go either way · normal = usually unchanged · no specific change = sources describe no typical finding. Patterns are typical, not universal: dose, timing, age and co‑ingestants change them. The combination of vital signs, pupils, gut and skin is more reliable than any single sign; a known ingestion does not exclude a second agent.

How the colors work: the color shows the state of the child — red · orange · pink = excitedblue · gray = depressedgreen = wet (secretions)purple = metabolic (fast, deep breathing)
Then skin, gut, pupils and breathing separate patterns of the same color: excited + sweaty = sympathomimetic, or serotonin toxicity if there is clonus; excited + dry skin, quiet gut = anticholinergic; depressed + pinpoint pupils and slow breathing = opioid; depressed + near‑normal vital signs = sedative‑hypnotic (benzodiazepine alone; alcohol and barbiturates do slow breathing); wet + pinpoint pupils = cholinergic, though a young child may show only coma and floppiness. The line under each name (e.g. “hot, red, dry, blind, mad, full”) is the memory hook.,,,,

Toxidrome · agentsMental statusVital signs · breathingPupils · gut · skinClues
EXCITED — FAST, HOT, AGITATED
Sympatho­mimetic
amphetamines, cocaine, pseudo­ephedrine, caffeine, ADHD stimulants
🔥 fast, hot, wet, wild
Agitation, psychosis, halluci­nations; seizuresHR ↑ · BP ↑ · T ↑ (hyper­pyrexia) · RR ↑Pupils dilated · gut: no specific change · skin sweatyWet skin separates it from anti­cholinergic; clonus points to serotonin toxicity instead; tremor, hyper­reflexia, rhabdo­myolysis; tachycardia may be absent on β‑blockers,,,,
Anti­cholinergic
anti­histamines (diphen­hydramine), tricyclics, atropine/​scopolamine, anti­psychotics, Datura
🌵 hot, red, dry, blind, mad, full
Agitated delirium, halluci­nations, or drow­siness; seizures, comaHR ↑ · BP mildly ↑ (↓ if severe) · T ↑ (usually ≤ 38.8 °C) · RR ↑Pupils dilated, poorly reactive (may look fixed) · gut ↓ (bowel sounds ↓ or absent) · skin hot, flushed, dry; dry mouthUrinary retention (“full”); dry skin and a quiet gut separate it from sympatho­mimetic and serotonin toxicity; no clonus; wide QRS with diphen­hydramine or tricyclics (get an ECG); anti­histamine overdose in young children: excitation, halluci­nations, seizures,,,,,
Serotonin syndrome
SSRIs/SNRIs, alone or with linezolid, tramadol, dextro­methorphan, ondansetron or methylene blue; MDMA
⚡ clonus, sweat, hot, agitated
Agitation, hyper­vigilance, easy startle → agitated delirium, comaHR ↑ · BP ↑ (severe: may collapse into shock) · T normal (mild) to ↑ (> 41 °C life‑threat­ening) · RR ↑Pupils dilated · gut ↑, diarrhea · skin sweaty, shiveringClonus (inducible, sponta­neous, ocular), hyper­reflexia, tremor; legs > arms; rigidity in severe cases may mask clonus; about 60% present within 6 h of a new drug, dose change or overdose; Hunter criteria,,,,
DEPRESSED — SLOW, SLEEPY
Opioid
morphine, metha­done, fentanyl, codeine, tramadol, bupre­norphine
😴 slow, small pupils, not breathing
Sedation → stupor → comaHR normal or ↓ · BP normal or ↓ · T normal or ↓ · RR ↓ (apnea): the defining signPupils pinpoint (may be normal or dilated with tramadol, meperi­dine or co‑ingestants; dilated if hypoxic) · gut ↓ · skin cold, clammyNaloxone response. Children: toxicity may be delayed, severe and prolonged; admit children ≤ 3 y for 24 h after methadone, a fentanyl patch or an extended‑release opioid, and admit any toddler exposed to bupre­norphine. Clonidine, or imida­zoline eye‑drop / nasal‑spray, ingestion in young children mimics it: lethargy, bradycardia, hypo­tension, respira­tory depression; no worsening after 4 h; pupils small or dilated; naloxone response inconsistent,,,,,
Sedative‑­hypnotic
benzo­diazepines, Z‑drugs (zolpidem), barbiturates, alcohol
💤 asleep, near‑normal vital signs
Drow­siness → coma; dysarthria, ataxiaBenzo­diazepine alone: HR, BP, RR usually normal · barbiturates, alcohol: BP ↓ · RR ↓ · T ↓ · HR ±Pupils normal or small (dilated late in severe barbiturate poisoning) · gut and skin: no specific changeIsolated benzo­diazepine overdose rarely causes life‑threat­ening hypo­ventilation or hypo­tension; if present, look for a co‑ingestant (alcohol, opioid); miosis + coma without marked respira­tory depres­sion points away from opioid,,,,
WET — SECRETIONS EVERYWHERE
Cholin­ergic
organo­phosphate and carbamate pesticides
💧 wet everywhere: DUMBELS
Lethargy, confusion → coma; seizures in about 1 in 5 childrenHR ↓ or ↑ (tachycardia in about half of children) · BP ± · T: no specific change · broncho­rrhea, broncho­spasm → respira­tory failurePupils pinpoint (in about 3 of 4 children) · vomiting, diarrhea · sweating, sali­vation, tearsFascicu­lations, weakness; pesticide/solvent smell; carbamates look the same; atropine titrated to a dry chest (antidote table). Young children: CNS depression and floppiness may dominate and muscarinic signs may be missing, so their absence does not exclude it,,,,
METABOLIC — FAST DEEP BREATHING
Salicylate
aspirin, oil of winter­green, bismuth sub­salicylate
🌀 fast breathing, ringing ears, acidosis
Lethargy, confusion → seizures, comaRR ↑, deep (hyperpnea): respira­tory alkalosis early, then anion‑gap metabolic acidosis · T ↑ (hyper­pyrexia = advanced poisoning) · HR ↑ with fever or dehydration · BP: no specific changePupils: no specific change · vomiting, abdominal pain, hemat­emesis · skin sweatyTinnitus, deafness, dehy­dration; cerebral and non‑­cardiogenic pulmonary edema; oil of winter­green 1 mL ≈ aspirin 1.4 g, so more than a lick or taste in a child < 6 y needs ED assessment; a normal acid–base picture does not exclude toxicity: keep a low threshold for a salicylate level,
PoisonAntidote · doseRate · target · monitor
Acetaminophen (paracetamol)Acetylcysteine IV — total 300 mg/kg; dose weight capped at 100 kg
Two‑bag (20 h), preferred ≥ 41 kg: 200 mg/kg over 4 h → 100 mg/kg over 16 h
Three‑bag (21 h), use ≤ 40 kg: 150 mg/kg over 1 h → 50 mg/kg over 4 h → 100 mg/kg over 16 h
High‑risk ingestion: double the final 16‑h bag to 200 mg/kg over 16 h (the second bag of the two‑bag regimen; the third bag of the three‑bag regimen) — on toxicology advice,,
Treat if the level is on/above the nomogram treatment line (150 mg/L at 4 h). The high‑risk line (300 mg/L at 4 h) marks a large ingestion — give a higher acetylcysteine dose and call toxicology. Both regimens prevent liver injury equally; the two‑bag causes fewer anaphylactoid reactions, so it is preferred where weight allows., Dilute in 0.45% sodium chloride (preferred) or 5% dextrose; adjust the volume < 41 kg (≤ 20 kg loading bag 3 mL/kg) — unadjusted volumes cause hyponatremia, seizures. Monitor acetaminophen, ALT/AST, INR, electrolytes. Stop only when acetaminophen < 10 mg/L, INR < 2.0, ALT/AST normal or fallen 25–50% from peak, and the child is well — do not stop automatically at 20–21 h.,
AnticholinergicPhysostigmine 0.02 mg/kg IV; may repeat every 5–10 min to effect, up to a total of 2 mg
— or a benzodiazepine for agitation,,
Give by slow IV, ≤ 0.5 mg/min, for anticholinergic delirium/agitation; reverses central and peripheral signs and outperforms benzodiazepines, which do not reverse delirium., Keep atropine at the bedside. Do not give if the QRS is prolonged on the ECG; use caution after an overdose of a QRS‑prolonging drug (e.g., a tricyclic) and with known coronary disease — bradyasystolic arrest and seizures have been reported. Monitor ECG, heart rate and secretions; watch for cholinergic excess (bradycardia, bronchorrhea, vomiting).
BenzodiazepineSupportive care (airway, ventilation) — the mainstay
Flumazenil 0.01 mg/kg IV (max 0.2 mg per dose) over 15 s; may repeat every 60 s, up to 4 further doses — max total 0.05 mg/kg or 1 mg, whichever is lower — selected cases only,
Isolated benzodiazepine overdose is rarely fatal — observe and support breathing. Reserve flumazenil for reversing pure benzodiazepine respiratory depression in a benzodiazepine‑naïve child (e.g., iatrogenic procedural sedation). Avoid in undifferentiated overdose: it can precipitate seizures or dysrhythmias in benzodiazepine‑dependent patients or with co‑ingested tricyclics, and is contraindicated when a benzodiazepine is controlling a life‑threatening condition (e.g., status epilepticus, raised intracranial pressure) or with signs of serious tricyclic overdose., Observe for resedation up to ~2 h after use.
Beta‑blockerHigh‑dose insulin: 1 unit/kg IV bolus, then 1–10 units/kg/h
Vasopressors (norepinephrine/epinephrine), titrated
Glucagon 0.05–0.15 mg/kg IV bolus, then infusion 1–15 mg/h (adult range; do not exceed the adult dose),
Severe toxicity (hypotension, bradycardia, conduction block): call KPCC 1804774 and PICU early. Give vasopressors and high‑dose insulin for hypotension; insulin is an inotrope, so start it early, together with a vasopressor., Run dextrose to keep glucose normal (needed for ~24 h after insulin stops) and replace potassium. Monitor glucose and potassium frequently., Glucagon for bradycardia or hypotension; expect vomiting. Escalate to pacing or VA‑ECMO for refractory shock.
Calcium‑channel blockerCalcium chloride 10% 0.2 mL/kg (20 mg/kg) — or calcium gluconate 10% 0.6 mL/kg (60 mg/kg) — IV, repeat every 10–20 min or infuse
High‑dose insulin 1 unit/kg bolus then 1–10 units/kg/h
Vasopressors (norepinephrine/epinephrine),
Severe toxicity (hypotension, bradycardia, conduction block): call KPCC 1804774 and PICU early. Give calcium (central line preferred, especially in children), high‑dose insulin and vasopressors as first‑line for hypotension; the choice is led by the clinical picture., Titrate calcium to blood pressure; do not exceed ionized calcium 1.5–2× the upper normal. Run dextrose and replace potassium with high‑dose insulin — monitor glucose and potassium frequently., Lipid emulsion and VA‑ECMO are rescue options. These steps come from an adult expert consensus; pediatric data are limited.
Carbon monoxideOxygen 100% by non‑rebreather mask, or by endotracheal tube if intubated
Continue until symptom‑free
Hyperbaric oxygen (HBO) — consider for every acute symptomatic CO poisoning; children can be treated safely
Refer for HBO whatever the COHb if any loss of consciousness, neurologic signs, cardiovascular dysfunction or severe acidosis; COHb correlates poorly with severity, so use it as one factor, not a cut‑off (COHb ≥ 25% is one more reason to discuss HBO); the shortest delay gives the best result,
Children take up CO faster than adults but also clear it faster
Monitor — COHb by co‑oximetry on venous or arterial blood; COHb ≥ 2% supports the diagnosis in a non‑smoker
Pulse oximetry is falsely reassuring — a standard oximeter cannot tell COHb from oxyhemoglobin; a pulse CO‑oximeter (SpCO) cannot rule CO out
Fire victim → treat cyanide too (next row); HBO is also indicated for CO with cyanide poisoning — see Smoke Inhalation & Carbon Monoxide Poisoning
Cyanide (smoke inhalation, nitroprusside)Hydroxocobalamin 70 mg/kg IV/IO (max 5 g) over 15 min,,
Second dose if needed: 70 mg/kg (max 5 g) over 15 min (very unstable) to 2 h
Total max 140 mg/kg (max 10 g),
± Sodium thiosulfate 250 mg/kg = 1 mL/kg of 25% (max 12.5 g = 50 mL), slow IV, in a separate line,
Oxygen 100%
Treat empirically — fire/smoke exposure with cardiac arrest, altered mental status, raised lactate, severe metabolic acidosis or hypotension
Lactate > 10 mmol/L (fire victims) or ≥ 8 mmol/L (other cyanide poisoning) is a sensitive marker, but specificity is only moderate — do not rely on lactate alone,
Repeat — second dose according to severity and clinical response
Monitor — blood pressure (transient rise); renal function (urea, creatinine) for 7 days; skin discoloration; hydroxocobalamin interferes with colorimetric laboratory tests,
Never give thiosulfate or nitrite through the hydroxocobalamin line
Sodium nitrite only if hydroxocobalamin is unavailable — its methemoglobin may worsen oxygen delivery when CO is also present (smoke)
DigoxinDigoxin‑specific immune Fab (each vial binds ~0.5 mg)
Acute, amount known: vials = body load (mg) ÷ 0.5, where body load = mg ingested × 0.8 for tablets (no correction for capsules/IV); round up
Acute, unknown: 10–20 vials (start 10, repeat 10)
Chronic, unknown level: adults/children ≥ 20 kg 6 vials; < 20 kg 1 vial
By level: vials = level (ng/mL) × weight (kg) ÷ 100,
Give for life‑threatening cardiac‑glycoside toxicity — ventricular dysrhythmia, bradycardia/high‑grade block unresponsive to atropine, or potassium > 5.5 mEq/L (adults) / > 6 mEq/L (children). Infuse over ≥ 30 min (bolus if arrest is imminent). In small children reconstitute/dilute to avoid volume overload. Monitor potassium closely for several hours (can fall fast); serum digoxin becomes unreliable after Fab. Re‑dose if toxicity persists or recurs.,
IronDeferoxamine IV, infusion rate up to 15 mg/kg/h; max 6,000 mg/24 hRefer any ingestion ≥ 40 mg/kg elemental iron, or with severe or persistent symptoms (persistent vomiting or diarrhea, altered consciousness, hematemesis, bloody diarrhea). Chelate for systemic toxicity, on toxicology (KPCC) advice., Slow or stop the infusion for rate‑related hypotension. Limit continuous IV infusion to ~24 h — longer durations are linked to ARDS., Monitor blood pressure and urine colour (a reddish change may follow chelation); switch IV→IM once stable.
IsoniazidPyridoxine IV — amount known: 1 g for each 1 g of isoniazid ingested,
Amount unknown: 80 mg/kg (maximum = adult dose, 5 g)
Slow IV bolus over 3–5 min
Repeat if seizures continue (more than 10 g is rarely needed)
Diazepam if seizures continue after pyridoxine (doses: Convulsive Status Epilepticus)
Who — every symptomatic child, and any acute ingestion > 80 mg/kg even if well
Expect seizures, severe metabolic acidosis and coma 30 min–3 h after ingestion
Target — seizures stop; they may not respond to anticonvulsants until pyridoxine is given, so keep IV pyridoxine readily available
Phenytoin only with caution (isoniazid slows its metabolism) — see Isoniazid Poisoning
Local anesthetic systemic toxicity (LAST)Lipid emulsion 20%
Under 70 kg: bolus 1.5 mL/kg over 2–3 min, then 0.25 mL/kg/min
Over 70 kg: bolus ~100 mL over 2–3 min, then ~250 mL over 15–20 min
Still unstable: repeat the bolus and double the infusion (0.5 mL/kg/min)
Max 12 mL/kg,
Epinephrine — smaller than usual doses; start with < 1 mcg/kg
Seizures — benzodiazepine preferred
When — call for help, get the LAST rescue kit and give lipid early; LAST resuscitation is different from standard advanced life support
Continue the infusion for > 15 min after the circulation is stable
Avoid vasopressin, calcium‑channel blockers, β‑blockers and more local anesthetic
Monitor — ≥ 2 h after a seizure; 4–6 h after cardiovascular instability
Methanol / ethylene glycolFomepizole IV — loading 15 mg/kg
then 10 mg/kg every 12 h × 4 doses
then 15 mg/kg every 12 h
Each dose as a slow infusion over 30 min
During hemodialysis: every 4 h
Methanol — add folinic (or folic) acid,
Ethanol only if fomepizole is unavailable (harder dosing, more monitoring, more adverse effects)
Stop when methanol or ethylene glycol is undetectable or < 20 mg/dL and the child is symptom‑free with a normal pH
Monitor — blood gas and pH, electrolytes, urea, creatinine, urinalysis, methanol/ethylene glycol levels
Dialysis — methanol: coma, seizures, new visual loss, pH ≤ 7.15, acidosis despite antidote, anion gap > 24 mmol/L, methanol > 700 mg/L (21.8 mmol/L) on fomepizole, or impaired kidney function; stop when methanol < 200 mg/L (6.2 mmol/L) and the child is improving
Dialysis — ethylene glycol: coma, seizures or acute kidney injury; glycolate > 12 mmol/L or anion gap > 27 mmol/L; consider if ethylene glycol > 50 mmol/L or osmolal gap > 50 on fomepizole; stop when anion gap < 18 mmol/L
Adjust fomepizole doses during dialysis,
Methemo­globinemiaMethylene blue 1 mg/kg IV (range 1–2 mg/kg) over 5–30 min,,
Repeat 1 mg/kg after 30–60 min if MetHb stays > 30% or symptoms persist,
Max cumulative 5–7 mg/kg (toxicity from 7 mg/kg),,
G6PD deficiency — contraindicated (hemolysis; may not work) → ascorbic acid or exchange transfusion,
Treat when MetHb ≥ 20% with symptoms, or ≥ 30% without; 10–30% if symptomatic with heart or lung disease, significant anemia or CO poisoning
Stop the oxidant; give oxygen; make sure glucose is available
Target — MetHb falls within ~1 h; no response after 2 doses → exchange transfusion or hyperbaric oxygen (PICU),
Monitor — MetHb by co‑oximetry; pulse oximetry is unreliable (sticks near 85% with high MetHb) and methylene blue lowers the reading — use a blood gas,
MetHb may rebound after dapsone or aniline — recheck,
Serotonergic drugs or opioids — risk of serotonin syndrome; avoid the combination
Infants with diarrhea and acidosis and MetHb < 20% may improve with fluids and bicarbonate alone
OpioidsNaloxone 0.1 mg/kg IV/IO/IM (max 2 mg), repeat every 2–3 min
Small titrated increments if opioid‑dependent
Infusion: two‑thirds of the effective waking dose per hour,,
Titrate to adequate ventilation and airway reflexes, not full arousal. In a known opioid‑dependent child give gradual small increments to avoid precipitated withdrawal., Naloxone is shorter‑acting than most opioids, so observe until consciousness and vital signs normalise and start an infusion (⅔ of the effective dose per hour) if resedation occurs — longer for methadone, sustained‑release products or buprenorphine.,
Organo­phosphate / carbamateAtropine 0.02 mg/kg IV/IO (not above the adult 1–2 mg); double the dose every 5 min until the chest is dry
Then infusion 10–20% of the total loading dose per hour
Pralidoxime (organophosphate) 20–50 mg/kg (max 2 g/dose) IV over 15–30 min
then 10–20 mg/kg/h
or repeat 20–50 mg/kg after ~1 h if weakness persists, then every 10–12 h,
Diazepam for seizures or agitation (doses: Convulsive Status Epilepticus)
Target — bronchorrhea and bronchospasm reversed, bradycardia and hypotension corrected (adult targets: pulse > 80/min, systolic BP > 80 mm Hg),
Too much atropine → anticholinergic delirium
Pralidoxime — never as a rapid bolus (vomiting, tachycardia, laryngospasm, rigidity); max 200 mg/min; start once atropine is working,
Known carbamate: pralidoxime is not indicated (may increase carbaryl toxicity)
Succinylcholine — prolonged paralysis; use only with caution
Monitor ≥ 48–72 h — sudden respiratory muscle weakness (intermediate syndrome), recurrent cholinergic signs, changing atropine needs,
SalicylateSodium bicarbonate — IV bolus, then infusion (≈ 150 mEq/L in 5% dextrose with potassium) to alkalinize the urine
Hemodialysis for severe poisoning,,
Alkalinize to a urine pH 7.5–8.0, running the infusion to a urine output ~2–3 mL/kg/h; check urine pH frequently., Keep potassium normal/high‑normal — hypokalemia prevents urinary alkalinization; replace early., Maintain high minute ventilation if intubated (avoid respiratory acidosis). Hemodialysis for altered mental status, ARDS needing oxygen, failure of standard therapy, severe acidemia, or a very high level (≈ 100 mg/dL acute).,
Serotonin syndromeStop all serotonergic drugs,
Benzodiazepine for agitation (doses: Convulsive Status Epilepticus),
Active cooling,
Cyproheptadine — oral only; adult dose 4–12 mg for moderate toxicity; benefit unproven and dose not well defined,
Severe — temperature > 39 °C with agitation, reduced consciousness, rigidity, or no response to cooling → early paralysis and intubation (PICU); supportive care comes before any antidote,
Monitor — temperature (rapid rise), muscle rigidity, clonus
Expect improvement within 24 h of stopping the drug — see Drug‑Induced Hyperthermia Syndromes
Sodium‑channel blocker / tricyclicSodium bicarbonate 1–3 mEq/kg IV bolus, repeat to narrow the QRS
Lidocaine if refractory
Give for QRS > 100 ms, ventricular dysrhythmia or hypotension; repeat boluses (then an infusion) until the QRS narrows, avoiding excessive alkalemia., A class Ib agent (lidocaine) is a reasonable next step for refractory wide‑complex toxicity; lipid emulsion for life‑threatening cases unresponsive to other therapy. Monitor the ECG (QRS width), blood pressure, serum pH, sodium and potassium.
SulfonylureaOctreotide — children 1–1.5 µg/kg IV/SC, then 2–3 further doses 6 h apart (adults 50 µg)
Dextrose for hypoglycemia (bolus then infusion),
Treat hypoglycemia first with IV dextrose, then give octreotide to stop insulin release and prevent recurrent hypoglycemia; hypoglycemia recurred in half of the reported children, so repeat doses are often needed., Taper the dextrose infusion as octreotide takes effect. Check glucose frequently; do not give prophylactic IV dextrose. Observe ~12 h after the last octreotide/dextrose dose for relapse — longer for large or sustained‑release ingestions.,
Sympathomimetic (cocaine, amphetamines)Sedation first — IV benzodiazepine titrated to control agitation (doses: Convulsive Status Epilepticus),
Rapid external cooling for life‑threatening hyperthermia — ice‑water immersion or evaporative cooling (faster than cooling blankets or cold packs),
Sodium bicarbonate 1–3 mEq/kg IV for cocaine wide‑complex tachycardia or cardiac arrest (lidocaine is an alternative for the tachycardia)
Vasodilator (nitrate, phentolamine, calcium‑channel blocker) for coronary vasospasm or a hypertensive emergency that persists after sedation,
Target — benzodiazepines are the mainstay of initial control of agitation and blood pressure
Monitor — ECG, temperature; watch for seizures, hyperthermia, rhabdomyolysis, metabolic acidosis and myocardial infarction
β‑blockers — safety in cocaine toxicity is controversial (both benefit and harm reported)
⚠ Avoid
  • Flumazenil is generally avoided (seizure risk) — see the benzodiazepine row.
  • Several agents have delayed or biphasic toxicity (acetaminophen, iron, sustained‑release products, sulfonylureas) — observe and recheck.
◣ Admit · Discharge · Refer
  • Admit — symptomatic, a significant/unknown ingestion, or a delayed‑toxicity agent (observe).
  • Home from the emergency department — asymptomatic after the appropriate observation window with a non‑toxic exposure.
  • Refer — now — the poison center/toxicology; psychiatry for intentional ingestion; safeguarding as needed.

One Pill Can Kill — Toddler Alert

HOURS< 6 YR · AAPCC 2005–2007

One tablet or one teaspoon of these can seriously harm or kill a 10‑kg toddler — observe for the full period even if the child is well.

▸
◣ Recognize
  • One or two adult dose units can kill a 10‑kg toddler. The classic list includes tricyclic antidepressants, antipsychotics, antimalarials (quinine derivatives), calcium‑channel blockers, opioids, oral hypoglycemics, camphor and methyl salicylate.,
  • These few drugs caused 40% of toddler poisoning deaths reported to US poison centers in 1990–2000.
  • The list keeps growing. By 2018 it had doubled, adding newer anticoagulants, a PDE‑5 inhibitor, newer antiepileptics, antidiabetic drugs, multiple‑sclerosis drugs and second‑generation antipsychotics.
  • Toxicity can be delayed and prolonged (methadone, modified‑release products, sulfonylureas, diphenoxylate). A child who is well on arrival is not reassuring.,,,
Decide
  • Any possible ingestion of a listed agent by a child < 6 y = toxic, even if the ingestion is unconfirmed or the amount unknown.,,
  • Call KPCC 1804774. Check glucose and a 12‑lead ECG on arrival.,
  • Observe for the full period in the table even if the child looks well. Never send home early.
  • Do not induce emesis.,,,
Agents, danger dose and minimum observation
Medicine / productDanger at one doseObserve at leastFirst action
Antimalarials — chloroquine, hydroxychloroquine1–2 chloroquine tablets have caused serious toxicity
> 10 mg/kg chloroquine base or unknown amount: hospital
Treat hydroxychloroquine the same
4–6 h12‑lead ECG and cardiac monitor; call KPCC,,
Antipsychotics — second‑generation; phenothiazinesChild < 12 y, hospital at:
aripiprazole 15 mg
clozapine 50 mg
olanzapine 10 mg
quetiapine 100 mg
risperidone 1 mg
ziprasidone 80 mg
6 hContinuous cardiac monitoring (conduction disturbances),,
Buprenorphine (tablet, film)> 2 mg, or more than a lick or taste if < 2 y
Every child taking > 4 mg had some effect; most often drowsiness, vomiting, miosis; respiratory depression in 7%
Onset 20 min–3 h
Admit
Effects lasted 8–24 h in 26%, > 24 h in 4%,
Naloxone for respiratory depression (at least partial response in 67%); dose in the Poisoning antidote table,
Calcium‑channel blockers — amlodipine, nifedipine, verapamil, diltiazemAmlodipine 5 mg caused hypotension in a 2‑year‑oldImmediate‑release: 6–8 h
Modified‑release: 24 h,
Cardiac monitor, blood pressure; IV fluids, then IV calcium for hypotension (antidote table),,
Camphor — camphorated oil, rubs5 mL of 20% camphorated oil killed a 19‑month‑old
> 30 mg/kg: hospital
Toxic effects, including seizures, often within 10–20 min,
4–8 h (one seizure reported at 9 h),Benzodiazepine for seizures; no activated charcoal,,
Clonidine; imidazoline eye drops and nasal spraysClonidine 0.1 mg is toxic; one 0.3‑mg tablet caused coma
1–2 mL of drops or spray: coma, bradycardia, slow breathing (≤ 5 y)
Onset 30–90 min; may last 1–3 days,
4 h after arrival (no later deterioration in a pediatric series); admit if any symptomMonitor heart rate, blood pressure, breathing; support the airway — naloxone works inconsistently,,,
Diphenoxylate–atropine (Lomotil)Half a tablet has caused toxicity
Mainly opioid: coma, respiratory depression, cerebral edema, death,
24 h in a monitored bed (respiratory depression recurred at 13–24 h),IV naloxone, then a continuous infusion if needed,
Methadone, fentanyl patch, extended‑release opioidsOne methadone tablet can kill a toddler
In children, toxicity is delayed, severe and prolonged,
Admit for 24 h (≤ 3 y), even if the ingestion is unconfirmed. Older children: observe at least 6 h in the emergency department after any methadone exposure and consider admission; longer for extended‑release products and patches.,Naloxone (children may need larger doses; repeat or infuse if breathing slows again); undress the child and look for patches,
Methyl salicylate (oil of wintergreen)5 mL of 98% = 7,000 mg salicylate
< 5 mL has been fatal
More than a lick or taste (< 6 y): hospital,
Salicylate level every 2 h until improving and non‑toxicSalicylate level now; call KPCC,,
Sulfonylureas — glibenclamide, glipizideA single tablet can cause hypoglycemia
Hypoglycemia in 30% of exposed children (96% of them within 8 h); may be delayed and persistent,,
12–24 h; keep until morning rather than discharge at night,Glucose checks often; feed; no prophylactic IV dextrose. Hypoglycemia: IV dextrose bolus (Hypoglycemia), then octreotide (antidote table),,
Tricyclic antidepressants — amitriptyline, imipramine, nortriptyline> 5 mg/kg: hospital (nortriptyline, desipramine > 2.5 mg/kg)
One 50‑mg tablet = 5 mg/kg in a 10‑kg child
15–20 mg/kg potentially lethal,
6 h, with a normal ECG at the end,ECG: QRS > 100 ms → sodium bicarbonate (antidote table); benzodiazepine for seizures; no flumazenil,
⚠ Pitfalls
  • Naloxone wears off before methadone or diphenoxylate do, so respiratory depression returns. Re‑dose or start an infusion, and keep the child in a monitored bed.,
  • In clonidine poisoning, naloxone helps inconsistently; 6 of 47 children needed intubation.
  • Sulfonylureas: no prophylactic IV dextrose, and no discharge at night.
  • Ask about every adult’s medicines in the home — toddlers find and swallow them.
◣ Admit · Discharge · Refer
  • Admit — methadone, fentanyl patch or extended‑release opioid (≤ 3 y, 24 h; older children: observe at least 6 h and consider admission); any buprenorphine; diphenoxylate–atropine (24 h, monitored); modified‑release calcium‑channel blocker; sulfonylurea when the 12 h would end at night; any symptomatic child.,,,
  • Home from the emergency department — well at the end of the agent’s observation period, with normal vital signs, a normal ECG (tricyclics) and normal glucose (sulfonylureas), after KPCC advice. Advise storing medicines, eye drops and nasal sprays out of children’s reach.,,,
  • Refer — now — PICU for coma, apnea, hypotension, bradycardia, seizures, QRS widening or recurrent hypoglycemia. Involve child protection when supervision or malicious administration is a concern.,,,

Caustic (Corrosive) Ingestion

HOURS

Acid or alkali burns — protect the airway; do no harm.

▸
◢ Recognize
  • Drooling, dysphagia, painful swallowing, oral or lip burns, chest or abdominal pain. Stridor or respiratory distress means airway injury.
  • The absence of oral burns does not exclude esophageal injury. Alkali (drain cleaner) causes deep liquefactive necrosis; acid causes coagulative necrosis.
⚠ Do not
No induced emesis, no gastric lavage, no activated charcoal, no neutralizing or forced dilution — these re‑expose the esophagus and worsen injury.
Do
  • Airway first — anticipate swelling and intubate early if any compromise (by anesthesia/ENT/PICU)
  • Avoid blind nasogastric‑tube insertion unless directed after endoscopic/surgical assessment.
  • Keep nothing by mouth; give IV fluids, analgesia, antiemetics.
  • Chest and abdominal X‑ray for free air. If esophageal perforation is suspected (free air, severe chest or abdominal pain, or sepsis), keep nothing by mouth, start IV fluids and broad‑spectrum IV antibiotics (aerobic and anaerobic cover; WSES 2019), and consult pediatric surgery immediately. Contact poison control.
◈ Endoscopy
  • Any symptom or sign (mouth lesion, drooling, vomiting, dysphagia, hematemesis, breathing difficulty, abdominal pain) → upper endoscopy within 24 h, once stabilized with a secure airway; acid and alkali alike. Three or more symptoms predict severe injury.
  • No symptoms, no drooling and no mouth lesions → routine endoscopy is not needed, provided follow‑up is assured.
  • Best within 12–24 h (acceptable up to 48 h; reported safe up to 96 h). Avoid endoscopy from about day 5 to day 15, when the healing wall is weakest and perforation risk is highest.
  • Watch for delayed strictures over the following weeks.
  • Corticosteroids: not routine and not before endoscopy. Endoscopic grade IIb only — GI‑led high‑dose IV methylprednisolone 1 g/1.73 m2 per day for 3 days reduces stricture formation (Usta et al., Pediatrics 2014); no proven benefit in grades I, IIa or III.
  • A swallowed button battery is a separate emergency — see Button (Lithium) Battery Ingestion.
◣ Admit · Discharge · Refer
  • Disposition depends on agent, amount, intent, symptoms and poison‑center/GI assessment, and on the ability to tolerate oral intake.
  • Admit — all symptomatic or significant exposures → nil by mouth, plan imaging/endoscopy.
  • Home from the emergency department — asymptomatic minor exposure after observation.
  • Refer — now — ENT/GI/surgery (endoscopy) and PICU; do not blind‑pass a nasogastric tube.

Hydrocarbon Ingestion & Pneumonitis

HOURSYOUNG CHILDREN · Clin Toxicol 2014

The danger is the lungs, not the gut — observe 6–8 h, X‑ray at the end, never make the child vomit.

▸
◣ Recognize
  • High aspiration risk — thin, runny, volatile products: gasoline, kerosene, spot removers, mineral spirits. Lamp oil, kerosene and lighter fluid/naphtha cause most of the serious lung injury.
  • Extra danger beyond the lungs: camphor (toxic effects, including seizures, often within 10–20 min; > 30 mg/kg needs hospital care); halogenated solvents (they sensitize the heart to epinephrine and can trigger a non‑perfusing rhythm); products containing pesticides, metals or methanol.,,
  • Aspiration signs: cough, vomiting, drowsiness, fever, fast breathing, tachycardia, altered mentation. Wheeze, tachypnea or altered mentation within 2 h predicts the need for treatment.
  • Timeline: pneumonitis follows about 15% of ingestions and evolves over the first 6–8 h. It peaks within 48 h, then improves; up to 5% progress rapidly to respiratory failure. Chest X‑ray changes appear by 4–8 h and do not always match the clinical picture. Pneumatoceles can appear after 6–10 days and resolve within 6 months.,
  • Most children stay well: in a poison‑center cohort of all ages, 1% developed significant complications.,
Do
  • Airway and breathing first; give oxygen for hypoxemia; watch the work of breathing.,
  • Observe 6–8 h, then take a chest X‑ray at the end of observation. An early film can be falsely normal.,,
  • Call KPCC 1804774 with the product name. Ingredients such as camphor, pesticides, halogenated solvents or methanol change management.,
  • Halogenated or inhaled volatile hydrocarbon: continuous cardiac monitoring in a calm environment. Avoid epinephrine and other catecholamines where possible — they can precipitate ventricular arrhythmia in the sensitized heart; beta‑blockers have been suggested for these arrhythmias — discuss with KPCC/PICU.
⚠ Do not
  • No induced emesis and no gastric lavage — both cause aspiration. No activated charcoal — it provokes gagging and vomiting.,
  • No prophylactic corticosteroids (no benefit). No prophylactic antibiotics: fever and infiltrates are part of chemical pneumonitis. Give antibiotics only for bacterial superinfection.,
Treatment
TreatmentDose · routeEndpoint · monitoring
Activated charcoalNot indicated,Gagging and vomiting raise the risk of aspiration,
AntibioticsNot prophylactic
Only for bacterial superinfection,
Fever and infiltrates alone are not an indication,
Benzodiazepine (seizures, e.g. camphor)Dose as in Convulsive Status EpilepticusSeizure stops; watch breathing
CorticosteroidsNot indicated,No benefit shown,
OxygenSupplemental, to correct hypoxemia
Intubation and mechanical ventilation if hypoxemia does not respond or the CNS is severely involved,
SpO2, work of breathing, mental status. ECMO, surfactant and high‑frequency ventilation are reported only in case reports,
◣ Admit · Discharge · Refer
  • Admit — symptomatic on arrival or during the 6–8 h observation, or an abnormal chest X‑ray. About 90% of admitted children have a benign course.,
  • Home from the emergency department — well through at least 6 h of observation with a normal chest X‑ray. Children with early symptoms who settle within the 6 h and have a normal X‑ray also do well.,
  • Refer — now — PICU for increased work of breathing, altered sensorium, seizures, or hypoxemia despite oxygen. Discuss camphor, pesticide or halogenated products with KPCC.,

Isoniazid (INH) Poisoning — Refractory Seizures

MINUTESISONIAZID LABEL 2025

Seizures that will not stop, with acidosis and coma, in a child with TB medicine at home — give IV pyridoxine now.

▸
◣ Recognize
  • Who: a child taking INH for TB infection, or one with access to a household member’s TB medicine. Ingestion may be accidental or deliberate. With known access to INH, a seizure is INH toxicity until proved otherwise.,
  • Onset 30 min–3 h: nausea, vomiting, dizziness, slurred speech, blurred vision and visual hallucinations. These progress rapidly to stupor, coma, respiratory depression and severe, intractable seizures.
  • Triad: seizures that do not respond to anticonvulsants · severe metabolic acidosis · coma. Ketonuria and hyperglycemia are typical.,,
  • Dose: in a pediatric series, seizures followed ingestions of 14–99 mg/kg (mean 54 mg/kg). An acute ingestion of > 80 mg/kg needs IV pyridoxine even without symptoms.,
Do
  • Airway, breathing, oxygen. Give a benzodiazepine for the seizure together with pyridoxine; the two act synergistically in animal studies.,
  • IV pyridoxine now (dose below). Repeat it if seizures continue. A single gram‑for‑gram dose prevented recurrent seizures and shortened coma.,
  • Send blood gas, electrolytes, urea and glucose. Acidosis usually clears once seizures are controlled, so dialysis is rarely needed.,
  • Call KPCC 1804774 and ask pharmacy for the full pyridoxine dose at once.,
Medications
DrugDoseRoute · rate · repeatEndpoint · monitoring
Benzodiazepine (midazolam, lorazepam, diazepam)Dose as in Convulsive Status EpilepticusRoute as in that card
Give together with pyridoxine, not instead of it
Seizure stops
Watch breathing,
Pyridoxine (vitamin B6)Known amount: equal to the INH ingested (1 mg per mg)
Unknown amount: 80 mg/kg (maximum = adult dose, 5 g)
Well child, > 80 mg/kg ingested: equal to the INH ingested
Total > 10 g rarely needed; maximum safe dose unknown
IV
Seizing: slow bolus over 3–5 min
Not seizing: over 30–60 min
Repeat the dose if seizures continue
Seizures stop; acidosis and coma resolve
Monitor seizure activity, ventilation, blood gas, electrolytes, glucose,
◈ If IV pyridoxine is not in the department
  • Keep treating seizures with benzodiazepines; if they continue, give a GABA‑ergic agent — phenobarbital 15–20 mg/kg IV (as in the Convulsive Status Epilepticus card), then a midazolam or propofol infusion with a secured airway in PICU — while KPCC and pharmacy obtain pyridoxine. Do not rely on phenytoin/fosphenytoin (no role in INH seizures); levetiracetam and valproate are unproven here. Seizures may stop only once parenteral pyridoxine is given.,
  • When it was not stocked in the ED, pyridoxine was delayed by 5.8 h on average and one child had to be transferred. Pyridoxine should be immediately available in every ED.,
  • At 100 mg/mL in 1‑mL vials, a 5‑g dose is 50 vials.
⚠ Pitfalls
  • Under‑dosing: an infant given 70 mg/kg (650 mg) after a 290 mg/kg ingestion seized again and needed 2 g more. When the amount is known, dose gram‑for‑gram regardless of age.
  • Phenytoin/fosphenytoin: avoid — ineffective for INH seizures, and INH inhibits its metabolism.
  • Sodium bicarbonate in a hypoventilating child can worsen hypercarbia. Monitor CO2 and support ventilation first.
  • Missed diagnosis: INH was not suspected at a first seizure and the child returned with another. Ask about TB medicines in the home.
◣ Admit · Discharge · Refer
  • Admit — every symptomatic child. Seizures, coma or acidosis need intensive care with repeated blood gases to protect against hypoxia, hypotension and aspiration.
  • Home from the emergency department — only a well child after a small accidental ingestion, once the observation period agreed with KPCC has passed. Advise locked storage of TB medicines.
  • Refer — now — PICU for recurrent seizures, coma or respiratory insufficiency. Psychiatry after a deliberate ingestion (3 of 8 episodes in a pediatric series were suicide attempts).,

Burns

HOURS

Cool it, size it, replace fluid to urine output — and protect the airway.

▸
◣ Assess
  • Estimate % total body surface area (TBSA) with a Lund‑Browder chartLund‑Browder chart (age‑adjusted values are in the calculatorLund–Browder figure on this card; the child's palm including fingers ≈ 1%); assess depth and mechanism.
  • Airway red flags — stridor, hoarseness, respiratory distress, black sputum, singed nasal hairs, facial swelling or progressive airway edema → prepare pediatric airway equipment, involve anesthesia/airway expertise early; low threshold for early intubation. If intubated, do not trim the endotracheal tube (facial swelling can leave it too short) — secure it carefully and reassess.,,
  • Enclosed‑space flame/flash burn → 100 % oxygen; co‑oximetry for carboxyhemoglobin; consider cyanide (hydroxocobalamin) — see Smoke Inhalation & Carbon Monoxide Poisoning.
  • Elevate significantly burned limbs and the head of the bed for head/neck burns; document distal perfusion. Circumferential limb or chest burn → check distal perfusion / chest excursion frequently; urgent burns advice if perfusion or ventilation is compromised; escharotomy only with expert guidance.,
  • Mechanism suggesting trauma (fall, blast, vehicle) → trauma primary survey first (§13 Major Trauma); spinal precautions when indicated.
Burns — Lund–Browder estimate of % TBSAAge‑adjusted regions a, b, c; fixed regions carry their value per side and aspect; the child’s palm with fingers ≈ 1 %,. The calculator applies the same values.
Burns — Lund–Browder estimate of % total body surface area (TBSA) Values are per region for that aspect (front or back) · amber regions a, b, c change with age (table) · the child’s palm with fingers ≈ 1 % a neck 1 13 anterior trunk 1 genitalia 2 1½ 1¼ b c 1¾ 2 1½ 1¼ b c 1¾ Anterior a neck 1 13 posterior trunk 2½ 2½ buttocks 2 1½ 1¼ b c 1¾ 2 1½ 1¼ b c 1¾ Posterior Percentage of body surface by age 0 y 1 y 5 y 10 y 15 y adult a · ½ head 9½ 8½ 6½ 5½ 4½ 3½ b · ½ one thigh 2¾ 3¼ 4 4¼ 4½ 4¾ c · ½ one lower leg 2½ 2½ 2¾ 3 3¼ 3½ Fixed regions (blue; per side, per aspect) neck 1 · trunk 13 · genitalia 1 (anterior) buttock 2½ each (posterior) upper arm 2 · forearm 1½ · hand 1¼ foot 1¾ · front + back add up to 100 % How to count Count partial- and full-thickness burn only (ignore simple erythema). For a region that is partly burned, take that fraction of its value. Formal IV resuscitation when TBSA > 10 %. Source: Lund CC, Browder NC. The estimation of areas of burns. Surg Gynecol Obstet 1944;79:352–358; ISBI practice guidelines 2016. Age-adjusted values a, b, c from Lund & Browder. Original drawing for this guide.
First aid Stop the burning; cool with running water for 20 min — worthwhile even if started up to 3 h after the burn (not ice; no hydrogel products); then cool the burn, warm the child: remove wet clothing and jewelry, warm room, blankets (infants lose heat fastest); cover; analgesia.,,,
Fluids (TBSA > 10%)
  • Lactated Ringer's starting at 3 mL/kg × %TBSA for the first 24 h (sources give 2–4): ½ in the first 8 h from the time of the burn, ½ over the next 16 h, plus maintenance with dextrose (4‑2‑1); adjust the rate hourly to urine output — the formula is only a starting estimate.,
  • Shock at presentation is unusual from the burn alone in the first hours — look for hemorrhage/trauma, inhalation injury or sepsis; give 10–20 mL/kg isotonic crystalloid and reassess rather than repeated boluses (over‑resuscitation harms).,
  • Titrate to urine output 1 mL/kg/h if < 30 kg; 0.5 mL/kg/h if ≥ 30 kg.,
Refer to a burns center > 10% TBSA, full‑thickness, face/hands/feet/perineum/joints, electrical or chemical, inhalation injury, or suspected inflicted injury (expert consensus; the 10% threshold is ISBI’s cut‑off for formal fluid resuscitation in children).
⚠ Airway / circulation red flags
  • Enclosed‑space fire → 100 % O₂; consider carbon monoxide ± cyanide.
  • Hoarseness, stridor, respiratory distress, black sputum, singed nasal hairs or progressive facial swelling → early airway/anesthesia involvement; do not trim the tube.
  • Circumferential chest burn + impaired ventilation → urgent burn‑specialist advice.
  • Circumferential limb burn → check distal perfusion frequently.
  • Elevate significantly burned limbs and head/neck burns.
  • Cool the burn, but keep the child warm.
⚠ Avoid over‑resuscitation ("fluid creep")
  • The formula is only a starting estimate — titrate to urine output, not to the number.
  • Don't apply ice or home remedies.
⚠ Raise suspicion for inflicted injury
  • A significant share of pediatric burns are inflicted — most intentional burns are scalds.
  • Red flags: a well‑demarcated burn with uniform depth and no splash marks; a symmetric immersion (“stocking/glove”) pattern with a clear upper margin and skin‑fold sparing; burns in normally protected sites (groin, perineum, buttocks, back, thighs); a patterned contact burn reproducing the shape of an object (iron, cigarette, lighter, heater, hair dryer); delayed presentation or a history that does not fit the burn pattern or the child's developmental stage.
  • Look for other injuries and old fractures; safeguard.
◣ Admit · Discharge · Refer
  • Admit — large or deep burns, airway/inhalation injury, electrical/chemical burns, or a safeguarding concern → burns center.
  • Home from the emergency department — small superficial burns with dressing and review.
  • Refer — now — a burns unit per criteria; ophthalmology/surgery as needed.

Heat Stroke

MINUTES

A clinical diagnosis — core ≥ 40°C + CNS dysfunction after heat exposure. Cool fast; antipyretics do not work.

▸
◣ Diagnose clinically
  • Core temperature ≥ 40°C with CNS dysfunction after environmental heat exposure. Criteria and cooling evidence are largely adult/exertional and are extrapolated to children. Well‑hydrated older children and adolescents tolerate exercise in the heat about as well as adults, but infants and young children gain heat faster (larger surface‑area‑to‑mass ratio, higher metabolic heat production, less effective sweating) and cannot remove themselves from hot environments such as closed vehicles.
  • CNS: confusion, delirium, irritability, hallucinations, ataxia, slurred speech, seizures, coma. CVS: tachycardia, hypotension, dehydration/shock. GI: nausea, vomiting (± diarrhea). Other: hot skin, tachypnea.
Investigations — do not delay cooling RBS (hypoglycemia) · CBC · electrolytes (Na/K/Ca) · urea & creatinine · LFTs · coagulation (DIC) · blood gas (metabolic acidosis ± early respiratory alkalosis) · creatine kinase (rhabdomyolysis) · urinalysis (myoglobinuria).
◣ Management
  • 1 · ABCDE — secure airway, support breathing and circulation.
  • 2 · Immediate rapid cooling (do not delay). Ice‑water immersion (1–5°C) when feasible — the fastest method; aim to cool by ≥ 0.15°C/min. Otherwise immerse in cool water (8–17°C — the AHA’s “tepid”, not lukewarm) or use tarp‑assisted ice‑water cooling; only if immersion is not possible use evaporative cooling — remove clothing, spray/mist water, high‑flow fans, mesh stretcher/hammock — plus ice packs to neck, axillae, and groin. Room‑temperature 0.9% saline for dehydration/shock (avoid overload). Continuous rectal core‑temperature monitoring.,
  • 3 · Stop active cooling at a core temperature of 38.6°C to avoid overshoot hypothermia.
  • 4 · No antipyretics (acetaminophen/ibuprofen) — ineffective in heat stroke and may worsen liver, renal, or GI injury. Treat shivering cautiously with IV midazolam or lorazepam; treat seizures per the pediatric status epilepticus protocol (see Convulsive Status Epilepticus).
⚠ Disposition
  • Admit — children with true heat stroke (CNS dysfunction) go to a PICU or high‑dependency/PICU‑capable setting depending on severity and organ injury — thermal instability and organ injury (rhabdomyolysis, AKI, DIC) can evolve over days.
  • High‑yield in Kuwait's climate.
◣ Admit · Discharge · Refer
  • Admit — all with CNS dysfunction or organ injury → high‑dependency/PICU.
  • Home from the emergency department — mild heat exhaustion, resolved and hydrated with normal mentation.
  • Refer — now — PICU; nephrology for rhabdomyolysis/AKI.

