Ministry of Health, State of Kuwait Kuwait Pediatric CouncilCOMMON & EMERGENCY CARE
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Ministry of Health, State of Kuwait
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Kuwait Pediatric Council · Bedside reference

Pediatric & Neonatal
Common & Emergency Care Guide

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 JaafarSpecialist, 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 AlajmiSpecialist, 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, verified against the primary sources and current guidelines, and approved by the author and the review panel named below, who take full responsibility for the accuracy and integrity of the content. 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 and approved the final version.
The author and reviewers confirm they have read this version, verified the clinical content and references, and approve it for use.
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.
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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
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
AAF — amino acid formula
ABC — airway, breathing, circulation
ABCDE — airway, breathing, circulation, disability, exposure
ABO — ABO blood‑group system
ACS — acute chest syndrome
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
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
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
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
BWPS — Burch–Wartofsky Point Scale (for thyrotoxicosis)
BXO — balanitis xerotica obliterans
C1‑INH — C1‑esterase inhibitor
CAH — congenital adrenal hyperplasia
CAP — community‑acquired pneumonia
CBC — complete blood count
CCHD — critical congenital heart disease
CDH — congenital diaphragmatic hernia
CFU — colony‑forming units
CHD — congenital heart disease
CICO — can't intubate, can't oxygenate
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)
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)
DOPE — displacement, obstruction, pneumothorax, equipment (deterioration mnemonic)
DOPES — displacement, obstruction, pneumothorax, equipment, stacked breaths (ventilator mnemonic)
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
FHH — familial hypocalciuric hypercalcemia
FiO₂ — fraction of inspired oxygen
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
GAS — group A Streptococcus
GBS — group B Streptococcus; also Guillain–Barré syndrome
GCS — Glasgow Coma Scale
GER — gastresophageal reflux
GERD — gastresophageal reflux disease
GFR — glomerular filtration rate
GGT — gamma‑glutamyl transferase
GH — growth hormone
GI — gastrointestinal
GIR — glucose infusion rate
GJ — gastrojejunal (tube)
HA — hypoallergenic (partially hydrolyzed formula label)
HAE — hereditary angiedema
HAST — hypoxia‑altitude simulation test
HbA1c — glycated hemoglobin
HBO — hyperbaric oxygen
HCN — hydrogen cyanide
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
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
IBI — invasive bacterial infection (bacteremia or bacterial meningitis)
ICP — intracranial pressure
ICU — intensive care unit
ID — infectious diseases
IDM — infant of a diabetic mother
IEI — inborn errors of immunity
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
KCl — potassium chloride
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
LP — lumbar puncture
LOC — loss of consciousness
LRINEC — Laboratory Risk Indicator for Necrotizing Fasciitis (score)
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
MMA — methylmalonic acidemia
MMR — measles, mumps and rubella (vaccine)
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
OGT — orogastric tube
OHP — 17‑hydroxyprogesterone (17‑OHP)
OI — oxygenation index
OME — otitis media with effusion
OPA — oropharyngeal airway
OR — odds ratio
ORS — oral rehydration solution
ORT — oral rehydration therapy
OSA — obstructive sleep apnea
PA — propionic acidemia; also posteroanterior (radiograph view)
PALF — pediatric acute liver failure
PALS — Pediatric Advanced Life Support
PaO₂ — arterial partial pressure of oxygen
PAT — Pediatric Assessment Triangle
PCR — polymerase chain reaction
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)
PEG — percutaneous endoscopic gastrostomy
PEN‑FAST — penicillin‑allergy risk‑assessment score
PEP — post‑exposure prophylaxis
PEWS — Pediatric Early Warning Score
PICC — peripherally inserted central catheter
PICU — pediatric intensive care unit
PIGN — post‑infectious glomerulonephritis
PLP — pyridoxal‑5‑phosphate
PMA — postmenstrual age
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
PTU — propylthiouracil
PUCAI — Pediatric Ulcerative Colitis Activity Index
PVC — premature ventricular contraction
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
RCT — randomized controlled trial
RDS — respiratory distress syndrome
rFVIIa — recombinant activated factor VII
RIG — rabies immunoglobulin
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
SCFE — slipped capital femoral epiphysis
SCID — severe combined immunodeficiency
SCIWORA — spinal cord injury without radiographic abnormality
SGA — small for gestational age
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
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
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
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
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)
WBC — white blood cell (count)
WOB — work of breathing
WPW — Wolff–Parkinson–White (syndrome)

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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 2020Chemo‑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.
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▸
PresentationGo to
Bilious vomiting (green)Malrotation / Midgut Volvulus
The limping / non‑weight‑bearing childThe Limping Child · Transient Synovitis vs Septic Arthritis · Slipped Capital Femoral Epiphysis (SCFE)
Cyanosis / the blue babyHypercyanotic (Tet) Spell · Neonatal & Infant CHD · Critical CHD — Pulse Oximetry Screening
Floppy infant / acute weaknessGuillain–Barré Syndrome / Acute Flaccid Paralysis · The Child with Neuromuscular Disease · Neonatal Sepsis (rapid approach)
Petechiae / purpuraImmune Thrombocytopenia (ITP) · IgA Vasculitis (Henoch–Schönlein Purpura) · Septic Shock
StridorCroup · Choking (Foreign‑Body Obstruction) · Anaphylaxis · Retropharyngeal Abscess
WheezeAcute Asthma · Bronchiolitis · Anaphylaxis
SeizureConvulsive Status Epilepticus · Febrile Seizure · Neonatal Seizures
Fever + non‑blanching rashSeptic Shock · Bacterial Meningitis & Encephalitis
Acute scrotal painAcute Scrotum · Testicular Torsion
Jaundiced neonateNeonatal Hyperbilirubinemia · Neonatal Cholestasis
Bloody diarrheaHemolytic Uremic Syndrome · Acute IBD Flare & Toxic Megacolon · Gastroenteritis & Dehydration
Apnea / brief resolved eventBRUE (Brief Resolved Unexplained Event) · Pertussis (Whooping Cough)
Severe abdominal painAcute Appendicitis · Intussusception · Malrotation / Midgut Volvulus · Diabetic Ketoacidosis
Bruising / abnormal bleedingImmune Thrombocytopenia (ITP) · Acute Bleeding in Hemophilia · Vitamin K Deficiency Bleeding (VKDB) · Child Protection & Safeguarding
Fever in the young infantFever in the Young Infant
Shock / poor perfusionShock — Recognition & Type · Septic Shock
Poisoning / ingestionPoisoning & Toxic Ingestion · Button (Lithium) Battery Ingestion · Caustic (Corrosive) Ingestion
High glucose / ketonesDiabetic Ketoacidosis · Hyperglycemic Hyperosmolar State (HHS)
HypoglycemiaHypoglycemia (Beyond the Newborn) · Metabolic Crisis (Inborn Error) · Neonatal Hypoglycemia
Painful swollen joint + feverTransient Synovitis vs Septic Arthritis · Osteoarticular Infections
Dark / tea‑colored urineRhabdomyolysis · Acute Kidney Injury · Gross Hematuria
Agitation / behavioral crisisAcute Severe Agitation · Self‑Harm / Intentional Ingestion
Major hemorrhage / traumaMassive Transfusion & Blood Products · Major Trauma — Primary Survey & Resuscitation
Anaphylaxis / urticaria + collapseAnaphylaxis
The unwell child with a deviceTracheostomy Emergencies · Gastrostomy (Feeding) Tube Problems · The Child with Medical Complexity
◈ 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.
  • 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 node is a sentinel pattern — tap it to jump to the full card (workup + doses). Not exhaustive; the section cards remain the source of truth.
Cyanotic CHD Cyanosis unresponsive to O₂ Raised ICP / brain tumor Morning headache + vomiting Cord compression Night back pain + leg weakness Neuromuscular / botulism Floppy infant, weak cry Hypertensive emergency Very high BP + seizure DKA ± cerebral edema Vomiting + polyuria + high glucose Septic arthritis Limp + fever, won't bear weight Acute hemolysis Sudden pallor + jaundice Inflicted injury Bruise, non‑mobile infant Reconsider diagnosis “Gastroenteritis”, no diarrhea Malrotation + volvulus Bilious (green) vomiting, infant Testicular torsion Acute scrotal pain / swelling Caustic injury Button / lithium battery Meningococcal sepsis Fever + non‑blanching rash Serious bacterial infection Fever, infant < 90 days ITP vs meningococcemia Petechiae — well or unwell? Epiglottitis / deep‑neck Drooling + tripod + stridor Myocarditis Tachycardia + gallop, hepatomegaly Duct‑dependent CHD / IEM Neonate collapse / shock Surgical / abdomen Fever, rash & sepsis Heart / neonate Brain, cord & BP Metabolic, bone & blood CAN'T‑MISS PATTERNS SEE → NAME → ACT
01