Drowning

MINUTES

Respiratory impairment from submersion/immersion — ventilate first; rescue breaths are the key intervention.

▸
◣ Initial management (ABCDE)
  • Airway & breathing: start rescue breathing immediately (the single most important intervention); give 100% oxygen; support ventilation as needed. A Heimlich maneuver and postural drainage have no role in drowning — do not perform them; they delay ventilation and risk aspiration.
  • Circulation: check pulse; if no pulse, start CPR per the PALS cardiac‑arrest algorithm — rescue breaths and chest compressions (compressions only if the rescuer cannot give breaths). Start CPR before applying an AED and never delay CPR to get one; give oxygen as soon as available. In the ED, check the rhythm and give electrical therapy with a manual defibrillator if the rhythm is shockable.
  • Temperature: remove wet clothing; if core < 35°C, prevent further heat loss and begin active rewarming.
  • Post‑ROSC: manage per PALS post–cardiac‑arrest care.
Observe ALL in the emergency department for 6–8 h
  • Every submersion patient, even if asymptomatic: continuous pulse oximetry with serial respiratory and neurological exams, (delayed pulmonary edema can appear within 4–8 h)
  • No routine chest X‑ray or laboratory tests in an asymptomatic child.,
ASYMPTOMATIC
No cough, normal work of breathing, SpO₂ ≥ 95% on room air, normal mental status and lung exam.
No routine chest X‑ray or blood tests → well at 6–8 h → discharge with return precautions.,
MILD — NO ADMISSION NEEDED
Mild cough only; normal work of breathing; SpO₂ ≥ 95% on room air; normal mental status; normal or minimally abnormal lung exam; stable circulation.
Pulse oximetry, oxygen only if needed, chest X‑ray, serial exams; observe 6–8 h.
Symptoms resolved, SpO₂ ≥ 95% on room air, normal exams and chest X‑ray → discharge with return precautions. Symptoms persist or worsen → admit. Cough with a normal lung exam carried 0% mortality in 1,189 drowning patients.
MODERATE — ADMIT (WARD)
Persistent cough, increased work of breathing, abnormal lung exam, SpO₂ < 95% on room air that responds to oxygen, or GCS 13–14; stable circulation.
Oxygen, cardiorespiratory monitoring, glucose, blood gas, CBC, electrolytes, renal function, chest X‑ray, ECG; avoid fluid overload. CPAP/BiPAP for persistent hypoxemia if the airway is protected (HFNC if not tolerated).
PICU if the oxygen need rises, NIV is needed, or breathing or mental status worsens.
SEVERE — PICU
Severe distress or respiratory failure, SpO₂ < 90% despite oxygen/NIV, frothy secretions, significant altered mental status, shock, or ARDS.
Secure the airway; intubate with lung‑protective ventilation and PEEP, 100% oxygen initially; rewarm; cautious fluids ± vasopressors; consider ECMO where available.
⚠ Admit
  • Admit — moderate symptoms (ward); mild symptoms that persist or worsen after 6–8 h; severe symptoms, rising oxygen need or need for NIV/ventilation (PICU). Mild cases that recover during observation do not need admission.
◈ Not recommended
  • Heimlich maneuver
  • postural drainage
  • routine chest X‑ray or blood tests in an asymptomatic child
  • glucocorticoids
  • routine antibiotics
  • routine cervical‑spine immobilization unless trauma (e.g., a diving injury) is suspected.,
◣ Admit · Discharge · Refer
  • Admit — moderate symptoms → ward; severe → PICU; mild symptoms only if they persist or worsen after 6–8 h observation.
  • Home from the emergency department — asymptomatic or mild, well after 6–8 h observation with SpO₂ ≥ 95% on room air and a normal exam (and a normal chest X‑ray if mild). Return at once for increasing or persistent cough, difficulty breathing, cyanosis or chest pain, persistent vomiting, drowsiness or seizure, or fever after the first 24 h.
  • Refer — now — PICU for severe or worsening respiratory compromise; child protection when the history, supervision, delay in presentation or injury pattern raises concern.

Smoke Inhalation & Carbon Monoxide Poisoning

MINUTESFIRE / SMOKE

Fire injures three ways — airway, carbon monoxide, cyanide. Look for and treat all three.

▸
◣ Define
  • Fire/smoke injures by three mechanisms: (1) thermal / chemical airway injury, (2) carbon monoxide (CO), (3) hydrogen cyanide (HCN). Suspect all three after any enclosed‑space fire, especially with altered mental status.
◣ Approach — the airway first
  • Signs of inhalation injury: facial/neck burns, singed nasal hairs, soot in the mouth or sputum, carbonaceous sputum, hoarseness, stridor, oropharyngeal edema or blistering.
  • Airway injury is progressive — edema worsens over hours. Reassess continuously.
⚠ Secure the airway early
  • Deep facial/neck burns, oropharyngeal blistering or edema, hoarseness/stridor, or large cutaneous burns → intubate early (call PICU/anesthesia urgently — expert airway control) before edema makes the airway impassable.
  • Avoid over‑aggressive IV fluids — they worsen airway edema.
Carbon monoxide
◣ Recognize & measure
  • CO binds hemoglobin ~200–250× more avidly than oxygen → tissue hypoxia plus direct cellular toxicity; symptoms and COHb level correlate poorly.
  • Pulse oximetry reads falsely normal (it cannot distinguish carboxyhemoglobin) — measure COHb by co‑oximetry (blood gas). COHb ≥ 2% (non‑smoker) or ≥ 9% (smoker) supports the diagnosis.
  • Symptoms: headache, nausea, dizziness, confusion, syncope, seizure, cardiac ischemia, coma.
◈ Hyperbaric oxygen (HBO) — available locally
  • High‑flow 100% oxygen via a non‑rebreather (or ventilator) is first‑line and cuts COHb half‑life from ~4–5 h to ~60–90 min.
  • With a chamber on site, consider HBO for severe poisoning: loss of consciousness/syncope, seizure or altered mental status, cardiac ischemia or arrhythmia, persistent metabolic acidosis, end‑organ damage, a markedly raised COHb, or pregnancy (COHb > 15%) — decide early; the Undersea and Hyperbaric Medical Society (UHMS) advises considering HBO for any acute symptomatic CO poisoning. Pediatric COHb cut‑offs are not established.,
  • HBO speeds elimination and may reduce delayed neurocognitive sequelae; trial evidence is mixed, so weigh case by case.
  • In children benefit is extrapolated from adult trials (the pivotal RCT excluded patients under 16 years and pregnant women); let CO exposure duration, COHb level, neurologic signs, and lactate guide the decision.
⚠ Cyanide — don't miss it
  • Suspect HCN co‑poisoning in an enclosed‑space fire with soot, altered mental status, hemodynamic instability, or severe lactic acidosis (lactate ≥ 10 mmol/L in a fire victim; ≥ 8 mmol/L applies to cyanide exposure without smoke).
  • Treat empirically — do not wait for levels.
  • Use hydroxocobalamin; avoid nitrite‑based kits in smoke victims (induced methemoglobinemia worsens hypoxia).,
Management
InterventionDoseNotes
Oxygen100% via non‑rebreather (or intubate)Continue until symptom‑free and COHb < 5%.,
Hydroxo­cobalamin (suspected cyanide)70 mg/kg IV/IO (max 5 g) over 15 min; may repeat once — 70 mg/kg (max 5 g) over 15 min to 2 h (total max 140 mg/kg, 10 g). Separate line from sodium thiosulfate/nitrite.Empiric in smoke inhalation with shock, or lactate ≥ 10 mmol/L plus compatible clinical findings (do not rely on lactate alone); repeat once if needed.
HBO (severe CO)Per hyperbaric‑unit protocol (pressure and number of sessions set by the unit)Refer to the hyperbaric unit for the criteria above; the pivotal adult RCT gave three sessions within 24 h.
◣ Also
  • Cardiac monitoring + ECG, serial lactate and COHb, cautious fluid resuscitation; ICU/burns referral.
  • See also Burns and Poisoning & Toxic Ingestion for concurrent burn and antidote management.
✦ Pearl — the oximeter lies
  • A normal SpO₂ does not exclude CO poisoning — measure carboxyhemoglobin.
  • In a fire victim with shock and a high lactate, give hydroxocobalamin without waiting for confirmation.
◣ Admit · Discharge · Refer
  • Admit — respiratory symptoms, altered mentation, or a significant carboxyhemoglobin → oxygen and monitoring.
  • Home from the emergency department — asymptomatic with normal levels after observation.
  • Refer — now — hyperbaric/PICU for severe CO; burns/ENT for airway injury.

Envenomation — Scorpion Sting & Snakebite

MINUTESWHO 2016 · regional

Two regional envenomations: scorpion sting = an autonomic storm; snakebite = local tissue injury and coagulopathy (± neurotoxicity).

▸
◣ Scorpion sting
  • Severe local pain, then an autonomic storm: sweating, salivation, vomiting, hypertension and tachycardia, agitation, and in severe cases pulmonary edema, myocardial dysfunction and cardiogenic shock (severity depends on venom dose, time to care and the victim’s age).,
  • Supportive care and analgesia. Hypertension is usually transient and may be followed by hypotension: do not treat it routinely; give an antihypertensive (prazosin is the most studied) only for a hypertensive crisis or pulmonary edema. Pulmonary edema or cardiogenic shock: intensive care, oxygen (target SpO₂ ≥ 92%), non‑invasive or invasive ventilation, and dobutamine 5–15 mcg/kg/min. Give antivenom for systemic envenomation per local protocol — with prazosin it hastened recovery in an Indian RCT (Mesobuthus tamulus), but evidence for other Old World species is weaker., Benzodiazepines for agitation, severe neuromuscular excitation or seizures.
◣ Snakebite
  • Look for local swelling/necrosis and systemic effects — coagulopathy/bleeding, neurotoxicity (ptosis, bulbar/respiratory weakness) or rhabdomyolysis, depending on species.
  • First aid: reassure; immobilize/splint the bitten limb and minimize movement; remove constrictions; move to hospital. Give species‑appropriate IV antivenom for systemic envenomation (shock, spontaneous bleeding or incoagulable blood, neurotoxicity, dark urine/acute kidney injury) or severe local envenomation (rapidly progressive swelling, bite on a digit, species known to cause necrosis). Children receive the same antivenom dose as adults — do not reduce it by weight. Monitor the airway and clotting.
⚠ Don’t make it worse
  • No tourniquets, incision, suction or ice on snakebites — they increase harm.
  • Watch for delayed coagulopathy and compartment syndrome; recheck clotting serially.
  • Anticipate anaphylaxis to antivenom and have epinephrine ready.
◈ Local The national/KPCC protocol and species‑specific antivenom take precedence over generic international regimens. Call KPCC 1804774 early for species identification and antivenom dosing.
◣ Workup
  • Snakebite: 20‑minute whole‑blood clotting test, CBC/platelets, PT/INR + fibrinogen, D‑dimer, renal function + potassium, CK, urinalysis (myoglobin), ECG, serial limb marking, group & crossmatch.
  • Scorpion: continuous cardiac/BP monitoring, serial ECG, cardiac enzymes (troponin/CK‑MB) + echocardiogram if cardiac signs (stress‑type cardiomyopathy), glucose, electrolytes, blood gas (pulmonary edema).,
◣ Admit · Refer
  • Admit — observe every child with a suspected snakebite for at least 24 h, even if initially well (repeat the 20‑minute whole‑blood clotting test/clotting screen and neurological checks); admit all systemic envenomation and any child with progressing local signs. Acetaminophen or an opioid for pain — no aspirin or NSAIDs; tetanus booster once clotting is normal; antibiotics only for infection or necrosis; fasciotomy only for proven compartment syndrome after antivenom and correction of coagulopathy.
  • Refer — now — call critical care and Poison Control; surgery for compartment syndrome/necrosis.
★

Quick Reference

Weight · airway · vital signs · master doses
Time‑critical emergencies — quick referenceSolid bar = knowable clock / deadline · dashed bar = unknown onset / prognosis. See each condition's card for detail.
The Golden WindowWhat must be done — and by when — for the guide’s time‑critical emergencies. The intervention above each bar is what the window governs.▸ Red “now” = a step that starts immediately, before any window applies (e.g. 100% O₂ in CO poisoning).Solid = clock starts at a knowable moment (recognition / arrival) — a real deadline to beat.Dashed = onset usually unknown — the window is prognosis; act on suspicion, do not treat it as a countdown.MINUTES1–2 HOURSWITHIN HOURS5 min15 min30 min1 h2 h4 h6 h8 hCardiac arrestHigh‑quality CPR + early defibrillationstart immediately AHA / ILCORAnaphylaxisIM epinephrinegive immediately EAACI / WAOConvulsive status epilepticusBenzodiazepine (then escalate)by 5 min NCS / ILAESickle vaso‑occlusive crisisParenteral analgesiawithin 30–60 min ASH / NHLBIMajor traumaHemorrhage control + definitive carewithin the 'golden hour' ATLS / RCSSeptic shock / meningococcemia▸ now: O₂ + IV/IO access nowIV fluid boluses + broad‑spectrum antibioticswithin 1 h Surviving Sepsis 2026Chemo‑induced febrile neutropeniaEmpiric antibioticswithin 1 h IDSA / NICEBacterial meningitisAntibiotics — LP first unless it delays themwithin 1 h IDSAButton / lithium battery▸ now: Honey if ≥12 mo & <12 hEndoscopic removalwithin ~2 h NASPGHAN / ESPGHANIschemic priapismAspiration ± phenylephrineafter ~4 h risk climbs AUA / EAUCO poisoning (severe)▸ now: 100% O₂ immediatelyHyperbaric O₂ (if indicated)greater benefit within ~6 h UHMSTesticular torsion▸ now: Manual detorsion (temporizing)Surgical detorsionsalvage falls after ~6 h EAU / AUAMidgut volvulus (bilious vomiting)Emergency laparotomyinfarcts within hours APSA / ACSAcute compartment syndromeFasciotomyirreversible by ~6–8 h Orthopedic consensusSolid‑bar windows are consensus targets for starting the named intervention; dashed‑bar figures are prognostic. Always act as early as possible. Immediate ABC resuscitation is assumed for every row. Built from the guide’s own time‑critical cards.

When to Admit

General triggers first, then condition‑specific thresholds.

▸
◢ Any acutely unwell child
Toxic or septic appearance; shock or unstable vital signs; hypoxia (SpO₂ < 92%); unable to tolerate oral fluids or medicines; moderate to severe dehydration; fever under 3 months; diagnostic uncertainty in an unwell child; or unreliable follow‑up.
ConditionAdmit if
Febrile young infant≤ 28 days: admit all; 29–60 days: admit unless low‑risk on screening; 61–90 days: admit if ill‑appearing, abnormal screening tests or unreliable follow‑up.
UTIUnder 3 months; toxic; vomiting or unable to take oral; no response by 48 h or a resistant organism; known uropathy, obstruction, chronic kidney disease, or transplant; suspected renal abscess; acute kidney injury.
Gastroenteritis / dehydrationShock or severe dehydration; failed oral or nasogastric rehydration; persistent vomiting; significant electrolyte disturbance; under 6 months with heavy losses; possible surgical abdomen.
BronchiolitisApnea; SpO₂ persistently under 90–92%; feeding under 50–75% or dehydration; severe respiratory distress; under 3 months or comorbidity (prematurity, congenital heart disease, chronic lung disease).
CroupStridor at rest persisting after a corticosteroid; repeated nebulized L‑epinephrine; hypoxia, exhaustion, or toxic appearance.
AsthmaIncomplete response to bronchodilators; ongoing oxygen need; needing bronchodilator more often than every 3–4 h; silent chest, exhaustion, or altered consciousness (→ critical care).
PneumoniaSustained SpO₂ under 90%; moderate to severe distress; under 3–6 months; not tolerating oral; dehydration; moderate‑to‑large effusion or empyema; or failed oral antibiotics.
Nephrotic syndromeFirst presentation; hypovolemia (abdominal pain, cool peripheries, hypotension, oliguria); peritonitis or sepsis; thromboembolism; severe edema with respiratory compromise; acute kidney injury; relapse not responding to oral steroids.
BRUEUnder 2 months; prematurity; more than one event; event needed CPR or vigorous stimulation; or a concerning history or examination (higher‑risk).

Rabies Post‑Exposure Prophylaxis

HOURSWHO 2018

Dog, cat, or bat bite/scratch — wash, risk‑stratify, give vaccine ± immunoglobulin same day.

▸
◣ First — wound care (most important)
  • Wash/flush the wound ~15 minutes with soap and running water, then apply a virucidal (povidone‑iodine or 70% alcohol).
  • Avoid early suturing; if unavoidable, suture loosely after immunoglobulin infiltration.
  • Give tetanus prophylaxis; add antibiotics for a deep or contaminated bite (e.g., amoxicillin‑clavulanate).
WHO categoryExposureAction
ITouching/feeding, licks on intact skinNo PEP — wash only
IINibbling of uncovered skin; minor scratch/abrasion without bleedingWound care + vaccine
IIITransdermal bite/scratch, lick on broken skin, mucous‑membrane contamination, or any bat contactWound care + vaccine + immunoglobulin
◣ Vaccine & immunoglobulin
  • Never previously vaccinated — cell‑culture vaccine IM into the deltoid (anterolateral thigh in infants and young children; never the gluteal area) on days 0, 3, 7, 14 (add day 28 if immunocompromised; CDC/ACIP schedule — WHO 2018 IM: days 0, 3, 7 and one dose between days 14–28); the WHO 1‑week 2‑site intradermal schedule (days 0, 3, 7) is an accepted dose‑sparing option.
  • Previously fully vaccinated — 2 doses only (days 0 and 3); no immunoglobulin.
  • Rabies immunoglobulin (category III, or category II if immunocompromised) — human RIG 20 IU/kg (equine 40 IU/kg) as a single day‑0 dose; infiltrate as much of the calculated dose as is anatomically possible into and around every wound (dilute with saline if the volume is too small for multiple wounds). WHO 2018 no longer advises injecting any remainder IM at a distant site; CDC/ACIP still does — if the local protocol follows ACIP, give the remainder IM away from the vaccine site. Never give RIG in the same syringe or site as the vaccine. If unavailable on day 0, RIG can be given up to day 7 after the first vaccine dose, not later.
  • Repeat exposure within 3 months of a complete course → wound care only (no vaccine or RIG).
⚠ Do not delay
  • Start PEP the same day — rabies is almost always fatal once symptomatic.
  • Immunoglobulin can blunt live vaccines (separate MMR/varicella by ~4 months).
  • Follow the Kuwait MOH / local rabies protocol and notify public health.

IV → Oral Switch & the DIVA Patient

ASSESS

In difficult access, every lost cannula is a switch decision — not an automatic re‑stick.

▸
◣ Why it matters in DIVA
  • In difficult intravenous access (DIVA), each re‑cannulation means pain, delay, distress, and line risk. Reassess switch eligibility at every line failure rather than reflexively re‑sticking — for many infections, evidence supports switching to oral earlier than previously recommended.
DIVA score — predict difficult access
Variable (add the points)Points
History of prematurity3
Age: < 1 yr / 1–2 yr / ≥ 3 yr3 / 1 / 0
Vein not palpable (after tourniquet)2
Vein not visible (after tourniquet)2
◈ Interpretation
  • Score ≥ 4 (max 10) → > 50% chance of first‑attempt cannulation failure.
  • Use it early: escalate to an ultrasound‑guided / senior inserter or vein‑finder — and in a child improving and able to take oral, favor an IV→oral switch over repeated sticks.
  • The simpler DIVA‑3 (age + vein visibility + palpability, dropping prematurity) performs as well.
◣ Switch criteria — all should be met (COMS)
  • Clinically improving and responding to treatment.
  • Oral route works — functioning gut, tolerating intake, not vomiting, no malabsorption.
  • Markers settling — defervescing, hemodynamically stable, no ongoing sepsis (± falling CRP/white count).
  • Suitable oral agent — adequate spectrum and bioavailability.
Deep‑seated / high‑risk infection?
SWITCH EARLY
Uncomplicated CAP, UTI/pyelonephritis, uncomplicated skin/soft‑tissue infection, and acute osteomyelitis/septic arthritis (early oral non‑inferior, with fewer line complications).
KEEP IV
Bacterial meningitis/brain abscess, endocarditis, S. aureus bacteremia, febrile neutropenia (until low‑risk/recovery criteria), undrained deep abscess, septic shock until stabilized.
◈ Lean on high oral‑bioavailability agents
  • Near‑IV exposure, ideal in DIVA: ciprofloxacin, levofloxacin, linezolid, metronidazole, fluconazole, trimethoprim‑sulfamethoxazole, clindamycin, doxycycline, rifampicin.
  • Beta‑lactams (e.g., high‑dose amoxicillin) are usable but dose adequately for their lower oral absorption.
⚠ DIVA rule of thumb
  • Do not place a PICC or midline solely to finish an IV course that an oral agent could complete.
  • Weigh the procedural burden of central access against the switch criteria above.

Weight & Airway Sizing

Quick estimates — a length‑based tape is more reliable.

▸
EstimateFormula
Weight (1–5 yr)(age × 2) + 8 kg
Weight (6–12 yr)(age × 3) + 7 kg
Endotracheal tube (uncuffed)(age ÷ 4) + 4 mm
Endotracheal tube (cuffed)(age ÷ 4) + 3.5 mm
Tube depth at liptube size × 3 cm
Hypotension (< 1 yr)< 1 month: systolic BP < 60 mmHg · 1–12 months: < 70 mmHg
Hypotension (1–10 yr)systolic BP < 70 + (2 × age) mmHg
Hypotension (> 10 yr)systolic BP < 90 mmHg
◈ Growth charts

Oxygen Delivery Systems & Cylinder Duration

Device → flow → approximate FiO₂ → when to escalate; and how long a cylinder will last.

▸
Oxygen delivery systems
DeviceFlow · FiO₂Notes & escalation
LOW Nasal cannula (low‑flow)Infant 1–2 L/min
Child up to 4 L/min
Older child up to 6 L/min
FiO₂ ~24–45%
Variable — FiO₂ rises with flow, falls with high inspiratory demand / mouth‑breathing. Above ~2 L/min the dry gas irritates and dries the nasal mucosa — add humidification (and warming) at these flows.
LOW Simple face mask5–10 L/min
FiO₂ ~40–60%
Minimum 5 L/min to flush CO₂ (avoid rebreathing). Variable performance.
HIGH O₂ Non‑rebreather (reservoir) mask10–15 L/min
keep the bag inflated
FiO₂ ~60–90%
Highest FiO₂ without support — resuscitation / emergency.
FIXED Venturi (air‑entrainment) mask2–15 L/min per valve
fixed FiO₂ 24 / 28 / 31 / 35 / 40 / 60%
Delivers a precise FiO₂ regardless of breathing pattern — when a controlled FiO₂ matters.
SUPPORT High‑flow nasal cannula (HFNC)≈ 2 L/kg/min
(to device max, up to ~60 L/min)
FiO₂ 21–100% (titratable)
Warmed & humidified; adds 1–3 cmH₂O PEEP + deadspace washout. Can be run on the ward where a clear written escalation protocol exists (defined limits, monitoring, and criteria to step up); otherwise HDU / PICU.
SUPPORT CPAP / BiPAP (NIV)Device‑set flow
set FiO₂
Non‑invasive support for rising work of breathing, recurrent apnea, or hypoxemia despite O₂. PICU‑directed.
◎ Reading the table
  • LOW low‑flow, variable FiO₂ · HIGH O₂/FIXED high or controlled FiO₂ · SUPPORT also provides pressure / washout → escalation.
  • Target SpO₂: give O₂ for SpO₂ < 90% (consider < 92% in young infants, prematurity, or cardiac / lung disease); titrate to target and wean.
  • Infants: if prongs/mask are not tolerated use blow‑by; a head box / hood gives up to ~80–90% FiO₂ but needs a gas flow of 2–3 L/kg/min to avoid CO₂ rebreathing (WHO 2016, which prefers nasal prongs or catheters). Neonatal resuscitation: T‑piece or self‑inflating bag with reservoir.
  • Low‑flow FiO₂ figures are estimates — the faster the child breathes, the lower the true delivered FiO₂.
Reading the pulse oximeter — practical notes
◣ Get a reliable number
  • Trust it only with a good trace. Confirm a clean plethysmograph waveform and that the oximeter's pulse rate matches the palpated / ECG rate — a damped or absent trace means the number is unreliable.
  • Weak signal = poor perfusion. Cold, shock, vasoconstriction or hypotension drop the signal (under‑reads or fails) — warm the hand, try another site (toe, earlobe), check the perfusion index if shown.
  • Motion and bright / ambient light cause erratic or false readings — settle the limb, shield the probe, use motion‑tolerant sensors.
  • Nail polish, henna, dirt — remove them or turn the probe sideways. In darker skin oximeters can overestimate true saturation (occult hypoxemia) — correlate with the clinical picture and a blood gas if in doubt.
⚠ When the number lies — falsely reassuring
  • Carbon monoxide poisoning: a standard oximeter reads carboxyhemoglobin as oxyhemoglobin, so SpO₂ looks normal / high despite real hypoxia. Suspect it by history; confirm with co‑oximetry / ABG and give 100% O₂ regardless of the SpO₂.
  • Methemoglobinemia pins SpO₂ around ~85% whatever the true saturation (a “saturation gap” vs the ABG) — suspect it with cyanosis unresponsive to O₂ (topical anesthetics, dapsone).
  • Severe anemia / blood loss: SpO₂ measures saturation, not oxygen content — it can read normal while oxygen delivery is inadequate.
✦ SpO₂ is not PaO₂ — and it lags
  • On the dissociation curve, SpO₂ 90% ≈ PaO₂ 60 mmHg; below 90% a small SpO₂ fall means a large PaO₂ drop — act quickly. The curve is flat near the top, so “100%” hides the reserve and cannot detect hyperoxia (important in preterm / neonates).
  • SpO₂ lags real change by seconds (longer if poorly perfused) — a falling number can already be a late sign.
  • Neonates — pre- vs post‑ductal: right hand = pre‑ductal, foot = post‑ductal; a difference > 3% (or lower post‑ductal) suggests a right‑to‑left shunt / critical CHD (CCHD screening).
Oxygen cylinder — content & how long it lasts
StepEquation
Usable duration (quick · psi)(gauge psi − 200) × cylinder factor ÷ flow (L/min)
Usable content (metric)capacity (L) × (gauge bar − 14) ÷ full pressure (bar)
Duration (metric)usable content (L) ÷ flow (L/min)
◎ What the terms mean
  • psi = pounds per square inch, a unit of gas pressure (what the cylinder gauge reads); 1 bar ≈ 14.5 psi.
  • Cylinder factor = liters of oxygen released per 1 psi of pressure (= the cylinder's full capacity ÷ its full pressure). Multiply the usable pressure (gauge − 200 psi safe residual) by this factor to get the liters available.
◎ Safe residual & cylinder data
  • Safe residual ≈ 200 psi (~14 bar) — a cylinder is treated as empty at this pressure; subtract it from the gauge before calculating, and do not run lower.
  • Content when full (BOC): CD 460 L (230 bar) · D 340 L (137 bar) · E 680 L (137 bar) · F 1360 L (137 bar). US E ≈ 625–680 L at ~2000 psi. 1 bar ≈ 14.5 psi. Check the label — capacity/pressure vary by supplier.
  • Cylinder factors (L/psi): D 0.16 · E 0.28 · M 1.56 · G 2.41 · H/K 3.14.
✦ Worked examples
  • Imperial: E cylinder, gauge 1800 psi, flow 6 L/min → (1800 − 200) × 0.28 ÷ 6 ≈ 75 min.
  • Metric: BOC E cylinder (in the calculator choose Custom / metric, water capacity 4.7 L → ≈ 101 min; the E preset is the smaller US cylinder → ≈ 88 min), gauge 100 bar, flow 4 L/min → 680 × ((100 − 14) ÷ 137) ≈ 427 L → ÷ 4 ≈ 107 min.
  • High flow drains fast: at 30–60 L/min a full E cylinder lasts only ~10–20 min — use wall O₂ or a large cylinder (and an air blender) for transport.
  • An interactive calculator is in the Bedside Calculators section (app / web).
⚠ Safety margin
Do not use a cylinder below the safe residual (~200 psi / ~14 bar) — treat it as empty. Change or refill at about ~500 psi / ~35 bar to keep a working reserve, and for transport carry ≥ 2× the calculated requirement (account for device / blender flush).
◎ Best clinical resources (open‑access)
  • Open Critical Care — Oxygen delivery devices (evidence‑based, WHO‑aligned): opencriticalcare.orgQR
  • WHO — Oxygen therapy for children (2016 manual): who.intQR

Normal Vital Signs by Age

Reference ranges (awake, at rest) — PALS 2020 age bands, the same set as the red‑zone figure.

▸
AgeHeart rate /minRespiratory rate /minSystolic BP mmHg
< 1 month100–20530–5367–84
1–12 months100–18030–5372–104
1–2 years98–14022–3786–106
3–5 years80–12020–2889–112
6–11 years75–11818–2597–120
≥ 12 years60–10012–20110–131
Source: PALS Provider Manual 2020 (awake heart rate, respiratory rate, systolic BP by age).
◈ Blood‑pressure percentiles Age-, sex-, and height‑based BP centiles (elevated BP ≥ 90th; hypertension ≥ 95th) — AAP 2017 BP tablesQR.

Scales, Equations & Synonyms

The scores, formulas, and drug names you reach for at the bedside.

▸
Glasgow Coma Scale — child values in brackets (best 15, worst 3)
PtsEyeVerbal (<2 y)Motor (infant)
6——Obeys (spontaneous movement)
5—Oriented (coos, babbles)Localizes (withdraws to touch)
4SpontaneousConfused (irritable cry)Withdraws to pain
3To voiceWrong words (cries to pain)Abnormal flexion
2To painSounds only (moans)Extension
1NoneNoneNone
APGAR — score at 1 and 5 minutes (≤3 low, 4–6 moderate, 7–10 reassuring)
Sign012
Appearanceblue / palebody pink, limbs blueall pink
Pulseabsent< 100≥ 100
Grimacenonegrimacecry / cough
Activity (tone)limpsome flexionactive
Respirationabsentslow, irregularstrong cry
Dehydration — severe means shock; give 20 mL/kg
SignMild ~3–5%Moderate ~6–9%Severe ≥10%
Generalalert, thirstyrestless, irritablelethargic, floppy
Eyes / mucosanormal, moistsunken, drydeeply sunken, parched
Skin pinchinstant< 2 s> 2 s
Cap refill / pulsenormalprolonged> 3 s, weak, cool
Urinenormalreducedminimal or none
Quick equations
ForFormula
Maintenance fluid4·2·1: 4 mL/kg/h first 10 kg + 2 next 10 + 1 each kg over 20 (Holliday–Segar)
Fluid deficit (mL)% dehydration × weight (kg) × 10
Corrected Na (high glucose)add 2.4 mmol/L per 5.6 mmol/L (100 mg/dL) glucose above 5.6 mmol/L (Hillier; the older 1.6 factor underestimates at high glucose)
CalciumMeasure ionized calcium — albumin‑corrected calcium is unreliable (misses hypocalcemia in critical illness and kidney disease)
Anion gapNa − (Cl + HCO₃); normal about 12 ± 2 mmol/L (ISPAD 2022) — use your laboratory’s reference range
Serum osmolality2 × Na + glucose + urea (mmol/L). Osmolar gap = measured − calculated osmolality; > 10 suggests an unmeasured osmole (methanol, ethylene glycol, ethanol, mannitol).
Expected pCO₂ (met. acidosis)Winter: 1.5 × HCO₃ + 8 ± 2 (mmHg) — the expected respiratory compensation for a metabolic acidosis; measured PaCO₂ above the range = added respiratory acidosis, below = added respiratory alkalosis.
QTc (Bazett)QTc (Bazett)QT ÷ √RR (s); prolonged > 0.45 s in children before puberty, infants and post‑pubertal males, > 0.46 s in post‑pubertal females (see QTc calculator)
eGFR (Schwartz)eGFR (Schwartz)36.5 × height (cm) ÷ creatinine (µmol/L) — i.e. 0.413 × height ÷ creatinine (mg/dL)
Glucose infusion rateGlucose infusion ratemg/kg/min = dextrose% × rate (mL/h) ÷ (6 × weight kg)
Names & synonyms
Generic (US)Also known as
Epinephrineadrenaline
Norepinephrinenoradrenaline
Albuterolsalbutamol
Acetaminophenparacetamol
Furosemidefrusemide
Lidocainelignocaine
Acycloviraciclovir
Amoxicillin–clavulanateco‑amoxiclav
Valproic acidsodium valproate
Regular insulinsoluble insulin
Normal saline (0.9% NaCl)isotonic saline
Lactated Ringer’sHartmann’s, compound sodium lactate
Succinylcholinesuxamethonium
Chlorpheniraminechlorphenamine

Procedural Sedation, RSI & Analgesia

Quick weight‑based doses — prepare airway, suction, and monitoring first.

▸
◈ Neonatal intubation — premedicate?
  • Emergency (delivery room, life‑threatening airway) → intubate now; no premedication.
  • All other intubations → premedicate every time, IV, in this order:
    1. Atropine 20 mcg/kg — prevents severe bradycardia,
    2. Fentanyl, slow IV: < 28 wk 1–2 mcg/kg · 28–32 wk 2–3 mcg/kg · > 32 wk 3–4 mcg/kg
    3. Succinylcholine 2 mg/kg — not in hyperkalemia, malignant‑hyperthermia risk or neuromuscular disease,
  • Do not use an opioid alone (morphine or remifentanil) as the only premedication.
  • Alternative if blood pressure is normal: propofol — ≥ 28 wk 2 mg/kg (repeat 1 mg/kg if needed); < 28 wk 1 mg/kg steps, max 2 mg/kg.
Analgesia
DrugDoseRoute & notes
AcetaminophenPO/PR: 15 mg/kg/dose every 4–6 h (max 1 g/dose; ≤ 75 mg/kg/day, not > 4 g/day)
IV, > 10 kg: 15 mg/kg/dose every 6 h (max 60 mg/kg/day; ≥ 50 kg: 1 g/dose, max 4 g/day)
IV, ≤ 10 kg: 7.5 mg/kg/dose, max 30 mg/kg/day (UK SmPC) — US label: neonates 12.5 mg/kg/dose every 6 h (max 50 mg/kg/day), 29 days–2 y 15 mg/kg/dose every 6 h (max 60 mg/kg/day)
PO/PR/IV; mild–moderate pain. IV in neonates and infants: follow the local formulary and prescribe the dose in mg and mL (10‑fold mg/mL errors have caused overdoses)
Ibuprofen10 mg/kg/dose every 6–8 h (max 400 mg/dose, 40 mg/kg/day)PO; age ≥ 6 months; mild–moderate pain (avoid in dehydration, renal impairment, GI bleeding)
Morphine0.05–0.1 mg/kgIV, titrate; for moderate–severe pain
Fentanyl1–2 mcg/kg IV; 1.5 mcg/kg intranasalRapid onset; useful when no IV access
Procedural sedation

Procedural sedation and RSI by credentialed clinicians only — airway‑rescue capability, full monitoring, and an institutional sedation policy.

DrugDoseRoute & notes
Ketamine1–2 mg/kg IV; 4–5 mg/kg IMDissociative; usually preserves airway reflexes/respiratory drive — but airway obstruction, laryngospasm, and apnea can still occur
MidazolamIV, titrated slowly: 6 months–5 y 0.05–0.1 mg/kg (total max 6 mg); 6–12 y 0.025–0.05 mg/kg (total max 10 mg)
Buccal/intranasal: 0.3–0.5 mg/kg (max 10 mg)
Anxiolysis; respiratory depression with opioids; not recommended < 6 months
Rapid sequence intubation
StepDoseRoute & notes
InductionKetamine 1–2 mg/kg
Propofol 2–3 mg/kg
Etomidate 0.3 mg/kg (avoid in septic shock)
Midazolam 0.1–0.3 mg/kg
± Fentanyl 1–2 mcg/kg (pre‑treatment)
Choose by hemodynamics
ParalyticRocuronium 1–1.2 mg/kg
Succinylcholine 1–2 mg/kg
IV
Atropine (pre‑treatment)0.02 mg/kgIV in young infants if bradycardia risk
⚠ Before any sedation/RSI
  • Have oxygen, suction, bag‑mask, the right tube size [(age ÷ 4) + 4 uncuffed], monitoring, and a reversal plan ready.
  • See Weight & Airway Sizing.

Emergency Drug Doses

MINUTESPALS 2025

Resuscitation doses by rule and by weight — use measured weight or a length‑based tape; cross‑check weight, concentration and the local chart before every dose.

▸
Drug · indicationRule (per kg · max)NotesDose for this child
Epinephrine — cardiac arrest0.01 mg/kg IV/IO = 0.1 mL/kg of 0.1 mg/mL (max 1 mg)Repeat every 3–5 min. Only if IV/IO access cannot be obtained (least‑preferred route): endotracheal 0.1 mg/kg (0.1 mL/kg of 1 mg/mL; PALS 2020 figure).—
Epinephrine — anaphylaxis0.01 mg/kg IM = 0.01 mL/kg of 1 mg/mL (max 0.3 mg before puberty; 0.5 mg in adolescents)Anterolateral thigh; repeat every 5–15 min.,—
Amiodarone — VF / pulseless VT5 mg/kg IV/IO bolus (max 300 mg; repeat doses max 150 mg)May repeat up to twice for refractory VF/pVT (3 doses total); repeat doses max 150 mg each (PALS 2025). Perfusing tachycardia: give over 20–60 min.—
Adenosine — SVT, 1st dose0.1 mg/kg rapid push (max 6 mg)Immediate saline flush; use the line closest to the heart.—
Adenosine — SVT, 2nd dose0.2 mg/kg rapid push (max 12 mg)If the first dose fails.—
Atropine — bradycardia0.02 mg/kg IV/IO (min 0.1 mg, max 0.5 mg)May repeat once.—
Calcium gluconate 10% — hyperkalemia, Ca‑channel‑blocker toxicity, hypocalcemia50 mg/kg = 0.5 mL/kg slow IV/IO (max 2 g = 20 mL)Calcium chloride 10% 20 mg/kg (0.2 mL/kg) only via a central line — sclerosing, high extravasation risk.—
Dextrose 10% — hypoglycemia2 mL/kg (0.2 g/kg) slow IV (max 200 mL = 20 g, the adult dose)Recheck glucose in 15 min; see Hypoglycemia. Adult dose: 200 mL of 10% glucose over 15 min (JBDS‑IP 2022).—
Magnesium sulfate — torsades, severe asthma25–50 mg/kg IV/IO (max 2 g)Torsades: rapid. Severe asthma (≥ 2 y): 40–50 mg/kg over 20 min.,—
Naloxone — opioid toxicity0.1 mg/kg IV/IM/IN (max 2 mg)Titrate to breathing; re‑dose (short half‑life).,—
Sodium bicarbonate 8.4%1 mEq/kg slowly IV/IO (max 50 mEq) = 1 mL/kg of 8.4%; neonates and children < 2 years: use 4.2% (0.5 mEq/mL → 2 mL/kg) and give slowlyTricyclic toxicity (QRS > 100 ms), severe acidosis, hyperkalemia.—
Lidocaine — VF/pVT (alternative to amiodarone)1 mg/kg IV/IO (max 100 mg)Then infusion 20–50 mcg/kg/min.—
Isotonic fluid bolus — shock10–20 mL/kg per bolus — no fixed volume cap in PALS/SSC; reassess after each10 mL/kg in neonates, cardiac disease or severe malnutrition; DKA: 10–20 mL/kg over 20–30 min (20 mL/kg boluses only if shocked — see Diabetic Ketoacidosis); reassess after each bolus.,—
Defibrillation — VF/pVT2 J/kg → 4 J/kg → ≥ 4 J/kgMax 10 J/kg or the adult dose (≈ 200 J biphasic).—
Synchronized cardioversion — unstable SVT/VT0.5–1 J/kg → 2 J/kgSedate if conscious and time permits.—
Doses by weight — pick the column nearest the weight
Drug · rule (per dose)  · kg▸510203050
Epinephrine (adrenaline) 0.01 mg/kg IV/IO — mg (mL of 0.1 mg/mL)0.05
(0.5)
0.1
(1)
0.2
(2)
0.3
(3)
0.5
(5)
Amiodarone 5 mg/kg (arrest) — mg2550100150250
Adenosine 0.1 mg/kg (1st, max 6) — mg0.51235
Atropine 0.02 mg/kg (0.1–0.5) — mg0.10.20.40.50.5
Calcium gluconate 10% 0.5 mL/kg (max 20) — mL2.55101520
Dextrose 10% 2 mL/kg — mL10204060100
Fluid bolus 20 mL/kg (10 if neonate/cardiac; DKA see card) — mL1002004006001000
Defibrillation — 1st shock 2 J/kg — J10204060100
Defibrillation — 2nd shock 4 J/kg (max 200) — J204080120200

Numbers are per single dose, already capped. Pick the nearest column and adjust to the child’s actual weight.

◣ Vasoactive infusions — weight‑based prep (verify locally)
InfusionMake up to 50 mLRate → dose
Epinephrine—1 mL/h = 0.1 mcg/kg/min · usual 0.05–0.3 mcg/kg/min (0.5–3 mL/h); higher doses on PICU advice,
Norepinephrine—1 mL/h = 0.1 mcg/kg/min · start 0.05–0.1 mcg/kg/min (0.5–1 mL/h) and titrate with the PICU; a second agent is commonly considered at about 0.1–0.3 mcg/kg/min (1–3 mL/h; American and Asian/Middle‑East practice — European units often wait until ~0.3–1 mcg/kg/min)
Milrinone—1 mL/h = 0.1 mcg/kg/min · usual 0.25–0.75 mcg/kg/min (2.5–7.5 mL/h); load 50 mcg/kg over 30–60 min,
Dopamine / Dobutamine—1 mL/h = 1 mcg/kg/min · usual 5–20 mcg/kg/min (5–20 mL/h),,

Central line for these concentrations,; the rule‑of‑6 preparation is for children up to 40 kg — above 40 kg use your unit’s standard fixed‑concentration chart (local policy).,

Concentrations & pitfalls
  • Epinephrine 0.1 mg/mL (old 1:10 000) is for IV/IO; 1 mg/mL (old 1:1000) is for IM and endotracheal use — confirm the ampoule before every dose.
  • Amiodarone is 150 mg/3 mL.
  • Use a length‑based (Broselow) tape when weight is unknown.
⚠ Always cross‑check
  • Confirm weight, ampoule concentration, and the local resuscitation chart before every dose.
  • If weight is unknown, entering length gives a Broselow length‑based estimate — confirm with a scale.
  • From 40 kg, weight‑based doses apply only until the adult maximum is reached (rows then show “(max)”) — PALS 2025: dose by weight without exceeding the adult dose; PPAG 2024: 40 kg threshold.,

Anticoagulation — VTE Prophylaxis & Treatment

ASSESSASH/ISTH 2024 · 2026

Who to treat, for how long, who needs prophylaxis — and enoxaparin doses with anti‑Xa targets.

▸
RegimenDoseMonitoring / notes
Enoxaparin — treatment, < 2 months1.5 mg/kg/dose SC every 12 hAnti‑Xa target 0.5–1.0 IU/mL, drawn 4–6 h post‑dose (after the 3rd–4th dose). Treatment anticoagulation is hematology‑guided with anti‑Xa monitoring; adjust for renal function, age, weight, and bleeding risk,
Enoxaparin — treatment, ≥ 2 months1.0 mg/kg/dose SC every 12 hInfants often need more: term up to 1.7, preterm up to 2 mg/kg/dose
Enoxaparin — prophylaxis, < 2 months0.75 mg/kg/dose SC every 12 hAnti‑Xa 0.1–0.3 IU/mL if monitored
Enoxaparin — prophylaxis, ≥ 2 months0.5 mg/kg/dose SC every 12 hRoutine anti‑Xa not required
◣ Treat — who
  • Anticoagulate: symptomatic DVT or PE; cerebral sinovenous thrombosis (CSVT); neonatal renal vein thrombosis.
  • Individualize: DVT or PE found by chance on imaging — anticoagulation or none are both acceptable.
  • No thrombolysis for proximal DVT or for PE without hemodynamic compromise; thrombolysis, then anticoagulation, only for PE with hemodynamic compromise.
  • Line‑related clot: if the central line is no longer needed or is not functioning, remove it — either immediately or after a few days of anticoagulation (both acceptable; favor a few days first with a large clot or a right‑to‑left shunt). A functioning line that is still needed can stay in place under anticoagulation. No IVC filter.,
◣ Treat — how long
  • Provoked, risk factor resolved: 6 weeks — continue to 3 months if the 6‑week scan still shows an occlusive clot.,
  • 3 months for PE, cancer‑associated VTE, recurrent VTE, a persisting risk factor, major thrombophilia, or persistently positive antiphospholipid antibodies.
  • Unprovoked: 6–12 months, not indefinite.
  • Agent: rivaroxaban or dabigatran is suggested over LMWH or warfarin, started after ≥ 5 days of parenteral anticoagulation; not in preterm neonates, eGFR < 30, significant liver disease or active bleeding. Hematology sets the dose.
◣ Prophylaxis — who
  • Give: TPN for more than 60 days (home TPN or intestinal failure; not neonates); antiphospholipid syndrome (secondary prevention).
  • Either: leukemia or lymphoblastic lymphoma, during asparaginase cycles only — favor prophylaxis if age ≥ 10 y, obesity, T‑cell or high‑risk disease, or a personal or family history of thrombosis. No antithrombin supplements.
  • Not routinely: general ward patients, critically ill children, trauma, noncardiac surgery, solid tumors, central lines, or positive antiphospholipid antibodies without a past clot. Consider case by case when several risk factors combine (adolescence, immobility, mechanical ventilation, a central line > 7 days, obesity, estrogen or the combined pill, thrombophilia, previous VTE, major surgery) and bleeding risk is low.
  • Before starting: weigh bleeding risk — do not start if it is high; reassess regularly; plan doses around lumbar puncture and spinal procedures. Continue only while the risk lasts (e.g., the asparaginase cycle, long‑term TPN).
Before starting
  • Baseline complete blood count, renal function, and coagulation screen.
  • Reduce dose if creatinine clearance < 30 mL/min.
Reversal & alternatives
  • Protamine partially reverses enoxaparin (1 mg per 1 mg enoxaparin given in the prior 8 h; 0.5 mg per 1 mg if > 8 h or a second dose is needed) — anti‑Xa activity is only partly neutralized (maximum ~60%).
  • Use an IV unfractionated heparin infusion instead of enoxaparin when rapid reversal may be needed (high bleeding risk or an imminent procedure) or creatinine clearance is < 30 mL/min — half‑life 0.5–2 h, cleared by the liver, neutralized by protamine (1 mg per 100 units; no more than 50 mg in 10 min).,

Maximum Local Anesthetic Doses

ASSESS

Single‑dose ceilings — count total mg/kg across all sites. Use lower limits in neonates/infants, liver disease, or low cardiac output; count the total across all injection sites and when agents are combined.