Resuscitation

PALS 2025 (AHA/AAP)

Cardiopulmonary Arrest

MINUTES

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

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◣ 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, go IO if IV fails after 2 attempts or 90 s); 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.
  • Reassess rhythm and a central pulse (brachial in infants; femoral/carotid in children) every 2 min, pausing compressions ≤ 10 s. 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; 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 or 90 s); 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).
  • Discharge — not applicable — care after unsuccessful resuscitation follows the death‑confirmation and bereavement pathway.
  • Refer — 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.

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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) Second‑generation antipsychotics first‑line; benzodiazepines where intoxication/anxiety predominates. Physical restraint = brief last resort, continuous monitoring.
DrugDose (approximate)Route & notes
Olanzapine2.5–5 mg (< 40 kg); 5–10 mg (≥ 40 kg)PO/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
Haloperidol0.025–0.05 mg/kg (max 5 mg)IM; watch for dystonia/QT — second‑generation agents preferred
Diphen­hydramine1–2 mg/kg/dose (max 50 mg)IV/IM/PO; antidote for an acute dystonic reaction from an antipsychotic (haloperidol/risperidone) — not a treatment for agitation itself
⚠ 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.
  • Discharge — settled, medically cleared, with a safety plan and follow‑up.
  • Refer — psychiatry; medical/toxicology for organic causes.

Self‑Harm / Intentional Ingestion

HOURS

Stabilize the patient medically first, then address psychological safety.

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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 acetaminophen and salicylate levels, contact poisons information. 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.
  • Discharge — medically cleared AND psychiatrically assessed as safe, with follow‑up and means restriction.
  • Refer — psychiatry (risk assessment), social work/safeguarding, and toxicology.

Drug‑Induced Hyperthermia Syndromes

MINUTES

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

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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; aggressive cooling; treat hyperkalemia/rhabdomyolysis; urgent PICU/toxicology/anesthesia — antidotes per local protocol
⚠ 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).
  • Discharge — not acutely; after resolution and review of the causative agent.
  • Refer — 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.

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◣ 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; packed red cells 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 — start epinephrine or norepinephrine early (PALS). May start peripherally with close observation for extravasation until central access is obtained
Norepinephrine (noradrenaline) infusion0.05–0.3 mcg/kg/minTitrate to response; first‑line alternative — warm/cold classification no longer directs the choice. 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.
  • Discharge — only once the cause is treated and perfusion is normal off vasoactive support.
  • Refer — 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 (≥ 2 points = sepsis; ≥ 1 cardiovascular point = septic shock).

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⚠ 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
  • two IV/IO
  • antibiotics within 1 hour
  • 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.
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, repeat up to ~40 mL/kg.
  • Watch for fluid overload — new hepatomegaly, crackles, gallop, or B‑lines on lung POCUS. Third bolus only if still dehydrated without overload.
  • Start vasoactives if shock persists after ~40 mL/kg, or earlier if overload develops.
fluid‑refractory
Vasoactive
  • Call PICU immediately.
  • Start epinephrine or norepinephrine (either is acceptable first‑line; not dopamine) — the warm/cold picture (norepinephrine if warm/vasodilated with bounding pulses, epinephrine if cold/low‑output) can guide but no longer strictly directs the choice; a well‑sited peripheral IV is acceptable, with close extravasation monitoring while central access is arranged.
  • Catecholamine‑resistant shock → consider early hydrocortisone, especially with adrenal‑insufficiency risk (purpura fulminans, recent/chronic steroids, hypothalamic–pituitary–adrenal disease): stress dose ≈ 50 mg/m² then 50–100 mg/m²/day
  • OR 1–2 mg/kg then ≈ 2–4 mg/kg/day.
  • Give stress‑dose hydrocortisone for suspected/documented adrenal insufficiency. In catecholamine‑resistant shock, hydrocortisone may restore vascular responsiveness to catecholamines — adult data suggest a mortality benefit, but pediatric evidence remains limited. Call PICU (SSC).
  • Refractory shock — persisting despite fluids, ≥ 2 vasoactives, and hydrocortisone, or low cardiac output on high inotropic support → consider VA‑ECMO early and activate an ECMO center; survival falls the longer cannulation is delayed. SSC 2020 suggests VA‑ECMO in children with septic shock refractory to all other treatments.
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. Meningitic ceftriaxone dose 50 mg/kg/dose every 12 h (max 2 g/dose)
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/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
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
  • Adrenaline and noradrenaline infusions should be given via a central venous catheter wherever possible. Do not delay initiation of vasoactive support to obtain central access (SSC Pediatric 2020).
  • 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 exceeding the stated 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) as the bitartrate 1 mg/mL (2 mg/2 mL, 4 mg/4 mL). Dose norepinephrine as base — a 4 mg/4 mL bitartrate ampoule = 2 mg base.
  • 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% (or 0.9% saline) — 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.
  • Sources: BNF for Children; ASHP/ISMP Standardize 4 Safety pediatric infusion standards; ANMF adrenaline & noradrenaline standard‑concentration monographs (2025–26).
◣ Admit · Discharge · Refer
  • Admit — all → PICU/high‑dependency; fluid‑refractory or vasoactive‑requiring shock is always PICU.
  • Discharge — not from the acute episode — step down once off vasoactives with a controlled source.
  • Refer — 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 minutesTwo agents IV/IO, 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. Use10 mL/kg if cardiac or no ICU.3≤ 15 minREASSESS + REPEATRepeat to ~40 mL/kg — STOP at overload (hepatomegaly,crackles, gallop, B‑lines). Correct glucose + calcium.415–40 minSTART VASOACTIVEEpinephrine (cold) or norepinephrine (warm) — 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.

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◢ 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 monitor with caution; may need positive‑pressure ventilation — call PICU.
  • Do not give large fluid boluses.
  • 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 — preferred if the blood pressure allows. Consider omitting the 50 mcg/kg loading dose in acute shock to avoid hypotension.
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.
◣ Admit · Discharge · Refer
  • Admit — all suspected cases → PICU/cardiology; arrhythmia, low output, or a troponin/BNP rise mandates continuous monitoring.
  • Discharge — only after cardiology review, recovered function, and a heart‑failure plan.
  • Refer — 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.