▸
AgentMax single doseNotes
Lidocaine 1% (plain)4.5 mg/kg (max 300 mg)
= 0.45 mL/kg of 1% (max 30 mL)
Onset fast; ~30–60 min duration. 1% = 10 mg/mL.
Lidocaine 1% + epinephrine7 mg/kg (max 500 mg)
= 0.7 mL/kg of 1% (max 50 mL)
Longer duration. Lidocaine ceilings (4.5 mg/kg, max 300 mg plain; 7 mg/kg, max 500 mg with epinephrine) are the US-label adult maximums applied per kg — adult-derived (the label sets pediatric doses by age and weight). Caution with epinephrine on end‑arteries (digits, pinna, penis).
Neonates and young infantsLower ceilingUse a lower ceiling (local practice 3–4 mg/kg for a neonatal penile block — see Circumcision).
Toxicity (LAST)
  • Perioral numbness, tinnitus, and agitation progress to seizures, then arrhythmia or arrest.
  • Stop injection, secure airway and oxygen, treat seizures with a benzodiazepine, and give 20% lipid emulsion (see Poisoning & Toxic Ingestion).
  • Dilute to the least concentrated effective solution, aspirate before injecting, and inject slowly in divided doses; reduce maximums in neonates.
Vital signs — normal vs red zone by ageThe escalation threshold, not just the normal range. Normal ranges: PALS 2020.
Vital Signs — Normal vs Red Zone by AgeThe number that should trigger escalation. Red‑zone values are concern thresholds, not just “abnormal.”Compensated pediatric shock is often normotensive — tachycardia + poor perfusion precede hypotension, which is a late, pre‑arrest sign.AgeNormal HRHR red zoneNormal RRRR red zoneHypotension SBP< 1 month100–205<100 or >20530–53>60<601–12 months100–180<100 or >18030–53>60<701–2 years98–140<90 or >14022–37>40<70+(2×age)3–5 years80–120<80 or >12020–28>34<70+(2×age)6–11 years75–118<60 or >12018–25>30<70+(2×age)≥ 12 years60–100<60 or >10012–20>20<90Hypotension (5th‑centile SBP): 70 + (2 × age in years) for 1–10 y; < 90 mmHg for ≥ 10 y. Example — 4‑year‑old: < 78 mmHg.Sepsis/shock red flags (any): capillary refill > 2–3 s or flash, mottled/cold or bounding pulses, altered mental status, lactate > 2 mmol/L, reduced urine output.Normal ranges: PALS Provider Manual 2020; red‑zone thresholds: escalation triggers (PALS hypotension definitions). Bradycardia and bradypnea in a sick child are ominous late signs — treat as pre‑arrest.

Kuwait Childhood Immunization Schedule

REFERENCEMOH Kuwait 2025

The routine schedule at a glance — and the ages a missed dose should prompt catch‑up.

▸
AgeVaccineRoute
Pregnant motherTdap — one dose in this pregnancy, and every subsequent pregnancyIM
Within 24 h of birthHepatitis B (HBV) — 1st doseIM
End of 2 monthsHexa (1st) · Pneumococcal (1st) · Rotavirus (1st)IM · IM · Oral
End of 3 monthsBCGID
End of 4 monthsHexa (2nd) · Pneumococcal (2nd) · Rotavirus (2nd)IM · IM · Oral
End of 6 monthsHexa (3rd) · Pneumococcal (3rd) · Rotavirus (3rd)*IM · IM · Oral
End of 12 monthsOPV (1st) · MMR (1st) · Varicella (1st) · Meningococcal conjugate (ACWY)Oral · SC · SC · IM
At 18 monthsOPV (2nd) · Hexa booster · Pneumococcal boosterOral · IM · IM
End of 2 yearsMMRV (1st)SC
End of 3.5 yearsDTaP boosterIM
4–6 years (preschool)Check immunization status before school admission—
10–12 years (school)Tdap boosterIM
16–18 years (school)Tdap boosterIM
◈ Vaccine key
  • Hexa = diphtheria, tetanus, acellular pertussis, hepatitis B, inactivated poliovirus (IPV) & Hib
  • MMRV = measles, mumps, rubella, varicella
  • DTaP/Tdap = diphtheria, tetanus, acellular pertussis
  • OPV = oral polio
  • * rotavirus is 2 or 3 doses according to the vaccine type used; give the first dose by 14 weeks 6 days (do not start at 15 weeks or older) and the last dose by 8 months 0 days (ACIP 2009).
✦ What changed in the 2025 schedule
  • Hexa replaces the pentavalent (adds IPV)
  • MMRV at 2 years replaces the old separate 2nd MMR + varicella
  • DTaP replaces DPT at 3.5 years
  • Tdap replaces Td at 10–12 and 16–18 years and is now given in every pregnancy
  • the old OPV booster at 3.5 years and the girls‑only MMR booster at 10–12 years were dropped.
✦ Use every emergency visit as a catch‑up trigger
  • An unwell or injured child is a chance to check the card.
  • A missed MMR/MMRV in an outbreak, an incomplete primary series in a young infant with a fever, or no tetanus‑containing cover before a dirty wound all change management on the spot.

Kuwait Newborn Screening Panel

REFERENCEKuwait program · since Oct 2014

What the heel‑prick looks for, how the result reaches you — and why a sick newborn is treated before it does.

▸
◣ The national dried‑blood‑spot panel — 22 disorders
GroupDisorders screenedMarker · what a positive means for you
Amino acid disorders (6)Phenylketonuria · maple syrup urine disease · classical homocystinuria · citrullinemia (types I and II) · tyrosinemia type I · argininosuccinic aciduriaTandem mass spectrometry amino acids; MSUD, citrullinemia and argininosuccinic aciduria can present as a neonatal encephalopathy before the result — see Metabolic Crisis
Organic acid disorders (8)Propionic acidemia · methylmalonic acidemia · isovaleric acidemia · glutaric acidemia type I · 3‑methylcrotonyl‑CoA carboxylase deficiency · β‑ketothiolase deficiency · multiple (holo)carboxylase deficiency · HMG‑CoA lyase deficiencyAcylcarnitines; acidosis, hyperammonemia and lethargy in the first week — treat on suspicion
Fatty acid oxidation disorders (4)MCAD deficiency · VLCAD deficiency · LCHAD deficiency · trifunctional protein deficiencyAcylcarnitines (C8; C14:1 for VLCAD). VLCAD is the commonest in Kuwait (1 in 8,290 births; 1 in 5,405 Kuwaiti newborns; founder variant c.65C>A) — hypoketotic hypoglycemia, cardiomyopathy, arrhythmia; never let these infants fast
Other metabolic (2)Classical galactosemia · biotinidase deficiencyGalactosemia: stop lactose feeds at once if suspected (E. coli sepsis, jaundice, cataract)
Endocrine (2)Congenital hypothyroidism · congenital adrenal hyperplasiaTSH; 17‑hydroxyprogesterone. Salt‑wasting CAH collapses at 1–3 weeks — see Adrenal Crisis
  • Not in the panel: hemoglobinopathies, G6PD deficiency, cystic fibrosis, SCID and lysosomal disorders — do not assume a "normal screen" covers them.
◣ How the program runs
  • Sample: dried blood spot 24–72 h after birth (ideally 48–72 h, after at least 2–3 feeds), accepted up to 1 month; a sample taken before 24 h is repeated within 7 days; preterm infants give three samples (72 h, 2 weeks, 1 month).,
  • Laboratory: every sample — public and private hospitals — goes to the Newborn Screening Laboratory, Kuwait Medical Genetics Center (coverage 100 % since 2019); results are available at a median of about 4 days of age.,
  • Positive screen: the hospital’s newborn screening office recalls the infant for a confirmatory sample (second blood spot for acylcarnitines/amino acids, urine organic acids at the Al‑Sabah biochemistry laboratory); a confirmed result goes to the metabolic team. A recall that is not completed is a missed diagnosis — one VLCAD infant, not followed up after a positive screen, presented at 3 months with dilated cardiomyopathy needing PICU admission.
⚠ In the emergency department
  • A pending or normal screen never excludes disease: a newborn with poor feeding, vomiting, lethargy, hypoglycemia, acidosis, hyperammonemia, seizures or cardiomyopathy is a metabolic emergency now — stop feeds/protein, give 10 % dextrose, send glucose, gas, ammonia, lactate and the newborn‑screening sample if not yet taken, and call the metabolic team (Metabolic Crisis, Neonatal Hypoglycemia).
  • A phone call about a positive screen for MSUD, an organic acidemia, a fatty acid oxidation disorder, galactosemia or CAH means same‑day assessment, not a clinic appointment.

Think Here — Consanguinity & Gulf‑Prevalent Conditions

REFERENCEGulf pre‑test probability

The same presentation carries a different differential in Kuwait — recessive disease is not rare here.

▸
◣ Why the baseline differs
  • Consanguineous marriage is common in Kuwait — 54% of marriages in a 1983 national sample, mostly first cousins; 23% (Capital) to 42% (Jahra) for first‑ and second‑cousin marriages among Kuwaiti nationals in a 1999 two‑governorate survey., Homozygosity sharply raises the pre‑test probability of autosomal‑recessive disease.,
✦ Raise these on the differential earlier than the textbook would
  • Inborn errors of metabolism in the encephalopathic / acidotic / hypoglycemic neonate or the child who decompensates with fasting or intercurrent illness — check gas, glucose, ammonia, lactate and start IV dextrose early.,, Hemoglobinopathies (sickle cell, β-thalassemia) and G6PD deficiency in the pale, jaundiced, or acutely hemolyzing child.,,
  • A recessive syndrome when a sick infant has an affected sibling or known parental consanguinity.

High‑Alert Drugs & Fluid Safety

EVERY SHIFTISMP 2024 · AAP 2018

The commonest pediatric harm is not the missed diagnosis — it’s the decimal point.

▸
◣ High‑alert drugs — where a decimal kills
  • Insulin (units, U‑100 vs U‑500) · opioids (mcg vs mg) · concentrated KCl / K‑phosphate (never IV push) · heparin / LMWH (1,000 vs 10,000 units/mL) · chemotherapy (intrathecal vincristine = fatal) · digoxin / milrinone · magnesium sulfate (mg vs mmol vs mEq) · hypertonic saline / dextrose · neuromuscular blockers · oral methotrexate (weekly, not daily).
  • Epinephrine concentration: 1 mg/mL (old 1:1,000, IM) vs 0.1 mg/mL (old 1:10,000, IV) — the classic 10‑fold pediatric error., State the concentration, never the ratio.,
⚠ The three error modes to double‑check
  • 10‑fold / decimal errors,
  • mg vs mL vs microgram vs unit confusion
  • concentration mix‑ups.,
  • For any high‑alert drug: independent double‑check of dose, concentration and pump rate.,,
◣ Sodium — correct within the safe rails
  • Hyponatremia: raise Na ≤ 8 mmol/L per 24 h (a conservative expert limit; NICE pediatric ceiling 12 mmol/L per 24 h), to avoid osmotic demyelination., Acute symptomatic (seizing): 3% saline 2 mL/kg (max 100 mL) IV over 10 min, repeated once or twice until symptoms improve; each bolus raises Na by about 2 mmol/L., Full protocol: Acute Electrolyte Emergencies.
  • Hypernatremia: lower Na ≤ 10–12 mmol/L per 24 h (≈ 0.5 mmol/L/h), to avoid cerebral edema (pediatric correction‑rate evidence is evolving).
◣ Fluids & potassium
  • Maintenance fluids (AAP 2018): for children 28 days–18 years, use isotonic fluid (0.9% saline or a balanced solution) with KCl and dextrose — hypotonic maintenance caused iatrogenic hyponatremia. Volume still by Holliday‑Segar.
  • IV potassium: peripheral ≤ 40 mmol/L, (40–60 mmol/L only where local protocol allows); ward rate ≤ 0.5 mmol/kg/h (max 10 mmol/h); faster rates only with continuous ECG — PICU rates up to 1 mmol/kg/h are local practice (not guideline‑stated). Never IV push: direct injection of the concentrate can be instantly fatal. Confirm concentration/rate ceilings against local protocol.
✦ Extravasation — stop, aspirate, and know the two antidotes
  • Vesicants: calcium, concentrated potassium, vasopressors, hypertonic dextrose/saline, TPN, chemotherapy.,,,
  • Immediately stop the infusion, aspirate, elevate.
  • Antidotes: hyaluronidase (most hyperosmolar/calcium/TPN infiltrations), and phentolamine (vasopressor extravasation, e.g. norepinephrine/dopamine).,,

Must‑Avoid Drugs — Conditions & Serious Interactions

EVERY SHIFTFDA · EMA · SOCIETY GUIDELINES

The diagnosis on the chart decides what you must not prescribe — check this list before the first dose.

▸
⚠ How to read this card
  • Not exhaustive. This card covers the conditions, ages and drug combinations that most often cause serious harm in children, but no list can be complete — read around each patient’s condition and check every new drug against its current product information and an interaction checker, especially in rare diseases or polypharmacy.
  • ⛔ label contraindication or boxed warning · ⚠ guideline or label "avoid" / "not recommended" / Class III (Harm) · △ caution or monitor.
  • Rows are alphabetical; within a row drugs are listed from the most to the least frequently used in pediatric practice. Every row carries its primary source (regulator label, society guideline or GeneReviews).
  • A listed drug may still be given when it is the only effective treatment — the decision belongs to the treating consultant, documented in the notes.
AAvoid because of the child’s conditionFind the diagnosis (alphabetical) — 28 conditions
ConditionAvoid — most to least frequently usedWhy · use instead
Acute hepatic porphyria (AIP, VP, HCP) — rare in children⚠ Metoclopramide · co‑trimoxazole and other sulfonamides · phenytoin · phenobarbital and other barbiturates · valproate · rifampicin · progestins
Avoid fasting — IV dextrose, including before surgery
Why: can precipitate an acute attack.
Use instead: opioids, benzodiazepines, phenothiazines, levetiracetam, gabapentin, lamotrigine and vigabatrin are considered safe; check a porphyria drug database (NAPOS / APF) before any new drug.,,
Acute kidney injury · dehydration/hypovolemia · CKD⚠ NSAIDs — ibuprofen · diclofenac · ketorolac (⛔ with volume depletion or advanced renal impairment)
Highest risk when also on diuretics and ACE inhibitors/ARBs
Why: NSAID‑induced AKI occurs even at correct doses; children < 5 y more often need dialysis or PICU.
Use instead: correct the volume deficit first.,,,,
Adrenal insufficiency (CAH, hypopituitarism, chronic steroids)Never omit stress‑dose hydrocortisone — crisis: 50 mg/m² IV, then 50–100 mg/m²/24 h; fever > 38.5 °C, gastroenteritis, surgery, trauma = increase the dose
Never stop chronic steroids abruptly
△ Etomidate — use with caution (see Why)
Why: adrenal crisis. A single dose of etomidate blocks cortisol production (11β‑hydroxylase) for up to 48 h in critically ill patients and can trigger a crisis in a child who cannot raise cortisol.
Use instead: another induction agent; if etomidate must be used, give stress‑dose hydrocortisone and discuss with endocrinology.,,,,
Asthma / history of bronchospasm⛔ Propranolol (tablets; Hemangeol) · ⛔ timolol eye drops · △ metoprolol, atenolol (β1‑selective) only with caution
⛔ Ibuprofen and other NSAIDs only in a child who has reacted to an NSAID before
Hemangioma propranolol: give with/after feeds; skip the dose if not eating or vomiting (hypoglycemia); interrupt for lower‑respiratory infection with wheeze
Why: β‑blockers cause bronchospasm and mask hypoglycemia. NSAID‑induced bronchospasm is uncommon in children (about 2% of school‑age children with asthma on challenge), and as‑needed ibuprofen did not increase attacks in young children with mild persistent asthma.
Use instead: acetaminophen at standard doses for a child who has reacted to an NSAID; if a β‑blocker is essential, a β1‑selective one at the lowest dose, with a bronchodilator at hand.,,,,,,,,,
Burns · major trauma · denervation (spinal cord injury, spinal muscular atrophy, Guillain–Barré) · upper‑motor‑neuron injury⛔ Succinylcholine after the acute phase of injury — risk rises over time, peaks day 7–10
△ Great caution in chronic abdominal infection, subarachnoid hemorrhage, neurodegenerative disease
Why: hyperkalemic cardiac arrest.
Use instead: rocuronium (sugammadex available).
Chickenpox (varicella)⚠ Ibuprofen and other NSAIDs
⛔ Aspirin and other salicylates, including bismuth subsalicylate
Why: ibuprofen — in observational studies, children who took NSAIDs during chickenpox had more severe group A streptococcal skin and soft‑tissue infection, including necrotizing fasciitis; this does not prove the NSAID caused it, but the UK product information advises avoiding ibuprofen during chickenpox. Aspirin — Reye syndrome (see Age‑based rules).
Use instead: acetaminophen for fever or pain.,,,
Cockayne syndrome⛔ Metronidazole — FDA contraindicationWhy: acute, irreversible liver failure with very rapid onset — 8 of about 100 patients in a cohort, 3 deaths, 6–11 days after the first dose.
Use instead: an antibiotic from another class — the contraindication also covers tinidazole and other nitroimidazoles, including topical and vaginal forms.,,
Dravet syndrome (SCN1A)Maintenance: ⚠ carbamazepine · ⚠ lamotrigine · ⚠ oxcarbazepine · ⚠ phenytoin (all contraindicated as maintenance therapy by international consensus — not a label contraindication) · △ vigabatrin, rufinamide (review level)Why: sodium‑channel blockers typically make seizures worse.
Use instead: in status epilepticus, a benzodiazepine → IV valproate or levetiracetam → IV phenytoin/fosphenytoin may be considered (not contraindicated — strong consensus).,
Duchenne/Becker muscular dystrophy and other myopathies⛔ Succinylcholine — boxed warning: hyperkalemic rhabdomyolysis → ventricular dysrhythmia, cardiac arrest, death (most often undiagnosed Duchenne, boys ≤ 8 y)
⚠ Volatile (inhalational) anesthetics
Why: in children succinylcholine is reserved for emergency intubation.
Use instead: rocuronium, with sugammadex for reversal.,,
Fatty acid oxidation disorders (MCAD; VLCAD, LCHAD/TFP, CPT II)Never fast — when feeds stop give ≥ 10 % dextrose at ≥ 1.5 × maintenance (10–12 mg/kg/min glucose)
Long‑chain defects: ⚠ propofol · ⚠ etomidate (lipid load) · high long‑chain fat · dehydration · myocardial irritation (e.g., catheterization)
MCAD: ⚠ aspirin · MCT‑based formula/coconut oil
Why: fasting or illness → hypoglycemia, coma and death; long‑chain defects also → rhabdomyolysis, cardiomyopathy and arrhythmias.
Use instead: ≥ 10 % IV dextrose with electrolytes whenever feeds stop, and an anesthetic plan agreed in advance with the metabolic center.
Note: MCT oil is treatment in long‑chain defects but must be avoided in MCAD. Valproate: case reports only.,,
G6PD deficiency⛔ rasburicase (boxed warning) · ⛔ primaquine in severe deficiency (test G6PD first) · ⚠ dapsone · ⛔ methylene blue (also ineffective) · ⛔ tafenoquine · ⚠ nitrofurantoin (CPIC medium risk — avoid when an alternative exists) · △ Co‑trimoxazole (CPIC 2023: low‑to‑no risk at standard doses — may be used; label caution: dose‑related hemolysis, monitor at high dose, e.g., PJP treatment)
Non‑drug: fava beans, naphthalene (mothballs)
Why: acute hemolysis ± methemoglobinemia.
Use instead: for tumor lysis, allopurinol instead of rasburicase (CPIC, strong) — allopurinol is less effective than rasburicase, so weigh the tumor‑lysis risk with oncology.,,,,,,,,,
Hemophilia and other bleeding disorders⚠ Ibuprofen, diclofenac, aspirin and other NSAIDs (selective COX‑2 inhibitors excepted)
⚠ No intramuscular analgesia
Vaccines preferably subcutaneous; if IM is unavoidable: factor dose, 25–27 G needle, ice 5 min before, firm pressure ≥ 10 min
Why: platelet inhibition; intramuscular injection → muscle hematoma.
Use instead: acetaminophen or opioids for pain.
Note: ITP: ASH 2019 makes no NSAID/IM statement — expert practice.
Hereditary angioedema (C1‑inhibitor deficiency)⛔ ACE inhibitors — captopril, enalapril, lisinopril (label contraindication; guideline: strictly avoid)
⚠ Estrogen‑containing contraceptives / HRT
Why: ACE inhibitors and estrogens can trigger attacks or make them more frequent (ACE normally breaks down bradykinin, which causes the swelling).
Use instead: progestin‑only pills for contraception; treat an attack with IV C1‑inhibitor, icatibant or ecallantide.
Note: attacks do not respond to antihistamines, corticosteroids or epinephrine.,,
Hereditary fructose intolerance · classical galactosemiaHFI: sucrose · fructose · sorbitol · sucralose · polysorbate — enteral or parenteral — can be fatal: ⛔ IV sorbitol/fructose‑containing medicines (EMA: "must not receive"); check oral syrups, enemas, some immunoglobulin solutions
Galactosemia: lactose and galactose
Why: hypoglycemia, lactic acidosis and liver failure (HFI).
Use instead: galactosemia — soy, casein‑hydrolysate or elemental formula from the time it is suspected.,,
Hypertrophic cardiomyopathy — obstructive⚠ Verapamil — Class 3: Harm with rest dyspnea, hypotension, resting gradient > 100 mmHg, or any infant < 6 weeks
Stop/avoid: ACE inhibitors, ARBs, amlodipine/nifedipine (dihydropyridines), digoxin (Class 2b)
Why: these drugs worsen dynamic outflow obstruction.
Use instead: for hypotension unresponsive to fluid, IV phenylephrine (vasoconstrictor without inotropy) — not inotropes (Class 1).,
Infant botulism⚠ Aminoglycosides (gentamicin, amikacin) — respiratory failure, deaths
△ Clindamycin, magnesium, calcium, tetracycline only after careful consideration with monitoring
Why: aminoglycosides potentiate the paralysis; antibiotics do not treat the botulism itself.
Use instead: BabyBIG (human botulism immune globulin), started on clinical suspicion.,,,
Inherited arrhythmia syndromes — long QT syndrome · Brugada syndrome · catecholaminergic polymorphic ventricular tachycardia (CPVT)Long QT syndrome (Class I): ⚠ QT‑prolonging drugs — ondansetron · azithromycin, clarithromycin, erythromycin · ciprofloxacin, levofloxacin · domperidone · fluconazole · haloperidol, droperidol · citalopram, escitalopram · methadone (CredibleMeds known‑risk list); correct K⁺/Mg²⁺ losses in vomiting/diarrhea
Brugada syndrome (Class I): ⚠ propofol · tricyclic antidepressants · oxcarbazepine · lithium · flecainide, propafenone · procainamide (brugadadrugs.org); treat fever promptly with antipyretics
CPVT: ⚠ digoxin · limit/avoid competitive sports and strenuous exercise (Class I)
Why: long QT syndrome — torsades de pointes. Brugada syndrome — sodium‑channel blockers and fever unmask the Brugada pattern and can trigger ventricular fibrillation. CPVT — adrenaline surges with exercise or emotion trigger polymorphic ventricular tachycardia; digoxin promotes the same arrhythmia mechanism.
Use instead: a drug that is not on the CredibleMeds (long QT) or brugadadrugs.org (Brugada) list; if none is suitable, prescribe only with cardiology advice.,,,,
Ketogenic diet (epilepsy)⚠ Glucose‑containing IV fluids — use 0.45–0.9 % saline or Ringer’s lactate; carbohydrate only for hypoglycemia or excess ketosis
Prefer tablets/sugar‑free formulations; count carbohydrate in medicines
△ Topiramate, zonisamide, acetazolamide (carbonic‑anhydrase inhibitors): monitor bicarbonate and stones · △ propofol
Why: loss of ketosis → seizures; acidosis.
Use instead: tablets rather than liquid or chewable medicines, choosing formulations without added carbohydrate.
Note: check glucose and ketones often when unwell. The diet can be stopped abruptly in an emergency (preferably inpatient).,
Malignant hyperthermia susceptibility (RYR1/CACNA1S; central core disease, King–Denborough; family history)⛔ Sevoflurane, isoflurane, desflurane, halothane (all volatile anesthetics) · ⛔ succinylcholineWhy: these are malignant hyperthermia triggers.
Use instead: total intravenous anesthesia, with dantrolene immediately available.
Note: do not combine dantrolene with calcium‑channel blockers (life‑threatening hyperkalemia).,
Mitochondrial disease⚠ Aminoglycosides (gentamicin, amikacin, tobramycin) with MT‑RNR1 m.1555A>G, m.1494C>T or m.1095T>C — irreversible deafness — unless no safe alternative
⛔ Valproate in POLG‑related disease (boxed warning — fatal liver failure) and in children < 2 y clinically suspected of a mitochondrial disorder
△ Linezolid: monitor lactate
Never fast — give IV glucose
Why: aminoglycosides → permanent deafness in carriers of the listed MT‑RNR1 variants; valproate → fatal liver failure in POLG disease.
Use instead: generally safe by international consensus (De Vries 2020): metformin, propofol (including ≤ 48 h infusion), volatile agents, ketamine, levetiracetam, NSAIDs, steroids and ceftriaxone.,,,
Myasthenia gravis (including juvenile MG)⚠ Fluoroquinolones — ciprofloxacin, levofloxacin (boxed warning: exacerbation, ventilation, deaths) · △ macrolides (azithromycin, clarithromycin) · △ aminoglycosides (gentamicin, amikacin) · ⚠ IV magnesium only if absolutely necessary · △ β‑blockers · ⚠ botulinum toxin · △ hydroxychloroquine, procainamide · ⚠ D‑penicillamine · telithromycin (withdrawn)
Anesthesia: profound sensitivity to non‑depolarizing blockers (reduce dose); resistance to succinylcholine. Corticosteroids may worsen weakness in the first 2 weeks
Why: myasthenic crisis / respiratory failure.
Use instead: an alternative outside these drug classes when one exists; if a listed drug is essential, give it and watch closely for worsening weakness or breathing.,,,,,
Pheochromocytoma / paraganglioma (suspected catecholamine crisis)Never give β‑blockers (propranolol, labetalol) before α‑blockade — unopposed α‑stimulation → hypertensive crisis
Crisis‑precipitating drugs: metoclopramide · corticosteroids (dexamethasone, prednisolone, hydrocortisone) · pseudoephedrine, ephedrine (decongestants) · morphine, tramadol, pethidine · succinylcholine · glucagon · methylphenidate · droperidol, prochlorperazine, chlorpromazine · tricyclics · ACTH
Why: hypertensive crisis / arrhythmia.
Use instead: α‑blockade first (phenoxybenzamine or doxazosin), adding a β‑blocker for tachycardia only after α‑blockade.
Note: the Hemangeol label lists pheochromocytoma as a contraindication.,,
Phenylketonuria⚠ Aspartame (E951) — a phenylalanine source: choose aspartame‑free medicines and drinks (labels must state "contains phenylalanine")Why: aspartame is broken down in the gut to phenylalanine, which builds up in PKU.
Use instead: aspartame‑free medicines; if none exists, give the needed medicine (e.g., an antibiotic) rather than withhold treatment.,,
SCID / severe T‑cell immunodeficiency (incl. complete DiGeorge) · high‑dose immunosuppression (prednisone ≥ 2 mg/kg/day or ≥ 20 mg/day for ≥ 14 days, chemotherapy, HSCT)⛔ All live vaccines — rotavirus (label contraindication in SCID) · BCG · MMR · varicella · OPV · LAIV · yellow fever · oral typhoid
Irradiated cellular blood components in suspected/confirmed SCID (start while tests are pending), after intrauterine transfusion (to 6 months post‑EDD), donations from relatives or HLA‑selected, Hodgkin lymphoma, purine analogues, allogeneic HSCT
Why: vaccine‑strain disease; transfusion‑associated GvHD.
Use instead: non‑live vaccines, which are safe in these children, and full vaccination of household contacts.
Note: irradiation is not required for HIV, solid‑organ transplant, routine chemotherapy or immunocompetent DiGeorge > 2 y.,,,
Sickle cell disease — vaso‑occlusive crisis⚠ Meperidine (pethidine) — do not use unless it is the only effective opioid for that patient (normeperidine → seizures)
IV fluids at no more than the maintenance rate · NSAIDs only as a short course (5–7 days) after assessing renal risk
Why: normeperidine accumulates (seizures); over‑hydration → acute chest syndrome.
Use instead: another parenteral opioid, started promptly and given by patient‑controlled analgesia or scheduled doses rather than as needed.,,
Urea cycle disorders / known hyperammonemia⛔ Valproate · ⚠ L‑asparaginase/pegaspargase
△ Also associated with hyperammonemic decompensation: furosemide · phenobarbital · phenytoin · carbamazepine · topiramate · salicylates · hydrochlorothiazide · primidone
Avoid fasting, protein loads, chemotherapy and high‑dose glucocorticoids
Why: these drugs, fasting and protein loads can raise ammonia → encephalopathy, coma and death.
Use instead: in a crisis, stop protein and give IV glucose to prevent catabolism; ammonia scavengers/dialysis per the metabolic team.,
Williams syndrome⚠ Multivitamins containing vitamin D in early childhood · △ vitamin D supplements with caution later · calcium at the reference daily intake — do not exceed, do not restrict without supervision
Sedation/anesthesia: risk of myocardial ischemia, hemodynamic collapse and sudden death — plan with pediatric anesthesia and cardiology
Why: hypercalcemia; supravalvar aortic stenosis / coronary ostial narrowing.
Use instead: no substitute needed — give vitamin D only for a proven deficiency, and monitor calcium during treatment.,
Wolff–Parkinson–White with pre‑excited atrial fibrillation (irregular wide‑complex tachycardia)Class III — Harm: IV/oral β‑blockers · IV digoxin · IV amiodarone · verapamil (⛔ label: AF/flutter with an accessory pathway) · diltiazem
△ Adenosine: avoid when the resting ECG shows pre‑excitation and the tachycardia is pre‑excited (ESC 2019)
Why: AV‑nodal block accelerates conduction down the accessory pathway → ventricular fibrillation.
Use instead: unstable → synchronized cardioversion; stable → IV procainamide or ibutilide (Class I — adult ACC/AHA/HRS and ESC grades; pediatric use is extrapolated).,,
BAvoid because of the child’s ageFind the drug — 12 rules
DrugAge limitWhy · use instead
Aspirin / salicylates (incl. bismuth subsalicylate)⛔ Children or teenagers with, or recovering from, chickenpox or flu‑like illness — Reye syndrome (FDA‑mandated label warning)Why: Reye syndrome — encephalopathy with fatty liver, fatal in about a third of reported US cases.
Use instead: acetaminophen for fever or pain; ibuprofen is an alternative except in chickenpox.
Note: Kawasaki disease and rheumatic indications are the exception (treating team; see the IVIG/vaccine interaction).,,,
Benzocaine · viscous lidocaine (teething)⚠ OTC benzocaine gels/liquids: not < 2 years (methemoglobinemia) · ⛔ viscous lidocaine 2 %: never for teething (boxed warning — seizures, severe brain injury, deaths)Why: benzocaine → methemoglobinemia (can be fatal); swallowed viscous lidocaine → seizures, brain injury, death.
Use instead: a chilled teething ring or gum massage.,
Codeine · tramadol⛔ < 12 years (pain or cough) · ⛔ < 18 years after tonsillectomy/adenoidectomy · ⚠ 12–18 y if obese, obstructive sleep apnea or severe lung diseaseWhy: ultra‑rapid CYP2D6 metabolism → fatal respiratory depression.
Use instead: acetaminophen, ibuprofen or both for pain, including after tonsillectomy.,,,
Cough‑and‑cold products (OTC antihistamine/decongestant/antitussive combinations)⚠ Not < 4 years (manufacturer labels; FDA: not < 2 y; AAP: not recommended < 4 y, unproven benefit at any age) · ⛔ codeine/hydrocodone cough products < 18 yWhy: serious and fatal adverse effects; no efficacy data.
Use instead: saline nose drops with suction, fluids, a cool‑mist humidifier, and honey for cough from 12 months.,
Diphenhydramine · dimenhydrinate (OTC)⚠ Diphenhydramine: do not use < 2 years; 2–5 y only if directed by a doctor; never to make a child sleepy · dimenhydrinate < 2 y only if directed by a doctorWhy: paradoxical excitation, anticholinergic toxicity; infant deaths.
Use instead: a non‑sedating (second‑generation) antihistamine for allergy symptoms.
Note: OTC labeling limits, not formal contraindications.,
Honey⚠ Not for infants < 12 months (including in remedies or on pacifiers)Why: infant botulism (C. botulinum spores).
Use instead: for an infant’s cold, saline nose drops with bulb suction and plenty of fluids — no honey before 12 months.,
Ibuprofen in young infants (licensing)UK: not suitable < 3 months or < 5 kg · US OTC from 6 months ("under 6 months: ask a doctor")Why: under 6 months, ibuprofen pharmacokinetics may differ and kidney function is still immature.
Use instead: acetaminophen below these ages.
Note: a licensing threshold, not a toxicity rule.,,
Loperamide⛔ < 2 years · OTC 2–5 y only on medical advice · never exceed recommended dosesWhy: respiratory depression; torsades/cardiac arrest with high doses.
Use instead: oral rehydration solution for acute diarrhea; antidiarrheal drugs are not recommended.,
Metoclopramide⛔ < 1 year (EMA) · 1–18 y second‑line only — established post‑operative vomiting or prevention of delayed chemotherapy‑induced vomiting — 0.1–0.15 mg/kg up to 3 ×/day, max 5 days · US label: not recommended in children at allWhy: acute dystonia / extrapyramidal reactions (more common in children); neonatal methemoglobinemia.
Use instead: ondansetron — one oral dose reduces vomiting and helps oral rehydration in gastroenteritis (trial ages 6 months–10 years).,,
Neonates (≤ 28 days)⛔ Ceftriaxone if calcium‑containing IV fluids are needed (fatal ceftriaxone–calcium precipitates) and in hyperbilirubinemic or premature neonates (EU: up to 41 weeks postmenstrual age) · ⛔ co‑trimoxazole < 2 months (kernicterus) · ⛔ benzyl‑alcohol‑preserved ("bacteriostatic") saline/flushes (gasping syndrome) · ⛔ nitrofurantoin < 1 month · ⚠ chloramphenicol (gray syndrome, fatalities)Why: immature drug clearance and red‑cell enzymes (gray syndrome, benzyl‑alcohol toxicity, nitrofurantoin hemolysis), and bilirubin displacement by ceftriaxone and sulfonamides (kernicterus).
Use instead: cefotaxime in place of ceftriaxone; preservative‑free 0.9 % saline for flushes and dilution.,,,,,,,
Promethazine⛔ < 2 years (any route) — boxed warning · ≥ 2 y lowest dose, avoid with other respiratory depressantsWhy: fatal respiratory depression.
Use instead: ondansetron for vomiting in gastroenteritis (studied from 6 months); a non‑sedating antihistamine for allergy.,,
Tetracyclines < 8 years⚠ Use in children < 8 y only for severe/life‑threatening infection without alternative (permanent tooth staining) — but doxycycline is the drug of choice for suspected rickettsial disease at any age; short courses have not caused stainingWhy: permanent yellow‑gray‑brown staining of developing teeth, and enamel hypoplasia.
Use instead: an antibiotic from another class when one is suitable; if a tetracycline is needed, doxycycline at the recommended dose and duration.
Note: tetracycline and minocycline are not covered by the doxycycline data.,,
CAvoid these drug combinationsFind either drug — 20 interactions
DrugsCombination — most to least frequently usedWhy · notes
β‑Blocker therapy + anaphylaxisβ‑blockers may blunt the response to epinephrine. Epinephrine‑refractory anaphylaxis with hypotension/bradycardia in a β‑blocked patient: IV glucagon 20–30 µg/kg (max 1 mg), repeat or infusionWhy: β‑blockers may worsen the outcome of anaphylaxis and its response to epinephrine (effect not fully established).
Use instead: intramuscular epinephrine first, as for any anaphylaxis; add IV glucagon only if the response is poor.
Note: very limited evidence (case reports); glucagon causes vomiting — protect the airway.,,
CarbamazepineLevels ↑ (toxicity — dizziness, drowsiness, ataxia): clarithromycin · erythromycin · fluconazole · itraconazole · voriconazole · ketoconazole · grapefruit juice (CYP3A4 inhibitors)
Carbamazepine lowers: hormonal contraceptives (unintended pregnancy) · itraconazole · ⛔ voriconazole is contraindicated with carbamazepine
Why: potent CYP3A4 inducer.
Use instead: with an interacting drug, monitor carbamazepine levels and adjust the dose; for contraception, an alternative or back‑up method.,
Ceftriaxone + calcium‑containing IV solutions (any age)⛔ Never mix, Y‑site or give simultaneously (including parenteral nutrition) · beyond the neonatal period (> 28 days): sequential administration only after thoroughly flushing the line with 0.9 % NaCl or D5W · neonates: contraindicated (see age rules)Why: ceftriaxone–calcium precipitates in the lungs and kidneys (fatal cases in neonates).
Use instead: beyond 28 days, give them one after the other with the line flushed in between, or through separate lines at different sites; in neonates, choose another antibiotic.,
Clonidine · dexmedetomidine + β‑blockers / digoxin / calcium‑channel blockers△ Clonidine with β‑blockers, digoxin, diltiazem/verapamil: monitor heart rate (bradycardia, AV block) · abrupt clonidine withdrawal → rebound hypertension — withdraw a β‑blocker several days before tapering clonidine (missed doses in children on clonidine for ADHD/tics) · dexmedetomidine: bradycardia/sinus arrest with high vagal tone, bolus dosing or other negative chronotropesWhy: additive slowing of heart rate and AV conduction; stopping clonidine suddenly → rapid rise in blood pressure, worse if a β‑blocker is continued.
Use instead: if both are needed, monitor heart rate; to stop, withdraw the β‑blocker several days first, then taper clonidine over 2–4 days (immediate‑release; the extended‑release label advises steps of no more than 0.1 mg/day every 3–7 days).
Note: the labels advise monitoring and caution; these are not contraindications.
Colchicine (familial Mediterranean fever)Strong CYP3A4 inhibitors — clarithromycin · itraconazole · ketoconazole · ritonavir — or the P‑gp inhibitor ciclosporin: fatal toxicity — ⛔ with renal or hepatic impairment; otherwise reduce or interrupt colchicine
Moderate inhibitors — erythromycin · fluconazole · verapamil · diltiazem · grapefruit juice: dose reduction · azithromycin: no adjustment
Why: fatal colchicine toxicity at therapeutic doses.
Use instead: azithromycin when a macrolide is needed (no colchicine dose change); with the other listed inhibitors, reduce or interrupt colchicine.,,
DigoxinLevels ↑ > 50 % — amiodarone · clarithromycin · erythromycin · verapamil · itraconazole · propafenone · quinidine: measure the level first, reduce digoxin 30–50 % · spironolactone ↑ 25 % (reduce 15–30 %)
Hypokalemia/hypomagnesemia (e.g., diuretics) predispose to toxicity · ⚠ rapid IV calcium → serious arrhythmias in digitalized patients
Why: narrow therapeutic index.
Use instead: if the combination is needed, measure the digoxin level first, cut the dose by about 30–50 % and keep monitoring.
Immunoglobulin (IVIG) + live vaccines · aspirin + varicella vaccineAfter IVIG defer measles‑ and varicella‑containing vaccines: 8 months after 400 mg/kg, 10 months after 1 g/kg, 11 months after 2 g/kg (Kawasaki disease); if given earlier, revaccinate or check seroconversion after the interval
⚠ Salicylates for 6 weeks after varicella vaccine · give annual inactivated influenza vaccine to children on chronic aspirin
Why: antibody interference with vaccine take; Reye syndrome.
Use instead: non‑live vaccines, which can be given at any interval before or after IVIG.,,
Isotretinoin (adolescent acne)⚠ Doxycycline, minocycline and other tetracyclines — intracranial hypertension (pseudotumor cerebri: headache, papilledema, visual change) · ⚠ vitamin A supplements (additive toxicity)Why: isotretinoin can cause intracranial hypertension, and some cases involved a tetracycline; vitamin A adds to its side effects.
Use instead: stop the oral tetracycline before starting isotretinoin, and avoid vitamin A–containing supplements.
Note: the label says "avoid", not "contraindicated".
Linezolid · methylene blue · tramadol + serotonergic drugs (serotonin syndrome)⚠ Linezolid and IV methylene blue are MAO inhibitors: avoid with SSRIs (fluoxetine, sertraline, escitalopram), tramadol, other opioids, SNRIs, tricyclics, triptans unless urgent (methylene blue boxed warning; linezolid ⛔ within 2 weeks of an MAOI, monitor with other serotonergic drugs) · elective use: stop the serotonergic drug ≥ 2 weeks (fluoxetine 5 weeks) before
△ Tramadol + SSRIs/tricyclics: seizures and serotonin syndrome
Why: serotonin syndrome (serious CNS reactions, deaths).
Use instead: another antibiotic or treatment when available; if linezolid or methylene blue is urgent, stop the serotonergic drug and monitor closely for CNS toxicity.,,,
Methotrexate (high‑dose oncology; weekly low‑dose rheumatology)⚠ Ibuprofen, aspirin and other NSAIDs · co‑trimoxazole and other sulfonamides · amoxicillin, piperacillin and other penicillins · omeprazole and other proton‑pump inhibitors · probenecid — reduce methotrexate clearance ("unexpectedly severe and fatal" toxicity, mainly high‑dose methotrexate + NSAIDs): reconcile and hold before HD‑MTX · ⚠ nitrous oxide anesthesia · co‑trimoxazole prophylaxis in ALL: deferral during HD‑MTX is protocol‑dependentWhy: reduced renal tubular secretion of methotrexate.
Use instead: a non‑interacting alternative from the day before high‑dose methotrexate until it has cleared.,
Ondansetron + other QT‑prolonging drugs⚠ Avoid in congenital long QT syndrome · ECG monitoring with hypokalemia/hypomagnesemia, heart failure, bradyarrhythmias or other QT‑prolonging drugs — azithromycin, clarithromycin, erythromycin · ciprofloxacin, levofloxacin, moxifloxacin · domperidone · fluconazole · haloperidol, droperidol · citalopram, escitalopram · methadone (known risk; hydroxyzine and other azoles: conditional risk) · no single IV dose > 16 mg (32 mg dose withdrawn 2012)Why: torsades de pointes.
Use instead: if both are needed, give ondansetron with ECG monitoring.,
Pimozide (Tourette)⛔ Clarithromycin, erythromycin, azithromycin · itraconazole, ketoconazole · sertraline, citalopram, escitalopram, paroxetine, fluvoxamine · protease inhibitors · nefazodone (QT prolongation, sudden death) · clarithromycin and voriconazole are likewise contraindicated with pimozide and ergot alkaloidsWhy: sudden deaths reported when clarithromycin was added to pimozide.
Use instead: an antibiotic, antifungal or antidepressant that the pimozide label does not contraindicate, with an ECG at baseline and during dose adjustment.,,
Propofol — prolonged infusion · PICU sedation · egg/soy allergy⚠ Propofol infusion syndrome (severe metabolic acidosis, hyperkalemia, rhabdomyolysis, lipemia, Brugada‑like ECG, cardiac failure) — risk with > 5 mg/kg/h for > 48 h, reported below 4 mg/kg/h · not indicated for PICU sedation (trial mortality 9 % vs 4 %) · ⛔ after anaphylaxis to egg or soy (US label); non‑anaphylactic egg/soy allergy is not a contraindication (adult data)Why: propofol infusion syndrome, which has caused deaths, and higher mortality when used for PICU sedation.
Use instead: an α2‑agonist (e.g., dexmedetomidine) as the main sedative for ventilated children; if propofol is used, keep it < 4 mg/kg/h for < 48 h.
Note: UK/EU product information has no egg contraindication but does contraindicate propofol in soya or peanut hypersensitivity, and contraindicates propofol for ICU sedation in children ≤ 16 years; follow the locally registered label.,,,
Rifampicin (enzyme inducer)Lowers: corticosteroids · ondansetron · fluconazole and other azoles (⛔ voriconazole) · clarithromycin · phenytoin · doxycycline · fluoroquinolones · tacrolimus/ciclosporin/sirolimus (rejection) · hormonal contraceptives (use a non‑hormonal method) · warfarin and other coumarins · methadone; several antivirals contraindicated · re‑titrate doses when starting and stopping rifampicinWhy: potent CYP/P‑gp induction.
Use instead: a non‑hormonal method of birth control; adjust doses of other affected drugs when rifampicin starts and again when it stops.,,
Sildenafil / tadalafil (pulmonary hypertension)⛔ Organic nitrates in any form (GTN, isosorbide; regular or intermittent) · ⛔ riociguatWhy: profound hypotension.
Use instead: a non‑nitrate alternative; after tadalafil, give no nitrate within 48 hours of the last dose.
Tacrolimus / ciclosporin (transplant, nephrotic syndrome, autoimmune disease)Levels ↑ (nephro‑/neurotoxicity): fluconazole · clarithromycin, erythromycin · voriconazole, posaconazole (give one‑third tacrolimus dose) · itraconazole, ketoconazole · diltiazem, verapamil · grapefruit
Levels ↓ (rejection): rifampicin · phenytoin · carbamazepine · phenobarbital · St John’s wort
△ Ciclosporin + ibuprofen/NSAIDs → renal dysfunction · ⚠ ciclosporin + spironolactone and other potassium‑sparing diuretics (should not be used) · △ ACE inhibitors/ARBs → hyperkalemia · tacrolimus prolongs QT (avoid in congenital LQTS)
Why: CYP3A4/P‑gp substrates with a narrow therapeutic index.
Use instead: if both are needed, adjust the dose and check tacrolimus or ciclosporin trough levels frequently.,
Theophylline / aminophylline⚠ Ciprofloxacin: serious and fatal reactions (cardiac arrest, seizures, status epilepticus, respiratory failure) — avoid; if unavoidable, monitor theophylline levels and adjust · △ clarithromycin raises theophylline — monitor with high dosesWhy: CYP1A2 inhibition (ciprofloxacin‑specific; levofloxacin/moxifloxacin have little effect).
Use instead: another antibiotic; if ciprofloxacin cannot be avoided, monitor theophylline levels and adjust the dose.,
Trimethoprim (co‑trimoxazole) + ACE inhibitor/ARB or spironolactone (± renal impairment, potassium supplements, NSAIDs)△ Trimethoprim blocks the distal‑nephron sodium channel (amiloride‑like) → hyperkalemia, especially at high dose (PJP treatment), with renal insufficiency or other potassium‑raising drugs: monitor potassium or choose another antibioticWhy: trimethoprim acts like amiloride and reduces renal potassium excretion, adding to the potassium rise from these drugs.
Use instead: an alternative antibiotic when appropriate; if co‑trimoxazole is needed, monitor potassium closely.
Note: the sudden‑death signal is from adults ≥ 66 y (BMJ 2014, CMAJ 2015); pediatric data are limited.,,,
Valproate + carbapenems (meropenem, imipenem, ertapenem)⚠ Valproate level falls 60–100 % within ~2 days → breakthrough seizures — not recommended; increasing the valproate dose does not compensate: use a non‑carbapenem antibiotic or add another anticonvulsantWhy: inhibition of valproate‑glucuronide hydrolysis.
Use instead: a non‑carbapenem antibiotic; if a carbapenem is essential, consider adding another anticonvulsant.,,
Valproate + lamotrigineLamotrigine concentrations rise > 2‑fold — lamotrigine dose with valproate is less than half the usual (label pediatric "with valproate" tables) · boxed warning: serious rash/SJS risk is higher in children (0.3–0.8 %) and with valproate or rapid escalationWhy: inhibition of lamotrigine glucuronidation.
Use instead: if both are needed, follow the label’s "with valproate" schedule — less than half the usual lamotrigine dose — and never exceed its starting dose or escalation.

Report an Error

FEEDBACK
▸
⚠ Report an error
  • Found a wrong dose, a broken link, or an out‑of‑date threshold? Report it — corrections are logged and issued between scheduled reviews.
  • Email Ayalmajed@moh.gov.kw with the topic name and what needs correcting.
✚

Bedside Calculators

Offline calculators — every result shows its formula and source. Decision support only; confirm against the drug chart and local protocol before administration.