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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, max 0.5 mg)IV/IO; for vagal cause, AV block, or cholinergic/organophosphate toxicity
◣ 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; modified Valsalva in older children — 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: synchronized cardioversion, or an antiarrhythmic infusion — amiodarone 5 mg/kg over 20–60 min OR procainamide 15 mg/kg over 30–60 min. 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, 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.
  • Discharge — a stable child who reverts and stays in sinus rhythm, feeding and well, with cardiology follow‑up and a clear return plan.
  • Refer — 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 no delay (short‑acting agent, e.g., IV fentanyl). 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.
  • Discharge — not from the acute episode — only after cardiology work‑up and a management plan.
  • Refer — cardiology urgently (structural disease, channelopathy, QT/electrolytes); 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 — duct‑dependent pulmonary flow / mixing ("5 T's + 1")
  • Transposition of the great arteries (duct‑dependent for mixing)
  • Truncus arteriosus
  • Total anomalous pulmonary venous drainage (obstructed type = emergency)
  • 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)start 0.05–0.1 → maintenance 0.01–0.02 mcg/kg/minIV infusion; two IV lines; never interrupt; once responding, titrate to the lowest effective dose (low dose maintains patency in ~80% with less apnea and fever). Watch for apnea (~12%), hypotension, and 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.
  • In duct‑dependent systemic lesions keep SpO₂ targets modest.
◈ 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.
  • Discharge — only under cardiology, with a feeding/oxygen/weight plan and clear red‑flag advice.
  • Refer — 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; beta‑blocker (propranolol or esmolol). 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.
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
Propranolol0.05–0.1 mg/kgslow IV; alternative to esmolol
Esmolol500 mcg/kg IV load over 1 min, then 50–300 mcg/kg/min infusionIV beta‑blocker alternative to propranolol
Sodium bicarbonate1 mmol/kgIV, if significant metabolic acidosis
◣ Admit · Discharge · Refer
  • Admit — any spell → monitored bed/PICU; recurrent or severe spells need urgent intervention.
  • Discharge — only after cardiology review, a spell‑management plan (knee‑chest, hydration, propranolol as advised), and caregiver education.
  • Refer — 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.
  • Loss of the continuous shunt murmur — the single most useful sign (a patent shunt murmurs continuously).
  • 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 (FiO2 ≈ 10% above the child's baseline) 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 3–10 mcg/kg slow IV, or norepinephrine 0.1 mcg/kg/min, or epinephrine up to 0.05 mcg/kg/min.
③ LOWER PVR (unload the lungs) — Deepen sedation + paralysis; hyperventilate to lower PaCO2 (mild respiratory alkalosis); keep well oxygenated; magnesium sulfate 0.4 mmol/kg (50%).
④ ANTICOAGULATE (stop the clot) — Heparin 100 units/kg IV bolus, then 20 units/kg/h infusion; an optional second 50 units/kg bolus at 15 min. 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 — confirm against your cardiac center's protocol
Drug / productDoseNotes
▮ SVR Phenylephrine3–10 mcg/kg slow IVRaises SVR; dilute before use (e.g., 10 mg in 100 mL, then 1 mL made up to 10 mL)
▮ SVR Norepinephrine (noradrenaline)0.1 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 IVPulmonary vasodilator — helps lower PVR
▮ CLOT Heparin100 units/kg IV bolus → 20 units/kg/h; ± 50 units/kg at 15 minPrevents 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 theatre. A lost shunt murmur in a cyanotic child is the shunt occluding until proven otherwise.
◈ Sources
  • NHS Greater Glasgow & Clyde paediatric guideline — immediate management of the modified Blalock–Taussig / central shunt (Paediatrics 386); PIER Network — acute management of the cyanosed infant with a systemic‑to‑pulmonary (BT/Sano) shunt in the ED; shunt‑thrombolysis case & review data (heparin/urokinase; catheter‑directed thrombolysis).
  • Confirm all doses against your formulary and cardiac center's protocol.