APGAR

▸
—
Score at 1 and 5 min; if < 7, repeat every 5 min to 20 min.
Does not guide resuscitation — never delay NRP steps to score. Not evidence of asphyxia; does not predict individual outcome.
During resuscitation, record the interventions with the score (expanded Apgar form).
Source: Apgar 1953; AAP/ACOG 2015; NRP 9th ed / AHA‑AAP 2025.

Blood pressure percentile

▸
Enter sex, age and height — add the blood pressure to stage it.
Tables: AAP 2017 values for normal‑weight children aged 1–17 years, by sex, age (completed years) and height; the measured‑height column nearest to the child's height is used. Without a height, the 5th height‑percentile column is used — screening only.
Stages, 1 to < 13 years (whichever threshold is lower): elevated ≥ 90th percentile or ≥ 120/80; stage 1 ≥ 95th percentile or ≥ 130/80; stage 2 ≥ 95th percentile + 12 mmHg or ≥ 140/90. ≥ 13 years: elevated 120–129/< 80; stage 1 130–139/80–89; stage 2 ≥ 140/90.
Percentiles of the reading and the 5th percentile (not listed in the AAP tables) are estimated from the table's 50th, 90th and 95th percentile values (normal approximation); the stage uses the table values directly.
Hypotension (PALS): systolic < 70 + 2 × age (1–10 years), < 90 mmHg (≥ 10 years).
Measure: cuff bladder length 80–100% and width ≥ 40% of the arm circumference; confirm a raised oscillometric reading by auscultation. Hypertension = auscultatory readings ≥ 95th percentile on 3 different visits.
Emergency: symptomatic, or > 30 mmHg above the 95th percentile (> 180/120 in adolescents) → emergency department — see Hypertensive Emergency.
Source: Flynn/AAP 2017; PALS 2020 (hypotension).

Blood products — volumes & rates

▸
Red cells — non‑bleeding child (top‑up)
Restrictive threshold: transfuse a stable critically ill child (no cyanotic heart disease, hemoglobinopathy or severe hypoxemia) when Hb < 70 g/L.
Enter weight, current and target Hb.
Platelets · FFP · cryoprecipitate
Enter weight.
Major hemorrhage — per‑kg aliquots (see Massive Transfusion)
Enter weight.
Neonatal exchange transfusion
Enter weight.
Red cells (mL) = weight (kg) × desired Hb increment (g/dL) × 3 ÷ hematocrit of the unit (Davies 2007, PICU data: with Hct 0.6 the factor is 5, so 10 mL/kg raises Hb by 2 g/dL = 20 g/L). Enter the hematocrit printed on the unit (default 0.6); recheck Hb 1 h after the transfusion (same as at 7 h). Expected effect: 10 mL/kg red cells raise Hb by about 2–3 g/dL (20–30 g/L); one adult unit ≈ 260 mL. Transfuse over 4 h (10 mL/kg ≈ 2.5 mL/kg/h).
Limits: restrictive threshold Hb < 70 g/L in a stable critically ill child (no cyanotic heart disease, hemoglobinopathy or severe hypoxemia; TAXI 2018; AABB 2023). Aim ≤ 20 g/L above the threshold; ≤ 20 mL/kg, usually ≤ 1 adult unit (≈ 280 mL); usual maximum rate 150 mL/h; finish each pack within 4 h of leaving the fridge.
Circulatory‑overload risk (severe chronic anemia, heart or kidney failure, fluid overload): smaller aliquots (≤ 10 mL/kg) over 4 h (≈ 2.5 mL/kg/h); with impaired cardiac function 1 mL/kg/h (expert practice); consider a diuretic; reassess before each aliquot (BSH; SHOT TACO checklist).
Non‑bleeding neonate: 15 mL/kg over 4 h.
Other products: platelets 10–20 mL/kg (max one adult therapeutic dose, ≈ 200 mL apheresis); FFP 15–20 mL/kg; cryoprecipitate 5–10 mL/kg (higher volumes when bleeding; max 2 pools); each at 10–20 mL/kg/h. Expected effect: 10 mL/kg platelets raise the count by about 50–100 ×10⁹/L; cryoprecipitate 5–10 mL/kg raises fibrinogen by about 0.5–1 g/L (one unit ≈ 25 mL; neonates/infants 1 unit per 5 kg); typical unit sizes FFP 200–250 mL, apheresis platelets 200–400 mL.
Major hemorrhage: blood volume ≈ 80 mL/kg (90 in term newborns, 70–80 in older children). Massive hemorrhage is defined as blood loss of 80 mL/kg in 24 h, 40 mL/kg in 3 h or 2–3 mL/kg/min (a definition of loss, not a transfusion volume). Aliquots: RBC 20 mL/kg (max 4 units) · FFP 20 mL/kg (max 4 units) · platelets 15–20 mL/kg (max 1 adult dose) after every 40 mL/kg RBC · cryo 10 mL/kg (max 2 pools). Targets: Hb 80 g/L, fibrinogen > 1.5 g/L, PT ratio < 1.5, platelets > 75 ×10⁹/L.
Exchange: double‑volume 160–200 mL/kg by gestational age (removes 85–90 % of red cells, ≈ 50 % of bilirubin).
Source: Davies 2007 (volume formula); BSH guideline on transfusion for fetuses, neonates and older children (New 2016); BSH administration of blood components (Robinson 2018); TAXI 2018; AABB 2023 (Carson); SHOT 2020.

Body surface area & hyperhydration

▸
Enter height and weight.
BSA (m²) = √(height cm × weight kg ÷ 3600).
Tumor‑lysis hyperhydration: established TLS 3 L/m²/day initially, up to 4 L/m²/day in children by renal function and fluid status (BSH 2025); prophylaxis 2–3 L/m²/day; 200 mL/kg/day if ≤ 10 kg (Coiffier).
No potassium, phosphate or calcium in the fluid initially. Target urine output ≈ 100 mL/m²/h (80–100; 4–6 mL/kg/h if ≤ 10 kg), specific gravity ≤ 1.010. Loop diuretic only for fluid overload.
Source: Mosteller 1987; BSH 2025 (Chan); Coiffier 2008.

Burns — Lund–Browder TBSA & resuscitation fluid

▸
For each area, enter the percentage of that area with partial‑ or full‑thickness burn (ignore simple erythema). Weight: enter the actual pre‑burn (dry) body weight in kg at every age, including Adult. The area's share of the body for the chosen age is shown in brackets.
Choose age, enter weight and the burned areas.
Lund–Browder (% of body, both sides combined, by age < 1 / 1 / 5 / 10 / 15 / adult): head 19 / 17 / 13 / 11 / 9 / 7 · thighs 11 / 13 / 16 / 17 / 18 / 19 · lower legs 10 / 10 / 11 / 12 / 13 / 14. Fixed: neck 2, anterior trunk 13, posterior trunk 13, buttocks 5, genitalia 1, upper arms 8, forearms 6, hands 5, feet 7.
Children with > 10% TBSA: Ringer's lactate 2–4 mL/kg/%TBSA over 24 h — the guide starts at 3 mL/kg/%TBSA; Parkland formula: 4 mL/kg × %TBSA.
Adults (≥ 16 y) with ≥ 20% TBSA: start at 2 mL/kg/%TBSA (ABA 2023); below 20% no formula.
Half in the first 8 h from the time of the burn, the rest over 16 h. Add maintenance fluid with glucose.
Limits: no hourly rate is shown when less than 2 h of the first 8 h remain or the rate would exceed 20 mL/kg/h or 1000 mL/h (no rapid catch‑up — burns center); the formula does not apply from 24 h after the burn.
Starting estimate only — titrate to urine output 1 mL/kg/h if < 30 kg, 0.5 mL/kg/h if ≥ 30 kg.
Source: Lund & Browder 1944; ISBI 2016; RCH Melbourne burns guideline.

Corrected age for preterm infants

▸
Enter date of birth and gestation at birth.
Chronological age = time since birth. Postmenstrual age = gestational age + chronological age. Corrected age = chronological age − weeks born before 40 weeks.
Use corrected age for growth and development in children born preterm, up to 3 years of age.
Source: AAP Committee on Fetus and Newborn (Engle 2004).

DKA — orders: fluids, insulin & cerebral injury (TREKK 2023 · ISPAD 2022)

▸
Fluid orders (TREKK)
Enter weight.
Insulin, potassium, monitoring & escalation
Enter weight.
Suspected cerebral injury
Enter weight.
Orders follow TREKK 2023 (Physician Orders, Pediatric DKA in the ED, v2.1).
Bolus: NS or RL 20 mL/kg (max 1,000 mL) over 20 min — rapid push over 5–10 min if hypotensive — repeated if capillary refill ≥ 3 s or extremities are cool.
Rehydration rate = the guide's DKA algorithm table: 6.5 mL/kg/h (5 to < 10 kg) · 6 mL/kg/h (10 to < 20 kg) · 5 mL/kg/h (20 to < 40 kg) · 4 mL/kg/h (≥ 40 kg, max 500 mL/h). The same rate is kept when KCl 40 mmol/L is added (once K⁺ < 5.5 mmol/L and urine is passed) and when fluids change to D5 (or D10) NS/RL with KCl 40 mmol/L (glucose < 17 mmol/L or a fall > 5 mmol/L/h). The table = a 7% deficit, minus a 10 mL/kg bolus, plus maintenance (Holliday–Segar) over 24 h — the ISPAD 2022 method (deficit minus bolus plus maintenance, evenly over 24–48 h).
Limits: below 5 kg the table does not apply — the senior clinician / PICU sets the rate.
Insulin: regular insulin 1 unit/mL (50 units in 50 mL) at 0.1 unit/kg/h (0.05 if < 5 y or pH > 7.15), started 1 h after IV fluids (not before 1 h, always before 2 h); never a bolus. K⁺ < 3.5 mmol/L: give potassium first (≤ 0.5 mmol/kg/h) and defer insulin.
Monitoring: bedside glucose hourly; glucose, electrolytes, urea, creatinine and venous gas every 2 h; neuro observations and fluid balance hourly.
Escalation: consult the pediatric diabetes team; PICU or the referral/transport team if pH < 7.1, age < 5 y, hypotension or suspected cerebral injury.
Bicarbonate: only for life‑threatening hyperkalemia or pH < 6.9 with compromised contractility.
Cerebral injury: head of bed 30° midline; mannitol 0.5–1 g/kg (max 100 g) over 10–15 min or 3% NaCl 2.5–5 mL/kg (max 250 mL; TREKK 5 mL/kg) over 10–15 min, repeat once after 30 min or use the other agent; then reduce IV fluids to 60% of the table rate, as in the guide's algorithm (TREKK uses 75%).
In PICU the Kuwait PICU Task Force protocol governs.
Source: TREKK 2023; ISPAD 2022; Kuwait PICU Task Force; CPS 2023.

eGFR — CKiD U25 (bedside Schwartz shown)

▸
Enter height and creatinine.
CKiD U25: eGFR (mL/min/1.73 m²) = K × height (m) ÷ creatinine (mg/dL); with creatinine in µmol/L, eGFR = K × 0.884 × height (cm) ÷ creatinine.
K, males: 39.0 × 1.008(age − 12) under 12 y; 39.0 × 1.045(age − 12) at 12–18 y; 50.8 from 18 y.
K, females: 36.1 × 1.008(age − 12) under 12 y; 36.1 × 1.023(age − 12) at 12–18 y; 41.4 from 18 y.
Valid for ages 1–25 y; derived in children and young adults with CKD using enzymatic, IDMS‑traceable creatinine.
Bedside Schwartz 2009 = 0.413 × height (cm) ÷ creatinine (mg/dL) (36.5 with µmol/L); overestimates GFR under 5 y, underestimates it from 18 y.
No creatinine equation is well validated at normal GFR; none is valid when creatinine is changing (AKI).
Source: Pierce 2021 (Kidney Int); Schwartz 2009 (J Am Soc Nephrol).

Anion gap, osmolality & corrected sodium

▸
Corrected sodium (hyperglycemia — DKA, HHS)
—
Anion gap
—
Calcium
Measure ionized calcium — albumin‑corrected calcium is unreliable (it misses hypocalcemia, especially in critical illness and chronic kidney disease).
Serum osmolality (calculated and effective)
—
Corrected Na = measured Na + 2.4 × (glucose − 5.6) ÷ 5.6 (mmol/L; Hillier — the older 1.6 factor underestimates at high glucose); applied only when glucose > 5.6 mmol/L.
Anion gap = Na − (Cl + HCO₃); use your laboratory's reference range (ISPAD: 12 ± 2). Albumin‑corrected anion gap = anion gap + 2.5 × (40 − albumin g/L) ÷ 10.
Osmolality = 2 × Na + glucose + urea; effective osmolality = 2 × Na + glucose (mmol/L; > 320 in HHS). Osmolar gap = measured − calculated osmolality (> 10 suggests an unmeasured osmole).
Calcium: measure ionized calcium — albumin‑corrected calcium is unreliable.
Source: ISPAD 2022; Figge 1998; Slomp 2003; Gauci 2008.

Endotracheal tube — size & depth

▸
Enter age (≥ 1 year). For neonates use weight‑based sizing.
Age 1–14 y: cuffed ID (mm) = age ÷ 4 + 3.5; uncuffed = age ÷ 4 + 4; shown rounded to 0.5 mm — have the 0.5 mm smaller and larger tubes ready. Depth at lip (cm) = age ÷ 2 + 12, or 3 × tube ID.
The age formula is not valid under 1 year or above 14 years (adult sizing). Cuff pressure < 20–25 cm H₂O. Depth formulas misplace 15–25% of tubes — confirm with capnography and chest X‑ray.
Neonate: ID ≈ 2.5–3.5 by weight; depth from a gestational‑age/weight table or nasal–tragus length + 1 cm; weight + 6 cm tends to place tubes too deep.
Source: APLS; AHA/AAP PALS 2025; AHA PALS 2020.

Glasgow Coma Scale

▸
—
Pediatric verbal responses are shown for pre‑verbal children.
Report E, V and M with the total; mark an untestable component NT. GCS ≤ 8 = threatened airway → involve PICU/anesthesia.
Source: Teasdale & Jennett 1974; Teasdale 2014; pediatric modification (James 1986).

Glucose infusion rate (GIR)

▸
Enter weight, then any two of dextrose %, rate and target GIR (or just one for a dextrose table).
GIR (mg/kg/min) = dextrose % × rate (mL/h) ÷ (6 × weight kg) (1% dextrose = 10 mg/mL; 1 h = 60 min).
Enter weight plus any two of dextrose %, rate and target GIR — the calculator solves the third (rate in mL/h or mL/kg/day).
Neonatal IV dextrose: GIR 5–8 mg/kg/min; escalate in 2 mg/kg/min steps. > 12.5% dextrose needs central access.
Persistently higher requirement: suspect hyperinsulinism or another persistent hypoglycemia disorder — send a critical sample during hypoglycemia and involve endocrinology.
Source: AAP (Adamkin 2011); Pediatric Endocrine Society (Thornton 2015).

HLH criteria (2004, revised 2024) · MAS‑2016 · MS score

▸
HLH criteria — HLH‑2004, revised 2024 (5 of 7; hematology pathway, not MAS in sJIA)
0 of 7 criteria.
Systemic JIA — MAS‑2016 classification & MS score
Enter the laboratory values.
HLH‑2004, revised 2024: molecular diagnosis, an affected sibling, or 5 of 7 criteria (NK‑cell activity no longer counted). Validated for familial HLH against infection and sJIA controls — exclude malignancy. No criteria set fits every setting (EULAR/ACR 2022).
MAS‑2016 (febrile child with known or suspected sJIA; fever is required): ferritin > 684 ng/mL plus any 2 of platelets ≤ 181 ×10⁹/L, AST > 48 U/L, triglycerides > 156 mg/dL (1.76 mmol/L), fibrinogen ≤ 360 mg/dL (3.6 g/L), not explained otherwise. Missing results = incomplete, not negative.
MS score = CNS × 2.44 + hemorrhage × 1.54 + arthritis × (−1.30) + platelets (×10⁹/L) × (−0.003) + LDH (U/L) × 0.001 + fibrinogen (mg/dL) × (−0.004) + ferritin (ng/mL) × 0.0001; possible range −8.4 to 41.8; ≥ −2.1 indicates MAS in a patient with active sJIA (validation sensitivity 89%, specificity 99%).
Criteria support, never delay, treatment (see Cytokine Storm card).
Source: Henter 2007; Henter 2024; Ravelli 2016; Minoia 2019; Shakoory 2023 (EULAR/ACR).

Hyponatremia — 3% saline & correction ceiling

▸
Enter weight.
Correction tracker
Enter the starting and current sodium and the hours between them.
Next fluid & rate (estimate)
Enter weight and the sodium values above.
Symptomatic (hyponatremic encephalopathy): 3% NaCl 2 mL/kg (max 100 mL) over 10 min; repeat 1–2 times until symptoms improve. Goal: 5–6 mmol/L rise in the first 1–2 h (each bolus raises Na by at most ~2 mmol/L).
Limits: stop boluses once symptoms resolve or Na has risen 10 mmol/L in the first 5 h; total rise in the first 48 h ≤ 15–20 mmol/L. Chronic or asymptomatic: ≤ 8 mmol/L in 24 h (the guide's cautious ceiling; see Acute Electrolyte Emergencies); NICE: ≤ 12 mmol/L in 24 h once symptoms resolve.
Next fluid & rate (Adrogué–Madias estimate): change in Na per litre = (fluid Na − serum Na) ÷ (total body water + 1); total body water ≈ 0.6 L/kg. It plans only the rise still allowed within the 24‑h limit (and ≤ 18 mmol/L in 48 h).
The estimate ignores urine and ongoing losses and underestimates the rise, especially once a water diuresis starts: recheck Na every 2–4 h (every 1–2 h on hypertonic saline) and adjust. The tracker uses one start/current pair and cannot exclude a faster rise within any 24‑h window.
Overcorrection: recheck Na every 1–2 h; a rise > 1 mmol/L per hour with urine output > 1 mL/kg/h signals a water diuresis — restrict sodium‑containing fluids and seek expert advice.
Source: Moritz & Ayus 2010 (Pediatr Nephrol); Sterns 2024 (CJASN); NICE NG29; Mohmand 2007 (Clin J Am Soc Nephrol).

Infusion calculator — dose ↔ rate

▸
Typical dose range appears here.
Your preparation — enter the actual concentration (nothing is assumed)
or
Enter weight, your preparation, and a dose or a rate.
Rate (mL/hr) = dose (mcg/kg/hr) × weight (kg) ÷ concentration (mcg/mL). Per‑minute dose × 60; mg/kg/hr × 1000.
Concentrations are never assumed: edit a preset or type your own. Titrate the dose to response. A red warning appears if the dose is more than 2× the typical upper limit or the rate is above 50 mL/hr.
Source: AHA/AAP PALS 2025; pediatric Surviving Sepsis Campaign (Weiss, 2026).

Maintenance fluids & bolus

▸
Enter weight.
Maintenance (Holliday–Segar): 100‑50‑20 mL/kg/day for the first 10 / next 10 / each further kg; hourly rate = daily volume ÷ 24 (≈ 4‑2‑1 mL/kg/hr).
Cap (NICE NG29, children and young people): about 2,000 mL/day for girls and 2,500 mL/day for boys — reached only above ≈ 45 kg; both caps are then shown.
ADH excess likely (postoperative, pain, nausea, CNS or lung disease): consider 50–80% of this rate.
Fluid: isotonic with glucose (AAP 2018). The recommendation excludes neonates < 28 days and neurosurgical, cardiac, hepatic or renal disease, cancer, diabetes insipidus, voluminous watery diarrhea and severe burns.
Bolus: 10–20 mL/kg balanced crystalloid (usual maximum per bolus 500–1000 mL in adult‑sized patients); reassess after each.
Source: Holliday & Segar 1957; NICE NG29; AAP Clinical Practice Guideline 2018; PALS 2025.

Modified Tal score — bronchiolitis severity

▸
Enter the respiratory rate.
Four items scored 0–3, total 0–12; validated in infants under 12 months with bronchiolitis.
Respiratory rate points: under 6 months ≤ 40 = 0 · 41–55 = 1 · 56–70 = 2 · ≥ 71 = 3; from 6 months ≤ 30 = 0 · 31–45 = 1 · 46–60 = 2 · ≥ 61 = 3. Count for 30 seconds and double.
Bands: ≤ 5 mild · 6–10 moderate · ≥ 11 severe.
Limit: the score supports documentation and trend; it does not replace clinical review. Apnea, exhaustion, or poor feeding need escalation whatever the score.
Source: Golan‑Tripto 2018 (Pediatr Pulmonol 53:796–801).

Oxygen cylinder duration

▸
Choose a cylinder, then enter the gauge pressure and flow.
Usable duration = (gauge pressure − safe residual) × cylinder factor ÷ flow.
Safe residual 200 psi (~14 bar) — treat as empty; change / refill at ~500 psi (~35 bar).
Presets are US (CGA) cylinders — factors (L/psi): D 0.16 · E 0.28 · M 1.56 · G 2.41 · H/K 3.14.
BOC/UK or other metric cylinders: choose Custom / metric — usable liters ≈ water capacity on the label (L) × (gauge pressure in bar − 14 bar). BOC oxygen, full at 137 bar: E 4.7 L water capacity = 680 L · F 9.4 L = 1360 L · G 23.6 L = 3400 L · J 47.2 L = 6800 L (a BOC G is not a US G).
Source: Egan's Fundamentals of Respiratory Care 12e; AARC; BOC cylinder data.

Paracetamol & iron ingestion

▸
Paracetamol (acetaminophen) — acute single ingestion
Enter weight and the amount taken.
Enter the hours since ingestion and the level.
Enter weight for the acetylcysteine doses (two‑bag and three‑bag).
Iron
Enter weight and the elemental iron taken (from the label).
Paracetamol — refer to hospital: ≥ 200 mg/kg or ≥ 10 g (whichever is less) within 24 h, unknown amount, or any self‑harm.
Nomogram: treatment line 150 mg/L at 4 h, halving every 4 h (37.5 mg/L at 12 h) to 24 h. High‑risk line 300 mg/L at 4 h (double the treatment line) — call toxicology; a higher acetylcysteine dose is often used (e.g., the final 16‑h bag doubled to 200 mg/kg over 16 h — the second bag of the two‑bag regimen, the third bag of the three‑bag regimen). µmol/L = mg/L × 6.614.
Do not use for: a level drawn before 4 h (cannot be plotted); repeated supratherapeutic or unknown‑time ingestions (treat if level > 20 mg/L or transaminases abnormal).
Acetylcysteine IV: total 300 mg/kg (dose weight capped at 100 kg). Dilute in 0.45% sodium chloride (preferred) or 5% dextrose; unadjusted volumes cause hyponatremia and seizures. Not studied under 5 kg.
≥ 41 kg — two‑bag (20 h), preferred: 200 mg/kg in 1,000 mL over 4 h → 100 mg/kg in 500 mL over 16 h. Fewer anaphylactoid reactions than three‑bag, similar liver outcomes in cohort studies. Three‑bag gives more drug in the first hours: preferred with early liver injury or a large ingestion.
≤ 40 kg — three‑bag (21 h): 150 mg/kg over 1 h → 50 mg/kg over 4 h → 100 mg/kg over 16 h; diluent ≤ 20 kg 3 / 7 / 14 mL/kg; 21–40 kg 100 / 250 / 500 mL (≥ 41 kg 200 / 500 / 1,000 mL). Two‑bag alternative under 41 kg (limited data): 200 mg/kg in 7 mL/kg (max 500 mL) → 100 mg/kg in 14 mL/kg (max 1,000 mL).
Stop only when: acetaminophen < 10 mg/L, INR < 2.0, ALT/AST normal or falling, and the child is well; otherwise continue at the second‑bag rate and call KPCC 1804774.
Iron: ≥ 40 mg/kg elemental iron, or severe/persistent symptoms → hospital; < 40 mg/kg with mild symptoms may be observed (call KPCC 1804774). The 40 mg/kg threshold applies to adult ferrous‑salt products; children's chewable multivitamins with iron, carbonyl iron and polysaccharide–iron complex can usually be observed at home.
Source: Fox 2025 (out‑of‑hospital, Clin Toxicol); Dart 2023 consensus; acetylcysteine prescribing information; Australia/New Zealand guideline (Chiew 2020); two‑bag vs three‑bag meta‑analysis (Nakatsu 2025); Manoguerra 2005.

PARDS — oxygenation index (PALICC‑2)

▸
Choose the support and enter FiO₂ with PaO₂ and/or SpO₂.
OI = mean airway pressure × FiO₂ (%) ÷ PaO₂ (mmHg). OSI = mean airway pressure × FiO₂ (%) ÷ SpO₂ (use only when SpO₂ ≤ 97%). Enter FiO₂ as a percentage; a fraction (0.21–1.0) is converted to %.
Invasive ventilation: PARDS if OI ≥ 4 or OSI ≥ 5; mild–moderate OI < 16 / OSI < 12; severe OI ≥ 16 / OSI ≥ 12 (stratify after ≥ 4 h).
Non‑invasive (full face mask CPAP ≥ 5 cmH₂O): PaO₂/FiO₂ ≤ 300 or SpO₂/FiO₂ ≤ 250; severe if PaO₂/FiO₂ ≤ 100 or SpO₂/FiO₂ ≤ 150.
Possible PARDS: nasal CPAP/BiPAP or high‑flow ≥ 1.5 L/kg/min (or ≥ 30 L/min) meeting the same oxygenation thresholds.
Applies to: < 18 y without active perinatal lung disease, within 7 days of a known insult, with new infiltrates not fully explained by cardiac failure or overload.
Source: PALICC‑2 (Emeriaud 2023).

Pediatric Appendicitis Score (PAS)

▸
PAS 0 / 10.
Eight items, total 0–10; derived in children 4–15 y.
Bands (Ebell 2014, systematic review of 26 prospective cohorts): ≤ 3 low (likelihood ratio 0.13) · 4–7 equivocal (0.70) · ≥ 8 high (8.1).
Limit: at usual pre‑test probabilities no PAS cut‑off rules appendicitis in or out on its own — use with ultrasound and clinical review.
Single‑center validations used ≤ 2 / 3–6 / ≥ 7 (Goldman 2008) and ≤ 4 / 5–7 / ≥ 8 (Bhatt 2009).
Source: Samuel 2002; Ebell 2014 systematic review (Ann Emerg Med); Goldman 2008 (J Pediatr); Bhatt 2009.

PRAM — asthma severity score

▸
PRAM 0 / 12 — mild (0–3).
Five items, total 0–12; validated at 2–17 y.
Bands: 0–3 mild · 4–7 moderate · 8–12 severe.
Use: score at triage and again after each treatment step. If the two sides differ, score the worse side.
Limit: drowsiness, confusion, or a silent chest means life‑threatening asthma whatever the score.
Source: Ducharme 2008 (J Pediatr); Chalut 2000.

PUCAI — Pediatric Ulcerative Colitis Activity Index

▸
PUCAI 0 — remission (< 10).
Six clinical items, no laboratory values; total 0–85.
< 10 remission · 10–34 mild · 35–64 moderate · ≥ 65 severe = acute severe colitis (admit, IV corticosteroids).
On IV steroids: day 3 > 45 → plan second‑line therapy; day 5 > 65 → start second‑line; 35–65 on day 5 → continue steroids with daily scoring, deciding on second‑line therapy within 7–10 days of IV steroids in total; < 35 → responding.
Source: Turner 2007 (Gastroenterology); ESPGHAN/ECCO acute severe colitis guideline 2025 (Assa et al., JPGN).

QTc (corrected QT)

▸
Enter QT and the RR interval (or heart rate).
Bazett: QTc = QT ÷ √RR. Fridericia: QTc = QT ÷ RR^⅓. RR (s) = 60 ÷ HR.
Measure QT in lead II or V5 and use the RR interval immediately before it — sinus arrhythmia is common in children, so a heart rate gives only an estimate. QT and RR may be entered in ms or seconds.
Prolonged: > 450 ms in children before puberty, infants and post‑pubertal males, > 460 ms in post‑pubertal females; ≥ 500 ms = high risk of torsades.
Long QT syndrome: Bazett QTc ≥ 500 ms on repeated ECGs, or 480–499 ms with unexplained syncope (or a Schwartz score ≥ 3.5), without a secondary cause.
Limit: Bazett overestimates QTc at fast heart rates and underestimates it at slow rates — repeat at a slower rate or compare with Fridericia.
Source: Bazett 1920; Rautaharju/AHA 2009; Priori/HRS 2013; Phan 2015 (J Pediatr).

Shock index, pediatric age‑adjusted (SIPA)

▸
Enter age, heart rate and systolic BP.
Shock index = heart rate ÷ systolic BP.
Elevated SIPA: > 1.22 at 4–6 y, > 1.0 at 7–12 y, > 0.9 at 13–16 y.
Derived in blunt trauma, ages 4–16 (injury severity score > 15): identified more children with ISS > 30, transfusion in 24 h, high‑grade liver/spleen injury needing transfusion, and in‑hospital death than the unadjusted index.
Limits: not validated outside 4–16 y or for non‑trauma shock. A normal SIPA does not exclude serious injury (sensitivity about 37%).
Source: Acker 2015 (J Pediatr Surg); Ramgopal 2024 (Injury).

Westley croup score

▸
—
Score: ≤ 2 mild · 3–5 moderate · 6–11 severe · ≥ 12 impending respiratory failure (conventional bands — not stated by Westley 1978 or by Bjornson & Johnson 2008/2013, who grade severity clinically: mild = no stridor at rest; moderate = stridor and indrawing at rest without sustained agitation; severe = sustained agitation; impending failure = lethargy or cyanosis in room air).
Limits: croup scores are research tools — not shown to improve routine care and unreliable across clinicians. Use for documentation; treat by clinical severity (stridor at rest, chest‑wall indrawing, agitation, lethargy).
Treatment: dexamethasone 0.15–0.6 mg/kg for all; nebulized L‑epinephrine 1:1000 (1 mg/mL) 0.5 mL/kg (max 5 mL) for moderate–severe.
Source: Westley 1978; Bjornson & Johnson 2008 (Lancet).
§

References

Primary guidelines & landmark trials (Vancouver)

Sources

Tap to view the full reference list.