Acute Rheumatic Fever

DIAGNOSEJones 2015 · AHA

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, or positive throat swab/RADT, or recent scarlet fever) 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
  • Gulf / Middle‑East children are a moderate‑to‑high‑risk population — applying low‑risk thresholds under‑diagnoses ARF.
  • 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, polyarthritis, or polyarthralgia
MinorPolyarthralgia · fever ≥ 38.5 °C · ESR ≥ 60 mm/h and/or CRP ≥ 3.0 mg/dL · prolonged PR (if carditis not a major)Mono‑arthralgia · fever ≥ 38 °C · ESR ≥ 30 mm/h and/or CRP ≥ 3.0 mg/dL · 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 carditisAspirin 80–100 mg/kg/day PO divided every 6 h for 2–6 weeks, then taper; watch for tinnitus/hyperpnea (salicylate toxicity).
Moderate–severe carditis / heart failureAdd prednisone/prednisolone ~2 mg/kg/day (max ~60 mg) 2–3 weeks then taper, overlapping aspirin. Diuretic + ACE inhibitor for heart failure; bed rest.
Sydenham choreaUsually self‑limited — quiet environment, protect from injury. If disabling: valproate or carbamazepine (off‑label). Salicylates/steroids do not help the chorea itself.
Secondary prophylaxis — benzathine penicillin G IM every 3–4 weeks (< 27 kg 600,000 u; ≥ 27 kg 1,200,000 u)
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 — often lifelong
◈ If the IM injection is declined Oral penicillin V 250 mg twice daily is an accepted alternative for secondary prophylaxis (sulfadiazine if penicillin‑allergic) — but adherence is worse and it is less effective than IM benzathine, which remains preferred.
✦ 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.
◈ Sources
  • AHA 2015 Revised Jones Criteria (Gewitz, Circulation 2015); AHA/AAP prevention statement (Gerber, Circulation 2009); WHO RHD guidance; SPIDS Gulf prophylaxis guidance.
  • Confirm doses against your formulary.

Pericarditis & Cardiac Tamponade

MINUTESESC 2015

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

▸
◣ Pericarditis — 2 of 4
  • 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.
  • Supportive: raised CRP/ESR.
  • 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. 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). Avoid intubation / positive‑pressure ventilation — it drops preload and can cause arrest; if unavoidable, drain first, low tidal volume/PEEP, keep volume‑loaded. Avoid diuretics/vasodilators. Call cardiology + cardiac surgery + PICU in parallel.
NO
Uncomplicated pericarditis: NSAID (ibuprofen) + colchicine — colchicine halves recurrence. Treat the cause; restrict strenuous exercise until symptom‑free with normal CRP/ECG/echo. Steroids are second‑line (increase recurrence).
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 dividedFirst‑line adjunct — halves recurrence; reduce in renal impairment.
Purulent pericarditisUrgent drainage + IV vancomycin + 3rd‑gen cephalosporin, ~3–4 weeksSurgical 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.
◈ Sources
  • ESC 2015 pericardial diseases guidelines (Adler, Eur Heart J); pediatric echo/tamponade reviews (Frontiers Pediatr 2017); pediatric colchicine data (Pediatr Cardiol 2024).
  • Confirm doses against your formulary.

Infective Endocarditis (incl. Subacute)

HOURSModified Duke / AHA

Fever + a new murmur + positive cultures — think endocarditis; diagnose by the modified Duke 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 of subacute native‑valve disease; S. aureus dominates acute disease.
  • Peripheral stigmata (late, immune‑mediated): 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.
◣ Modified Duke 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 two MAJOR criteria
MICROBIOLOGY
Typical organism from ≥ 2 separate blood cultures (viridans streptococci, S. gallolyticus/bovis, HACEK group, S. aureus, or community‑acquired enterococci with no primary focus), or persistently positive cultures of a compatible organism.
ENDOCARDIAL
Echo evidence of endocardial involvement: vegetation, abscess, new partial dehiscence of a prosthetic valve, or new valvular regurgitation (worsening of an existing murmur is not enough).
◣ 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.
⚠ 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, FBC, 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. Ventricular assist device (VAD) — added by ESC 2023.
◆ 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). Routine fillings, radiographs, 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). Cover staphylococci if the airway procedure treats an established infection (add anti‑staphylococcal agent).
  • 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 more restrictive for non‑dental procedures — it advises prophylaxis for respiratory, GI, GU, skin, or musculoskeletal procedures only when performed at an infected or colonized site. 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.
◈ Sources
  • AHA prevention of IE statement (Wilson, Circulation 2007) and 2021 update (Wilson, Circulation 2021), and AHA IE wallet card; 2023 ESC endocarditis guidelines (Delgado & Ajmone Marsan, Eur Heart J 2023;44:3948); Modified Duke criteria (Li, Clin Infect Dis 2000); 2023 Duke‑ISCVID criteria (Fowler, Clin Infect Dis 2023).
  • Confirm doses against your formulary.
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 carries the same risk — manage identically.
  • This pathway does not apply to the ill‑appearing at any age.
  • Risk factors that are not applicable to this pathway: 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 100 mg/kg/dose q8h (reduced neonatal renal clearance; Lexicomp) + gentamicin 4 mg/kg/dose q24hMeningitis: add — or replace the aminoglycoside with — cefotaxime 50 mg/kg/dose q8h. HSV risk: add acyclovir 20 mg/kg/dose q8h.
8–28 daysAmpicillin 75 mg/kg/dose q6h + gentamicin 5 mg/kg/dose q24hMeningitis: 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. Low‑risk UTI: cefixime 8 mg/kg/dose q24h PO.
Source
Canadian Pediatric Society — Management of well‑appearing febrile young infants aged ≤ 90 days (updated May 2026); AAP — Pantell et al., Evaluation and Management of Well‑Appearing Febrile Infants 8–60 Days Old, Pediatrics 2021.
◈ 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. Test selectively (urinalysis ± inflammatory markers) and use clinical judgment; escalate only the ill‑appearing or those with a positive screen.
◈ See also For the neonate (≤ 28 days), see Neonatal Sepsis — rapid approach for neonatal‑specific empiric therapy (ampicillin + gentamicin/cefotaxime ± acyclovir).

Gastroenteritis & Dehydration

HOURS

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

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◣ 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)10 mg/day (< 6 mo)
20 mg/day (≥ 6 mo)
Oral, 10–14 days. A WHO/UNICEF measure for low- and middle‑income settings where zinc deficiency is common — shortens diarrhea by ~½ day (~1 day if malnourished) concentrates at ≥ 6 months in zinc‑deficient or malnourished children. 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.
  • Red flags: bilious or bloody vomit, severe pain/distension (think surgical), inability to tolerate ORS.
  • Zinc dosing & evidence: WHO eLENAQR.
◣ Admit · Discharge · Refer
  • Admit — shock or severe dehydration, failed oral/NG rehydration, intractable vomiting, dangerous electrolyte derangement, or diagnostic uncertainty.
  • Discharge — minimal or mild dehydration tolerating oral rehydration, with carers confident on fluids and red‑flag advice.
  • Refer — surgical review if a surgical abdomen is suspected; PICU for refractory shock or severe electrolyte disturbance.

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) ± increased work of breathing, chest or abdominal pain, poor feeding. Wheeze + hypoxia points to bronchiolitis or asthma, not bacterial CAP.
  • Tachypnea cut‑offs (breaths/min):
  • < 2 mo > 60
  • 2–12 mo > 50
  • 1–5 yr > 40
  • > 5 yr > 30.
  • Check SpO₂ in everyone — hypoxemia may not be clinically obvious; give oxygen for SpO₂ < 92%.
  • 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.
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 day 1, then 5 mg/kg × 4 d (max 500 mg)School‑age with atypical features. Macrolide resistance rising; doxycycline (any age, short courses).
⚠ 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 (SpO₂ < 90%; < 92% in high-risk infants), respiratory distress, dehydration or feeding failure, an effusion/empyema, or failure of outpatient therapy.
  • Discharge — well child maintaining saturations in air, feeding, on oral antibiotics with follow‑up arranged.
  • Refer — 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.