▸
  1. State of Kuwait. Law No. 70 of 2020 on the Practice of the Medical Profession and its Auxiliary Professions, the Rights of Patients and Health Facilities. Official Gazette (Kuwait Al‑Youm), 2020.
  2. State of Kuwait. Child Rights Law No. 21 of 2015. Kuwait National Child Protection Program, Ministry of Health. kncpp.moh.gov.kw
  3. Lasa JJ, Dhillon GS, Duff JP, et al.; American Heart Association and American Academy of Pediatrics. Part 8: Pediatric Advanced Life Support: 2025 American Heart Association and American Academy of Pediatrics Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2025;152(16 Suppl 2):S479–S537. doi:10.1161/CIR.0000000000001368
  4. Kleinman ME, Buick JE, Huber N, et al. Part 7: Adult Basic Life Support: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2025;152(16 suppl 2):S448–S478. doi:10.1161/CIR.0000000000001369
  5. Van de Voorde P, Turner NM, Djakow J, et al. European Resuscitation Council Guidelines 2021: paediatric life support. Resuscitation. 2021;161:327–387. doi:10.1016/j.resuscitation.2021.02.015
  6. 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. doi:10.5811/westjem.2019.1.41344
  7. Shain B; American Academy of Pediatrics Committee on Adolescence. Suicide and suicide attempts in adolescents. Pediatrics. 2016;138(1):e20161420. doi:10.1542/peds.2016-1420
  8. Kuwait Poison Control Center (KPCC), Ministry of Health — 24/7 toxicology hotline: 1804774.
  9. Simon LV, Hashmi MF, Callahan AL. Neuroleptic malignant syndrome. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2026 (updated Apr 2023). NBK482282
  10. Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med. 2005;352(11):1112–1120. doi:10.1056/NEJMra041867
  11. Rosenberg H, Pollock N, Schiemann A, Bulger T, Stowell K. Malignant hyperthermia: a review. Orphanet J Rare Dis. 2015;10:93. doi:10.1186/s13023-015-0310-1
  12. Weiss SL, Peters MJ, Oczkowski SJW, et al. Surviving Sepsis Campaign international guidelines for the management of sepsis and septic shock in children 2026. Pediatr Crit Care Med. 2026;27(4):379–434. doi:10.1097/PCC.0000000000003927
  13. Davis AL, Carcillo JA, Aneja RK, et al. American College of Critical Care Medicine Clinical Practice Parameters for Hemodynamic Support of Pediatric and Neonatal Septic Shock. Crit Care Med. 2017;45(6):1061–1093. doi:10.1097/CCM.0000000000002425
  14. Guarino A, Ashkenazi S, Gendrel D, Lo Vecchio A, Shamir R, Szajewska H; ESPGHAN/ESPID. Evidence‑Based Guidelines for the Management of Acute Gastroenteritis in Children in Europe: Update 2014. J Pediatr Gastroenterol Nutr. 2014;59(1):132–152. doi:10.1097/MPG.0000000000000375
  15. Russell RT, Esparaz JR, Beckwith MA, et al. Pediatric traumatic hemorrhagic shock consensus conference recommendations. J Trauma Acute Care Surg. 2023;94(1S):S2–S10. doi:10.1097/TA.0000000000003805
  16. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support (ATLS) Course Manual. 11th ed. Chicago, IL: American College of Surgeons; 2025.
  17. Law YM, Lal AK, Chen S, et al. Diagnosis and management of myocarditis in children: a scientific statement from the American Heart Association. Circulation. 2021;144(6):e123–e135. doi:10.1161/CIR.0000000000001001
  18. Centers for Disease Control and Prevention. Health Alert Network HAN‑00476: Clinical guidance for carbon monoxide (CO) poisoning (Hurricanes Fiona and Ian). Atlanta: CDC; 1 Oct 2022. archive.cdc.gov
  19. Cao D, Arens AM, Chow SL, et al. Part 10: Adult and Pediatric Special Circumstances of Resuscitation: 2025 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2025;152(16 suppl 2):S578–S672. doi:10.1161/CIR.0000000000001380
  20. Cyanokit (hydroxocobalamin for injection): US prescribing information. BTG International Inc.; revised Apr 2023. DailyMed
  21. PROVAYBLUE (methylene blue) injection — US prescribing information (boxed warning; §4; §5.1). Provepharm; revised 02/2024. www.accessdata.fda.gov
  22. Goyer I, Thibault C, Marquis C, et al. Use of norepinephrine in the pediatric intensive care unit: an international survey of prescription and administration habits in case of pediatric hypotensive shock. Eur J Pediatr. 2025;184(7):392. doi:10.1007/s00431-025-06205-6
  23. Schlapbach LJ, Watson RS, Sorce LR, et al; SCCM Pediatric Sepsis Definition Task Force. International consensus criteria for pediatric sepsis and septic shock. JAMA. 2024;331(8):665–674. doi:10.1001/jama.2024.0179
  24. American Heart Association. Pediatric Advanced Life Support (PALS) Provider Manual. Dallas, TX: American Heart Association; 2020. Part: Recognition of shock (age‑based hypotension and urine‑output thresholds).
  25. Ceftriaxone for injection, USP — US prescribing information (Contraindications; §5.2 interaction with calcium‑containing products). DailyMed, revised 1/2023; Rocephin Core Data Sheet v9.0, Roche, January 2024. DailyMed
  26. Maitland K, Kiguli S, Opoka RO, et al. (FEAST) Mortality after fluid bolus in African children with severe infection. N Engl J Med. 2011;364(26):2483–2495. doi:10.1056/NEJMoa1101549
  27. Kuwait Pediatric Council. Pediatric Antibiotic Policy (Ministry of Health, Kuwait) — internal Council document (current edition), not published online.
  28. Kuwait PICUs Taskforce. PICU Septic Shock Approach and Management. Version 2.0. Kuwait Ministry of Health; October 2025.
  29. Epinephrine Injection, USP 1 mg/mL — US prescribing information (§2.2 dilution for hypotension associated with septic shock; §16 storage and handling). BPI Labs; revised 3/2024. www.accessdata.fda.gov
  30. Epinephrine Injection USP, 1 mg/10 mL (0.1 mg/mL) ABBOJECT prefilled syringe — US prescribing information (dosage forms and strengths). Hospira; revised 6/2025. labeling.pfizer.com
  31. LEVOPHED (norepinephrine bitartrate) injection — US prescribing information (dosage forms and strengths — strength as norepinephrine base; dilution; storage and handling). Hospira; revised 5/2024. labeling.pfizer.com
  32. Noradrenaline (Norepinephrine) 1 mg/ml concentrate for solution for infusion — Summary of Product Characteristics (§2 composition; §6.2 incompatibilities; §6.4 storage; §6.6 dilution). AS Kalceks; emc (SmPC), revised 16 Apr 2022. medicines.org.uk/emc/product/13172
  33. Irwin D, Vaillancourt R, Dalgleish D, et al. Standard concentrations of high-alert drug infusions across paediatric acute care. Paediatr Child Health. 2008;13(5):371–376. doi:10.1093/pch/13.5.371
  34. American Society of Health-System Pharmacists. Standardize 4 Safety: Pediatric Continuous Infusion Standards. Bethesda, MD: ASHP; updated June 2026. ashp.org/standardize4safety
  35. Fazio S, Blackmon E, Doroy A, Vu AN, MacDowell P. An inadvertent bolus of norepinephrine. PSNet WebM&M case. Rockville, MD: Agency for Healthcare Research and Quality; 26 May 2021. psnet.ahrq.gov
  36. Institute for Safe Medication Practices. ISMP List of High-Alert Medications in Acute Care Settings. Plymouth Meeting, PA: ISMP; 2024. ISMP/ECRI
  37. Magor NRE, Elhalafawy SEH, Ads SEM, Abdelfattah ME, Melika SWM. Efficacy of modified versus standard Valsalva maneuvers on clinical outcomes and satisfaction of children with paroxysmal supraventricular tachycardia: a randomized controlled trial. BMC Pediatr. 2025;25(1):1003. doi:10.1186/s12887-025-06396-9
  38. Appelboam A, Reuben A, Mann C, et al. Postural modification to the standard Valsalva maneuver for emergency treatment of supraventricular tachycardias (REVERT): a randomized controlled trial. Lancet. 2015;386(10005):1747–1753. doi:10.1016/S0140-6736(15)61485-4
  39. Singh Y, Mikrou P. Use of prostaglandins in duct‑dependent congenital heart conditions. Arch Dis Child Educ Pract Ed. 2018;103(3):137–140. doi:10.1136/archdischild-2017-313654
  40. Kliegman RM, St Geme JW, Blum NJ, et al., eds. Nelson Textbook of Pediatrics. 22nd ed. Philadelphia, PA: Elsevier; 2024. Part XIX, Section 3 (Congenital heart disease: acyanotic lesions). ISBN 978‑0‑323‑88305‑4.
  41. Bailliard F, Anderson RH. Tetralogy of Fallot. Orphanet J Rare Dis. 2009;4:2. doi:10.1186/1750-1172-4-2
  42. Taketomo CK, Hodding JH, Kraus DM. Pediatric & Neonatal Dosage Handbook. 31st ed. Hudson, OH: Lexicomp (Wolters Kluwer); 2024.
  43. Rudd NA, Ghanayem NS, Hill GD, et al. Interstage home monitoring for infants with single ventricle heart disease: education and management: a scientific statement from the American Heart Association. J Am Heart Assoc. 2020;9(16):e014548. doi:10.1161/JAHA.119.014548
  44. Marino BS, Tabbutt S, MacLaren G, et al. Cardiopulmonary resuscitation in infants and children with cardiac disease: a scientific statement from the American Heart Association. Circulation. 2018;137(22):e691–e782. doi:10.1161/CIR.0000000000000524
  45. Stevenson JG, Kawabori I, Bailey WW. Noninvasive evaluation of Blalock-Taussig shunts: determination of patency and differentiation from patent ductus arteriosus by Doppler echocardiography. Am Heart J. 1983;106(5 Pt 1):1121–1132. doi:10.1016/0002-8703(83)90661-0
  46. Heparin Sodium Injection, USP — US prescribing information (Clinical Pharmacology — half-life 0.5–2 h, hepatic/reticuloendothelial clearance; Overdosage — protamine neutralization). Pfizer/Hospira. pfizermedical.com
  47. Vaughn GR, Moore JW, Mallula KK, Lamberti JJ, El-Said HG. Transcatheter stenting of the systemic-to-pulmonary artery shunt: a 7-year experience from a single tertiary center. Catheter Cardiovasc Interv. 2015;86(3):454–462. doi:10.1002/ccd.25926
  48. Patange A, Blake J, Gowda S. Complete Blalock-Taussig shunt obstruction in < 24 hours post-operative period in a neonate treated emergently using transcatheter angioplasty and low dose local recombinant TPA. Catheter Cardiovasc Interv. 2014;83(6):964–967. doi:10.1002/ccd.25281
  49. Abu-Osba YK, Galal O, Manasra K, Rejjal A. Treatment of severe persistent pulmonary hypertension of the newborn with magnesium sulphate. Arch Dis Child. 1992;67(1 Spec No):31–35. doi:10.1136/adc.67.1_spec_no.31
  50. Monagle P, Chan AKC, Goldenberg NA, et al. Antithrombotic therapy in neonates and children: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012;141(2 Suppl):e737S–e801S. doi:10.1378/chest.11-2308
  51. Gewitz MH, Baltimore RS, Tani LY, et al. Revision of the Jones criteria for the diagnosis of acute rheumatic fever in the era of Doppler echocardiography: a scientific statement from the American Heart Association. Circulation. 2015;131(20):1806–1818. doi:10.1161/CIR.0000000000000205
  52. Carapetis JR, Beaton A, Cunningham MW, et al. Acute rheumatic fever and rheumatic heart disease. Nat Rev Dis Primers. 2016;2:15084. doi:10.1038/nrdp.2015.84
  53. Gerber MA, Baltimore RS, Eaton CB, et al. Prevention of rheumatic fever and diagnosis and treatment of acute streptococcal pharyngitis: a scientific statement from the American Heart Association. Circulation. 2009;119(11):1541–1551. doi:10.1161/CIRCULATIONAHA.109.191959
  54. RHDAustralia (ARF/RHD writing group). The 2020 Australian guideline for prevention, diagnosis and management of acute rheumatic fever and rheumatic heart disease. 3rd ed. Darwin: Menzies School of Health Research; 2020. Summary: Ralph AP, Noonan S, Wade V, Currie BJ. Med J Aust. 2021;214(5):220–227. doi:10.5694/mja2.50851
  55. Adler Y, Charron P, Imazio M, et al. 2015 ESC guidelines for the diagnosis and management of pericardial diseases. Eur Heart J. 2015;36(42):2921–2964. doi:10.1093/eurheartj/ehv318
  56. Schulz-Menger J, Collini V, Gröschel J, et al. 2025 ESC Guidelines for the management of myocarditis and pericarditis. Eur Heart J. 2025;46(40):3952–4041. doi:10.1093/eurheartj/ehaf192
  57. Adler Y, Ristić AD, Imazio M, et al. Cardiac tamponade. Nat Rev Dis Primers. 2023;9(1):36. doi:10.1038/s41572-023-00446-1
  58. COLCRYS (colchicine) tablets — US prescribing information (§4; §5.3; §7 Table 1). Takeda; label file 2019. www.accessdata.fda.gov
  59. Baltimore RS, Gewitz M, Baddour LM, et al. Infective endocarditis in childhood: 2015 update: a scientific statement from the American Heart Association. Circulation. 2015;132(15):1487–1515. doi:10.1161/CIR.0000000000000298
  60. Holland TL, Baddour LM, Bayer AS, Hoen B, Miro JM, Fowler VG. Infective endocarditis. Nat Rev Dis Primers. 2016;2:16059. doi:10.1038/nrdp.2016.59
  61. Gupta S, Sakhuja A, McGrath E, Asmar B. Trends, microbiology, and outcomes of infective endocarditis in children during 2000–2010 in the United States. Congenit Heart Dis. 2017;12(2):196–201. doi:10.1111/chd.12425
  62. Li JS, Sexton DJ, Mick N, et al. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. Clin Infect Dis. 2000;30(4):633–638. doi:10.1086/313753
  63. Lamas CC, Eykyn SJ. Suggested modifications to the Duke criteria for the clinical diagnosis of native valve and prosthetic valve endocarditis: analysis of 118 pathologically proven cases. Clin Infect Dis. 1997;25(3):713–719. doi:10.1086/513765
  64. Fowler VG, Durack DT, Selton‑Suty C, et al. The 2023 Duke‑ISCVID criteria for infective endocarditis: updating the modified Duke criteria. Clin Infect Dis. 2023;77(4):518–526. doi:10.1093/cid/ciad271
  65. Delgado V, Ajmone Marsan N, de Waha S, et al. 2023 ESC guidelines for the management of endocarditis. Eur Heart J. 2023;44(39):3948–4042. doi:10.1093/eurheartj/ehad193
  66. Wilson WR, Gewitz M, Lockhart PB, et al. Prevention of viridans group streptococcal infective endocarditis: a scientific statement from the American Heart Association. Circulation. 2021;143(20):e963–e978. doi:10.1161/CIR.0000000000000969
  67. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Circulation. 2007;116(15):1736–1754. doi:10.1161/CIRCULATIONAHA.106.183095
  68. Pantell RH, Roberts KB, Adams WG, et al. Evaluation and Management of Well‑Appearing Febrile Infants 8 to 60 Days Old (AAP). Pediatrics. 2021;148(2):e2021052228. doi:10.1542/peds.2021-052228
  69. Burstein B, Lirette MP, Beck C, Chauvin‑Kimoff L, Chan K; Canadian Pediatric Society, Acute Care Committee. Management of well‑appearing febrile young infants aged ≤ 90 days. Paediatr Child Health. 2024;29(1):50–66. doi:10.1093/pch/pxad085. Online version updated 27 May 2026: cps.ca
  70. Burstein B, Waterfield T, Umana E, Xie J, Kuppermann N. Prediction of bacteremia and bacterial meningitis among febrile infants aged 28 days or younger. JAMA. 2026;335(5):425–433. doi:10.1001/jama.2025.21454
  71. Gomez B, Mintegi S, Bressan S, et al. Validation of the “Step‑by‑Step” approach in the management of young febrile infants. Pediatrics. 2016;138(2):e20154381. doi:10.1542/peds.2015-4381
  72. Aronson PL, Shabanova V, Shapiro ED, et al. A prediction model to identify febrile infants ≤60 days at low risk of invasive bacterial infection. Pediatrics. 2019;144(1):e20183604. doi:10.1542/peds.2018-3604
  73. Dandona P, Nix D, Wilson MF, et al. Procalcitonin increase after endotoxin injection in normal subjects. J Clin Endocrinol Metab. 1994;79(6):1605–1608. doi:10.1210/jcem.79.6.7989463
  74. ZOFRAN (ondansetron) — US prescribing information (§5.2 QT prolongation; §5.3 serotonin syndrome). Novartis/Sandoz; revised 02/2025. FDA Drug Safety Communication, 32 mg IV dose, 4 Dec 2012. www.accessdata.fda.gov
  75. Lazzerini M, Wanzira H. Oral zinc for treating diarrhea in children. Cochrane Database Syst Rev. 2016;(12):CD005436. doi:10.1002/14651858.CD005436.pub5
  76. Liang Y, Zhang L, Zeng L, Gordon M, Wen J. Racecadotril for acute diarrhoea in children. Cochrane Database Syst Rev. 2019;12(12):CD009359. doi:10.1002/14651858.CD009359.pub2
  77. Lieberthal AS, Carroll AE, Chonmaitree T, et al. The Diagnosis and Management of Acute Otitis Media (AAP). Pediatrics. 2013;131(3):e964–e999. doi:10.1542/peds.2012-3488
  78. Le Saux N, Robinson JL; Canadian Pediatric Society, Infectious Diseases and Immunization Committee. Management of acute otitis media in children six months of age and older. Paediatr Child Health. 2016;21(1):39–50 (reaffirmed Nov 2024). doi:10.1093/pch/21.1.39
  79. Linder JA, Watson ME Jr, Wessels MR, et al. 2025 Clinical Practice Guideline Update by the Infectious Diseases Society of America on Group A Streptococcal (GAS) Pharyngitis: Risk Assessment Using Clinical Scoring Systems in Children and Adults. Clin Infect Dis. 2026;82(Suppl 3):i97–i104. doi:10.1093/cid/ciaf668
  80. Shulman ST, Bisno AL, Clegg HW, et al. Clinical Practice Guideline for the Diagnosis and Management of Group A Streptococcal Pharyngitis: 2012 Update (IDSA). Clin Infect Dis. 2012;55(10):e86–e102. doi:10.1093/cid/cis629
  81. Mattoo TK, Shaikh N, Nelson CP. Contemporary Management of Urinary Tract Infection in Children. Pediatrics. 2021;147(2):e2020012138. doi:10.1542/peds.2020-012138
  82. Alverson BK, Hains DS, Downs SM, et al. Clinical practice guideline for the diagnosis and treatment of urinary tract infection in children from 8 days to 5 years of age. Pediatrics. 2026;158(4):e2026078565. doi:10.1542/peds.2026-078565
  83. National Institute for Health and Care Excellence. Urinary tract infection in under 16s: diagnosis and management (NG224). London: NICE; 2022, updated May 2023. nice.org.uk/guidance/ng224
  84. Alsubaie MA, Alsuheili AZ, Aljehani MN, et al. Pediatric community‑acquired urinary tract infections due to extended‑spectrum beta‑lactamase versus non‑extended‑spectrum beta‑lactamase producing bacteria. Pediatr Int. 2023;65(1):e15620. doi:10.1111/ped.15620
  85. He XT, Chang CN, Yu CH, et al. The risk factors, antimicrobial resistance patterns, and outcomes associated with extended‑spectrum β‑lactamase‑producing pathogens in pediatric urinary tract infection. Pediatr Neonatol. 2024;65(3):242–248. doi:10.1016/j.pedneo.2023.04.021
  86. Eltai NO, Al Thani AA, Al‑Ansari K, et al. Molecular characterization of extended spectrum β‑lactamases Enterobacteriaceae causing lower urinary tract infection among pediatric population. Antimicrob Resist Infect Control. 2018;7:90. doi:10.1186/s13756-018-0381-6
  87. Jackson MA, Schutze GE; AAP Committee on Infectious Diseases. The use of systemic and topical fluoroquinolones. Pediatrics. 2016;138(5):e20162706. doi:10.1542/peds.2016-2706
  88. Amikacin 250 mg/mL Injection — Summary of Product Characteristics (§4.2 paediatric posology; §4.4 serum concentration monitoring). Hospira UK Ltd; emc (SmPC). medicines.org.uk
  89. Subcommittee on Urinary Tract Infection. Reaffirmation of AAP Clinical Practice Guideline: The Diagnosis and Management of the Initial UTI in Febrile Infants and Young Children 2–24 Months of Age. Pediatrics. 2016;138(6):e20163026. doi:10.1542/peds.2016-3026
  90. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis. 2014;59(2):e10–e52. doi:10.1093/cid/ciu444
  91. Penner J, Fanella S; Canadian Pediatric Society, Infectious Diseases and Immunization Committee. Management of community‑associated bacterial skin and soft tissue infections in children and prevention of recurrence. 2026. cps.ca
  92. Yagupsky P. Review highlights the latest research in Kingella kingae and stresses that molecular tests are required for diagnosis. Acta Paediatr. 2021;110(6):1750–1758. doi:10.1111/apa.15773
  93. Woods CR, Bradley JS, Chatterjee A, et al. Clinical practice guideline by PIDS and IDSA: 2021 guideline on diagnosis and management of acute hematogenous osteomyelitis in pediatrics. J Pediatric Infect Dis Soc. 2021;10(8):801–844. doi:10.1093/jpids/piab027
  94. Weinstock MS, Patel NA, Smith LP. Pediatric cervical lymphadenopathy. Pediatr Rev. 2018;39(9):433–443. doi:10.1542/pir.2017-0249
  95. Friedmann AM. Evaluation and management of lymphadenopathy in children. Pediatr Rev. 2008;29(2):53–60. doi:10.1542/pir.29-2-53
  96. Gaddey HL, Riegel AM. Unexplained lymphadenopathy: evaluation and differential diagnosis. Am Fam Physician. 2016;94(11):896–903. PMID 27929264 (no DOI assigned)
  97. Viard E, Gazagne C, Petit P, et al. From pathology back to the clinic: refining indications for paediatric cervical lymph node biopsy. Eur J Pediatr. 2026;185(6). doi:10.1007/s00431-026-07085-0
  98. Dulin MF, Kennard TP, Leach L, Williams R. Management of cervical lymphadenitis in children. Am Fam Physician. 2008;78(9):1097–1098. PMID 19007057 (no DOI assigned)
  99. American Academy of Pediatrics. Red Book: 2024–2027 Report of the Committee on Infectious Diseases. 33rd ed. Itasca, IL: American Academy of Pediatrics; 2024.
  100. Lindeboom JA, Kuijper EJ, Bruijnesteijn van Coppenraet ES, Lindeboom R, Prins JM. Surgical excision versus antibiotic treatment for nontuberculous mycobacterial cervicofacial lymphadenitis in children: a multicenter, randomized, controlled trial. Clin Infect Dis. 2007;44(8):1057–1064. doi:10.1086/512675
  101. Bass JW, Freitas BC, Freitas AD, et al. Prospective randomized double blind placebo-controlled evaluation of azithromycin for treatment of cat-scratch disease. Pediatr Infect Dis J. 1998;17(6):447–452. doi:10.1097/00006454-199806000-00002
  102. Locke R, Comfort R, Kubba H. When does an enlarged cervical lymph node in a child need excision? A systematic review. Int J Pediatr Otorhinolaryngol. 2014;78(3):393–401. doi:10.1016/j.ijporl.2013.12.011
  103. PDQ® Pediatric Treatment Editorial Board. Childhood Hodgkin Lymphoma Treatment (PDQ®)–Health Professional Version. Bethesda, MD: National Cancer Institute; updated April 2025. cancer.gov/types/lymphoma/hp/child-hodgkin-treatment-pdq
  104. National Institute for Health and Care Excellence. Suspected cancer: recognition and referral (NG12). London: NICE; 2015, last reviewed May 2025. nice.org.uk/guidance/ng12
  105. Soldes OS, Younger JG, Hirschl RB. Predictors of malignancy in childhood peripheral lymphadenopathy. J Pediatr Surg. 1999;34(10):1447–1452. doi:10.1016/s0022-3468(99)90101-x
  106. Falk N, Joseph R, Dieujuste M. Lymphadenopathy: evaluation and differential diagnosis. Am Fam Physician. 2025;112(3):286–293. PMID 40961306 (no DOI assigned)
  107. Barmayehvar B, Keay AAR, Elsegood R, Parmar A. Paediatric cervical lymphadenopathy: an evidence‑based approach for GPs. Br J Gen Pract. 2026;76(764):137–140. doi:10.3399/BJGP.2025.0666
  108. Farndon S, Behjati S, Jonas N, Messahel B. How to use… lymph node biopsy in paediatrics. Arch Dis Child Educ Pract Ed. 2017;102(5):244–248. doi:10.1136/archdischild-2015-309634
  109. McCrindle BW, Rowley AH, Newburger JW, et al. Diagnosis, Treatment, and Long‑Term Management of Kawasaki Disease (AHA). Circulation. 2017;135(17):e927–e999. doi:10.1161/CIR.0000000000000484
  110. Tan A, Nolan JA. Anesthesia for children with anterior mediastinal masses. Paediatr Anaesth. 2022;32(1):4–9. doi:10.1111/pan.14319
  111. National Institute for Health and Care Excellence. Fever in under 5s: assessment and initial management (NG143). London: NICE; 2019, updated March 2024. nice.org.uk/guidance/ng143
  112. Sullivan JE, Farrar HC; American Academy of Pediatrics, Section on Clinical Pharmacology and Therapeutics, Committee on Drugs. Fever and antipyretic use in children. Pediatrics. 2011;127(3):580–587. doi:10.1542/peds.2010-3852
  113. OFIRMEV (acetaminophen) injection — US prescribing information (§2.2 dosing: adults and adolescents ≥50 kg; adults and adolescents <50 kg and children 2–12 years). Mallinckrodt Hospital Products; revised 03/2018. mallinckrodt.com
  114. Hay AD, Costelloe C, Redmond NM, et al. Paracetamol plus ibuprofen for the treatment of fever in children (PITCH): randomized controlled trial. BMJ. 2008;337:a1302. doi:10.1136/bmj.a1302
  115. Thompson MJ, Ninis N, Perera R, et al. Clinical recognition of meningococcal disease in children and adolescents. Lancet. 2006;367(9508):397‑403. doi:10.1016/S0140-6736(06)67932-4
  116. National Institute for Health and Care Excellence. Meningitis (bacterial) and meningococcal disease: recognition, diagnosis and management (NG240). London: NICE; March 2024. nice.org.uk/guidance/ng240
  117. Georgesen C, Fox LP, Harp J. Retiform purpura: a diagnostic approach. J Am Acad Dermatol. 2020;82(4):783–796. doi:10.1016/j.jaad.2019.07.112
  118. De Rose DU, Bosco A, Braguglia A, et al. Neonatal herpes simplex virus infection: from the maternal infection to the child outcome. J Med Virol. 2023;95(8):e29024. doi:10.1002/jmv.29024
  119. Gill PJ, Buba M, Krueger C, Wolter NE, Reginald YA; Canadian Paediatric Society, Hospital Paediatrics Section. Preseptal and orbital cellulitis in otherwise healthy children and youth. Paediatr Child Health. 2026;31(6):670–675. doi:10.1093/pch/pxag024 · cps.ca
  120. Kornelsen E, Mahant S, Parkin P, et al. Corticosteroids for periorbital and orbital cellulitis. Cochrane Database Syst Rev. 2021;4(4):CD013535. doi:10.1002/14651858.CD013535.pub2
  121. Tieder JS, Bonkowsky JL, Etzel RA, et al. Brief Resolved Unexplained Events (formerly ALTE) and evaluation of lower‑risk infants: AAP clinical practice guideline. Pediatrics. 2016;137(5):e20160590. doi:10.1542/peds.2016-0590
  122. Tieder JS, Sullivan E, Stephans A, et al; Brief Resolved Unexplained Event Research and Quality Improvement Network. Risk Factors and Outcomes After a Brief Resolved Unexplained Event: A Multicenter Study. Pediatrics. 2021;148(1):e2020036095. doi:10.1542/peds.2020-036095
  123. American College of Obstetricians and Gynecologists. Committee Opinion No. 785: Screening and management of bleeding disorders in adolescents with heavy menstrual bleeding. Obstet Gynecol. 2019;134(3):e71–e83. doi:10.1097/AOG.0000000000003411
  124. American College of Obstetricians and Gynecologists. Committee Opinion No. 760: Dysmenorrhea and endometriosis in the adolescent. Obstet Gynecol. 2018;132(6):e249–e258. doi:10.1097/AOG.0000000000002978
  125. American College of Obstetricians and Gynecologists. Committee Opinion No. 651: Menstruation in girls and adolescents: using the menstrual cycle as a vital sign (reaffirmed 2025). Obstet Gynecol. 2015;126(6):e143–e146. doi:10.1097/AOG.0000000000001215
  126. Klein DA, Sylvester JE, Paradise SL. Amenorrhea: a practical approach to diagnosis and management. Am Fam Physician. 2026;114(1):72–85. aafp.org
  127. LYSTEDA (tranexamic acid) tablets — US prescribing information (§2 dosage for cyclic heavy menstrual bleeding; §8.4 pediatric use). Ferring/Xanodyne; 2009 (NDA 022430). www.accessdata.fda.gov
  128. CYKLOKAPRON (tranexamic acid) injection and tablets — US prescribing information (dosage and administration; pediatric use). Pfizer; revised January 2026. labeling.pfizer.com
  129. State of Kuwait. Law No. 14 of 2019 on Mental Health. Official Gazette (Kuwait Al‑Youm), 2019.
  130. Hampl SE, Hassink SG, Skinner AC, et al. Clinical Practice Guideline for the Evaluation and Treatment of Children and Adolescents With Obesity. Pediatrics. 2023;151(2):e2022060640. doi:10.1542/peds.2022-060640
  131. Gaeta F, Conti V, Pepe A, Vajro P, Filippelli A, Mandato C. Drug dosing in children with obesity: a narrative updated review. Ital J Pediatr. 2022;48(1):168. doi:10.1186/s13052-022-01361-z
  132. Glaser N, Fritsch M, Priyambada L, et al. ISPAD Clinical Practice Consensus Guidelines 2022: Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatr Diabetes. 2022;23(7):835–856. doi:10.1111/pedi.13406
  133. Perry DC, Metcalfe D, Lane S, Turner S. Childhood obesity and slipped capital femoral epiphysis. Pediatrics. 2018;142(5):e20181067. doi:10.1542/peds.2018-1067
  134. US Food and Drug Administration. FDA Drug Safety Communication: FDA restricts use of prescription codeine pain and cough medicines and tramadol pain medicines in children; recommends against use in breastfeeding women. 20 Apr 2017. fda.gov
  135. Centers for Disease Control and Prevention. Pertussis (whooping cough): postexposure antimicrobial prophylaxis. Atlanta: CDC; reviewed 2 Dec 2025. cdc.gov/pertussis
  136. Cohen E, Kuo DZ, Agrawal R, et al. Children with medical complexity: an emerging population for clinical and research initiatives. Pediatrics. 2011;127(3):529–538. doi:10.1542/peds.2010-0910
  137. Kuo DZ, Houtrow AJ; Council on Children With Disabilities. Recognition and management of medical complexity. Pediatrics. 2016;138(6):e20163021. doi:10.1542/peds.2016-3021
  138. Resuscitation Council UK. Paediatric life support (basic and advanced). 2025 Resuscitation Guidelines. London: Resuscitation Council UK; 27 Oct 2025. resus.org.uk
  139. Doherty C, Neal R, English C, et al. Multidisciplinary guidelines for the management of paediatric tracheostomy emergencies. Anaesthesia. 2018;73(11):1400–1417. doi:10.1111/anae.14307
  140. Sherman JM, Davis S, Albamonte-Petrick S, et al. Care of the child with a chronic tracheostomy. Am J Respir Crit Care Med. 2000;161(1):297–308. doi:10.1164/ajrccm.161.1.ats1-00
  141. Mitchell RB, Hussey HM, Setzen G, et al. Clinical consensus statement: tracheostomy care. Otolaryngol Head Neck Surg. 2013;148(1):6–20. doi:10.1177/0194599812460376
  142. Smiths Medical. Bivona® TTS™ neonatal and pediatric tracheostomy tubes — instructions for use (MR safety information; cuff inflation with sterile water). Document PKG‑DFU‑PNT‑2, Rev 004. Smiths Medical; 2013. manufacturer IFU (PDF)
  143. McGrath BA, Bates L, Atkinson D, Moore JA; National Tracheostomy Safety Project. Multidisciplinary guidelines for the management of tracheostomy and laryngectomy airway emergencies. Anaesthesia. 2012;67(9):1025–1041. doi:10.1111/j.1365-2044.2012.07217.x
  144. Grant CA, Dempsey G, Harrison J, Jones T. Tracheo‑innominate artery fistula after percutaneous tracheostomy: three case reports and a clinical review. Br J Anaesth. 2006;96(1):127–131. doi:10.1093/bja/aei282
  145. Lee DJ, Yang W, Propst EJ, et al. Tracheo‑innominate fistula in children: a systematic review of literature. Laryngoscope. 2020;130(1):217–224. doi:10.1002/lary.27765
  146. Amin R, Agarwal A, Chiang J, et al. Care of Infants and Children with Tracheostomies: an Official American Thoracic Society Clinical Practice Guideline. Am J Respir Crit Care Med. 2025;211(11):2001–2020. doi:10.1164/rccm.202508-2055ST
  147. Morrison JM, Hassan A, Kysh L, et al. Diagnosis, management, and outcomes of pediatric tracheostomy‑associated infections: a scoping review. Pediatr Pulmonol. 2022;57(5):1145–1156. doi:10.1002/ppul.25873
  148. Volsko TA, Parker SW, Deakins K, et al. AARC Clinical Practice Guideline: Management of Pediatric Patients With Tracheostomy in the Acute Care Setting. Respir Care. 2021;66(1):144–155. doi:10.4187/respcare.08137
  149. Homan M, Hauser B, Romano C, et al. Percutaneous endoscopic gastrostomy in children: an update to the ESPGHAN position paper. J Pediatr Gastroenterol Nutr. 2021;73(3):415–426. doi:10.1097/MPG.0000000000003207
  150. Bhambani S, Phan TH, Brown L, Thorp AW. Replacement of dislodged gastrostomy tubes after stoma dilation in the pediatric emergency department. West J Emerg Med. 2017;18(4):770–774. doi:10.5811/westjem.2017.3.31796
  151. NHS Improvement. Patient safety alert NHS/PSA/RE/2016/006: Nasogastric tube misplacement — continuing risk of death and severe harm (gastric aspirate pH 1–5.5 or X‑ray before use). London: NHS Improvement; 22 July 2016. england.nhs.uk
  152. Watson J, McGuire W. Nasal versus oral route for placing feeding tubes in preterm or low birth weight infants. Cochrane Database Syst Rev. 2013;(2):CD003952. doi:10.1002/14651858.CD003952.pub3
  153. Klang MG. Developing guidance for feeding tube administration of oral medications. JPEN J Parenter Enteral Nutr. 2023;47(4):519–540. doi:10.1002/jpen.2490
  154. Extracorporeal Life Support Organization (ELSO). ELSO general guidelines for all ECLS cases. Version 1.4. Ann Arbor (MI): ELSO; August 2017. elso.org
  155. Brown G, Moynihan KM, Deatrick KB, et al. Extracorporeal Life Support Organization (ELSO): guidelines for pediatric cardiac failure. ASAIO J. 2021;67(5):463–475. doi:10.1097/MAT.0000000000001431
  156. Extracorporeal Life Support Organization (ELSO). ELSO guidelines for pediatric respiratory failure (Oct 2020) and pediatric cardiac failure (May 2021). Ann Arbor (MI): ELSO. elso.org
  157. Wild KT, Rintoul N, Kattan J, Gray B. Extracorporeal Life Support Organization (ELSO): guidelines for neonatal respiratory failure. ASAIO J. 2020;66(5):463–470. doi:10.1097/MAT.0000000000001153
  158. Ijsselstijn H, Schiller RM, Holder C, Shappley RKH, Wray J, Hoskote A. Extracorporeal Life Support Organization (ELSO) guidelines for follow-up after neonatal and pediatric extracorporeal membrane oxygenation. ASAIO J. 2021;67(9):955–963. doi:10.1097/MAT.0000000000001525
  159. Manning JC, Pinto NP, Rennick JE, Colville G, Curley MAQ. Conceptualizing Post Intensive Care Syndrome in Children — the PICS‑p Framework. Pediatr Crit Care Med. 2018;19(4):298–300. doi:10.1097/PCC.0000000000001476
  160. Chareyre J, Pouletty M, Morin L, et al. Diagnosis and management of children with post-intensive care syndrome in paediatrics: clinical practice guidelines by the French National Authority for Health (HAS). Ann Intensive Care. 2026;16:100097. doi:10.1016/j.aicoj.2026.100097
  161. Pande CK, Risen S, LaRosa JM, Kudchadkar SR. Post intensive care syndrome in pediatrics — what the general pediatrician needs to know about life after critical illness. Pediatr Rev. 2026;47(10):557–567. doi:10.1542/pir.2024-006723
  162. Killien EY, Maddux AB, Tse SM, Watson RS; Second Pediatric Acute Lung Injury Consensus Conference (PALICC-2) Group on behalf of the Pediatric Acute Lung Injury and Sepsis Investigators (PALISI) Network. Outcomes of children surviving pediatric acute respiratory distress syndrome: from the Second Pediatric Acute Lung Injury Consensus Conference. Pediatr Crit Care Med. 2023;24(2 Suppl 1):S28–S44. doi:10.1097/PCC.0000000000003157
  163. Colville G, Kerry S, Pierce C. Children’s factual and delusional memories of intensive care. Am J Respir Crit Care Med. 2008;177(9):976–982. doi:10.1164/rccm.200706-857OC
  164. Bone MF, Feinglass JM, Goodman DM. Risk factors for acquiring functional and cognitive disabilities during admission to a PICU. Pediatr Crit Care Med. 2014;15(7):640–648. doi:10.1097/PCC.0000000000000199
  165. Woolgar FA, Wilcoxon L, Pathan N, et al. Screening for factors influencing parental psychological vulnerability during a child’s PICU admission. Pediatr Crit Care Med. 2022;23(4):286–295. doi:10.1097/PCC.0000000000002905
  166. Rennick JE, Dougherty G, Dryden-Palmer K, et al. The Caring Intensively Study: three-year follow-up findings from a mixed methods study of children’s psychological and behavioral responses after PICU hospitalization. Pediatr Crit Care Med. 2025;26(4):e516–e530. doi:10.1097/PCC.0000000000003701
  167. Ahmedzai S, Balfour‑Lynn IM, Bewick T, et al.; British Thoracic Society Standards of Care Committee. Managing passengers with stable respiratory disease planning air travel: British Thoracic Society recommendations. Thorax. 2011;66(Suppl 1):i1–i30. doi:10.1136/thoraxjnl-2011-200295
  168. Israëls J, Nagelkerke AF, Markhorst DG, van Heerde M. Fitness to fly in the paediatric population, how to assess and advice. Eur J Pediatr. 2018;177(5):633–639. doi:10.1007/s00431-018-3119-9
  169. Coker RK, Armstrong A, Church AC, et al. BTS clinical statement on air travel for passengers with respiratory disease. Thorax. 2022;77(4):329–350. doi:10.1136/thoraxjnl-2021-218110
  170. State of Kuwait, Ministry of Health. Aeromedical evacuation & transport policy (A‑ADM‑014). Kuwait: MOH; 2025 (effective Oct 2025; review 2027).
  171. Federal Aviation Administration. PackSafe: oxygen (compressed or liquid). Washington (DC): FAA; updated 13 April 2026. faa.gov/hazmat/packsafe/oxygen-compressed-or-liquid
  172. Royal College of Physicians. National Early Warning Score (NEWS) 2: standardising the assessment of acute‑illness severity in the NHS. Updated report of a working party. London: RCP; 2017. rcp.ac.uk (executive summary PDF)
  173. Desmond M, von Ungern‑Sternberg BS. Pediatric endotracheal tube cuff management at altitude: implications for aeromedical retrieval and other austere environments. Paediatr Anaesth. 2025;35(7):504–510. doi:10.1111/pan.15123
  174. TREKK (Translating Emergency Knowledge for Kids). Pediatric diabetic ketoacidosis (DKA) algorithm, version 2.0. Winnipeg: TREKK; January 2023. trekk.ca
  175. Kuppermann N, Ghetti S, Schunk JE, et al. (PECARN) Clinical trial of fluid infusion rates for pediatric DKA. N Engl J Med. 2018;378(24):2275–2287. doi:10.1056/NEJMoa1716816
  176. Kuwait PICUs Taskforce. PICU Management of Diabetic Ketoacidosis (DKA). Version 2.0. Kuwait Ministry of Health; November 2025.
  177. Speiser PW, Arlt W, Auchus RJ, et al. Congenital Adrenal Hyperplasia Due to Steroid 21‑Hydroxylase Deficiency: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2018;103(11):4043–4088. doi:10.1210/jc.2018-01865
  178. Bornstein SR, Allolio B, Arlt W, et al. Diagnosis and treatment of primary adrenal insufficiency: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2016;101(2):364–389. doi:10.1210/jc.2015-1710
  179. Mushtaq T, Ali SR, Boulos N, et al. Emergency and perioperative management of adrenal insufficiency in children and young people: British Society for Paediatric Endocrinology and Diabetes consensus guidance. Arch Dis Child. 2023;108(11):871–878. doi:10.1136/archdischild-2022-325156
  180. Thornton PS, Stanley CA, De León DD, Harris D, Haymond MW, Hussain K, 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. doi:10.1016/j.jpeds.2015.03.057
  181. Lehnhardt A, Kemper MJ. Pathogenesis, diagnosis and management of hyperkalemia. Pediatr Nephrol. 2011;26(3):377–384. doi:10.1007/s00467-010-1699-3
  182. Moritz ML, Ayus JC. New aspects in the pathogenesis, prevention, and treatment of hyponatremic encephalopathy in children. Pediatr Nephrol. 2010;25(7):1225–1238. doi:10.1007/s00467-009-1323-6
  183. National Institute for Health and Care Excellence. Intravenous fluid therapy in children and young people in hospital (NG29). London: NICE; 2015, updated June 2020; fluid‑bolus recommendation amended October 2022. nice.org.uk/guidance/ng29
  184. National Institute for Health and Care Excellence. Diarrhoea and vomiting caused by gastroenteritis in under 5s: diagnosis and management (CG84). London: NICE; 2009. nice.org.uk/guidance/cg84
  185. Calcium Gluconate 10% w/v Injection BP — Summary of Product Characteristics (§4.2 paediatric posology; §4.4 extravasation and monitoring). B. Braun Melsungen AG; emc (SmPC), revised 7 Mar 2024. medicines.org.uk/emc/product/15226
  186. Huang CL, Kuo E. Mechanism of hypokalemia in magnesium deficiency. J Am Soc Nephrol. 2007;18(10):2649–2652. doi:10.1681/ASN.2007070792
  187. Suh SM, Tashjian AH Jr, Matsuo N, et al. Pathogenesis of hypocalcemia in primary hypomagnesemia: normal end‑organ responsiveness to parathyroid hormone, impaired parathyroid gland function. J Clin Invest. 1973;52(1):153–160. doi:10.1172/JCI107159
  188. Spasovski G, Vanholder R, Allolio B, et al; Hyponatremia Guideline Development Group. Clinical practice guideline on diagnosis and treatment of hyponatremia. Eur J Endocrinol. 2014;170(3):G1–G47. doi:10.1530/EJE-13-1020
  189. Davies JH, Shaw NJ. Investigation and management of hypercalcaemia in children. Arch Dis Child. 2012;97(6):533–538. doi:10.1136/archdischild-2011-301284
  190. Major P, Lortholary A, Hon J, et al. Zoledronic acid is superior to pamidronate in the treatment of hypercalcemia of malignancy: a pooled analysis of two randomized, controlled clinical trials. J Clin Oncol. 2001;19(2):558–567. doi:10.1200/JCO.2001.19.2.558
  191. Ross DS, Burch HB, Cooper DS, et al. 2016 American Thyroid Association guidelines for diagnosis and management of hyperthyroidism and other causes of thyrotoxicosis. Thyroid. 2016;26(10):1343–1421. doi:10.1089/thy.2016.0229
  192. Mooij CF, Cheetham TD, Verburg FA, et al. 2022 European Thyroid Association guideline for the management of pediatric Graves’ disease. Eur Thyroid J. 2022;11(1):e210073. doi:10.1530/ETJ-21-0073
  193. Lee SY, Modzelewski KL, Law AC, Walkey AJ, Pearce EN, Bosch NA. Comparison of propylthiouracil vs methimazole for thyroid storm in critically ill patients. JAMA Netw Open. 2023;6(4):e238655. doi:10.1001/jamanetworkopen.2023.8655
  194. Häberle J, Burlina A, Chakrapani A, et al. Suggested guidelines for the diagnosis and management of urea cycle disorders: first revision. J Inherit Metab Dis. 2019;42(6):1192–1230. doi:10.1002/jimd.12100
  195. Forny P, Hörster F, Ballhausen D, et al. Guidelines for the diagnosis and management of methylmalonic acidaemia and propionic acidaemia: first revision. J Inherit Metab Dis. 2021;44(3):566–592. doi:10.1002/jimd.12370
  196. Servais A, Abi‑Wardé MT, Arnoux JB, et al. Management of acute metabolic decompensation in maple syrup urine disease: guidance based on international clinical practice. Orphanet J Rare Dis. 2026;21(1). doi:10.1186/s13023-026-04418-y
  197. Shah SM, Khanna CL. Ophthalmic emergencies for the clinician. Mayo Clin Proc. 2020;95(5):1050–1058. doi:10.1016/j.mayocp.2020.03.018
  198. American Academy of Pediatrics, Section on Ophthalmology; American Association for Pediatric Ophthalmology and Strabismus; American Academy of Ophthalmology; American Association of Certified Orthoptists. Red reflex examination in neonates, infants, and children. Pediatrics. 2008;122(6):1401–1404. doi:10.1542/peds.2008-2624
  199. Faiq M, Sharma R, Dada R, et al. Genetic, biochemical and clinical insights into primary congenital glaucoma. J Curr Glaucoma Pract. 2013;7(2):66–84. doi:10.5005/jp-journals-10008-1140
  200. Christian CW, Levin AV; AAP Council on Child Abuse and Neglect, Section on Ophthalmology; American Association of Certified Orthoptists; American Association for Pediatric Ophthalmology and Strabismus; American Academy of Ophthalmology. The eye examination in the evaluation of child abuse. Pediatrics. 2018;142(2):e20181411. doi:10.1542/peds.2018-1411
  201. Fouad AF, Abbott PV, Tsilingaridis G, et al. International Association of Dental Traumatology guidelines for the management of traumatic dental injuries: 2. Avulsion of permanent teeth. Dent Traumatol. 2020;36(4):331–342. doi:10.1111/edt.12573
  202. Amir J, Harel L, Smetana Z, Varsano I. Treatment of herpes simplex gingivostomatitis with aciclovir in children: a randomized double blind placebo controlled study. BMJ. 1997;314(7097):1800–1803. doi:10.1136/bmj.314.7097.1800
  203. American Academy of Pediatric Dentistry. Useful medications for oral conditions. In: The Reference Manual of Pediatric Dentistry 2025–2026. Chicago (IL): AAPD; 2025:669–677. aapd.org
  204. Lin HW, O'Neill A, Cunningham MJ. Ludwig's angina in the pediatric population. Clin Pediatr (Phila). 2009;48(6):583–587. doi:10.1177/0009922809333095
  205. McPherson T, Exton LS, Biswas S, et al. British Association of Dermatologists' guidelines for the management of Stevens‑Johnson syndrome/toxic epidermal necrolysis in children and young people, 2018. Br J Dermatol. 2019;181(1):37–54. doi:10.1111/bjd.17841
  206. Gray L, Hansen AM, Cipriano SD. Pediatric staphylococcal scalded skin syndrome: a systematic review of the literature to inform work‑up and management. Pediatr Dermatol. 2025;42(5):978–984. doi:10.1111/pde.16029
  207. Syed HA, Tsuchiya A. Eczema herpeticum. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2026 (updated Aug 2024). NBK560781
  208. Kuyucu S, Blanca‑Lopez N, Caubet JC, Moral L, et al. Clinical diagnosis and management of drug reaction with eosinophilia and systemic symptoms (DRESS) in children: an EAACI position paper. Pediatr Allergy Immunol. 2025;36(7):e70103. doi:10.1111/pai.70103
  209. Damari D, et al. Diagnosis and management of reactive infectious mucocutaneous eruption. J Hosp Med. 2025;20(11):1212–1216. doi:10.1002/jhm.70099 (PMID 40619921)
  210. Heuer R, Paulmann M, Annecke T, Behr B, et al. S3 guideline: Diagnosis and treatment of epidermal necrolysis (Stevens‑Johnson syndrome and toxic epidermal necrolysis) — Part 1: Diagnosis, initial management, and immunomodulating systemic therapy. J Dtsch Dermatol Ges. 2024;22(10):1448–1466. doi:10.1111/ddg.15515
  211. Zimmermann S, Sekula P, Venhoff M, et al. Systemic immunomodulating therapies for Stevens‑Johnson syndrome and toxic epidermal necrolysis: a systematic review and meta‑analysis. JAMA Dermatol. 2017;153(6):514–522. doi:10.1001/jamadermatol.2016.5668
  212. Ramien ML. Reactive infectious mucocutaneous eruption: Mycoplasma pneumoniae‑induced rash and mucositis and other parainfectious eruptions. Clin Exp Dermatol. 2021;46(3):420–429. doi:10.1111/ced.14404
  213. Yan S, Chen G, Zeng N, Gao C, et al. Characteristics and treatment of pediatric nasal foreign bodies with button batteries: a retrospective analysis of 176 cases. PLoS One. 2024;19(8):e0309261. doi:10.1371/journal.pone.0309261
  214. Hankey PB, Tracy M, Arganbright JM. Emerging findings for the assessment and treatment of pediatric deep neck abscesses. Curr Opin Otolaryngol Head Neck Surg. 2023;31(6):407–411. doi:10.1097/MOO.0000000000000937
  215. Children’s Hospital of Philadelphia. Ventricular shunt obstruction/infection clinical pathway — emergency, ICU and inpatient (revised Sep 2026). Philadelphia: CHOP Clinical Pathways. chop.edu
  216. Tunkel AR, Hasbun R, Bhimraj A, et al. 2017 Infectious Diseases Society of America's Clinical Practice Guidelines for Healthcare‑Associated Ventriculitis and Meningitis. Clin Infect Dis. 2017;64(6):e34–e65. doi:10.1093/cid/ciw861
  217. Kochanek PM, Tasker RC, Carney N, et al. Guidelines for the Management of Pediatric Severe Traumatic Brain Injury, Third Edition: Update of the Brain Trauma Foundation Guidelines, Executive Summary. Pediatr Crit Care Med. 2019;20(3):280–289. doi:10.1097/PCC.0000000000001736
  218. Thomson M, Amil‑Dias J, Assa A, et al. A management strategy for nonvariceal gastrointestinal bleeding in children: an ESPGHAN position paper. J Pediatr Gastroenterol Nutr. 2026;82(3):895–915. doi:10.1002/jpn3.70278
  219. Romano C, Oliva S, Martellossi S, et al. Pediatric gastrointestinal bleeding: Perspectives from the Italian Society of Pediatric Gastroenterology. World J Gastroenterol. 2017;23(8):1328–1337. doi:10.3748/wjg.v23.i8.1328
  220. Valentine SL, Bembea MM, Muszynski JA, et al; Pediatric Critical Care Transfusion and Anemia Expertise Initiative (TAXI). Consensus recommendations for RBC transfusion practice in critically ill children. Pediatr Crit Care Med. 2018;19(9):884–898. doi:10.1097/PCC.0000000000001613
  221. Ukarapol N, Poddar U, et al.; Asian Pan‑Pacific Society for Pediatric Gastroenterology, Hepatology and Nutrition. APSPGHAN statement on endoscopic variceal bleeding hemostasis. Pediatr Gastroenterol Hepatol Nutr. 2026;29(1):1–21. doi:10.5223/pghn.2026.29.1.1
  222. Villanueva C, Colomo A, Bosch A, et al. Transfusion strategies for acute upper gastrointestinal bleeding. N Engl J Med. 2013;368(1):11–21. doi:10.1056/NEJMoa1211801
  223. Taher KW, Yaseen R, Alnan M, Aburas W, Khalil H, Alabdulsalam M. Efficacy and safety of empiric treatment with omeprazole continuous infusion in critically ill children with gastrointestinal bleeding. Front Pediatr. 2024;12:1270911. doi:10.3389/fped.2024.1270911
  224. Gralnek IM, Morris J, Laursen SB, et al. Endoscopic diagnosis and management of peptic ulcer bleeding: European Society of Gastrointestinal Endoscopy (ESGE) Guideline – Update 2026. Endoscopy. 2026;58(8):899–924. doi:10.1055/a-2863-8314
  225. Eroglu Y, Emerick KM, Whitington PF, Alonso EM. Octreotide therapy for control of acute gastrointestinal bleeding in children. J Pediatr Gastroenterol Nutr. 2004;38(1):41–47. doi:10.1097/00005176-200401000-00011
  226. Gralnek IM, Stanley AJ, Morris AJ, et al. Endoscopic diagnosis and management of nonvariceal upper gastrointestinal hemorrhage (NVUGIH): European Society of Gastrointestinal Endoscopy (ESGE) Guideline – Update 2021. Endoscopy. 2021;53(3):300–332. doi:10.1055/a-1369-5274
  227. Rockey DC, Ahn C, de Melo SW Jr. Randomized pragmatic trial of nasogastric tube placement in patients with upper gastrointestinal tract bleeding. J Investig Med. 2017;65(4):759–764. doi:10.1136/jim-2016-000375
  228. Squires RH Jr, Shneider BL, Bucuvalas J, et al. Acute liver failure in children: the first 348 patients in the pediatric acute liver failure study group. J Pediatr. 2006;148(5):652–658. doi:10.1016/j.jpeds.2005.12.051
  229. Squires JE, Alonso EM, Ibrahim SH, et al. North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition Position Paper on the Diagnosis and Management of Pediatric Acute Liver Failure. J Pediatr Gastroenterol Nutr. 2022;74(1):138–158. doi:10.1097/MPG.0000000000003268
  230. Squires RH, Dhawan A, Alonso E, et al. Intravenous N‑acetylcysteine in pediatric patients with nonacetaminophen acute liver failure: a placebo‑controlled clinical trial. Hepatology. 2013;57(4):1542–1549. doi:10.1002/hep.26001
  231. Abu‑El‑Haija M, Kumar S, Quiros JA, et al. Management of Acute Pancreatitis in the Pediatric Population: A Clinical Report From the NASPGHAN Pancreas Committee. J Pediatr Gastroenterol Nutr. 2018;66(1):159–176. doi:10.1097/MPG.0000000000001715
  232. Chen HL, Taylor SA, Lee WS, et al. Diagnostic approaches for infants with cholestatic liver diseases: position paper and perspectives of the Federation of International Societies of Pediatric Gastroenterology, Hepatology, and Nutrition (FISPGHAN). J Pediatr Gastroenterol Nutr. 2025;81(5):1360–1377. doi:10.1002/jpn3.70207
  233. Fawaz R, Baumann U, Ekong U, et al. Guideline for the evaluation of cholestatic jaundice in infants: joint recommendations of the North American Society for Pediatric Gastroenterology, Hepatology, and Nutrition and the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition. J Pediatr Gastroenterol Nutr. 2017;64(1):154–168. doi:10.1097/MPG.0000000000001334
  234. Kramer RE, Lerner DG, Lin T, et al; NASPGHAN Endoscopy Committee. Management of ingested foreign bodies in children: a clinical report of the NASPGHAN Endoscopy Committee. J Pediatr Gastroenterol Nutr. 2015;60(4):562–574. doi:10.1097/MPG.0000000000000729
  235. Ledder O, Furlano R, Papadopoulou A, et al. Foreign body ingestions in children and adolescents: a position paper of the European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN) endoscopy special interest group. J Pediatr Gastroenterol Nutr. 2026;83(3):539–554. doi:10.1002/jpn3.70485
  236. Cho J, Kogosov A, Scheinfeld L, et al. What to do after it's swallowed? Management strategies after superabsorbent polymer bead ingestion: a scoping review. J Pediatr Surg. 2026;61(6):162957. doi:10.1016/j.jpedsurg.2026.162957
  237. Expert Panel on Pediatric Imaging; Meyers ML, Moore MM, Baker JB, et al. ACR Appropriateness Criteria® Ingested or Aspirated Foreign Body—Child. J Am Coll Radiol. 2026;23(4):732–747. doi:10.1016/j.jacr.2025.12.013
  238. Mubarak A, Benninga MA, Broekaert I, et al. Diagnosis, management, and prevention of button battery ingestion in childhood: a European Society for Paediatric Gastroenterology Hepatology and Nutrition position paper. J Pediatr Gastroenterol Nutr. 2021;73(1):129–136. doi:10.1097/MPG.0000000000003048
  239. Tabbers MM, DiLorenzo C, Berger MY, et al. Evaluation and treatment of functional constipation in infants and children: evidence‑based recommendations from ESPGHAN and NASPGHAN. J Pediatr Gastroenterol Nutr. 2014;58(2):258–274. doi:10.1097/MPG.0000000000000266
  240. Rodriguez L, Ambartsumyan L, Baumgartner K, et al. American Gastroenterological Association–North American Society for Pediatric Gastroenterology, Hepatology and Nutrition Pediatric Functional Constipation Clinical Care Pathway. Clin Gastroenterol Hepatol. 2026;24(10):2839–2851. doi:10.1016/j.cgh.2026.03.003
  241. National Institute for Health and Care Excellence (NICE). Constipation in children and young people: diagnosis and management. Clinical guideline [CG99]. London: NICE; 2010 (updated 2017). nice.org.uk/guidance/cg99
  242. FLEET ENEMA FOR CHILDREN (sodium phosphates) rectal enema — product label (Directions; Warnings). C.B. Fleet Co. DailyMed. dailymed.nlm.nih.gov
  243. Bekkali NLH, Hoekman DR, Liem O, et al. Polyethylene glycol 3350 with electrolytes versus polyethylene glycol 4000 for constipation: a randomized, controlled trial. J Pediatr Gastroenterol Nutr. 2018;66(1):10–15. doi:10.1097/MPG.0000000000001726
  244. Mínguez M, López Higueras A, Júdez J. Use of polyethylene glycol in functional constipation and fecal impaction. Rev Esp Enferm Dig. 2016;108(12):790–806. doi:10.17235/reed.2016.4571/2016
  245. Candy DCA, Edwards D, Geraint M. Treatment of faecal impaction with polyethylene glycol plus electrolytes (PEG+E) followed by a double‑blind comparison of PEG+E versus lactulose as maintenance therapy. J Pediatr Gastroenterol Nutr. 2006;43(1):65–70. doi:10.1097/01.mpg.0000228097.58960.e6
  246. Rosen R, Vandenplas Y, Singendonk M, et al. Pediatric Gastroesophageal Reflux Clinical Practice Guidelines: Joint NASPGHAN–ESPGHAN Recommendations. J Pediatr Gastroenterol Nutr. 2018;66(3):516–554. doi:10.1097/MPG.0000000000001889
  247. Assa A, Aloi M, Van Biervliet S, et al. Management of paediatric ulcerative colitis, part 2: Acute severe colitis—An updated evidence‑based consensus guideline from the European Society of Paediatric Gastroenterology, Hepatology and Nutrition and the European Crohn's and Colitis Organization. J Pediatr Gastroenterol Nutr. 2025;81(3):816–851. doi:10.1002/jpn3.70096 (supersedes Turner et al. 2018, JPGN 67:292–310)
  248. Turner D, Otley AR, Mack D, et al. Development, validation, and evaluation of a pediatric ulcerative colitis activity index: a prospective multicenter study. Gastroenterology. 2007;133(2):423–432. doi:10.1053/j.gastro.2007.05.029
  249. Lirette MP, Wright N, Trottier ED, Beck CE; Canadian Paediatric Society, Acute Care Committee. Management of febrile neutropenia in immunocompetent children and youth. Paediatr Child Health. 2023;28(5):324–330. doi:10.1093/pch/pxac127
  250. Hao R, Saleh M, Liang T, et al. The prevalence of serious bacterial infections in neutropenic immunocompetent febrile children. Am J Emerg Med. 2021;45:1–6. doi:10.1016/j.ajem.2021.02.017
  251. Lehrnbecher T, Robinson PD, Ammann RA, et al. Guideline for the Management of Fever and Neutropenia in Pediatric Patients With Cancer and HCT Recipients: 2023 Update. J Clin Oncol. 2023;41(9):1774–1785. doi:10.1200/JCO.22.02224
  252. Alghounaim M, Alonaizi E, Hussain E, Burhamah M. Guideline for the Management of Fever and Neutropenia in Children with Cancer or Bone Marrow Failure Syndromes. Version 4. Kuwait: NBK Children’s Hospital; 2019.
  253. Coiffier B, Altman A, Pui CH, et al. Guidelines for the management of pediatric and adult tumor lysis syndrome. J Clin Oncol. 2008;26(16):2767–2778. doi:10.1200/JCO.2007.15.0177
  254. Chan YLT, El-Sharkawi D, Shah P, et al.; British Society for Haematology. British Society for Haematology updated guidelines for the diagnosis and management of tumour lysis syndrome in adults and children with haematological malignancies: a focus on patient safety. Br J Haematol. 2025;207(4):1248–1258. doi:10.1111/bjh.70092
  255. Labonté S, Bergeron É, Laverdière I, et al. Rasburicase real‑world usage for the prevention and treatment of tumor lysis syndrome in adults and children. Ann Pharmacother. 2026;60(10):950–961. doi:10.1177/10600280251391871
  256. ELITEK (rasburicase) for injection — US prescribing information (boxed warning; §4 Contraindications). sanofi-aventis; revised 5/2025. DailyMed
  257. Brandow AM, Carroll CP, Creary S, et al. American Society of Hematology 2020 guidelines for sickle cell disease: management of acute and chronic pain. Blood Adv. 2020;4(12):2656–2701. doi:10.1182/bloodadvances.2020001851
  258. Gwarzo I, Coleman KD, McKinley K, et al. Opioid timeliness in the emergency department and hospitalizations for acute sickle cell pain. JAMA Pediatr. 2025;179(11):1194–1202. doi:10.1001/jamapediatrics.2025.2967
  259. National Heart, Lung, and Blood Institute. Evidence‑Based Management of Sickle Cell Disease: Expert Panel Report, 2014 (Quick Guide pp. 14–17). Summary: Yawn BP, Buchanan GR, Afenyi‑Annan AN, et al. JAMA. 2014;312(10):1033–1048. doi:10.1001/jama.2014.10517
  260. Chou ST, Alsawas M, Fasano RM, et al. American Society of Hematology 2020 guidelines for sickle cell disease: transfusion support. Blood Adv. 2020;4(2):327–355. doi:10.1182/bloodadvances.2019001143
  261. DeBaun MR, Jordan LC, King AA, et al. American Society of Hematology 2020 guidelines for sickle cell disease: prevention, diagnosis, and treatment of cerebrovascular disease in children and adults. Blood Adv. 2020;4(8):1554–1588. doi:10.1182/bloodadvances.2019001142
  262. Yates AM, Aygun B, Nuss R, Rogers ZR, et al.; AAP Section on Hematology/Oncology. Health supervision for children and adolescents with sickle cell disease: clinical report. Pediatrics. 2024;154(2):e2024066842. doi:10.1542/peds.2024-066842
  263. Srivastava A, Santagostino E, Dougall A, et al. WFH Guidelines for the Management of Hemophilia, 3rd edition. Haemophilia. 2020;26(Suppl 6):1–158. doi:10.1111/hae.14046
  264. Kendel NE, et al. Increasing optimal coagulation factor dosing in the pediatric emergency department: update to a quality improvement study. Haemophilia. 2024;30(2):367–374. doi:10.1111/hae.14927
  265. Neunert C, Terrell DR, Arnold DM, et al. American Society of Hematology 2019 guidelines for immune thrombocytopenia. Blood Adv. 2019;3(23):3829–3866. doi:10.1182/bloodadvances.2019000966
  266. Cyklokapron 100 mg/mL solution for injection — Summary of Product Characteristics (§4.2 paediatric posology; §4.4 haematuria from the upper urinary tract). Pfizer Ltd; emc (SmPC). medicines.org.uk/emc/product/1077/smpc
  267. Stephanos K, Dubbs SB. Pediatric Hematologic and Oncologic Emergencies. Emerg Med Clin North Am. 2021;39(3):555–571. doi:10.1016/j.emc.2021.04.007
  268. Sanz MA, Fenaux P, Tallman MS, et al. Management of acute promyelocytic leukemia: updated recommendations from an expert panel of the European LeukemiaNet. Blood. 2019;133(15):1630–1643. doi:10.1182/blood-2019-01-894980
  269. Lee HC, Strand ML, Finan E, et al.; American Heart Association and American Academy of Pediatrics. Part 5: Neonatal Resuscitation: 2025 American Heart Association and American Academy of Pediatrics Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2025;152(16 Suppl 2):S385–S423. doi:10.1161/CIR.0000000000001367
  270. Oster ME, Pinto NM, Pramanik AK, et al; AAP Section on Cardiology and Cardiac Surgery, Section on Hospital Medicine, Committee on Fetus and Newborn. Newborn Screening for Critical Congenital Heart Disease: A New Algorithm and Other Updated Recommendations: Clinical Report. Pediatrics. 2025;155(1):e2024069667. doi:10.1542/peds.2024-069667
  271. Abman SH, Hansmann G, Archer SL, et al. Pediatric Pulmonary Hypertension: Guidelines From the American Heart Association and American Thoracic Society. Circulation. 2015;132(21):2037–2099. doi:10.1161/CIR.0000000000000329
  272. The Neonatal Inhaled Nitric Oxide Study Group. Inhaled nitric oxide in full‑term and nearly full‑term infants with hypoxic respiratory failure. N Engl J Med. 1997;336(9):597–604. doi:10.1056/NEJM199702273360901
  273. Tourneux P, Rakza T, Bouissou A, Krim G, Storme L. Pulmonary circulatory effects of norepinephrine in newborn infants with persistent pulmonary hypertension. J Pediatr. 2008;153(3):345–349. doi:10.1016/j.jpeds.2008.03.007
  274. Kelly LE, Ohlsson A, Shah PS. Sildenafil for pulmonary hypertension in neonates. Cochrane Database Syst Rev. 2017;8:CD005494. doi:10.1002/14651858.CD005494.pub4
  275. Narvey MR, Marks SD; Canadian Paediatric Society, Fetus and Newborn Committee. The screening and management of newborns at risk for low blood glucose. Paediatr Child Health. 2019;24(8):536–554. doi:10.1093/pch/pxz134
  276. Harris DL, Weston PJ, Signal M, Chase JG, Harding JE. Dextrose gel for neonatal hypoglycemia (the Sugar Babies Study): a randomized, double‑blind, placebo‑controlled trial. Lancet. 2013;382(9910):2077–2083. doi:10.1016/S0140-6736(13)61645-1
  277. Ng E, Altit G, Joynt C, Radziminski N, Narvey M; Canadian Paediatric Society, Fetus and Newborn Committee. Guidelines for detection and management of hyperbilirubinemia in term and late preterm newborns (≥ 35 weeks gestational age). Paediatr Child Health. 2026;31(5):496–526. doi:10.1093/pch/pxaf034
  278. Kemper AR, Newman TB, Slaughter JL, et al. Clinical Practice Guideline Revision: Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation (AAP). Pediatrics. 2022;150(3):e2022058859. doi:10.1542/peds.2022-058859
  279. Puopolo KM, Benitz WE, Zaoutis TE; Committee on Fetus and Newborn, Committee on Infectious Diseases. Management of Neonates Born at ≥35 0/7 Weeks' Gestation With Suspected or Proven Early‑Onset Bacterial Sepsis. Pediatrics. 2018;142(6):e20182894. doi:10.1542/peds.2018-2894
  280. Shane AL, Sánchez PJ, Stoll BJ. Neonatal sepsis. Lancet. 2017;390(10104):1770–1780. doi:10.1016/S0140-6736(17)31002-4
  281. Mak GK, Shah M. Omphalitis. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2026 (updated Aug 2026). NBK513338
  282. Fraser N, Davies BW, Cusack J. Neonatal omphalitis: a review of its serious complications. Acta Paediatr. 2006;95(5):519–522. doi:10.1080/08035250600640422
  283. Stewart D, Benitz W; Committee on Fetus and Newborn. Umbilical cord care in the newborn infant. Pediatrics. 2016;138(3):e20162149. doi:10.1542/peds.2016-2149
  284. Muniraman H, Sardesai T, Sardesai S. Disorders of the umbilical cord. Pediatr Rev. 2018;39(7):332–341. doi:10.1542/pir.2017-0202
  285. Inarejos Clemente EJ, Navarro OM, Navallas Irujo M, et al. Omphalomesenteric duct anomalies in children: a multimodality overview. RadioGraphics. 2021;41(7):2090–2110. doi:10.1148/rg.2021210048
  286. Naiditch JA, Radhakrishnan J, Chin AC. Current diagnosis and management of urachal remnants. J Pediatr Surg. 2013;48(10):2148–2152. doi:10.1016/j.jpedsurg.2013.02.069
  287. Solomon‑Cohen E, Lapidoth M, Snast I, et al. Cutaneous presentations of omphalomesenteric duct remnant: a systematic review of the literature. J Am Acad Dermatol. 2019;81(5):1120–1126. doi:10.1016/j.jaad.2019.02.033
  288. Neu J, Walker WA. Necrotizing enterocolitis. N Engl J Med. 2011;364(3):255–264. doi:10.1056/NEJMra1005408
  289. Walsh MC, Kliegman RM. Necrotizing enterocolitis: treatment based on staging criteria. Pediatr Clin North Am. 1986;33(1):179–201. doi:10.1016/S0031-3955(16)34975-6
  290. Cuna AC, Reddy N, Robinson AL, Chan SS. Bowel ultrasound for predicting surgical management of necrotizing enterocolitis: a systematic review and meta-analysis. Pediatr Radiol. 2018;48(5):658–666. doi:10.1007/s00247-017-4056-x
  291. Blakely ML, Tyson JE, Lally KP, et al. Initial laparotomy versus peritoneal drainage in extremely low birthweight infants with surgical necrotizing enterocolitis or isolated intestinal perforation: a multicenter randomized clinical trial. Ann Surg. 2021;274(4):e370–e380. doi:10.1097/SLA.0000000000005099
  292. Pressler RM, Abend NS, Auvin S, et al. Treatment of seizures in the neonate: Guidelines and consensus‑based recommendations — Special report from the ILAE Task Force on Neonatal Seizures. Epilepsia. 2023;64(10):2550–2570. doi:10.1111/epi.17745
  293. Sharpe C, Reiner GE, Davis SL, et al; NEOLEV2 Investigators. Levetiracetam Versus Phenobarbital for Neonatal Seizures: A Randomized Controlled Trial. Pediatrics. 2020;145(6):e20193182. doi:10.1542/peds.2019-3182
  294. Hand I, Noble L, Abrams SA; Committee on Fetus and Newborn. Vitamin K and the Newborn Infant. Pediatrics. 2022;149(3):e2021056036. doi:10.1542/peds.2021-056036
  295. Young LW, Ounpraseuth ST, Merhar SL, et al. Eat, Sleep, Console Approach or Usual Care for Neonatal Opioid Withdrawal. N Engl J Med. 2023;388(25):2326–2337. doi:10.1056/NEJMoa2214470
  296. Hudak ML, Tan RC; Committee on Drugs; Committee on Fetus and Newborn. Neonatal drug withdrawal. Pediatrics. 2012;129(2):e540–e560. doi:10.1542/peds.2011-3212
  297. Patrick SW, Barfield WD, Poindexter BB; Committee on Fetus and Newborn, Committee on Substance Use and Prevention. Neonatal opioid withdrawal syndrome. Pediatrics. 2020;146(5):e2020029074. doi:10.1542/peds.2020-029074
  298. Engle WA; American Academy of Pediatrics Committee on Fetus and Newborn. Age terminology during the perinatal period. Pediatrics. 2004;114(5):1362–1364. doi:10.1542/peds.2004-1915
  299. Fuchs A, Guidi M, Giannoni E, et al. Population pharmacokinetic study of gentamicin in a large cohort of premature and term neonates. Br J Clin Pharmacol. 2014;78(5):1090–1101. doi:10.1111/bcp.12444
  300. Frymoyer A, Hersh AL, El-Komy MH, et al. Association between vancomycin trough concentration and area under the concentration-time curve in neonates. Antimicrob Agents Chemother. 2014;58(11):6454–6461. doi:10.1128/AAC.03620-14
  301. Välitälo PAJ, van den Anker JN, Allegaert K, et al. Novel model-based dosing guidelines for gentamicin and tobramycin in preterm and term neonates. J Antimicrob Chemother. 2015;70(7):2074–2077. doi:10.1093/jac/dkv052
  302. Frymoyer A, Stockmann C, Hersh AL, Goswami S, Keizer RJ. Individualized empiric vancomycin dosing in neonates using a model-based approach. J Pediatric Infect Dis Soc. 2019;8(2):97–104. doi:10.1093/jpids/pix109
  303. Micromedex NeoFax [online neonatal drug reference]. Ann Arbor, MI: Merative US L.P.; 2026.
  304. Paediatric Formulary Committee. BNF for Children 2025–2026. London: BMJ Group, Pharmaceutical Press and RCPCH Publications; 2025.
  305. Schmidt B, Roberts RS, Davis P, et al; Caffeine for Apnea of Prematurity Trial Group. Caffeine therapy for apnea of prematurity. N Engl J Med. 2006;354(20):2112–2121. doi:10.1056/NEJMoa054065
  306. Glauser T, Shinnar S, Gloss D, et al. Evidence‑based guideline: treatment of convulsive status epilepticus in children and adults (AES). Epilepsy Curr. 2016;16(1):48–61. doi:10.5698/1535-7597-16.1.48
  307. National Institute for Health and Care Excellence. Epilepsies in children, young people and adults (NG217). London: NICE; 2022, updated January 2025. nice.org.uk/guidance/ng217
  308. Kapur J, Elm J, Chamberlain JM, et al. Randomized trial of three anticonvulsant medications for status epilepticus (ESETT). N Engl J Med. 2019;381(22):2103–2113. doi:10.1056/NEJMoa1905795
  309. Becker LL, et al. Treatment of pediatric convulsive status epilepticus. Front Neurol. 2023;14:1175370. doi:10.3389/fneur.2023.1175370
  310. Subcommittee on Febrile Seizures, American Academy of Pediatrics. Neurodiagnostic evaluation of the child with a simple febrile seizure. Pediatrics. 2011;127(2):389–394. doi:10.1542/peds.2010-3318
  311. Steering Committee on Quality Improvement and Management, Subcommittee on Febrile Seizures; American Academy of Pediatrics. Febrile seizures: clinical practice guideline for the long‑term management of the child with simple febrile seizures. Pediatrics. 2008;121(6):1281–1286. doi:10.1542/peds.2008-0939
  312. Le Saux N; Canadian Paediatric Society, Infectious Diseases and Immunization Committee. Guidelines for the management of suspected and confirmed bacterial meningitis in Canadian children older than one month of age. Paediatr Child Health. 2014;19(3):141–152. doi:10.1093/pch/19.3.141
  313. Tunkel AR, Hartman BJ, Kaplan SL, et al. Practice guidelines for the management of bacterial meningitis. Clin Infect Dis. 2004;39(9):1267–1284. doi:10.1086/425368
  314. Venkatesan A, Tunkel AR, Bloch KC, et al; International Encephalitis Consortium. Case definitions, diagnostic algorithms, and priorities in encephalitis: consensus statement. Clin Infect Dis. 2013;57(8):1114–1128. doi:10.1093/cid/cit458
  315. Nigrovic LE, Kuppermann N, Macias CG, et al. Clinical prediction rule for identifying children with cerebrospinal fluid pleocytosis at very low risk of bacterial meningitis. JAMA. 2007;297(1):52–60. doi:10.1001/jama.297.1.52
  316. Nigrovic LE, Kuppermann N, Malley R. Development and validation of a multivariable predictive model to distinguish bacterial from aseptic meningitis in children in the post-Haemophilus influenzae era. Pediatrics. 2002;110(4):712–719. doi:10.1542/peds.110.4.712
  317. Nigrovic LE, Malley R, Kuppermann N. Meta-analysis of bacterial meningitis score validation studies. Arch Dis Child. 2012;97(9):799–805. doi:10.1136/archdischild-2012-301798
  318. Rees CA, Cruz AT, Freedman SB, et al. Application of the bacterial meningitis score for infants aged 0 to 60 days. J Pediatric Infect Dis Soc. 2019;8(6):559–562. doi:10.1093/jpids/piy126
  319. Rybak MJ, Le J, Lodise TP, et al. Executive Summary: Therapeutic Monitoring of Vancomycin for Serious Methicillin‑Resistant Staphylococcus aureus Infections: A Revised Consensus Guideline and Review (ASHP/IDSA/PIDS/SIDP). J Pediatric Infect Dis Soc. 2020;9(3):281–284. doi:10.1093/jpids/piaa057
  320. Berry I, Rubis AB, Howie RL, et al. Selection of antibiotics as prophylaxis for close contacts of patients with meningococcal disease in areas with ciprofloxacin resistance — United States, 2024. MMWR Morb Mortal Wkly Rep. 2024;73(5):99–103. doi:10.15585/mmwr.mm7305a2
  321. Wilne S, Collier J, Kennedy C, Koller K, Grundy R, Walker D. Presentation of childhood CNS tumours: a systematic review and meta‑analysis. Lancet Oncol. 2007;8(8):685–695. doi:10.1016/S1470-2045(07)70207-3
  322. Wilne S, Koller K, Collier J, et al. The diagnosis of brain tumours in children: a guideline to assist healthcare professionals in the assessment of children who may have a brain tumour (RCPCH guideline; basis of the HeadSmart campaign). Arch Dis Child. 2010;95(7):534–539. doi:10.1136/adc.2009.162057
  323. Brouwer MC, Tunkel AR, McKhann GM 2nd, van de Beek D. Brain abscess. N Engl J Med. 2014;371(5):447‑456. doi:10.1056/NEJMra1301635
  324. Bodilsen J, D'Alessandris QG, Humphreys H, et al; ESCMID Study Group for Infections of the Brain (ESGIB). European Society of Clinical Microbiology and Infectious Diseases guidelines on diagnosis and treatment of brain abscess in children and adults. Clin Microbiol Infect. 2024;30(1):66‑89. doi:10.1016/j.cmi.2023.08.016
  325. van Doorn PA, Van den Bergh PYK, Hadden RDM, et al. European Academy of Neurology/Peripheral Nerve Society Guideline on diagnosis and treatment of Guillain‑Barré syndrome. Eur J Neurol. 2023;30(12):3646–3674. doi:10.1111/ene.16073
  326. Lawn ND, Fletcher DD, Henderson RD, Wolter TD, Wijdicks EF. Anticipating mechanical ventilation in Guillain‑Barré syndrome. Arch Neurol. 2001;58(6):893–898. doi:10.1001/archneur.58.6.893
  327. Global Polio Eradication Initiative (World Health Organization). Surveillance indicators: acute flaccid paralysis (AFP) surveillance and stool specimen adequacy. Geneva: WHO/GPEI. polioeradication.org
  328. Birnkrant DJ, Bushby K, Bann CM, et al. Diagnosis and management of Duchenne muscular dystrophy, part 2: respiratory, cardiac, bone health, and orthopaedic management. Lancet Neurol. 2018;17(4):347–361. doi:10.1016/S1474-4422(18)30025-5
  329. Khan A, Frazer-Green L, Amin R, et al. Respiratory management of patients with neuromuscular weakness: an American College of Chest Physicians clinical practice guideline and expert panel report. Chest. 2023;164(2):394–413. doi:10.1016/j.chest.2023.03.011
  330. Racca F, Conti E, Racca G, et al. A multidisciplinary approach to the anesthetic management of patients with Duchenne muscular dystrophy. Pediatr Pulmonol. 2026;61(10):e71833. doi:10.1002/ppul.71833
  331. Feingold B, Mahle WT, Auerbach S, et al. Management of cardiac involvement associated with neuromuscular diseases: a scientific statement from the American Heart Association. Circulation. 2017;136(13):e200–e231. doi:10.1161/CIR.0000000000000526
  332. Birnkrant DJ, Bushby K, Bann CM, et al. Diagnosis and management of Duchenne muscular dystrophy, part 1: diagnosis, and neuromuscular, rehabilitation, endocrine, and gastrointestinal and nutritional management. Lancet Neurol. 2018;17(3):251–267. doi:10.1016/S1474-4422(18)30024-3
  333. Sanders DB, Wolfe GI, Benatar M, et al. International consensus guidance for management of myasthenia gravis: executive summary. Neurology. 2016;87(4):419–425. doi:10.1212/WNL.0000000000002790
  334. Myasthenia Gravis Foundation of America. Cautionary drugs. MGFA
  335. Parikh S, Goldstein A, Koenig MK, et al. Diagnosis and management of mitochondrial disease: a consensus statement from the Mitochondrial Medicine Society. Genet Med. 2015;17(9):689–701. doi:10.1038/gim.2014.177
  336. Woods CR, Bradley JS, Chatterjee A, et al. Clinical practice guideline by PIDS and IDSA: 2023 guideline on diagnosis and management of acute bacterial arthritis in pediatrics. J Pediatric Infect Dis Soc. 2024;13(1):1–59. doi:10.1093/jpids/piad089
  337. Caird MS, Flynn JM, Leung YL, et al. Factors distinguishing septic arthritis from transient synovitis of the hip in children: a prospective study. J Bone Joint Surg Am. 2006;88(6):1251–1257. doi:10.2106/JBJS.E.00216
  338. Kocher MS, Zurakowski D, Kasser JR. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence‑based clinical prediction algorithm. J Bone Joint Surg Am. 1999;81(12):1662–1670. doi:10.2106/00004623-199912000-00002
  339. Zaoutis T, Localio AR, Leckerman K, et al. Prolonged intravenous therapy versus early transition to oral antimicrobial therapy for acute osteomyelitis in children. Pediatrics. 2009;123(2):636–642. doi:10.1542/peds.2008-0596
  340. Peltola H, Pääkkönen M, Kallio P, Kallio MJT; OM‑SA Study Group. Prospective, randomized trial of 10 days versus 30 days of antimicrobial treatment, including a short‑term course of parenteral therapy, for childhood septic arthritis. Clin Infect Dis. 2009;48(9):1201–1210. doi:10.1086/597582
  341. Naranje S, Kelly DM, Sawyer JR. A systematic approach to the evaluation of a limping child. Am Fam Physician. 2015;92(10):908–916. PMID 26554284 (no DOI assigned)
  342. Haney S, Scherl S, DiMeglio L, Perez‑Rossello J, Servaes S, Merchant N; AAP Council on Child Abuse and Neglect, Section on Orthopaedics, Section on Endocrinology, Section on Radiology. Evaluating young children with fractures for child abuse: clinical report. Pediatrics. 2025;155(2):e2024070074. doi:10.1542/peds.2024-070074
  343. Morancie NA, Helton MR. Evaluating the child with a limp. Am Fam Physician. 2023;107(5):474–485. aafp.org/afp/2023/0500/evaluating-child-with-limp
  344. Bexkens R, Washburn FJ, Eygendaal D, van den Bekerom MPJ, Oh LS. Effectiveness of reduction maneuvers in the treatment of nursemaid's elbow: a systematic review and meta‑analysis. Am J Emerg Med. 2017;35(1):159–163. doi:10.1016/j.ajem.2016.10.059
  345. Webb CW, Liu R, Bouchereau-Lal N. Slipped capital femoral epiphysis: rapid evidence review. Am Fam Physician. 2025;112(4):414–423. aafp.org/afp/2025/1000/slipped-capital-femoral-epiphysis
  346. Loder RT, Richards BS, Shapiro PS, et al. Acute slipped capital femoral epiphysis: the importance of physeal stability. J Bone Joint Surg Am. 1993;75(8):1134–1140. doi:10.2106/00004623-199308000-00002
  347. Chasm RM, Swencki SA. Pediatric orthopedic emergencies. Emerg Med Clin North Am. 2010;28(4):907–926. doi:10.1016/j.emc.2010.06.003
  348. British Orthopaedic Association. BOAST: Supracondylar fractures of the humerus in children. London: BOA; updated October 2020. boa.ac.uk/resource/boast-11-pdf.html
  349. Livingston KS, Glotzbecker MP, Shore BJ. Pediatric acute compartment syndrome. J Am Acad Orthop Surg. 2017;25(5):358–364. doi:10.5435/JAAOS-D-15-00655
  350. Bae DS, Kadiyala RK, Waters PM. Acute compartment syndrome in children: contemporary diagnosis, treatment, and outcome. J Pediatr Orthop. 2001;21(5):680–688.
  351. Lin JS, Samora JB. Pediatric acute compartment syndrome: a systematic review and meta‑analysis. J Pediatr Orthop B. 2020;29(1):90–96. doi:10.1097/BPB.0000000000000593
  352. Garner MR, Sethuraman SA, Schade MA, Boateng H. Antibiotic prophylaxis in open fractures: evidence, evolving issues, and recommendations. J Am Acad Orthop Surg. 2020;28(8):309–315. doi:10.5435/JAAOS-D-18-00193
  353. British Orthopaedic Association. BOAST: Diagnosis and management of arterial injuries associated with musculoskeletal trauma. London: BOA; revised June 2026. boa.ac.uk (BOAST arterial injuries)
  354. Benedick A, Lopas L, Daley E, Jang Y. Traumatic hip dislocation: pediatric and adult evaluation and management. J Am Acad Orthop Surg. 2024;32(14):637–646. doi:10.5435/JAAOS-D-23-01013
  355. Kenawey M, Howard A, Tile M. Pediatric‑specific lesions in unstable pelvic ring fractures of skeletally immature children: impact on diagnosis and management decisions. J Am Acad Orthop Surg. 2024;32(14):e683–e694. doi:10.5435/JAAOS-D-23-01249
  356. Kwon BK, Tetreault LA, Martin AR, et al. A clinical practice guideline for the management of patients with acute spinal cord injury: recommendations on hemodynamic management. Global Spine J. 2024;14(3 Suppl):187S–211S. doi:10.1177/21925682231202348
  357. Fehlings MG, Vaccaro A, Wilson JR, et al. Early versus delayed decompression for traumatic cervical spinal cord injury: results of the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS). PLoS One. 2012;7(2):e32037. doi:10.1371/journal.pone.0032037
  358. Fehlings MG, Wilson JR, Tetreault LA, et al. A clinical practice guideline for the management of patients with acute spinal cord injury: recommendations on the use of methylprednisolone sodium succinate. Global Spine J. 2017;7(3 Suppl):203S–211S. doi:10.1177/2192568217703085
  359. American Academy of Pediatrics Committee on Pediatric Emergency Medicine, Council on Injury, Violence, and Poison Prevention, Section on Critical Care, Section on Orthopaedics, Section on Surgery, Section on Transport Medicine; Pediatric Trauma Society; Society of Trauma Nurses Pediatric Committee. Management of pediatric trauma (policy statement). Pediatrics. 2016;138(2):e20161569. doi:10.1542/peds.2016-1569
  360. Rossaint R, Afshari A, Bouillon B, et al. The European guideline on management of major bleeding and coagulopathy following trauma: sixth edition. Crit Care. 2023;27(1):80. doi:10.1186/s13054-023-04327-7
  361. Terboven T, Leonhard G, Wessel L, et al. Chest wall thickness and depth to vital structures in paediatric patients — implications for prehospital needle decompression of tension pneumothorax. Scand J Trauma Resusc Emerg Med. 2019;27(1):45. doi:10.1186/s13049-019-0623-5
  362. CRASH‑2 trial collaborators; Shakur H, Roberts I, et al. Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH‑2): a randomised, placebo‑controlled trial. Lancet. 2010;376(9734):23–32. doi:10.1016/S0140-6736(10)60835-5
  363. New HV, Berryman J, Bolton-Maggs PHB, et al; British Committee for Standards in Haematology. Guidelines on transfusion for fetuses, neonates and older children. Br J Haematol. 2016;175(5):784–828. doi:10.1111/bjh.14233
  364. Holcomb JB, Tilley BC, Baraniuk S, et al. Transfusion of plasma, platelets, and red blood cells in a 1:1:1 vs a 1:1:2 ratio and mortality in patients with severe trauma: the PROPPR randomized clinical trial. JAMA. 2015;313(5):471–482. doi:10.1001/jama.2015.12
  365. Eckert MJ, Wertin TM, Tyner SD, et al. Tranexamic acid administration to pediatric trauma patients in a combat setting: the pediatric trauma and tranexamic acid study (PED‑TRAX). J Trauma Acute Care Surg. 2014;77(6):852–858. doi:10.1097/TA.0000000000000443
  366. Holmes JF, Lillis K, Monroe D, et al; PECARN. Identifying children at very low risk of clinically important blunt abdominal injuries. Ann Emerg Med. 2013;62(2):107–116.e2. doi:10.1016/j.annemergmed.2012.11.009
  367. Stengel D, Leisterer J, Ferrada P, et al. Point‑of‑care ultrasonography for diagnosing thoracoabdominal injuries in patients with blunt trauma. Cochrane Database Syst Rev. 2018;12(12):CD012669. doi:10.1002/14651858.CD012669.pub2
  368. Leonard JC, et al; Pediatric Emergency Care Applied Research Network (PECARN). PECARN prediction rule for cervical spine imaging of children presenting to the emergency department with blunt trauma: a multicentre prospective observational study. Lancet Child Adolesc Health. 2024;8(7):482–490. doi:10.1016/S2352-4642(24)00104-4
  369. Rozzelle CJ, Aarabi B, Dhall SS, et al. Spinal cord injury without radiographic abnormality (SCIWORA). Neurosurgery. 2013;72(Suppl 2):227–233. doi:10.1227/NEU.0b013e3182770ebc
  370. Kuppermann N, Holmes JF, Dayan PS, et al; Pediatric Emergency Care Applied Research Network (PECARN). Identification of children at very low risk of clinically‑important brain injuries after head trauma: a prospective cohort study. Lancet. 2009;374(9696):1160–1170. doi:10.1016/S0140-6736(09)61558-0
  371. Suttipongkaset P, Chaikittisilpa N, Vavilala MS, et al. Blood pressure thresholds and mortality in pediatric traumatic brain injury. Pediatrics. 2018;142(2):e20180594. doi:10.1542/peds.2018-0594
  372. Pierce MC, Kaczor K, Lorenz DJ, et al. Validation of a Clinical Decision Rule to Predict Abuse in Young Children Based on Bruising Characteristics (TEN‑4‑FACESp). JAMA Netw Open. 2021;4(4):e215832. doi:10.1001/jamanetworkopen.2021.5832
  373. Narang SK, Fingarson A, Lukefahr J; AAP Council on Child Abuse and Neglect. Abusive head trauma in infants and children. Pediatrics. 2020;145(4):e20200203. doi:10.1542/peds.2020-0203
  374. Choudhary AK, Servaes S, Slovis TL, et al. Consensus statement on abusive head trauma in infants and young children. Pediatr Radiol. 2018;48(8):1048–1065. doi:10.1007/s00247-018-4149-1
  375. Kuwait National Child Protection Program (KNCPP), Ministry of Health — Child Protection Hotline 147. kncpp.moh.gov.kw
  376. Expert Panel on Pediatric Imaging; Mirsky DM, Bardo DME, Iyer RS, et al. ACR Appropriateness Criteria® Suspected Physical Abuse—Child: Update 2025. J Am Coll Radiol. 2026;23(8):1613–1646. doi:10.1016/j.jacr.2026.02.017
  377. Glenn K, Nickerson E, Bennett CV, et al. Head computed tomography in suspected physical abuse: time to rethink? Arch Dis Child. 2021;106(5):461–466. doi:10.1136/archdischild-2020-320192
  378. The Royal College of Radiologists, Society and College of Radiographers. The radiological investigation of suspected physical abuse in children. London: RCR; 2017 (revised 2018). rcr.ac.uk
  379. Rubin DM, Christian CW, Bilaniuk LT, Zazyczny KA, Durbin DR. Occult head injury in high‑risk abused children. Pediatrics. 2003;111(6 Pt 1):1382–1386. doi:10.1542/peds.111.6.1382
  380. Anderst J, Carpenter SL, Abshire TC, Killough E; AAP Section on Hematology/Oncology, Council on Child Abuse and Neglect. Evaluation for bleeding disorders in suspected child abuse. Pediatrics. 2022;150(4):e2022059276. doi:10.1542/peds.2022-059276
  381. Lindberg D, Makoroff K, Harper N, et al. Utility of hepatic transaminases to recognize abuse in children. Pediatrics. 2009;124(2):509–516. doi:10.1542/peds.2008-2348
  382. CRASH‑3 trial collaborators. Effects of tranexamic acid on death, disability, vascular occlusive events and other morbidities in patients with acute traumatic brain injury (CRASH‑3): a randomised, placebo‑controlled trial. Lancet. 2019;394(10210):1713–1723. doi:10.1016/S0140-6736(19)32233-0
  383. Calcium Gluconate in Sodium Chloride Injection — US prescribing information (§2.1 administration via a secure intravenous line; initial bolus dose table; §5.3 tissue necrosis and calcinosis). WG Critical Care; 2018 (NDA 210906). www.accessdata.fda.gov
  384. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney Int Suppl. 2012;2(1):1–138.
  385. Harbord N. Common toxidromes and the role of extracorporeal detoxification. Adv Chronic Kidney Dis. 2020;27(1):11–17. doi:10.1053/j.ackd.2019.08.016
  386. Fakhouri F, Zuber J, Frémeaux‑Bacchi V, Loirat C. Haemolytic uraemic syndrome. Lancet. 2017;390(10095):681–696. doi:10.1016/S0140-6736(17)30062-4
  387. Loirat C, Fakhouri F, Ariceta G, et al.; HUS International. An international consensus approach to the management of atypical hemolytic uremic syndrome in children. Pediatr Nephrol. 2016;31(1):15–39. doi:10.1007/s00467-015-3076-8
  388. Garnier A, Brochard K, Kwon T, et al. Efficacy and safety of eculizumab in pediatric patients affected by Shiga toxin‑related hemolytic and uremic syndrome: a randomized, placebo‑controlled trial. J Am Soc Nephrol. 2023;34(9):1561–1573. doi:10.1681/ASN.0000000000000182
  389. Centers for Disease Control and Prevention. Clinical guidance for managing meningococcal disease risk in patients receiving complement inhibitor therapy. Atlanta: CDC. cdc.gov
  390. McNamara LA, Topaz N, Wang X, Hariri S, Fox L, MacNeil JR. High risk for invasive meningococcal disease among patients receiving eculizumab (Soliris) despite receipt of meningococcal vaccine. MMWR Morb Mortal Wkly Rep. 2017;66(27):734–737. doi:10.15585/mmwr.mm6627e1
  391. Flynn JT, Kaelber DC, Baker‑Smith CM, et al. Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents (AAP). Pediatrics. 2017;140(3):e20171904. doi:10.1542/peds.2017-1904
  392. Trautmann A, Boyer O, Hodson E, et al; International Pediatric Nephrology Association. IPNA clinical practice recommendations for the diagnosis and management of children with steroid‑sensitive nephrotic syndrome. Pediatr Nephrol. 2023;38(3):877–919. doi:10.1007/s00467-022-05739-3
  393. American Academy of Pediatrics Task Force on Circumcision. Male circumcision. Pediatrics. 2012;130(3):e756‑e785. doi:10.1542/peds.2012-1990
  394. Brady‑Fryer B, Wiebe N, Lander JA. Pain relief for neonatal circumcision. Cochrane Database Syst Rev. 2004;(4):CD004217. doi:10.1002/14651858.CD004217.pub2
  395. Sharara‑Chami R, Lakissian Z, Charafeddine L, Milad N, El‑Hout Y. Combination Analgesia for Neonatal Circumcision: A Randomized Controlled Trial. Pediatrics. 2017;140(6):e20171935. doi:10.1542/peds.2017-1935
  396. Hayashi Y, Kojima Y, Mizuno K, Kohri K. Prepuce: phimosis, paraphimosis, and circumcision. ScientificWorldJournal. 2011;11:289–301. doi:10.1100/tsw.2011.31
  397. Qin KR, Qu LG. Diagnosing with a TWIST: systematic review and meta‑analysis of a testicular torsion risk score. J Urol. 2022;208(1):62–70. doi:10.1097/JU.0000000000002496
  398. European Association of Urology. EAU Guidelines on Paediatric Urology — Acute scrotum. Edn. presented at the EAU Annual Congress, London 2026. Arnhem: EAU Guidelines Office; 2026. ISBN 978‑94‑92671‑32‑5. uroweb.org
  399. Mellick LB, Sinex JE, Gibson RW, et al. A systematic review of testicle survival time after a torsion event. Pediatr Emerg Care. 2019;35(12):821–825. doi:10.1097/PEC.0000000000001287
  400. Bayne CE, Villanueva J, Davis TD, et al. Factors associated with delayed presentation and misdiagnosis of testicular torsion: a case‑control study. J Pediatr. 2017;186:200–204. doi:10.1016/j.jpeds.2017.03.037
  401. Bivalacqua TJ, Allen BK, Brock GB, et al. Acute ischemic priapism: an AUA/SMSNA guideline. J Urol. 2021;206(5):1114–1121. doi:10.1097/JU.0000000000002236
  402. European Association of Urology. EAU Guidelines on Sexual and Reproductive Health — Priapism. Edn. presented at the EAU Annual Congress, London 2026. Arnhem: EAU Guidelines Office; 2026. uroweb.org
  403. Bivalacqua TJ, Allen BK, Brock GB, et al. The diagnosis and management of recurrent ischemic priapism, priapism in sickle cell patients, and non‑ischemic priapism: an AUA/SMSNA guideline. J Urol. 2022;208(1):43–52. doi:10.1097/JU.0000000000002767
  404. Phillips M, Cara‑Fuentes G, Najjar M, Rheault MN, Kallash M. Evaluation and management of hematuria in children. Curr Treat Options Pediatr. 2024;10(4):237–246. doi:10.1007/s40746-024-00302-8
  405. Greenfield SP, Williot P, Kaplan D. Gross hematuria in children: a ten‑year review. Urology. 2007;69(1):166–169. doi:10.1016/j.urology.2006.10.018
  406. Kidney Disease: Improving Global Outcomes (KDIGO) Glomerular Diseases Work Group. KDIGO 2021 Clinical Practice Guideline for the Management of Glomerular Diseases. Kidney Int. 2021;100(4S):S1–S276. doi:10.1016/j.kint.2021.05.021
  407. Abugrain K, McCulloch MI, Muloiwa R, Luyckx VA, Buys H. A 6‑year review of acute post‑streptococcal glomerulonephritis at a public children's hospital in Cape Town, South Africa. Pediatr Nephrol. 2024;39(6):1809–1816. doi:10.1007/s00467-023-06247-8
  408. VanDeVoorde RG. Acute poststreptococcal glomerulonephritis: the most common acute glomerulonephritis. Pediatr Rev. 2015;36(1):3–12. doi:10.1542/pir.36-1-3
  409. Centers for Disease Control and Prevention. Clinical guidelines for post‑streptococcal glomerulonephritis. Atlanta, GA: CDC; updated August 5, 2025. www.cdc.gov
  410. Mannix R, Tan ML, Wright R, Baskin M. Acute pediatric rhabdomyolysis: causes and rates of renal failure. Pediatrics. 2006;118(5):2119–2125. doi:10.1542/peds.2006-1352
  411. Michelsen J, Cordtz J, Liboriussen L, et al. Prevention of rhabdomyolysis‑induced acute kidney injury – a DASAIM/DSIT clinical practice guideline. Acta Anaesthesiol Scand. 2019;63(5):576–586. doi:10.1111/aas.13308
  412. Brown CVR, Rhee P, Chan L, et al. Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference? J Trauma. 2004;56(6):1191–1196. doi:10.1097/01.ta.0000130761.78627.10
  413. Dribin TE, Muraro A, Camargo CA Jr, Turner PJ, et al. Anaphylaxis definition, overview, and clinical support tool: 2024 consensus report — a GA²LEN project. J Allergy Clin Immunol. 2025;156(2):406–417.e6. doi:10.1016/j.jaci.2025.01.021
  414. Golden DBK, Wang J, Waserman S, et al. Anaphylaxis: a 2023 practice parameter update. Ann Allergy Asthma Immunol. 2024;132(2):124–176. doi:10.1016/j.anai.2023.09.015
  415. Nowak‑Węgrzyn A, Chehade M, Groetch ME, et al. International consensus guidelines for the diagnosis and management of food protein‑induced enterocolitis syndrome: executive summary — Workgroup Report of the Adverse Reactions to Foods Committee, American Academy of Allergy, Asthma & Immunology. J Allergy Clin Immunol. 2017;139(4):1111–1126.e4. doi:10.1016/j.jaci.2016.12.966
  416. Cardona V, Ansotegui IJ, Ebisawa M, et al. World Allergy Organization anaphylaxis guidance 2020. World Allergy Organ J. 2020;13(10):100472. doi:10.1016/j.waojou.2020.100472
  417. National Institute for Health and Care Excellence. Anaphylaxis: assessment and referral after emergency treatment. NICE guideline NG258. London: NICE; May 2026. nice.org.uk/guidance/ng258
  418. Chalut DS, Ducharme FM, Davis GM. The Preschool Respiratory Assessment Measure (PRAM): a responsive index of acute asthma severity. J Pediatr. 2000;137(6):762–768. doi:10.1067/mpd.2000.110121
  419. Ducharme FM, Chalut D, Plotnick L, et al. The Pediatric Respiratory Assessment Measure: a valid clinical score for assessing acute asthma severity from toddlers to teenagers. J Pediatr. 2008;152(4):476–480. doi:10.1016/j.jpeds.2007.08.034
  420. Global Initiative for Asthma (GINA). Global Strategy for Asthma Management and Prevention, 2026 update. ginasthma.org/2026-gina-strategy-report
  421. National Asthma Education and Prevention Program. Expert Panel Report 3: Guidelines for the Diagnosis and Management of Asthma. Bethesda, MD: National Heart, Lung, and Blood Institute; 2007 (NIH publication 07‑4051). nhlbi.nih.gov
  422. Mitra A, Bassler D, Goodman K, Lasserson TJ, Ducharme FM. Intravenous aminophylline for acute severe asthma in children over two years receiving inhaled bronchodilators. Cochrane Database Syst Rev. 2005;(2):CD001276. doi:10.1002/14651858.CD001276.pub2
  423. Rodrigo GJ, Pollack CV, Rodrigo C, Rowe BH. Heliox for non‑intubated acute asthma patients. Cochrane Database Syst Rev. 2006;(4):CD002884. doi:10.1002/14651858.CD002884.pub2
  424. Kim IK, Phrampus E, Venkataraman S, et al. Helium/oxygen‑driven albuterol nebulization in the treatment of children with moderate to severe asthma exacerbations: a randomized, controlled trial. Pediatrics. 2005;116(5):1127–1133. doi:10.1542/peds.2004-2136
  425. Lew A, Morrison JM, Amankwah E, Sochet AA. Heliox for pediatric critical asthma: a multicenter, retrospective, registry‑based descriptive study. J Intensive Care Med. 2022;37(6):776–783. doi:10.1177/08850666211026550
  426. Keeney GE, Gray MP, Morrison AK, et al. Dexamethasone for acute asthma exacerbations in children: a meta‑analysis. Pediatrics. 2014;133(3):493–499. doi:10.1542/peds.2013-2273
  427. Barnett PL, Caputo GL, Baskin M, et al. Intravenous versus oral corticosteroids in the management of acute asthma in children. Ann Emerg Med. 1997;29(2):212–217. doi:10.1016/s0196-0644(97)70270-1
  428. Westley CR, Cotton EK, Brooks JG. Nebulized racemic epinephrine by IPPB for the treatment of croup: a double‑blind study. Am J Dis Child. 1978;132(5):484–487. doi:10.1001/archpedi.1978.02120300044008
  429. Ortiz‑Alvarez O; Canadian Paediatric Society, Acute Care Committee. Acute management of croup in the emergency department. Paediatr Child Health. 2017;22(3):166–173 (updated March 2026). doi:10.1093/pch/pxx019
  430. Aregbesola A, Tam CM, Kothari A, Le ML, Ragheb M, Klassen TP. Glucocorticoids for croup in children. Cochrane Database Syst Rev. 2023;1(1):CD001955. doi:10.1002/14651858.CD001955.pub5
  431. Bjornson C, Russell K, Vandermeer B, Klassen TP, Johnson DW. Nebulized epinephrine for croup in children. Cochrane Database Syst Rev. 2013;(10):CD006619. doi:10.1002/14651858.CD006619.pub3
  432. Klassen TP, Craig WR, Moher D, et al. Nebulized budesonide and oral dexamethasone for treatment of croup: a randomized controlled trial. JAMA. 1998;279(20):1629–1632. doi:10.1001/jama.279.20.1629
  433. Moraa I, Sturman N, McGuire TM, van Driel ML. Heliox for croup in children. Cochrane Database Syst Rev. 2021;(8):CD006822. doi:10.1002/14651858.CD006822.pub6
  434. Liu Y, Nicotera DJ, Islam AA, Dunsky K, Lieu JEC. Prognostic factors for retropharyngeal abscess in children receiving surgery or antibiotic therapy. Laryngoscope. 2024;134(4):1955–1960. doi:10.1002/lary.31064
  435. Wilkie MD, De S, Krishnan M. Defining the role of surgical drainage in paediatric deep neck space infections. Clin Otolaryngol. 2019;44(3):366–371. doi:10.1111/coa.13315
  436. Fiadjoe JE, Nishisaki A, Jagannathan N, et al. Airway management complications in children with difficult tracheal intubation from the Pediatric Difficult Intubation (PeDI) registry: a prospective cohort analysis. Lancet Respir Med. 2016;4(1):37–48. doi:10.1016/S2213-2600(15)00508-1
  437. Black AE, Flynn PER, Smith HL, Thomas ML, Wilkinson KA; Association of Paediatric Anaesthetists of Great Britain and Ireland. Development of a guideline for the management of the unanticipated difficult airway in pediatric practice. Paediatr Anaesth. 2015;25(4):346–362. doi:10.1111/pan.12615
  438. Disma N, Asai T, Cools E, et al. Airway management in neonates and infants: European Society of Anaesthesiology and Intensive Care and British Journal of Anaesthesia joint guidelines. Br J Anaesth. 2024;132(1):124–144. doi:10.1016/j.bja.2023.08.040
  439. Apfelbaum JL, Hagberg CA, Connis RT, et al. 2022 American Society of Anesthesiologists practice guidelines for management of the difficult airway. Anesthesiology. 2022;136(1):31–81. doi:10.1097/ALN.0000000000004002
  440. Kuwait pediatric difficult‑airway algorithm (Three‑Zones approach) — local anesthesia/critical‑care protocol; internal Council document, not published online.
  441. Peyton J, Park R, Staffa SJ, et al. Videolaryngoscopy using standard blades or non‑standard blades in children in the Pediatric Difficult Intubation Registry. Br J Anaesth. 2021;126(1):331–339. doi:10.1016/j.bja.2020.08.010
  442. Borland ML, Loveys K, Babl FE, et al; PREDICT network. Australasian Bronchiolitis Guideline: 2025 update. J Paediatr Child Health. 2025;61(8):1197–1215. doi:10.1111/jpc.70144
  443. Ralston SL, Lieberthal AS, Meissner HC, et al. Diagnosis, Management, and Prevention of Bronchiolitis (AAP). Pediatrics. 2014;134(5):e1474–e1502. doi:10.1542/peds.2014-2742
  444. Franklin D, Babl FE, Schlapbach LJ, et al. A randomized trial of high‑flow oxygen therapy in infants with bronchiolitis (PARIS). N Engl J Med. 2018;378(12):1121–1131. doi:10.1056/NEJMoa1714855
  445. Franklin D, Babl FE, George S, et al. Effect of early high‑flow nasal oxygen vs standard oxygen therapy on length of hospital stay in hospitalized children with acute hypoxemic respiratory failure: the PARIS‑2 randomized clinical trial. JAMA. 2023;329(3):224–234. doi:10.1001/jama.2022.21805
  446. National Institute for Health and Care Excellence. Bronchiolitis in children: diagnosis and management. NICE guideline NG9. London: NICE; 2015, updated August 2021. nice.org.uk/guidance/ng9
  447. Cunningham S, Rodriguez A, Boyd KA, et al. Bronchiolitis of Infancy Discharge Study (BIDS): a multicentre, parallel‑group, double‑blind, randomised controlled, equivalence trial with economic evaluation. Health Technol Assess. 2015;19(71):1–172. doi:10.3310/hta19710
  448. Bradley JS, Byington CL, Shah SS, et al. The management of community‑acquired pneumonia in infants and children older than 3 months of age (PIDS/IDSA). Clin Infect Dis. 2011;53(7):e25–e76. doi:10.1093/cid/cir531
  449. Le Saux N, Robinson JL; Canadian Pediatric Society, Infectious Diseases and Immunization Committee. Uncomplicated pneumonia in healthy Canadian children and youth: Practice points for management. Updated 2024. cps.ca
  450. Chibuk T, Cohen E, Robinson JL, Mahant S, Hartfield D; Canadian Paediatric Society, Hospital Paediatrics Section. Paediatric complicated pneumonia: Diagnosis and management of empyema. Updated May 2024. cps.ca
  451. St. Peter SD, Ampofo K, Brogan T, et al. Clinical practice guideline by the Infectious Diseases Society of America and the Pediatric Infectious Diseases Society: 2026 guideline update on the management of community‑acquired pneumonia in infants and children older than 3 months of age. Clin Infect Dis. 2026. doi:10.1093/cid/ciag186
  452. Balfour‑Lynn IM, Abrahamson E, Cohen G, et al. BTS guidelines for the management of pleural infection in children. Thorax. 2005;60(Suppl 1):i1–i21. doi:10.1136/thx.2004.030676
  453. Joyner BL, Dewan M, Bavare A, et al. Part 6: Pediatric Basic Life Support: 2025 American Heart Association and American Academy of Pediatrics Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2025;152(16 suppl 2):S424–S447. doi:10.1161/CIR.0000000000001370
  454. Cole S, Wilkinson S, Kubba H. Rigid bronchoscopy is the gold standard management of inhaled foreign bodies in children: myth or maxim? Breathe (Sheff). 2026;22(2):260039. doi:10.1183/20734735.0039-2026
  455. Fidkowski CW, Zheng H, Firth PG. The anesthetic considerations of tracheobronchial foreign bodies in children: a literature review of 12,979 cases. Anesth Analg. 2010;111(4):1016–1025. doi:10.1213/ANE.0b013e3181ef3e9c
  456. Marcus CL, Brooks LJ, Draper KA, et al. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics. 2012;130(3):576–584. doi:10.1542/peds.2012-1671
  457. Kaditis AG, Alonso Alvarez ML, Boudewyns A, et al. Obstructive sleep disordered breathing in 2- to 18‑year‑old children: diagnosis and management. Eur Respir J. 2016;47(1):69–94. doi:10.1183/13993003.00385-2015
  458. MacLean JE, Adeleye A, Van Dam A, et al. The Canadian Thoracic Society/Canadian Sleep Society guideline on the diagnosis of obstructive sleep apnea in children. Chest. 2026;170(2):565–582. doi:10.1016/j.chest.2025.12.017
  459. Evans HJ, Gibson NA, Bennett J, et al. British Thoracic Society guideline for diagnosing and monitoring paediatric sleep-disordered breathing. Thorax. 2023;78(Suppl 2):s1–s27. doi:10.1136/thorax-2022-218938
  460. Mitchell RB, Archer SM, Ishman SL, et al. Clinical practice guideline: tonsillectomy in children (update). Otolaryngol Head Neck Surg. 2019;160(1 Suppl):S1–S42. doi:10.1177/0194599818801757
  461. Brown KA, Laferrière A, Lakheeram I, Moss IR. Recurrent hypoxemia in children is associated with increased analgesic sensitivity to opiates. Anesthesiology. 2006;105(4):665–669. doi:10.1097/00000542-200610000-00009
  462. Ehsan Z, Ishman SL, Soghier I, et al. Management of persistent, post-adenotonsillectomy obstructive sleep apnea in children: an official American Thoracic Society clinical practice guideline. Am J Respir Crit Care Med. 2024;209(3):248–261. doi:10.1164/rccm.202310-1857ST
  463. Meyer R, Venter C, Bognanni A, et al. World Allergy Organization (WAO) Diagnosis and Rationale for Action against Cow’s Milk Allergy (DRACMA) guideline update – VII – Milk elimination and reintroduction in the diagnostic process of cow’s milk allergy. World Allergy Organ J. 2023;16(7):100785. doi:10.1016/j.waojou.2023.100785
  464. Vandenplas Y, Broekaert I, Domellöf M, et al. An ESPGHAN position paper on the diagnosis, management, and prevention of cow's milk allergy. J Pediatr Gastroenterol Nutr. 2024;78(2):386–413. doi:10.1097/MPG.0000000000003897
  465. Sathya P, Fenton TR; Canadian Paediatric Society, Nutrition and Gastroenterology Committee. Cow’s milk protein allergy in infants and children. Paediatr Child Health. 2024;29(6):382–396. doi:10.1093/pch/pxae043
  466. Cook VE, Connors LA, Vander Leek TK, Watson W. Non‑immunoglobulin E‑mediated food allergy. Allergy Asthma Clin Immunol. 2024;20(Suppl 3):70. doi:10.1186/s13223-024-00933-4
  467. Husby S, Koletzko S, Korponay-Szabó I, et al. European Society Paediatric Gastroenterology, Hepatology and Nutrition guidelines for diagnosing coeliac disease 2020. J Pediatr Gastroenterol Nutr. 2020;70(1):141–156. doi:10.1097/MPG.0000000000002497
  468. Venter C, Meyer R, Groetch M, et al. World Allergy Organization (WAO) Diagnosis and Rationale for Action against Cow’s Milk Allergy (DRACMA) guidelines update – XVI – Nutritional management of cow’s milk allergy. World Allergy Organ J. 2024;17(8):100931. doi:10.1016/j.waojou.2024.100931
  469. McWilliam V, Netting MJ, Volders E, Palmer DJ; WAO DRACMA Guideline Group. World Allergy Organization (WAO) Diagnosis and Rationale for Action against Cow's Milk Allergy (DRACMA) guidelines update – X – Breastfeeding a baby with cow's milk allergy. World Allergy Organ J. 2023;16(11):100830. doi:10.1016/j.waojou.2023.100830
  470. Leonard SA, Pecora V, Fiocchi AG, Nowak-Wegrzyn A. Food protein-induced enterocolitis syndrome: a review of the new guidelines. World Allergy Organ J. 2018;11(1):4. doi:10.1186/s40413-017-0182-z
  471. Wong T, Atkinson A, t’Jong G, et al; Canadian Paediatric Society. Beta‑lactam allergy in the paediatric population. Paediatr Child Health. 2020;25(1):62–63. doi:10.1093/pch/pxz179
  472. Khan DA, Banerji A, Blumenthal KG, et al. Drug allergy: A 2022 practice parameter update. J Allergy Clin Immunol. 2022;150(6):1333‑1393. doi:10.1016/j.jaci.2022.08.028
  473. Macy E, Contreras R. Health care use and serious infection prevalence associated with penicillin “allergy” in hospitalized patients: a cohort study. J Allergy Clin Immunol. 2014;133(3):790–796. doi:10.1016/j.jaci.2013.09.021
  474. Copaescu AM, Vogrin S, Shand G, et al. Validation of the PEN‑FAST score in a pediatric population. JAMA Netw Open. 2022;5(9):e2233703. doi:10.1001/jamanetworkopen.2022.33703
  475. Devchand M, Trubiano JA. Penicillin allergy: a practical approach to assessment and prescribing. Aust Prescr. 2019;42(6):192–199. doi:10.18773/austprescr.2019.065
  476. Children’s Hospital of Philadelphia. Penicillin drug allergy clinical pathway — all settings (revised November 2025). Philadelphia: CHOP Clinical Pathways. chop.edu
  477. Maurer M, Magerl M, Betschel S, et al. The international WAO/EAACI guideline for the management of hereditary angioedema—the 2021 revision and update. Allergy. 2022;77(7):1961–1990. doi:10.1111/all.15214
  478. Farkas H, Martinez‑Saguer I, Bork K, et al. International guideline on the diagnosis and management of pediatric patients with hereditary angioedema. Allergy. 2026;81(8):2744–2774. doi:10.1111/all.70207
  479. Aden A, Jemide I, Islam T, et al. Clinical warning signs in detecting inborn errors of immunity in children: a diagnostic accuracy systematic review. J Allergy Clin Immunol Pract. 2026;14(4):920–936.e1. doi:10.1016/j.jaip.2026.01.026
  480. Jeffrey Modell Foundation. 10 warning signs of primary immunodeficiency (children). New York: JMF; endorsed by the European Society for Immunodeficiencies. esid.org
  481. Kim VHD, Upton JEM, Derfalvi B, Hildebrand KJ, McCusker C. Inborn errors of immunity (primary immunodeficiencies). Allergy Asthma Clin Immunol. 2024;20(Suppl 3):76. doi:10.1186/s13223-024-00938-z
  482. Buckley RH. The long quest for neonatal screening for severe combined immunodeficiency. J Allergy Clin Immunol. 2012;129(3):597–604. doi:10.1016/j.jaci.2011.12.964
  483. Biggs CM, Haddad E, Issekutz TB, Roifman CM, Turvey SE. Newborn screening for severe combined immunodeficiency: a primer for clinicians. CMAJ. 2017;189(50):E1551–E1557. doi:10.1503/cmaj.170561
  484. Box 6.2 Clinical pearls: therapeutic principles — treatment of infants with SCID. Textbook chapter supplied by the section reviewer (Dr. Maysoon Al Rushood); internal copy, not available online.
  485. Lyng JW, Ward C, Angelidis M, et al. Prehospital Trauma Compendium: traumatic pneumothorax care — position statement and resource document of NAEMSP. Prehosp Emerg Care. 2024:1–21. doi:10.1080/10903127.2024.2416978
  486. Roberts ME, Rahman NM, Maskell NA, et al. British Thoracic Society Guideline for pleural disease. Thorax. 2023;78(11):1143–1156. doi:10.1136/thorax-2023-220304
  487. Speck KE, Kulaylat AN, Baerg JE, et al. Evaluation and management of primary spontaneous pneumothorax in adolescents and young adults: a systematic review from the APSA Outcomes & Evidence‑Based Practice Committee. J Pediatr Surg. 2023;58(10):1873–1885. doi:10.1016/j.jpedsurg.2023.03.018
  488. Flume PA, Mogayzel PJ Jr, Robinson KA, et al.; Clinical Practice Guidelines for Pulmonary Therapies Committee. Cystic fibrosis pulmonary guidelines: pulmonary complications: hemoptysis and pneumothorax. Am J Respir Crit Care Med. 2010;182(3):298–306. doi:10.1164/rccm.201002-0157OC
  489. Laan DV, Vu TDN, Thiels CA, et al. Chest wall thickness and decompression failure: a systematic review and meta‑analysis comparing anatomic locations in needle thoracostomy. Injury. 2016;47(4):797–804. doi:10.1016/j.injury.2015.11.045
  490. Leonhard G, Overhoff D, Wessel L, et al. Determining optimal needle size for decompression of tension pneumothorax in children — a CT‑based study. Scand J Trauma Resusc Emerg Med. 2019;27(1):90. doi:10.1186/s13049-019-0671-x
  491. Hossain R, Qadri U, Dembowski N, et al. Sound and Air: Ultrasonographic measurements of pediatric chest wall thickness and implications for needle decompression of tension pneumothorax. Pediatr Emerg Care. 2021;37(12):e1544–e1548. doi:10.1097/PEC.0000000000002112
  492. Alrajab S, Youssef AM, Akkus NI, et al. Pleural ultrasonography versus chest radiography for the diagnosis of pneumothorax: review of the literature and meta‑analysis. Crit Care. 2013;17(5):R208. doi:10.1186/cc13016
  493. Miscia ME, Lauriti G, Lisi G, Riccio A, Lelli Chiesa P. Management of spontaneous pneumothorax in children: a systematic review and meta‑analysis. Eur J Pediatr Surg. 2020;30(1):2–12. doi:10.1055/s-0039-3402522
  494. Brown SGA, Ball EL, Perrin K, et al. Conservative versus interventional treatment for spontaneous pneumothorax. N Engl J Med. 2020;382(5):405–415. doi:10.1056/NEJMoa1910775
  495. Walker S, Hallifax R, Ricciardi S, et al. Joint ERS/EACTS/ESTS clinical practice guidelines on adults with spontaneous pneumothorax. Eur Respir J. 2024;63(5):2300797. doi:10.1183/13993003.00797-2023
  496. Shakoory B, Geerlinks A, Wilejto M, et al. The 2022 EULAR/ACR points to consider at the early stages of diagnosis and management of suspected haemophagocytic lymphohistiocytosis/macrophage activation syndrome (HLH/MAS). Ann Rheum Dis. 2023;82(10):1271–1285. doi:10.1136/ard-2023-224123
  497. Henderson LA, Canna SW, Friedman KG, et al. American College of Rheumatology clinical guidance for multisystem inflammatory syndrome in children associated with SARS‑CoV‑2 and hyperinflammation in pediatric COVID‑19: version 3. Arthritis Rheumatol. 2022;74(4):e1–e20. doi:10.1002/art.42062
  498. Fautrel B, Mitrovic S, De Matteis A, et al. EULAR/PReS recommendations for the diagnosis and management of Still’s disease, comprising systemic juvenile idiopathic arthritis and adult‑onset Still’s disease. Ann Rheum Dis. 2024;83(12):1614–1627. doi:10.1136/ard-2024-225851
  499. Ravelli A, Minoia F, Davì S, et al. 2016 classification criteria for macrophage activation syndrome complicating systemic juvenile idiopathic arthritis: a EULAR/ACR/PRINTO collaborative initiative. Arthritis Rheumatol. 2016;68(3):566–576. doi:10.1002/art.39332
  500. Henter JI, Sieni E, Eriksson J, et al. Diagnostic guidelines for familial hemophagocytic lymphohistiocytosis revisited. Blood. 2024;144(22):2308–2318. doi:10.1182/blood.2024025077
  501. Henter JI, Horne A, Aricó M, et al. HLH‑2004: diagnostic and therapeutic guidelines for hemophagocytic lymphohistiocytosis. Pediatr Blood Cancer. 2007;48(2):124–131. doi:10.1002/pbc.21039
  502. Minoia F, Bovis F, Davì S, et al. Development and initial validation of the MS score for diagnosis of macrophage activation syndrome in systemic juvenile idiopathic arthritis. Ann Rheum Dis. 2019;78(10):1357–1362. doi:10.1136/annrheumdis-2019-215211
  503. Fardet L, Galicier L, Lambotte O, et al. Development and validation of the HScore, a score for the diagnosis of reactive hemophagocytic syndrome. Arthritis Rheumatol. 2014;66(9):2613–2620. doi:10.1002/art.38690
  504. Bergsten E, Horne A, Aricó M, et al. Confirmed efficacy of etoposide and dexamethasone in HLH treatment: long-term results of the cooperative HLH-2004 study. Blood. 2017;130(25):2728–2738. doi:10.1182/blood-2017-06-788349
  505. Bindoli S, De Matteis A, Mitrovic S, Fautrel B, Carmona L, De Benedetti F. Efficacy and safety of therapies for Still's disease and macrophage activation syndrome: a systematic review informing the EULAR/PReS guidelines. Ann Rheum Dis. 2024;83(12):1731‑1747. doi:10.1136/ard-2024-225854
  506. Gamifant (emapalumab‑lzsg) injection: US prescribing information. Swedish Orphan Biovitrum AB; revised Mar 2026. DailyMed
  507. Ehl S, Astigarraga I, von Bahr Greenwood T, et al. Recommendations for the use of etoposide-based therapy and bone marrow transplantation for the treatment of HLH: consensus statements by the HLH Steering Committee of the Histiocyte Society. J Allergy Clin Immunol Pract. 2018;6(5):1508–1517. doi:10.1016/j.jaip.2018.05.031
  508. Jone PN, Tremoulet A, Choueiter N, et al; American Heart Association. Update on diagnosis and management of Kawasaki disease: a scientific statement from the American Heart Association. Circulation. 2024;150(23):e481–e500. doi:10.1161/CIR.0000000000001295
  509. Kuo HC, Lin MC, Kao CC, et al. Intravenous immunoglobulin alone for coronary artery lesion treatment of Kawasaki disease: a randomized clinical trial. JAMA Netw Open. 2025;8(4):e253063. doi:10.1001/jamanetworkopen.2025.3063
  510. Huang YH, Hsin YC, Wang LJ, et al. Treatment of Kawasaki disease: a network meta‑analysis of four dosage regimens of aspirin combined with recommended intravenous immunoglobulin. Front Pharmacol. 2021;12:725126. doi:10.3389/fphar.2021.725126
  511. Jia X, Du X, Bie S, Li Q, Chen Y. What dose of aspirin should be used in the initial treatment of Kawasaki disease? A meta‑analysis. Rheumatology (Oxford). 2020;59(8):1826–1833. doi:10.1093/rheumatology/keaa050
  512. Chiang MH, Liu HE, Wang JL. Low‑dose or no aspirin administration in acute‑phase Kawasaki disease: a meta‑analysis and systematic review. Arch Dis Child. 2021;106(7):662–668. doi:10.1136/archdischild-2019-318245
  513. Thadani L, Khan H, Kim KY, et al. Lack of discernible benefit of high‑dose aspirin in the treatment of Kawasaki disease. J Pediatric Infect Dis Soc. 2026;15(2):piag002. doi:10.1093/jpids/piag002
  514. Hayashi K, Miyakoshi C, Hoshino S, et al. Initial intravenous immunoglobulin therapy without aspirin for acute Kawasaki disease: a retrospective cohort study with a Bayesian inference. BMJ Paediatr Open. 2024;8(1):e002312. doi:10.1136/bmjpo-2023-002312
  515. Suzuki T, Michihata N, Hashimoto Y, et al. Association between aspirin dose and outcomes in patients with acute Kawasaki disease: a nationwide retrospective cohort study in Japan. Eur J Pediatr. 2024;183(1):415–424. doi:10.1007/s00431-023-05302-8
  516. Ozen S, Pistorio A, Iusan SM, et al. EULAR/PRINTO/PRES criteria for Henoch‑Schönlein purpura, childhood polyarteritis nodosa, childhood Wegener granulomatosis and childhood Takayasu arteritis: Ankara 2008. Part II: final classification criteria. Ann Rheum Dis. 2010;69(5):798–806. doi:10.1136/ard.2009.116657
  517. Ozen S, Marks SD, Brogan P, et al. European consensus‑based recommendations for diagnosis and treatment of immunoglobulin A vasculitis — the SHARE initiative. Rheumatology (Oxford). 2019;58(9):1607–1616. doi:10.1093/rheumatology/kez041
  518. Oni L, Platt C, Marlais M, et al. National recommendations for the management of children and young people with IgA vasculitis: a best available evidence, group agreement‑based approach. Arch Dis Child. 2025;110(1):67–76. doi:10.1136/archdischild-2024-327364
  519. Vivarelli M, Samuel S, Coppo R, et al. IPNA clinical practice recommendations for the diagnosis and management of children with IgA nephropathy and IgA vasculitis nephritis. Pediatr Nephrol. 2025;40(2):533–569. doi:10.1007/s00467-024-06502-6
  520. Watson L, Richardson AR, Holt RC, Jones CA, Beresford MW. Henoch Schönlein purpura — a 5‑year review and proposed pathway. PLoS One. 2012;7(1):e29512. doi:10.1371/journal.pone.0029512
  521. Narchi H. Risk of long term renal impairment and duration of follow up recommended for Henoch‑Schönlein purpura with normal or minimal urinary findings: a systematic review. Arch Dis Child. 2005;90(9):916–920. doi:10.1136/adc.2005.074641
  522. Council of State and Territorial Epidemiologists / Centers for Disease Control and Prevention. Multisystem inflammatory syndrome in children (MIS‑C) associated with SARS‑CoV‑2 infection: 2023 case definition (CSTE position statement 22‑ID‑02). Atlanta (GA): CDC; 2023. cdc.gov
  523. Berard RA, Tam H, Scuccimarri R, et al.; Canadian Paediatric Society, Acute Care Committee. Paediatric inflammatory multisystem syndrome temporally associated with COVID-19 (spring 2021 update). Position statement, posted 6 Jul 2020, updated 3 May 2021. cps.ca
  524. Applegate KE, Anderson JM, Klatte EC. Intestinal malrotation in children: a problem‑solving approach to the upper gastrointestinal series. RadioGraphics. 2006;26(5):1485–1500. doi:10.1148/rg.265055167
  525. Langer JC. Intestinal rotation abnormalities and midgut volvulus. Surg Clin North Am. 2017;97(1):147–159. doi:10.1016/j.suc.2016.08.011
  526. Hwang J, Yoon HM, Kim PH, et al. Current diagnosis and image‑guided reduction for intussusception in children. Clin Exp Pediatr. 2023;66(1):12–21. doi:10.3345/cep.2021.01816
  527. Belkind‑Gerson J. Hypertrophic pyloric stenosis. In: Merck Manual Professional Edition. Rahway (NJ): Merck & Co.; revised Aug 2025. merckmanuals.com
  528. Podda M, et al. Diagnosis and treatment of acute appendicitis: 2025 edition of the WSES Jerusalem guidelines. JAMA Surg. 2026;161(3):283–295. doi:10.1001/jamasurg.2025.6218
  529. Green R, Bulloch B, Kabani A, et al. Early analgesia for children with acute abdominal pain. Pediatrics. 2005;116(4):978–983. doi:10.1542/peds.2005-0273
  530. Solomkin JS, Mazuski JE, Bradley JS, et al. Diagnosis and management of complicated intra-abdominal infection in adults and children: guidelines by the Surgical Infection Society and the Infectious Diseases Society of America. Clin Infect Dis. 2010;50(2):133–164. doi:10.1086/649554
  531. ZOSYN (piperacillin and tazobactam) for injection — US prescribing information (Dosage and Administration: pediatric patients with appendicitis and/or peritonitis). Pfizer (Wyeth). labeling.pfizer.com
  532. Sawyer RG, Claridge JA, Nathens AB, et al. Trial of short‑course antimicrobial therapy for intraabdominal infection. N Engl J Med. 2015;372(21):1996–2005. doi:10.1056/NEJMoa1411162
  533. Holcomb GW III, Murphy JP, St Peter SD, eds. Holcomb and Ashcraft’s Pediatric Surgery. 7th ed. Philadelphia, PA: Elsevier; 2020. Chapter: Inguinal and umbilical hernias. ISBN 978‑0‑323‑54940‑0.
  534. Inguinal hernia in neonates. In: Miscellaneous surgical emergencies in neonates. Merck Manual Professional Edition. Rahway (NJ): Merck & Co.; revised Aug 2025. merckmanuals.com
  535. Boyle JS, Bechtel LK, Holstege CP. Management of the critically poisoned patient. Scand J Trauma Resusc Emerg Med. 2009;17:29. doi:10.1186/1757-7241-17-29
  536. Dart RC, Mullins ME, Matoushek T, et al. Management of acetaminophen poisoning in the US and Canada: a consensus statement. JAMA Netw Open. 2023;6(8):e2327739. doi:10.1001/jamanetworkopen.2023.27739
  537. Hoegberg LCG, Gosselin S, Buckley NA, et al. Recommendations from the Clinical Toxicology Recommendations Collaborative on the administration of activated charcoal in acute oral overdose. Clin Toxicol (Phila). 2026;64(6):419–475. doi:10.1080/15563650.2025.2609807
  538. Thanacoody R, Caravati EM, Troutman B, et al. Position paper update: whole bowel irrigation for gastrointestinal decontamination of overdose patients. Clin Toxicol (Phila). 2015;53(1):5–12. doi:10.3109/15563650.2014.989326
  539. Chyka PA, Seger D, Krenzelok EP, et al.; American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Position paper: single-dose activated charcoal. Clin Toxicol (Phila). 2005;43(2):61–87 (update of the 1997 AACT/EAPCCT position statement, J Toxicol Clin Toxicol 1997;35(7):721–741). doi:10.1081/clt-200051867
  540. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Position paper: whole bowel irrigation. J Toxicol Clin Toxicol. 2004;42(6):843–854. doi:10.1081/clt-200035932
  541. American Academy of Clinical Toxicology; European Association of Poisons Centres and Clinical Toxicologists. Position statement and practice guidelines on the use of multi-dose activated charcoal in the treatment of acute poisoning. J Toxicol Clin Toxicol. 1999;37(6):731–751. doi:10.1081/clt-100102451
  542. Benson BE, Hoppu K, Troutman WG, et al. Position paper update: gastric lavage for gastrointestinal decontamination. Clin Toxicol (Phila). 2013;51(3):140–146. doi:10.3109/15563650.2013.770154
  543. Höjer J, Troutman WG, Hoppu K, et al. Position paper update: ipecac syrup for gastrointestinal decontamination. Clin Toxicol (Phila). 2013;51(3):134–139. doi:10.3109/15563650.2013.770153
  544. Isbister GK, Buckley NA, Whyte IM. Serotonin toxicity: a practical approach to diagnosis and treatment. Med J Aust. 2007;187(6):361–365. doi:10.5694/j.1326-5377.2007.tb01282.x
  545. Boyer EW. Management of opioid analgesic overdose. N Engl J Med. 2012;367(2):146–155. doi:10.1056/NEJMra1202561
  546. Hoffman RJ, Nillas A. Toxidromes and a general approach to poisoning. Arch Dis Child. 2025;110(9):681–686. doi:10.1136/archdischild-2024-326969
  547. Lifshitz M, Shahak E, Sofer S. Carbamate and organophosphate poisoning in young children. Pediatr Emerg Care. 1999;15(2):102–103. doi:10.1097/00006565-199904000-00006
  548. Holstege CP, Borek HA. Toxidromes. Crit Care Clin. 2012;28(4):479–498. doi:10.1016/j.ccc.2012.07.008
  549. Lavonas EJ, Akpunonu PD, Arens AM, et al. 2023 American Heart Association focused update on the management of patients with cardiac arrest or life-threatening toxicity due to poisoning: an update to the American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2023;148(16):e149–e184. doi:10.1161/CIR.0000000000001161
  550. DiphenhydrAMINE hydrochloride injection, USP — US prescribing information (Warnings — use in pediatric patients; Overdosage). Hospira; revised 05/2019. Pfizer labeling
  551. Dunkley EJC, Isbister GK, Sibbritt D, Dawson AH, Whyte IM. The Hunter Serotonin Toxicity Criteria: simple and accurate diagnostic decision rules for serotonin toxicity. QJM. 2003;96(9):635–642. doi:10.1093/qjmed/hcg109
  552. FDA Drug Safety Communication: Serious CNS reactions possible when methylene blue is given to patients taking certain psychiatric medications. 26 July 2011 (updated 20 Oct 2011); companion communication on linezolid (Zyvox), 20 Oct 2011. FDA
  553. Morphine sulfate injection — US prescribing information (§10 Overdosage — clinical presentation). Hospira; revised 12/2025. Pfizer labeling
  554. Klein-Schwartz W. Trends and toxic effects from pediatric clonidine exposures. Arch Pediatr Adolesc Med. 2002;156(4):392–396. doi:10.1001/archpedi.156.4.392
  555. Wiley JF, Wiley CC, Torrey SB, Henretig FM. Clonidine poisoning in young children. J Pediatr. 1990;116(4):654–658. doi:10.1016/s0022-3476(05)81621-x
  556. US Food and Drug Administration. FDA Drug Safety Communication: Serious adverse events from accidental ingestion by children of over-the-counter eye drops and nasal sprays. 25 Oct 2012. FDA
  557. Phenobarbital tablets, USP — US prescribing information (Overdosage — signs and symptoms of barbiturate poisoning). Hikma Pharmaceuticals USA; revised 7/2024. DailyMed
  558. Eddleston M, Buckley NA, Eyer P, Dawson AH. Management of acute organophosphorus pesticide poisoning. Lancet. 2008;371(9612):597–607. doi:10.1016/S0140-6736(07)61202-1
  559. Zwiener RJ, Ginsburg CM. Organophosphate and carbamate poisoning in infants and children. Pediatrics. 1988;81(1):121–126. PMID 3336578
  560. Chyka PA, Erdman AR, Christianson G, et al. Salicylate poisoning: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2007;45(2):95–131. doi:10.1080/15563650600907140
  561. Chiew AL, Reith D, Pomerleau A, et al. Updated guidelines for the management of paracetamol poisoning in Australia and New Zealand. Med J Aust. 2020;212(4):175–183. doi:10.5694/mja2.50428
  562. Acetadote (acetylcysteine) injection. Full prescribing information. Nashville: Cumberland Pharmaceuticals; revised 4/2025.
  563. Nakatsu L, Lopez JR, Garcia CM, et al. Comparison of two-bag and three-bag acetylcysteine regimens in the treatment of paracetamol poisoning: a systematic review and meta-analysis. Clin Toxicol (Phila). 2025;63(3):155–165. doi:10.1080/15563650.2025.2456116
  564. Wong A, Isbister G, McNulty R, et al. Efficacy of a two bag acetylcysteine regimen to treat paracetamol overdose (2NAC study). EClinicalMedicine. 2020;20:100288. doi:10.1016/j.eclinm.2020.100288
  565. Physostigmine salicylate injection — US prescribing information (Indications; Contraindications; Warnings; Dosage and Administration — adult and pediatric). HF Acquisition Co LLC (HealthFirst); revised 1/2023. DailyMed
  566. Wang GS, Baker K, Ng P, et al. A randomized trial comparing physostigmine vs lorazepam for treatment of antimuscarinic (anticholinergic) toxidrome. Clin Toxicol (Phila). 2021;59(8):698–704. doi:10.1080/15563650.2020.1854281
  567. Burns MJ, Linden CH, Graudins A, Brown RM, Fletcher KE. A comparison of physostigmine and benzodiazepines for the treatment of anticholinergic poisoning. Ann Emerg Med. 2000;35(4):374–381. doi:10.1016/S0196-0644(00)70057-6
  568. Arens AM, Kearney T. Adverse effects of physostigmine. J Med Toxicol. 2019;15(3):184–191. doi:10.1007/s13181-019-00697-z
  569. Flumazenil injection, USP — US prescribing information (boxed warning — seizures; Contraindications; Dosage and Administration; management of suspected benzodiazepine overdose; monitoring for resedation). Hikma; revised 12/2025. DailyMed
  570. Engebretsen KM, Kaczmarek KM, Morgan J, Holger JS. High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning. Clin Toxicol (Phila). 2011;49(4):277–283. doi:10.3109/15563650.2011.582471
  571. St-Onge M, Anseeuw K, Cantrell FL, et al. Experts consensus recommendations for the management of calcium channel blocker poisoning in adults. Crit Care Med. 2017;45(3):e306–e315. doi:10.1097/CCM.0000000000002087
  572. Weaver LK. Carbon monoxide poisoning (reprinted from the 2023 Hyperbaric Indications Manual, 15th edition). Undersea Hyperb Med. 2024;51(3):253–276. PMID 39348519 (no DOI assigned)
  573. Uysalol M, Gümüş S, Yıldız R. How to decide oxygen therapy in childhood carbon monoxide poisoning? Turk Arch Pediatr. 2023;58(3):282–288. doi:10.5152/TurkArchPediatr.2023.22189
  574. Cyanokit 5 g powder for solution for infusion (hydroxocobalamin) — Summary of Product Characteristics (§4.2 paediatric posology; §4.4 blood pressure and renal function monitoring; §6.2 incompatibilities). SERB S.A.; EMA EPAR product information. EMA
  575. Sodium Thiosulfate Injection, USP 12.5 g/50 mL (250 mg/mL) — US prescribing information (§2 Dosage and administration — pediatric dose; incompatibility with hydroxocobalamin; blood pressure monitoring). Hope Pharmaceuticals; revised 06/2020. www.accessdata.fda.gov
  576. Baud FJ, Barriot P, Toffis V, et al. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med. 1991;325(25):1761–1766. doi:10.1056/NEJM199112193252502
  577. Baud FJ, Borron SW, Mégarbane B, et al. Value of lactic acidosis in the assessment of the severity of acute cyanide poisoning. Crit Care Med. 2002;30(9):2044–2050. doi:10.1097/00003246-200209000-00015
  578. DIGIFAB (digoxin immune Fab [ovine]) for injection — US prescribing information (§1 Indications and Usage; §2 Dosage and Administration). Salvagenix Inc.; revised 4/2026. DailyMed
  579. DESFERAL (deferoxamine mesylate) for injection — US prescribing information (§2 acute iron intoxication; §5 rate-related hypotension and acute respiratory distress syndrome; §8.4 pediatric use). Novartis; revised 6/2025. DailyMed
  580. Manoguerra AS, Erdman AR, Booze LL, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005;43(6):553–570. doi:10.1081/clt-200068842
  581. Tenenbein M, Kowalski S, Sienko A, Bowden DH, Adamson IY. Pulmonary toxic effects of continuous desferrioxamine administration in acute iron poisoning. Lancet. 1992;339(8795):699–701. doi:10.1016/0140-6736(92)90598-W
  582. Isoniazid tablets, USP — US prescribing information (Overdosage: signs and symptoms; treatment of the asymptomatic and symptomatic patient). Chartwell RX; revised 02/2025. DailyMed
  583. Wason S, Lacouture PG, Lovejoy FH. Single high-dose pyridoxine treatment for isoniazid overdose. JAMA. 1981;246(10):1102–1104. PMID 7265398
  584. Shah BR, Santucci K, Sinert R, Steiner P. Acute isoniazid neurotoxicity in an urban hospital. Pediatrics. 1995;95(5):700–704. PMID 7724306
  585. Neal JM, Neal EJ, Weinberg GL. American Society of Regional Anesthesia and Pain Medicine Local Anesthetic Systemic Toxicity checklist: 2020 version. Reg Anesth Pain Med. 2021;46(1):81–82. doi:10.1136/rapm-2020-101986
  586. ANTIZOL (fomepizole) injection — US prescribing information (Dosage and administration — dosing with hemodialysis; Precautions — pediatric use). Revised 12/2020. www.accessdata.fda.gov
  587. Barceloux DG, Bond GR, Krenzelok EP, Cooper H, Vale JA; American Academy of Clinical Toxicology Ad Hoc Committee on the Treatment Guidelines for Methanol Poisoning. American Academy of Clinical Toxicology practice guidelines on the treatment of methanol poisoning. J Toxicol Clin Toxicol. 2002;40(4):415–446. doi:10.1081/clt-120006745
  588. Roberts DM, Yates C, Megarbane B, et al. Recommendations for the role of extracorporeal treatments in the management of acute methanol poisoning: a systematic review and consensus statement. Crit Care Med. 2015;43(2):461–472. doi:10.1097/CCM.0000000000000708
  589. Ghannoum M, Gosselin S, Hoffman RS, et al. Extracorporeal treatment for ethylene glycol poisoning: systematic review and recommendations from the EXTRIP workgroup. Crit Care. 2023;27(1):56. doi:10.1186/s13054-022-04227-2
  590. Iolascon A, Bianchi P, Andolfo I, et al. Recommendations for diagnosis and treatment of methemoglobinemia. Am J Hematol. 2021;96(12):1666–1678. doi:10.1002/ajh.26340
  591. American Academy of Pediatrics Committee on Drugs. Naloxone dosage and route of administration for infants and children: addendum to emergency drug doses for infants and children. Pediatrics. 1990;86(3):484–485. PMID 2388800
  592. PROTOPAM Chloride (pralidoxime chloride) for injection — US prescribing information (Dosage and administration — pediatric loading dose and infusion, maximum rate; Precautions — succinylcholine; carbamates). Baxter Healthcare; FDA‑approved labeling 8 Sep 2010. www.accessdata.fda.gov
  593. American College of Medical Toxicology. Guidance document: management priorities in salicylate toxicity. J Med Toxicol. 2015;11(1):149–152. doi:10.1007/s13181-013-0362-3
  594. Proudfoot AT, Krenzelok EP, Vale JA. Position paper on urine alkalinization. J Toxicol Clin Toxicol. 2004;42(1):1–26. doi:10.1081/clt-120028740
  595. Chiew AL, Isbister GK. Management of serotonin syndrome (toxicity). Br J Clin Pharmacol. 2025;91(3):654–661. doi:10.1111/bcp.16152
  596. Woolf AD, Erdman AR, Nelson LS, et al. Tricyclic antidepressant poisoning: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2007;45(3):203–233. doi:10.1080/15563650701226192
  597. Klein-Schwartz W, Stassinos GL, Isbister GK. Treatment of sulfonylurea and insulin overdose. Br J Clin Pharmacol. 2016;81(3):496–504. doi:10.1111/bcp.12822
  598. Glatstein M, Scolnik D, Bentur Y. Octreotide for the treatment of sulfonylurea poisoning. Clin Toxicol (Phila). 2012;50(9):795–804. doi:10.3109/15563650.2012.734626
  599. American Heart Association. Highlights of the 2023 American Heart Association focused update on the management of patients with cardiac arrest or life-threatening toxicity due to poisoning (sympathomimetics; cocaine). Dallas, TX: American Heart Association; 2023 (KJ‑1712). cpr.heart.org
  600. Koren G. Medications which can kill a toddler with one tablet or teaspoonful. J Toxicol Clin Toxicol. 1993;31(3):407–413. doi:10.3109/15563659309000409
  601. Bar-Oz B, Levichek Z, Koren G. Medications that can be fatal for a toddler with one tablet or teaspoonful: a 2004 update. Paediatr Drugs. 2004;6(2):123–126. doi:10.2165/00148581-200406020-00005
  602. Koren G, Nachmani A. Drugs that can kill a toddler with one tablet or teaspoonful: a 2018 updated list. Clin Drug Investig. 2019;39(2):217–220. doi:10.1007/s40261-018-0726-1
  603. Olson KR, Erdman AR, Woolf AD, et al. Calcium channel blocker ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2005;43(7):797–822. doi:10.1080/15563650500357404
  604. McCarron MM, Challoner KR, Thompson GA. Diphenoxylate-atropine (Lomotil) overdose in children: an update (report of eight cases and review of the literature). Pediatrics. 1991;87(5):694–700. PMID 2020516
  605. Smith ER, Klein-Schwartz W. Are 1-2 dangerous? Chloroquine and hydroxychloroquine exposure in toddlers. J Emerg Med. 2005;28(4):437–443. doi:10.1016/j.jemermed.2004.12.011
  606. Cobaugh DJ, Erdman AR, Booze LL, et al. Atypical antipsychotic medication poisoning: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila). 2007;45(8):918–942. doi:10.1080/15563650701665142
  607. Hayes BD, Klein-Schwartz W, Doyon S. Toxicity of buprenorphine overdoses in children. Pediatrics. 2008;121(4):e782–e786. doi:10.1542/peds.2007-1774
  608. Michael JB, Sztajnkrycer MD. Deadly pediatric poisons: nine common agents that kill at low doses. Emerg Med Clin North Am. 2004;22(4):1019–1050. doi:10.1016/j.emc.2004.05.004
  609. Manoguerra AS, Erdman AR, Wax PM, et al. Camphor poisoning: an evidence-based practice guideline for out-of-hospital management. Clin Toxicol (Phila). 2006;44(4):357–370. doi:10.1080/15563650600671696
  610. Sachdeva DK, Stadnyk JM. Are one or two dangerous? Opioid exposure in toddlers. J Emerg Med. 2005;29(1):77–84. doi:10.1016/j.jemermed.2004.12.015
  611. Spiller HA, Villalobos D, Krenzelok EP, et al. Prospective multicenter study of sulfonylurea ingestion in children. J Pediatr. 1997;131(1 Pt 1):141–146. doi:10.1016/s0022-3476(97)70138-0
  612. Contini S, Scarpignato C. Caustic injury of the upper gastrointestinal tract: a comprehensive review. World J Gastroenterol. 2013;19(25):3918–3930. doi:10.3748/wjg.v19.i25.3918
  613. Chirica M, Kelly MD, Siboni S, et al. Esophageal emergencies: WSES guidelines. World J Emerg Surg. 2019;14:26. doi:10.1186/s13017-019-0245-2
  614. Thomson M, Tringali A, Dumonceau JM, et al. Paediatric gastrointestinal endoscopy: European Society for Paediatric Gastroenterology Hepatology and Nutrition and European Society of Gastrointestinal Endoscopy guidelines. J Pediatr Gastroenterol Nutr. 2017;64(1):133–153. doi:10.1097/MPG.0000000000001408
  615. Tormoehlen LM, Tekulve KJ, Nañagas KA. Hydrocarbon toxicity: a review. Clin Toxicol (Phila). 2014;52(5):479–489. doi:10.3109/15563650.2014.923904
  616. Makrygianni EA, Palamidou F, Kaditis AG. Respiratory complications following hydrocarbon aspiration in children. Pediatr Pulmonol. 2016;51(6):560–569. doi:10.1002/ppul.23392
  617. Machado B, Cross K, Snodgrass WR. Accidental hydrocarbon ingestion cases telephoned to a regional poison center. Ann Emerg Med. 1988;17(8):804–807. doi:10.1016/s0196-0644(88)80558-4
  618. Anas N, Namasonthi V, Ginsburg CM. Criteria for hospitalizing children who have ingested products containing hydrocarbons. JAMA. 1981;246(8):840–843. PMID 7253158
  619. Minns AB, Ghafouri N, Clark RF. Isoniazid-induced status epilepticus in a pediatric patient after inadequate pyridoxine therapy. Pediatr Emerg Care. 2010;26(5):380–381. doi:10.1097/PEC.0b013e3181db24b6
  620. Dart RC, Goldfrank LR, Erstad BL, et al. Expert consensus guidelines for stocking of antidotes in hospitals that provide emergency care. Ann Emerg Med. 2018;71(3):314–325.e1. doi:10.1016/j.annemergmed.2017.05.021
  621. Pyridoxine hydrochloride injection, USP 100 mg/mL — US prescribing information (How supplied). Fresenius Kabi USA; revised 9/2019. DailyMed
  622. ISBI Practice Guidelines Committee. ISBI Practice Guidelines for Burn Care. Burns. 2016;42(5):953–1021. doi:10.1016/j.burns.2016.05.013
  623. Walker PF, Buehner MF, Wood LA, et al. Diagnosis and management of inhalation injury: an updated review. Crit Care. 2015;19(1):351. doi:10.1186/s13054-015-1077-4
  624. TREKK (Translating Emergency Knowledge for Kids). Bottom Line Recommendations: Pediatric Thermal Burns. Version 2.0, April 2025 (Malic C, Crombie T). trekk.ca
  625. Royal Children’s Hospital Melbourne. Clinical Practice Guideline: Burns — acute management. Updated April 2026. rch.org.au
  626. Lund CC, Browder NC. The estimation of areas of burns. Surg Gynecol Obstet. 1944;79:352–358.
  627. Griffin BR, Frear CC, Babl F, Oakley E, Kimble RM. Cool running water first aid decreases skin grafting requirements in pediatric burns: a cohort study of two thousand four hundred ninety-five children. Ann Emerg Med. 2020;75(1):75–85. doi:10.1016/j.annemergmed.2019.06.028
  628. American Burn Association. Advanced Burn Life Support Course: Provider Manual. 2023 update. Chicago (IL): American Burn Association; 2023.
  629. Maguire S, Moynihan S, Mann M, Potokar T, Kemp AM. A systematic review of the features that indicate intentional scalds in children. Burns. 2008;34(8):1072–1081. doi:10.1016/j.burns.2008.02.011
  630. Epstein Y, Yanovich R. Heatstroke. N Engl J Med. 2019;380(25):2449–2459. doi:10.1056/NEJMra1810762
  631. Bergeron MF, Devore C, Rice SG; American Academy of Pediatrics Council on Sports Medicine and Fitness and Council on School Health. Policy statement—Climatic heat stress and exercising children and adolescents. Pediatrics. 2011;128(3):e741–e747. doi:10.1542/peds.2011-1664
  632. Szpilman D, Bierens JJLM, Handley AJ, Orlowski JP. Drowning. N Engl J Med. 2012;366(22):2102–2110. doi:10.1056/NEJMra1013317
  633. State of Kuwait, Ministry of Health. National protocol for the evaluation and management of drowning (submersion injury) across the continuum of care. National Multidisciplinary Drowning Protocol Working Group. Kuwait: MOH; 2026 (draft pending approval).
  634. Szpilman D. Near-drowning and drowning classification: a proposal to stratify mortality based on the analysis of 1,831 cases. Chest. 1997;112(3):660–665. doi:10.1378/chest.112.3.660
  635. Buckley NA, Juurlink DN, Isbister G, Bennett MH, Lavonas EJ. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev. 2011;(4):CD002041. doi:10.1002/14651858.CD002041.pub3
  636. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002;347(14):1057–1067. doi:10.1056/NEJMoa013121
  637. Bawaskar HS, Bawaskar PH. Efficacy and safety of scorpion antivenom plus prazosin compared with prazosin alone for venomous scorpion (Mesobuthus tamulus) sting: randomised open label clinical trial. BMJ. 2011;342:c7136. doi:10.1136/bmj.c7136
  638. Abroug F, Ouanes-Besbes L, Tilouche N, et al. Scorpion envenomation: state of the art. Intensive Care Med. 2020;46(3):401–410. doi:10.1007/s00134-020-05924-8
  639. World Health Organization, Regional Office for South‑East Asia. Guidelines for the Management of Snakebites. 2nd ed. New Delhi: WHO‑SEARO; 2016. who.int
  640. World Health Organization. Rabies vaccines: WHO position paper – April 2018. Wkly Epidemiol Rec. 2018;93(16):201–220. who.int
  641. CDC/ACIP. General Best Practice Guidelines for Immunization: Altered Immunocompetence; Timing and Spacing of Immunobiologics (table of intervals between antibody‑containing products and measles‑ or varicella‑containing vaccine). Last reviewed 1 Aug 2023. CDC — Timing and Spacing (Table 3‑6); CDC — Altered Immunocompetence
  642. McMullan BJ, Andresen D, Blyth CC, et al; ANZPID‑ASAP group. Antibiotic duration and timing of the switch from intravenous to oral route for bacterial infections in children: systematic review and guidelines. Lancet Infect Dis. 2016;16(8):e139–e152. doi:10.1016/S1473-3099(16)30024-X
  643. Yen K, Riegert A, Gorelick MH. Derivation of the DIVA score: a clinical prediction rule for the identification of children with difficult intravenous access. Pediatr Emerg Care. 2008;24(3):143–147. doi:10.1097/PEC.0b013e3181666f32
  644. Riker MW, Kennedy C, Winfrey BS, Yen K, Dowd MD. Validation and refinement of the difficult intravenous access score. Acad Emerg Med. 2011;18(11):1129–1134. doi:10.1111/j.1553-2712.2011.01205.x
  645. Schwartz GJ, Muñoz A, Schneider MF, et al. New equations to estimate GFR in children with CKD. J Am Soc Nephrol. 2009;20(3):629–637. doi:10.1681/ASN.2008030287
  646. Durrmeyer X, Walter-Nicolet E, Chollat C, et al. Premedication before laryngoscopy in neonates: evidence-based statement from the French Society of Neonatology (SFN). Front Pediatr. 2023;10:1075184. doi:10.3389/fped.2022.1075184
  647. Afifi J, El-Naggar W, Hatfield T, et al. Atropine versus placebo for neonatal nonemergent intubation: a randomized clinical trial. J Pediatr. 2025;286:114719. doi:10.1016/j.jpeds.2025.114719
  648. ANECTINE (succinylcholine chloride) injection — US prescribing information (boxed warning; Contraindications; Warnings). Sandoz; revised November 2022. www.accessdata.fda.gov
  649. US Food and Drug Administration. Single entity injectable drug products — removal of ratio expressions of strength from labeling (e.g., Epinephrine Injection 1:1,000 now labeled 1 mg/mL). Silver Spring, MD: FDA; accessed 5 Oct 2026. fda.gov
  650. Monagle P, Azzam M, Bercovitz R, et al. American Society of Hematology/International Society on Thrombosis and Haemostasis 2024 updated guidelines for treatment of venous thromboembolism in pediatric patients. Blood Adv. 2025;9(10):2587–2636. doi:10.1182/bloodadvances.2024015328
  651. Monagle P, Cuello CA, Augustine C, et al. American Society of Hematology 2018 guidelines for management of venous thromboembolism: treatment of pediatric venous thromboembolism. Blood Adv. 2018;2(22):3292–3316. doi:10.1182/bloodadvances.2018024786
  652. Goldenberg NA, Kittelson JM, Abshire TC, et al. Effect of anticoagulant therapy for 6 weeks vs 3 months on recurrence and bleeding events in patients younger than 21 years of age with provoked venous thromboembolism: the Kids-DOTT randomized clinical trial. JAMA. 2022;327(2):129–137. doi:10.1001/jama.2021.23182
  653. Betensky M, Azzam M, Bercovitz R, et al. ASH/ISTH 2026 guidelines for anticoagulant prophylaxis in pediatric patients at risk of venous thromboembolism. Blood Adv. 2026;10(12):4303–4333. doi:10.1182/bloodadvances.2025019415
  654. LOVENOX (enoxaparin sodium injection) — US prescribing information (Dosage and Administration: severe renal impairment; Overdosage: protamine neutralization). sanofi-aventis U.S. label text (medlibrary.org)
  655. XYLOCAINE (lidocaine HCl) and XYLOCAINE with epinephrine injection — US prescribing information (Dosage and Administration: maximum recommended dosages, adults and children). Fresenius Kabi USA. label text (medlibrary.org)
  656. Ministry of Health, State of Kuwait (Public Health Sector). Kuwait Childhood Immunization Schedule 2025. Kuwait: MOH; 2025. Official national schedule (not published as an open web document; MOH preventive-vaccination service: e.gov.kw).
  657. Alsharhan H, Ahmed AA, Ali NM, et al. Early diagnosis of classic homocystinuria in Kuwait through newborn screening: a 6-year experience. Int J Neonatal Screen. 2021;7(3):56. doi:10.3390/ijns7030056
  658. Alsharhan H, Ahmed AA, Abdullah M, et al. Insights from the newborn screening program for very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency in Kuwait. Int J Neonatal Screen. 2025;11(1):19. doi:10.3390/ijns11010019
  659. Al‑Awadi SA, Moussa MA, Naguib KK, et al. Consanguinity among the Kuwaiti population. Clin Genet. 1985;27(5):483–486. doi:10.1111/j.1399-0004.1985.tb00236.x
  660. Radovanovic Z, Shah N, Behbehani J. Prevalence and social correlates to consanguinity in Kuwait. Ann Saudi Med. 1999;19(3):206–210. doi:10.5144/0256-4947.1999.206
  661. Teebi AS. Autosomal recessive disorders among Arabs: an overview from Kuwait. J Med Genet. 1994;31(3):224–233. doi:10.1136/jmg.31.3.224
  662. Marafi D. Founder mutations and rare disease in the Arab world. Dis Model Mech. 2024;17(6):dmm050715. doi:10.1242/dmm.050715
  663. Adekile AD, Al‑Sherida S, Marouf R, Mustafa N, Thomas D. The sub‑phenotypes of sickle cell disease in Kuwait. Hemoglobin. 2019;43(2):83–87. doi:10.1080/03630269.2019.1610427
  664. Adekile A, Sukumaran J, Thomas D, D’Souza T, Haider M. Alpha thalassemia genotypes in Kuwait. BMC Med Genet. 2020;21(1):170. doi:10.1186/s12881-020-01105-y
  665. Samilchuk E, Al‑Suliman I, Usanga E, Al Awadi S. Glucose‑6‑phosphate dehydrogenase (G6PD) mutations and UDP‑glucuronosyltransferase promoter polymorphism among G6PD deficient Kuwaitis. Blood Cells Mol Dis. 2003;31(2):201–205. doi:10.1016/s1079-9796(03)00125-6
  666. Adrenaline (Epinephrine) 1 mg/ml (1:1000) solution for injection (ampoule) — Summary of Product Characteristics (§4.1 indications; §4.2 intramuscular route in anaphylaxis; not suitable for IV use — dilute to 0.1 mg/ml (1:10000) before IV use). Macarthys Laboratories Ltd (Martindale Pharma); emc (SmPC), revised 7 Jul 2026. medicines.org.uk/emc/product/3673
  667. Hoyle JD, Ekblad G, Hover T, et al. Dosing errors made by paramedics during pediatric patient simulations after implementation of a state-wide pediatric drug dosing reference. Prehosp Emerg Care. 2020;24(2):204–213. doi:10.1080/10903127.2019.1619002
  668. Institute for Safe Medication Practices. ISMP List of Error-Prone Abbreviations, Symbols, and Dose Designations. Plymouth Meeting, PA: ISMP; 2024. ISMP/ECRI
  669. Doherty C, Mc Donnell C. Tenfold medication errors: 5 years’ experience at a university-affiliated pediatric hospital. Pediatrics. 2012;129(5):916–924. doi:10.1542/peds.2011-2526
  670. Benjamin L, Frush K, Shaw K, Shook JE, Snow SK; American Academy of Pediatrics, American College of Emergency Physicians, Emergency Nurses Association. Pediatric medication safety in the emergency department. Pediatrics. 2018;141(3):e20174066. doi:10.1542/peds.2017-4066
  671. Institute for Safe Medication Practices. Independent double checks: worth the effort if used judiciously and properly. ISMP Medication Safety Alert! Acute Care. 2019 Jun 6;24:1–7. ISMP/ECRI
  672. Sterns RH, Rondon-Berrios H, Adrogué HJ, et al. Treatment guidelines for hyponatremia: stay the course. Clin J Am Soc Nephrol. 2024;19(1):129–135. doi:10.2215/CJN.0000000000000244
  673. Didsbury M, See EJ, Cheng DR, Kausman J, Quinlan C. Correcting hypernatremia in children. Clin J Am Soc Nephrol. 2023;18(3):306–314. doi:10.2215/CJN.0000000000000077
  674. Feld LG, Neuspiel DR, Foster BA, et al.; Subcommittee on Fluid and Electrolyte Therapy. Clinical practice guideline: maintenance intravenous fluids in children. Pediatrics. 2018;142(6):e20183083. doi:10.1542/peds.2018-3083
  675. Potassium Chloride for Injection Concentrate, USP — US prescribing information (Dosage and Administration — dilution, rate and concentration limits, cardiac monitoring; Warnings — direct injection may be instantaneously fatal). Hospira; LAB-1319-3.0, revised 1/2026. pfizermedical.com
  676. Hackenberg RK, Kabir K, Müller A, Heydweiller A, Burger C, Welle K. Extravasation injuries of the limbs in neonates and children — development of a treatment algorithm. Dtsch Arztebl Int. 2021;118(33–34):547–554. doi:10.3238/arztebl.m2021.0220
  677. Ong J, Van Gerpen R. Recommendations for management of noncytotoxic vesicant extravasations. J Infus Nurs. 2020;43(6):319–343. doi:10.1097/NAN.0000000000000392
  678. Corbett M, Marshall D, Harden M, Oddie S, Phillips R, McGuire W. Treatment of extravasation injuries in infants and young children: a scoping review and survey. Health Technol Assess. 2018;22(46):1–112. doi:10.3310/hta22460
  679. Phentolamine Mesylate for Injection — US prescribing information (Indications and Usage — prevention or treatment of dermal necrosis and sloughing after extravasation of norepinephrine; Dosage and Administration). Hikma Pharmaceuticals USA; revised 3/2024. label text (medlibrary.org)
  680. Dopamine Hydrochloride Injection, USP (vial) — US prescribing information (extravasation; phentolamine infiltration, adult and pediatric doses). Hospira; LAB-1154-4.0, revised 9/2023. pfizermedical.com
  681. Anderson KE. Acute hepatic porphyrias: current diagnosis & management. Mol Genet Metab. 2019;128(3):219–227. doi:10.1016/j.ymgme.2019.07.002
  682. Balwani M, Wang B, Anderson KE, et al. Acute hepatic porphyrias: recommendations for evaluation and long-term management. Hepatology. 2017;66(4):1314–1322. doi:10.1002/hep.29313
  683. American Porphyria Foundation. Emergency room guidelines for acute porphyrias. APF
  684. Ketorolac tromethamine injection USP — US prescribing information (Contraindications; Warnings — renal effects). Hospira; revised 3/2014. www.accessdata.fda.gov
  685. CALDOLOR (ibuprofen) injection — US prescribing information (§2; §5.6 Renal toxicity and hyperkalemia). Cumberland; revised 01/2026. www.accessdata.fda.gov
  686. Ibuprofen oral suspension USP 100 mg/5 mL — US prescribing information (Contraindications; Warnings — preexisting asthma; renal effects). Padagis; revised 12/2024. DailyMed
  687. Misurac JM, Knoderer CA, Leiser JD, et al. Nonsteroidal anti-inflammatory drugs are an important cause of acute kidney injury in children. J Pediatr. 2013;162(6):1153–1159.e1. doi:10.1016/j.jpeds.2012.11.069
  688. AMIDATE (etomidate) injection — US prescribing information (Precautions — adrenal suppression; Pediatric use). Hospira text; revised 10/2023. DailyMed
  689. Vinclair M, Broux C, Faure P, et al. Duration of adrenal inhibition following a single dose of etomidate in critically ill patients. Intensive Care Med. 2008;34(4):714–719. doi:10.1007/s00134-007-0970-y
  690. Albert SG, Ariyan S, Rather A. The effect of etomidate on adrenal function in critical illness: a systematic review. Intensive Care Med. 2011;37(6):901–910. doi:10.1007/s00134-011-2160-1
  691. Propranolol hydrochloride tablets USP — US prescribing information (Contraindications — bronchial asthma). Mylan; revised 1/2026. DailyMed
  692. HEMANGEOL (propranolol hydrochloride) oral solution — US prescribing information (§4; §5.1 Hypoglycemia; §5.3 Bronchospasm). Pierre Fabre; revised 06/2021. www.accessdata.fda.gov
  693. TIMOPTIC (timolol maleate ophthalmic solution) — US prescribing information (Contraindications). Bausch + Lomb; revised 11/2021. www.accessdata.fda.gov
  694. LOPRESSOR (metoprolol tartrate) — US prescribing information (Warnings — bronchospastic diseases). Novartis; revised 12/2012. www.accessdata.fda.gov
  695. Krowchuk DP, Frieden IJ, Mancini AJ, et al. Clinical practice guideline for the management of infantile hemangiomas. Pediatrics. 2019;143(1):e20183475. doi:10.1542/peds.2018-3475
  696. Sheehan WJ, Mauger DT, Paul IM, et al. Acetaminophen versus ibuprofen in young children with mild persistent asthma. N Engl J Med. 2016;375(7):619–630. doi:10.1056/NEJMoa1515990
  697. Debley JS, Carter ER, Gibson RL, et al. The prevalence of ibuprofen-sensitive asthma in children: a randomized controlled bronchoprovocation challenge study. J Pediatr. 2005;147(2):233–238. doi:10.1016/j.jpeds.2005.03.055
  698. Kidon M, Blanca-Lopez N, Gomes E, et al. EAACI/ENDA position paper: diagnosis and management of hypersensitivity reactions to non-steroidal anti-inflammatory drugs (NSAIDs) in children and adolescents. Pediatr Allergy Immunol. 2018;29(5):469–480. doi:10.1111/pai.12915
  699. Romano A, Valluzzi RL, Alvarez-Cuesta E, et al. Updating the classification and routine diagnosis of NSAID hypersensitivity reactions: a WAO statement. World Allergy Organ J. 2025;18(8):101086. doi:10.1016/j.waojou.2025.101086
  700. Ibuprofen 100 mg/5 mL oral suspension — Summary of Product Characteristics (§4.4 varicella). Pinewood (UK), revised 27 Aug 2024; Nurofen for Children SmPC §4.3/§4.4, Reckitt (UK), 2024–2025. emc (SmPC)
  701. Zerr DM, Alexander ER, Duchin JS, et al. A case-control study of necrotizing fasciitis during primary varicella. Pediatrics. 1999;103(4 Pt 1):783–790. doi:10.1542/peds.103.4.783
  702. Lesko SM, O’Brien KL, Schwartz B, et al. Invasive group A streptococcal infection and nonsteroidal antiinflammatory drug use among children with primary varicella. Pediatrics. 2001;107(5):1108–1115. doi:10.1542/peds.107.5.1108
  703. Mikaeloff Y, Kezouh A, Suissa S. Nonsteroidal anti-inflammatory drug use and the risk of severe skin and soft tissue complications in patients with varicella or zoster disease. Br J Clin Pharmacol. 2008;65(2):203–209. doi:10.1111/j.1365-2125.2007.02997.x
  704. FLAGYL (metronidazole) capsules — US prescribing information (Contraindications — Cockayne syndrome). Pfizer; revised 07/2024. www.accessdata.fda.gov
  705. Wilson BT, Strong A, O’Kelly S, Munkley J, Stark Z. Metronidazole toxicity in Cockayne syndrome: a case series. Pediatrics. 2015;136(3):e706–e708. doi:10.1542/peds.2015-0531
  706. Swissmedic. HPC – Metronidazole and other nitroimidazoles: new contraindication in patients with Cockayne syndrome. Health Professional Communication; 23 December 2024. Swissmedic
  707. Wirrell EC, Hood V, Knupp KG, et al. International consensus on diagnosis and management of Dravet syndrome. Epilepsia. 2022;63(7):1761–1777. doi:10.1111/epi.17274
  708. Wirrell EC. Treatment of Dravet syndrome. Can J Neurol Sci. 2016;43(Suppl 3):S13–S18. doi:10.1017/cjn.2016.249
  709. Darras BT, Urion DK, Ghosh PS. Dystrophinopathies. In: GeneReviews® [Internet]. Seattle: University of Washington; last revision 20 January 2022. GeneReviews
  710. Leslie ND, Saenz-Ayala S. Very Long-Chain Acyl-Coenzyme A Dehydrogenase Deficiency. In: GeneReviews® [Internet]. Seattle: University of Washington; last revision 7 August 2025. GeneReviews
  711. Chang IJ, Lam C, Vockley J. Medium-Chain Acyl-Coenzyme A Dehydrogenase Deficiency. In: GeneReviews® [Internet]. Seattle: University of Washington; last revision 26 September 2024. GeneReviews
  712. Spiekerkoetter U, Lindner M, Santer R, et al. Treatment recommendations in long-chain fatty acid oxidation defects: consensus from a workshop. J Inherit Metab Dis. 2009;32(4):498–505. doi:10.1007/s10545-009-1126-8
  713. BACTRIM (sulfamethoxazole and trimethoprim) — US prescribing information (Contraindications; Precautions; Drug Interactions). Sun Pharmaceutical; revised February 2025. www.accessdata.fda.gov
  714. MACROBID (nitrofurantoin) capsules — US prescribing information (Contraindications; Warnings). Almatica; revised 12/2020. www.accessdata.fda.gov
  715. Primaquine phosphate tablets — US prescribing information (Contraindications; Warnings). sanofi-aventis; revised July 2016. www.accessdata.fda.gov
  716. Dapsone tablets USP — US prescribing information (Precautions). Westminster Pharmaceuticals; revised June 2025. DailyMed
  717. KRINTAFEL (tafenoquine) tablets — US prescribing information (§2.1; §4). GlaxoSmithKline; revised 8/2023. DailyMed
  718. Luzzatto L, Ally M, Notaro R. Glucose-6-phosphate dehydrogenase deficiency. Blood. 2020;136(11):1225–1240. doi:10.1182/blood.2019000944
  719. Relling MV, McDonagh EM, Chang T, et al. Clinical Pharmacogenetics Implementation Consortium (CPIC) guidelines for rasburicase therapy in the context of G6PD deficiency genotype. Clin Pharmacol Ther. 2014;96(2):169–174. doi:10.1038/clpt.2014.97
  720. Busse PJ, Christiansen SC, Riedl MA, et al. US HAEA Medical Advisory Board 2020 guidelines for the management of hereditary angioedema. J Allergy Clin Immunol Pract. 2021;9(1):132–150.e3. doi:10.1016/j.jaip.2020.08.046
  721. ZESTRIL (lisinopril) tablets — US prescribing information (§4 Contraindications — hereditary or idiopathic angioedema). AstraZeneca; revised 12/2014. www.accessdata.fda.gov
  722. Gaughan S, Ayres L, Baker PR II. Hereditary Fructose Intolerance. In: GeneReviews® [Internet]. Seattle: University of Washington; last revision 18 February 2021. GeneReviews
  723. European Commission / EMA. Annex to the European Commission guideline on ‘Excipients in the labelling and package leaflet of medicinal products for human use’ (SANTE‑2017‑11668), EMA/CHMP/302620/2017 Rev. 2, 22 November 2019 (sorbitol; aspartame). EMA
  724. Welling L, Bernstein LE, Berry GT, et al. International clinical guideline for the management of classical galactosemia: diagnosis, treatment, and follow-up. J Inherit Metab Dis. 2017;40(2):171–176. doi:10.1007/s10545-016-9990-5
  725. Ommen SR, Ho CY, Asif IM, et al. 2024 AHA/ACC/AMSSM/HRS/PACES/SCMR guideline for the management of hypertrophic cardiomyopathy. Circulation. 2024;149(23):e1239–e1311. doi:10.1161/CIR.0000000000001250
  726. LANOXIN (digoxin) tablets — US prescribing information (§5.3; §7.2 Drug interactions table; §7.3). Concordia; revised 08/2018. Digoxin oral solution label §5.4 (HCM), Hikma 04/2024. www.accessdata.fda.gov
  727. Rao AK, Sobel J, Chatham-Stephens K, Luquez C. Clinical guidelines for diagnosis and treatment of botulism, 2021. MMWR Recomm Rep. 2021;70(2):1–30. doi:10.15585/mmwr.rr7002a1
  728. L’Hommedieu C, Stough R, Brown L, et al. Potentiation of neuromuscular weakness in infant botulism by aminoglycosides. J Pediatr. 1979;95(6):1065–1070. doi:10.1016/S0022-3476(79)80314-5
  729. Arnon SS, Schechter R, Maslanka SE, et al. Human botulism immune globulin for the treatment of infant botulism. N Engl J Med. 2006;354(5):462–471. doi:10.1056/NEJMoa051926
  730. BabyBIG [Botulism Immune Globulin Intravenous (Human)] — package insert. California Department of Public Health; revised June 2021. CDPH
  731. Priori SG, Wilde AA, Horie M, et al. HRS/EHRA/APHRS expert consensus statement on the diagnosis and management of patients with inherited primary arrhythmia syndromes. Heart Rhythm. 2013;10(12):1932–1963. doi:10.1016/j.hrthm.2013.05.014
  732. Zeppenfeld K, Tfelt-Hansen J, de Riva M, et al. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2022;43(40):3997–4126. doi:10.1093/eurheartj/ehac262
  733. BrugadaDrugs.org (Amsterdam UMC with international Brugada experts). Drugs to be avoided by Brugada syndrome patients. brugadadrugs.org
  734. CredibleMeds (AZCERT). QTdrugs lists — medicines with known risk of torsades de pointes (registration required; list revised 22 May 2025). CredibleMeds
  735. Napolitano C, Mazzanti A, Bloise R, Priori SG. Catecholaminergic polymorphic ventricular tachycardia. In: Adam MP, et al., eds. GeneReviews® [Internet]. Seattle (WA): University of Washington; 2004, updated 23 June 2022. NBK1289.
  736. Kossoff EH, Zupec-Kania BA, Auvin S, et al. Optimal clinical management of children receiving dietary therapies for epilepsy: updated recommendations of the International Ketogenic Diet Study Group. Epilepsia Open. 2018;3(2):175–192. doi:10.1002/epi4.12225
  737. van der Louw E, van den Hurk D, Neal E, et al. Ketogenic diet guidelines for infants with refractory epilepsy. Eur J Paediatr Neurol. 2016;20(6):798–809. doi:10.1016/j.ejpn.2016.07.009
  738. Riazi S, Biesecker LG, Rosenberg H, Dirksen RT. Nonsyndromic Malignant Hyperthermia Susceptibility. In: GeneReviews® [Internet]. Seattle: University of Washington; last update 7 August 2025. GeneReviews
  739. DEPAKOTE (divalproex sodium) — US prescribing information (boxed warning; Contraindications; §5.15; §7). AbbVie; revised 3/2024. www.accessdata.fda.gov
  740. McDermott JH, Wolf J, Hoshitsuki K, et al. Clinical Pharmacogenetics Implementation Consortium guideline for the use of aminoglycosides based on MT-RNR1 genotype. Clin Pharmacol Ther. 2022;111(2):366–372. doi:10.1002/cpt.2309
  741. De Vries MC, Brown DA, Allen ME, et al. Safety of drug use in patients with a primary mitochondrial disease: an international Delphi-based consensus. J Inherit Metab Dis. 2020;43(4):800–818. doi:10.1002/jimd.12196
  742. Parikh S, Goldstein A, Karaa A, et al. Patient care standards for primary mitochondrial disease: a consensus statement from the Mitochondrial Medicine Society. Genet Med. 2017;19(12). doi:10.1038/gim.2017.107
  743. CIPRO (ciprofloxacin) — US prescribing information (boxed warning — myasthenia gravis; §5.9 theophylline). Bayer; revised 2016/2022. www.accessdata.fda.gov
  744. Narayanaswami P, Sanders DB, Wolfe G, et al. International consensus guidance for management of myasthenia gravis: 2020 update. Neurology. 2021;96(3):114–122. doi:10.1212/WNL.0000000000011124
  745. Rocuronium bromide injection — US prescribing information (Warnings — myasthenia gravis). Pfizer/Hospira. Pfizer labeling
  746. BOTOX (onabotulinumtoxinA) — US prescribing information (§5.5 Pre‑existing neuromuscular disorders). Allergan. label text
  747. Lenders JWM, Duh QY, Eisenhofer G, et al. Pheochromocytoma and paraganglioma: an Endocrine Society clinical practice guideline. J Clin Endocrinol Metab. 2014;99(6):1915–1942. doi:10.1210/jc.2014-1498
  748. Eisenhofer G, Rivers G, Rosas AL, et al. Adverse drug reactions in patients with phaeochromocytoma: incidence, prevention and management. Drug Saf. 2007;30(11):1031–1062. doi:10.2165/00002018-200730110-00004
  749. van Wegberg AMJ, MacDonald A, Ahring K, et al. The complete European guidelines on phenylketonuria: diagnosis and treatment. Orphanet J Rare Dis. 2017;12(1):162. doi:10.1186/s13023-017-0685-2
  750. 21 CFR § 201.21 — Declaration of presence of phenylalanine as a component of aspartame in over‑the‑counter and prescription drugs for human use. eCFR
  751. RotaTeq (rotavirus vaccine, live, oral, pentavalent) — US package insert (§4.2 SCID). Merck; revised 5/2026. FDA
  752. Rubin LG, Levin MJ, Ljungman P, et al. 2013 IDSA clinical practice guideline for vaccination of the immunocompromised host. Clin Infect Dis. 2014;58(3):e44–e100. doi:10.1093/cid/cit684
  753. Foukaneli T, Kerr P, Bolton-Maggs PHB, et al. Guidelines on the use of irradiated blood components. Br J Haematol. 2020;191(5):704–724. doi:10.1111/bjh.17015
  754. DEMEROL (meperidine) injection — US prescribing information (§5.13 normeperidine). Pfizer/Hospira; revised 9/2020. Pfizer labeling
  755. Morris CA, Braddock SR; AAP Council on Genetics. Health care supervision for children with Williams syndrome. Pediatrics. 2020;145(2):e20193761. doi:10.1542/peds.2019-3761
  756. Morris CA. Williams Syndrome. In: GeneReviews® [Internet]. Seattle: University of Washington; last update 13 April 2023. GeneReviews
  757. Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia. Circulation. 2016;133(14):e506–e574. doi:10.1161/CIR.0000000000000311
  758. Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. Eur Heart J. 2020;41(5):655–720. doi:10.1093/eurheartj/ehz467
  759. Verapamil hydrochloride injection — US prescribing information (Contraindications). Exela; revised November 2016. www.accessdata.fda.gov
  760. 21 CFR § 201.314(h) — Labeling of drug preparations containing salicylates (Reye’s syndrome warning). eCFR
  761. Belay ED, Bresee JS, Holman RC, Khan AS, Shahriari A, Schonberger LB. Reye’s syndrome in the United States from 1981 through 1997. N Engl J Med. 1999;340(18):1377–1382. doi:10.1056/NEJM199905063401801
  762. FDA Drug Safety Communication: Risk of serious and potentially fatal blood disorder prompts FDA action on oral over‑the‑counter benzocaine products used for teething and mouth pain and prescription local anesthetics. 23 May 2018; FDA Drug Safety Communication on oral viscous lidocaine for teething (boxed warning), 26 June 2014. FDA
  763. US Food and Drug Administration. Safely soothing teething pain in infants and children. FDA Consumer Update; content current as of 26 June 2024. FDA
  764. ULTRAM (tramadol) tablets — US prescribing information (§5.8; §5.9; Contraindications < 12 years). Janssen; revised 02/2023. www.accessdata.fda.gov
  765. European Medicines Agency. Codeine-containing medicines – Article 31 referral: restrictions on the use of codeine for pain relief in children (CMDh position, 26 June 2013). EMA
  766. FDA. Use caution when giving cough and cold products to kids (current as of 8 Feb 2018); FDA statement on OTC cough and cold medicines in children, 13 Oct 2008; AAP HealthyChildren.org, Coughs and colds: medicines or home remedies? (2 Dec 2022). FDA
  767. 21 CFR § 336.50 — Labeling of antiemetic drug products (dimenhydrinate); Children’s BENADRYL Drug Facts (Kenvue). eCFR
  768. Church MK, Maurer M, Simons FER, Bindslev-Jensen C, van Cauwenberge P, Bousquet J, et al. Risk of first-generation H1-antihistamines: a GA2LEN position paper. Allergy. 2010;65(4):459–466. doi:10.1111/j.1398-9995.2009.02325.x
  769. California Department of Public Health, Infant Botulism Treatment and Prevention Program. For parents and families (honey and infant botulism); AAP HealthyChildren.org (2022). CDPH
  770. MOTRIN Infants’ (ibuprofen oral suspension drops) — US OTC Drug Facts label (Directions: under 6 months, ask a doctor). Kenvue Brands LLC; revised May 2026. DailyMed
  771. Loperamide hydrochloride capsules USP 2 mg — US prescribing information (Contraindications — < 2 years); IMODIUM Drug Facts (OTC). label text
  772. European Medicines Agency. European Medicines Agency recommends changes to the use of metoclopramide. Press release, 26 July 2013. EMA
  773. REGLAN (metoclopramide) tablets — US prescribing information (§8.4 Pediatric use). ANI Pharmaceuticals; revised 08/2017. label text
  774. Freedman SB, Adler M, Seshadri R, Powell EC. Oral ondansetron for gastroenteritis in a pediatric emergency department. N Engl J Med. 2006;354(16):1698–1705. doi:10.1056/NEJMoa055119
  775. Rocephin 1 g — Summary of Product Characteristics (§4.3). Roche (UK), revised 03 Jan 2025; MHRA Drug Safety Update, ceftriaxone incompatible with calcium (2009/2014). emc (SmPC)
  776. Bacteriostatic 0.9% sodium chloride injection — US prescribing information (boxed statement: not for use in neonates). Pfizer/Hospira; revised 02/2019. Pfizer labeling
  777. Bacteriostatic Sodium Chloride Injection, USP, 0.9% — US prescribing information (benzyl alcohol; use in newborns: preservative-free Sodium Chloride Injection only). Fresenius Kabi USA. label text
  778. American Academy of Pediatrics, Committee on Fetus and Newborn and Committee on Drugs. Benzyl alcohol: toxic agent in neonatal units. Pediatrics. 1983;72(3):356–358. PubMed
  779. Chloramphenicol 1 g powder for solution for injection — Summary of Product Characteristics (§4.4 Grey syndrome). UK, revised 28 Mar 2022. emc (SmPC)
  780. Promethazine hydrochloride injection, USP — US prescribing information (boxed warning; Contraindications — children < 2 years). Hikma; FDA 2009 class labeling. www.accessdata.fda.gov
  781. VIBRAMYCIN (doxycycline) — US prescribing information (Warnings — tooth development). Pfizer. Pfizer labeling
  782. Biggs HM, Behravesh CB, Bradley KK, et al. Diagnosis and management of tickborne rickettsial diseases: Rocky Mountain spotted fever and other spotted fever group rickettsioses, ehrlichioses, and anaplasmosis — United States. MMWR Recomm Rep. 2016;65(RR-2):1–44. doi:10.15585/mmwr.rr6502a1
  783. Todd SR, Dahlgren FS, Traeger MS, et al. No visible dental staining in children treated with doxycycline for suspected Rocky Mountain spotted fever. J Pediatr. 2015;166(5):1246–1251. doi:10.1016/j.jpeds.2015.02.015
  784. Lieberman P, Nicklas RA, Randolph C, et al. Anaphylaxis — a practice parameter update 2015. Ann Allergy Asthma Immunol. 2015;115(5):341–384. doi:10.1016/j.anai.2015.07.019
  785. Australasian Society of Clinical Immunology and Allergy (ASCIA). Guidelines: Acute management of anaphylaxis. August 2019 (glucagon 20–30 microgram/kg up to 1 mg in children). ASCIA
  786. TEGRETOL (carbamazepine) — US prescribing information (Precautions — Drug interactions). Novartis; revised September 2025. www.accessdata.fda.gov
  787. VFEND (voriconazole) — US prescribing information (§4 Contraindications). Pfizer; revised 1/2019. www.accessdata.fda.gov
  788. KAPVAY (clonidine hydrochloride) extended‑release tablets — US prescribing information (Dosage and Administration — discontinuation). Concordia Pharmaceuticals; revised 2/2020. www.accessdata.fda.gov
  789. CATAPRES (clonidine hydrochloride) tablets — US prescribing information (Warnings — withdrawal; Precautions — Drug interactions). Boehringer Ingelheim; January 2010. PRECEDEX (dexmedetomidine) label §5.2, Hospira 5/2026. www.accessdata.fda.gov
  790. BIAXIN (clarithromycin) — US prescribing information (§4 Contraindications; §7 Drug interactions). AbbVie; revised 12/2018. www.accessdata.fda.gov
  791. Terkeltaub RA, Furst DE, Digiacinto JL, Kook KA, Davis MW. Novel evidence-based colchicine dose-reduction algorithm to predict and prevent colchicine toxicity in the presence of cytochrome P450 3A4/P-glycoprotein inhibitors. Arthritis Rheum. 2011;63(8):2226–2237. doi:10.1002/art.30389
  792. VARIVAX (varicella virus vaccine live) — US package insert (Warnings and Precautions — salicylates). Merck. FDA
  793. ABSORICA / ABSORICA LD (isotretinoin) capsules — US prescribing information (§5.5; §7.1; §7.2). Sun Pharma; revised 6/2026. www.accessdata.fda.gov
  794. ZYVOX (linezolid) — US prescribing information (§4.2; §5.3 Serotonin syndrome). Pfizer; revised 6/2026. www.accessdata.fda.gov
  795. Methotrexate injection, USP — US prescribing information (§7.1 Drug interactions). Pfizer/Hospira; revised 05/2025. RediTrex (methotrexate) label, boxed warning, Cumberland 11/2019. Pfizer labeling
  796. Howard SC, McCormick J, Pui CH, Buddington RK, Harvey RD. Preventing and managing toxicities of high-dose methotrexate. Oncologist. 2016;21(12):1471–1482. doi:10.1634/theoncologist.2015-0164
  797. Pimozide tablets USP — US prescribing information (Contraindications). Par; revised 08/2024. DailyMed
  798. DIPRIVAN (propofol) injectable emulsion — US prescribing information (Contraindications; Warnings — propofol infusion syndrome; pediatric ICU sedation). Fresenius Kabi; revised 8/2022. www.accessdata.fda.gov
  799. Krajčová A, Waldauf P, Anděl M, Duška F. Propofol infusion syndrome: a structured review of experimental studies and 153 published case reports. Crit Care. 2015;19:398. doi:10.1186/s13054-015-1112-5
  800. Asserhøj LL, Mosbech H, Krøigaard M, Garvey LH. No evidence for contraindications to the use of propofol in adults allergic to egg, soy or peanut. Br J Anaesth. 2016;116(1):77–82. doi:10.1093/bja/aev360
  801. Smith HAB, Besunder JB, Betters KA, Johnson PN, Srinivasan V, Stormorken A, et al. 2022 Society of Critical Care Medicine clinical practice guidelines on prevention and management of pain, agitation, neuromuscular blockade, and delirium in critically ill pediatric patients with consideration of the ICU environment and early mobility. Pediatr Crit Care Med. 2022;23(2):e74–e110. doi:10.1097/PCC.0000000000002873
  802. Rifadin 300 mg capsules (rifampicin) — Summary of Product Characteristics (§4.3; §4.5 Table 1). Sanofi (UK, MHRA‑authorised); revised 03 Jun 2026. emc (SmPC)
  803. PROGRAF (tacrolimus) — US prescribing information (§5.7; QT prolongation; §7 Table 15). Astellas; revised 08/2023. www.accessdata.fda.gov
  804. REVATIO (sildenafil) — US prescribing information (§4 Contraindications). Viatris; revised 1/2023. ADCIRCA (tadalafil) label §4, Lilly 09/2020. www.accessdata.fda.gov
  805. NEORAL (cyclosporine, modified) — US prescribing information (Warnings/Precautions — Drug interactions). Novartis; label file 2019. www.accessdata.fda.gov
  806. Fralick M, Macdonald EM, Gomes T, et al. Co-trimoxazole and sudden death in patients receiving inhibitors of renin-angiotensin system: population based study. BMJ. 2014;349:g6196. doi:10.1136/bmj.g6196
  807. Antoniou T, Hollands S, Macdonald EM, et al. Trimethoprim-sulfamethoxazole and risk of sudden death among patients taking spironolactone. CMAJ. 2015;187(4):E138–E143. doi:10.1503/cmaj.140816
  808. Velázquez H, Perazella MA, Wright FS, Ellison DH. Renal mechanism of trimethoprim-induced hyperkalemia. Ann Intern Med. 1993;119(4):296–301. doi:10.7326/0003-4819-119-4-199308150-00008
  809. MERREM (meropenem) for injection — US prescribing information (§5.4; §7.2 valproic acid). Pfizer; revised May 2022. Pfizer labeling
  810. MHRA. Carbapenems: concomitant use with valproic acid not recommended. Drug Safety Update, 11 December 2014 (originally February 2010). MHRA
  811. LAMICTAL (lamotrigine) — US prescribing information (boxed warning; §2.1; §5.12; §7 Table 13). GlaxoSmithKline; revised 10/2025. www.accessdata.fda.gov
  812. Bjornson CL, Johnson DW. Croup. Lancet. 2008;371(9609):329–339. doi:10.1016/S0140-6736(08)60170-1
  813. World Health Organization. WHO guideline on the prevention and diagnosis of rheumatic fever and rheumatic heart disease. Geneva: WHO; 2024. ISBN 978‑92‑4‑010007‑7. iris.who.int
  814. Perth Children’s Hospital, Child and Adolescent Health Service. Tranexamic acid — Medication Management Manual monograph. Perth: CAHS; issued January 2025, amended February 2026. pch.health.wa.gov.au (PDF)
  815. Cyklokapron 500 mg film‑coated tablets (tranexamic acid) — Summary of Product Characteristics. Viatris Healthcare Limited; Health Products Regulatory Authority (Ireland); text revised February 2025. assets.hpra.ie (PDF)
  816. Wells M, Goldstein LN, Bentley A, Basnett S, Monteith I. The accuracy of the Broselow tape as a weight estimation tool and a drug‑dosing guide — a systematic review and meta‑analysis. Resuscitation. 2017;121:9–33. doi:10.1016/j.resuscitation.2017.09.026
  817. Matson KL, Horton ER, Capino AC; Pediatric Pharmacy Association. Medication dosing for children with overweight and obesity. J Pediatr Pharmacol Ther. 2024;29(5):550–553. doi:10.5863/1551-6776-29.5.550
  818. Hodiamont CJ, van den Broek AK, de Vroom SL, Prins JM, Mathôt RAA, van Hest RM. Clinical pharmacokinetics of gentamicin in various patient populations and consequences for optimal dosing for Gram‑negative infections: an updated review. Clin Pharmacokinet. 2022;61(8):1075–1094. doi:10.1007/s40262-022-01143-0
  819. Lott C, Truhlář A, Alfonzo A, et al. European Resuscitation Council Guidelines 2021: cardiac arrest in special circumstances. Resuscitation. 2021;161:152–219. doi:10.1016/j.resuscitation.2021.02.011
  820. Bourguignon C, Cohenca N, Lauridsen E, et al. International Association of Dental Traumatology guidelines for the management of traumatic dental injuries: 1. Fractures and luxations. Dent Traumatol. 2020;36(4):314–330. doi:10.1111/edt.12578
  821. Day PF, Flores MT, O’Connell AC, et al. International Association of Dental Traumatology guidelines for the management of traumatic dental injuries: 3. Injuries in the primary dentition. Dent Traumatol. 2020;36(4):343–359. doi:10.1111/edt.12576
  822. Tsai TY, Huang IH, Chao YC, et al. Treating toxic epidermal necrolysis with systemic immunomodulating therapies: a systematic review and network meta‑analysis. J Am Acad Dermatol. 2021;84(2):390–397. doi:10.1016/j.jaad.2020.08.122
  823. Gordon M, de Geus A, Boruta M, et al. European Society for Paediatric Gastroenterology, Hepatology and Nutrition/North American Society for Pediatric Gastroenterology, Hepatology and Nutrition guidelines for treatment of functional constipation in children aged 0–18 years. J Pediatr Gastroenterol Nutr. 2026;83(2):335–366. doi:10.1002/jpn3.70447
  824. Freifeld AG, Bow EJ, Sepkowitz KA, et al. Clinical practice guideline for the use of antimicrobial agents in neutropenic patients with cancer: 2010 update by the Infectious Diseases Society of America. Clin Infect Dis. 2011;52(4):e56–e93. doi:10.1093/cid/cir073
  825. National Institute for Health and Care Excellence. Neutropenic sepsis: prevention and management in people with cancer. Clinical guideline CG151. London: NICE; 2012. nice.org.uk/guidance/cg151
  826. CRASH‑2 collaborators; Roberts I, Shakur H, Afolabi A, et al. The importance of early treatment with tranexamic acid in bleeding trauma patients: an exploratory analysis of the CRASH‑2 randomised controlled trial. Lancet. 2011;377(9771):1096–1101. doi:10.1016/S0140-6736(11)60278-X
  827. Peterson J, Johnson N, Deakins K, Wilson‑Costello D, Jelovsek JE, Chatburn R. Accuracy of the 7‑8‑9 Rule for endotracheal tube placement in the neonate. J Perinatol. 2006;26(6):333–336. doi:10.1038/sj.jp.7211503
  828. Harris EA, Arheart KL, Penning DH. Endotracheal tube malposition within the pediatric population: a common event despite clinical evidence of correct placement. Can J Anaesth. 2008;55(10):685–690. doi:10.1007/BF03017744
  829. Thayyil S, Nagakumar P, Gowers H, Sinha A. Optimal endotracheal tube tip position in extremely premature infants. Am J Perinatol. 2008;25(1):13–16. doi:10.1055/s-2007-995221
  830. Joint British Diabetes Societies for Inpatient Care. The hospital management of hypoglycaemia in adults with diabetes mellitus. Revised March 2022 (JBDS 01). JBDS‑01 HypoGuideline March 2022 (PDF)
  831. Gammal RS, Pirmohamed M, Somogyi AA, et al. Expanded Clinical Pharmacogenetics Implementation Consortium guideline for medication use in the context of G6PD genotype. Clin Pharmacol Ther. 2023;113(5):973–985. doi:10.1002/cpt.2735
  832. Dorsey MJ, Wright NAM, Chaimowitz NS, et al. Infections in infants with SCID: isolation, infection screening, and prophylaxis in PIDTC centers. J Clin Immunol. 2021;41(1):38–50. doi:10.1007/s10875-020-00865-9
  833. Trottier ED, Chan K, Allain D, Chauvin‑Kimoff L; Canadian Paediatric Society, Acute Care Committee. Managing an acute asthma exacerbation in children. Paediatr Child Health. 2021;26(7):438–439. doi:10.1093/pch/pxab058
  834. Djakow J, Turner NM, Skellett S, et al. European Resuscitation Council Guidelines 2025: paediatric life support. Resuscitation. 2025;215(Suppl 1):110767. doi:10.1016/j.resuscitation.2025.110767
  835. Jones JM, Fleming‑Dutra KE, Prill MM, et al. Use of nirsevimab for the prevention of respiratory syncytial virus disease among infants and young children: recommendations of the Advisory Committee on Immunization Practices — United States, 2023. MMWR Morb Mortal Wkly Rep. 2023;72(34):920–925. doi:10.15585/mmwr.mm7234a4
  836. Mowery NT, Gunter OL, Collier BR, et al. Practice management guidelines for management of hemothorax and occult pneumothorax. J Trauma. 2011;70(2):510–518. doi:10.1097/TA.0b013e31820b5c31
  837. Notrica DM, Garcia‑Filion P, Moore FO, et al. Management of pediatric occult pneumothorax in blunt trauma: a subgroup analysis of the American Association for the Surgery of Trauma multicenter prospective observational study. J Pediatr Surg. 2012;47(3):467–472. doi:10.1016/j.jpedsurg.2011.09.037
  838. National Asthma Council Australia. Australian Asthma Handbook, version 3.0. Melbourne: National Asthma Council Australia; 2025. Managing acute asthma in children 6–11 years in the emergency department. asthmahandbook.org.au
  839. Paediatric Research in Emergency Departments International Collaborative (PREDICT). Australasian bronchiolitis guideline. Melbourne: PREDICT; 2016 (initial assessment table).
  840. Bitnun A, Comeau J, Penner J, Barton M; Canadian Paediatric Society, Infectious Diseases and Immunization Committee. Clostridioides difficile in children. Position statement. Ottawa: Canadian Paediatric Society; posted 23 Sep 2026. cps.ca
  841. Grünert SC, Bhattacharya K, Karall D, et al. International guideline on the diagnosis, treatment, and monitoring of long-chain fatty acid oxidation disorders (LC-FAOD). J Inherit Metab Dis. 2026;49(5):e70251. doi:10.1002/jimd.70251
  842. Harding JE, Alsweiler JM, Brown GTL, et al. Prophylactic dextrose gel for neonatal hypoglycemia and neurocognitive function at 6 to 7 years of age: a secondary analysis of a randomized clinical trial. JAMA Pediatr. 2026;180(9):934–941. doi:10.1001/jamapediatrics.2026.2486
  843. American Academy of Pediatrics, Committee on Infectious Diseases. Recommendations for the prevention of RSV disease in infants and children: policy statement. Pediatrics. 2026; published online 2 Sep 2026:e2026079047. doi:10.1542/peds.2026-079047
  844. Zar HJ, Bont LJ, Manzoni P, et al. Clesrovimab in infants at increased risk for severe disease during 2 RSV seasons: a randomized clinical trial. JAMA Pediatr. 2026;180(9):951–960. doi:10.1001/jamapediatrics.2026.2760
  845. Harley A, George S, Phillips N, et al. Resuscitation with early adrenaline infusion for children with septic shock: a randomized pilot trial. Pediatr Crit Care Med. 2024;25(2):106–117. doi:10.1097/PCC.0000000000003351
  846. Primacor 1 mg/ml solution for injection (milrinone) — Summary of Product Characteristics (§4.2 paediatric population: loading dose and continuous infusion). Sanofi; emc (SmPC), revised 17 Sep 2019; identical paediatric wording in Milrinone 1 mg/ml solution for injection/infusion SmPC, Wockhardt UK, revised 23 Jul 2021. medicines.org.uk/emc/product/1460
  847. Hoffman TM, Wernovsky G, Atz AM, et al. Efficacy and safety of milrinone in preventing low cardiac output syndrome in infants and children after corrective surgery for congenital heart disease. Circulation. 2003;107(7):996–1002. doi:10.1161/01.CIR.0000051365.81920.28
  848. Ramaswamy KN, Singhi S, Jayashree M, Bansal A, Nallasamy K. Double-blind randomized clinical trial comparing dopamine and epinephrine in pediatric fluid-refractory hypotensive septic shock. Pediatr Crit Care Med. 2016;17(11):e502–e512. doi:10.1097/PCC.0000000000000954
  849. Dobutamine 5 mg/ml solution for infusion — Summary of Product Characteristics (§4.2 posology: paediatric population). hameln pharma ltd; emc (SmPC), revised 6 Aug 2024. medicines.org.uk/emc/product/6462
  850. American Academy of Pediatrics Committee on Fetus and Newborn; American College of Obstetricians and Gynecologists Committee on Obstetric Practice. The Apgar score. Pediatrics. 2015;136(4):819–822. doi:10.1542/peds.2015-2651
  851. Carson JL, Stanworth SJ, Guyatt G, et al. Red blood cell transfusion: 2023 AABB International Guidelines. JAMA. 2023;330(19):1892–1902. doi:10.1001/jama.2023.12914
  852. Robinson S, Harris A, Atkinson S, et al. The administration of blood components: a British Society for Haematology Guideline. Transfus Med. 2018;28(1):3–21. doi:10.1111/tme.12481
  853. Serious Hazards of Transfusion (SHOT). Paediatric transfusion bookmark: key information from the BSH paediatric transfusion guidelines (2016 guideline and 2020 addendum). Manchester: SHOT; 2020. shotuk.org
  854. Mosteller RD. Simplified calculation of body-surface area. N Engl J Med. 1987;317(17):1098. doi:10.1056/NEJM198710223171717
  855. Cartotto R, Johnson LS, Savetamal A, et al. American Burn Association clinical practice guidelines on burn shock resuscitation. J Burn Care Res. 2024;45(3):565–589. doi:10.1093/jbcr/irad125
  856. The Royal Children's Hospital Melbourne. Clinical practice guideline: burns. Melbourne: RCH; updated 2026. rch.org.au
  857. Gripp KE, Trottier ED, Thakore S, Sniderman J, Lawrence S; Canadian Paediatric Society, Acute Care Committee. Current recommendations for management of paediatric diabetic ketoacidosis. Paediatr Child Health. 2023;28(2):128–138. doi:10.1093/pch/pxac119
  858. Pierce CB, Muñoz A, Ng DK, Warady BA, Furth SL, Schwartz GJ. Age- and sex-dependent clinical equations to estimate glomerular filtration rates in children and young adults with chronic kidney disease. Kidney Int. 2021;99(4):948–956. doi:10.1016/j.kint.2020.10.047
  859. Figge J, Jabor A, Kazda A, Fencl V. Anion gap and hypoalbuminemia. Crit Care Med. 1998;26(11):1807–1810. doi:10.1097/00003246-199811000-00019
  860. Slomp J, van der Voort PH, Gerritsen RT, Berk JA, Bakker AJ. Albumin-adjusted calcium is not suitable for diagnosis of hyper- and hypocalcemia in the critically ill. Crit Care Med. 2003;31(5):1389–1393. doi:10.1097/01.CCM.0000063044.55669.3C
  861. Gauci C, Moranne O, Fouqueray B, et al. Pitfalls of measuring total blood calcium in patients with CKD. J Am Soc Nephrol. 2008;19(8):1592–1598. doi:10.1681/ASN.2007040449
  862. Topjian AA, Raymond TT, Atkins D, et al. Part 4: Pediatric basic and advanced life support: 2020 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2020;142(16 Suppl 2):S469–S523. doi:10.1161/CIR.0000000000000901
  863. Phipps LM, Thomas NJ, Gilmore RK, et al. Prospective assessment of guidelines for determining appropriate depth of endotracheal tube placement in children. Pediatr Crit Care Med. 2005;6(5):519–522. doi:10.1097/01.pcc.0000165802.32383.9e
  864. Kempley ST, Moreiras JW, Petrone FL. Endotracheal tube length for neonatal intubation. Resuscitation. 2008;77(3):369–373. doi:10.1016/j.resuscitation.2008.02.002
  865. Shukla HK, Hendricks-Munoz KD, Atakent Y, Rapaport S. Rapid estimation of insertional length of endotracheal intubation in newborn infants. J Pediatr. 1997;131(4):561–564. doi:10.1016/s0022-3476(97)70062-3
  866. Gill I, Stafford A, Murphy MC, et al. Randomised trial of estimating oral endotracheal tube insertion depth in newborns using weight or vocal cord guide. Arch Dis Child Fetal Neonatal Ed. 2018;103(4):F312–F316. doi:10.1136/archdischild-2017-312798
  867. Teasdale G, Maas A, Lecky F, Manley G, Stocchetti N, Murray G. The Glasgow Coma Scale at 40 years: standing the test of time. Lancet Neurol. 2014;13(8):844–854. doi:10.1016/S1474-4422(14)70120-6
  868. Adamkin DH; Committee on Fetus and Newborn. Postnatal Glucose Homeostasis in Late‑Preterm and Term Infants. Pediatrics. 2011;127(3):575–579. doi:10.1542/peds.2010-3851
  869. Mohmand HK, Issa D, Ahmad Z, Cappuccio JD, Kouides RW, Sterns RH. Hypertonic saline for hyponatremia: risk of inadvertent overcorrection. Clin J Am Soc Nephrol. 2007;2(6):1110–1117. doi:10.2215/CJN.00910207
  870. Golan‑Tripto I, Goldbart A, Akel K, Dizitzer Y, Novack V, Tal A. Modified Tal Score: validated score for prediction of bronchiolitis severity. Pediatr Pulmonol. 2018;53(6):796–801. doi:10.1002/ppul.24007
  871. Fox EJ, Dalton AM, Mullins ME, et al. Out-of-hospital assessment and triage of paracetamol (acetaminophen) exposure in the United States and Canada: a consensus guideline. Clin Toxicol (Phila). 2025;63(5):348–352. doi:10.1080/15563650.2025.2471915
  872. Emeriaud G, López-Fernández YM, Iyer NP, et al. Executive summary of the second international guidelines for the diagnosis and management of pediatric acute respiratory distress syndrome (PALICC-2). Pediatr Crit Care Med. 2023;24(2):143–168. doi:10.1097/PCC.0000000000003147
  873. Samuel M. Pediatric appendicitis score. J Pediatr Surg. 2002;37(6):877–881. doi:10.1053/jpsu.2002.32893
  874. Ebell MH, Shinholser J. What are the most clinically useful cutoffs for the Alvarado and Pediatric Appendicitis Scores? A systematic review. Ann Emerg Med. 2014;64(4):365–372.e2. doi:10.1016/j.annemergmed.2014.02.025
  875. Goldman RD, Carter S, Stephens D, et al. Prospective validation of the pediatric appendicitis score. J Pediatr. 2008;153(2):278–282. doi:10.1016/j.jpeds.2008.01.033
  876. Bhatt M, Joseph L, Ducharme FM, et al. Prospective validation of the pediatric appendicitis score in a Canadian pediatric emergency department. Acad Emerg Med. 2009;16(7):591–596. doi:10.1111/j.1553-2712.2009.00445.x
  877. Rautaharju PM, Surawicz B, Gettes LS, et al. AHA/ACCF/HRS recommendations for the standardization and interpretation of the electrocardiogram: part IV: the ST segment, T and U waves, and the QT interval. Circulation. 2009;119(10):e241–e250. doi:10.1161/CIRCULATIONAHA.108.191096
  878. Phan DQ, Silka MJ, Lan YT, Chang RK. Comparison of formulas for calculation of the corrected QT interval in infants and young children. J Pediatr. 2015;166(4):960–964.e2. doi:10.1016/j.jpeds.2014.12.037
  879. Acker SN, Ross JT, Partrick DA, Tong S, Bensard DD. Pediatric specific shock index accurately identifies severely injured children. J Pediatr Surg. 2015;50(2):331–334. doi:10.1016/j.jpedsurg.2014.08.009
  880. Ramgopal S, Gorski JK, Chaudhari PP, et al. Establishing thresholds for shock index in children to identify major trauma. Injury. 2024;56(1):111840. doi:10.1016/j.injury.2024.111840
  881. Davies P, Robertson S, Hegde S, Greenwood R, Massey E, Davis P. Calculating the required transfusion volume in children. Transfusion. 2007;47(2):212–216. doi:10.1111/j.1537-2995.2007.01091.x
  882. Wong Ramsey K. Transfusions in pediatrics. Pediatr Rev. 2025;46(9):531–533. doi:10.1542/pir.2024-006451
Back cover: Compassion, Knowledge, Better Tomorrow.