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◈ 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 0.1 mg/kg (max 4 mg) in normal saline instilled via the chest tube, clamp/dwell 1 hour, then drain — once daily for up to 3 days (a fixed 4 mg dose daily × 3 is an accepted alternative). 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 — clinically significant empyema or a moderate‑to‑large effusion, for IV antibiotics ± drainage. A small parapneumonic effusion in a well child can be managed as community‑acquired pneumonia with close follow‑up rather than admitted.
  • Discharge — not acutely; complete therapy with follow‑up imaging.
  • Refer — respiratory/surgery for drainage (chest drain ± fibrinolytics or VATS).

Acute Otitis Media

ASSESSINFANT–CHILD · CPS 2016 / AAP 2013

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

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◣ 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). 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, 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 BIDPO. Drug of choice — covers S. pneumoniae; excellent middle‑ear penetration.
Amoxicillin‑​clavulanate40–45 mg/kg/dose BID (amoxicillin component)PO. If AOM + purulent conjunctivitis, amoxicillin in the last 30 days, or failure at 48–72 h. Specify the 14:1 suspension.
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.
  • 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.
  • Discharge — uncomplicated disease — analgesia, with observation or antibiotics per age and severity, and safety‑netting.
  • Refer — ENT for suspected mastoiditis, recurrent or complicated 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.

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◣ 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: ≤1 low (~1–10%) → testing can be deferred; 2–3 intermediate (~11–35%) → test; ≥4 high (~50%) → 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 titres 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 penicillin V10 days
Poor adherence expectedBenzathine penicillin G IM — < 27 kg: 600,000 U; ≥ 27 kg: 1,200,000 U1 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‑labelled 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 days5–10 days
⚠ Why we treat
  • Antibiotics prevent suppurative complications and acute rheumatic fever (but not post‑streptococcal glomerulonephritis). All GAS is penicillin‑susceptible, but macrolide/clindamycin resistance reaches ~20% 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).
  • Discharge — most, with antibiotics and safety‑net advice.
  • Refer — ENT for abscess or recurrent tonsillitis.

Urinary Tract Infection

HOURS> 2 MONTHS

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

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◁ 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 (> 5 WBC/HPF, or ≥ 10/µL) supports infection.
Diagnostic colony‑count thresholds
Collection methodMinimum count (CFU/mL)Note
Clean catch / midstream≥ 10⁵Mixed growth usually = contamination.
In‑and‑out catheter≥ 5 × 10⁴Indwelling‑catheter specimens less reliable.
Suprapubic aspirateAny growthMost reliable method.
◣ Admit · Discharge · Refer
  • Admit — young infants, ill/septic, unable to tolerate oral, or complicated/obstructive UTI.
  • Discharge — well child on oral antibiotics with follow‑up.
  • Refer — 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). 2–4 days of an oral agent chosen by local E. coli susceptibility. No imaging needed.
FEBRILE UTI / PYELONEPHRITIS
Treat 7–10 days. Oral is as effective as IV in non‑toxic children likely to tolerate every dose. Use IV initially if toxic, < 2–3 months, vomiting, or unable to tolerate oral — then step down.
◈ 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.
Antimicrobial options — if the isolate is susceptible
DrugDoseNotes
Amikacin (IV)15 mg/kg once dailyESBL‑active empiric choice; 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) BIDPreferred oral step‑down once susceptible — covers many ESBL isolates if tested S.
Cefixime (PO)8 mg/kg/dose once dailyCommon 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 (7:1) TIDIf susceptible; amoxicillin alone often resisted.
Ciprofloxacin (PO) *15 mg/kg/dose BID* 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 < 2 yr (during, or within ~2 weeks of, the illness).
  • VCUG is not routine — obtain it only if RBUS shows marked hydronephrosis, a dilated ureter, a duplex system / ureterocele, or obstruction, or after a second febrile UTI. 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.

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◣ 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, IV antibiotics, urgent surgery. Add an anti‑toxin agent (clindamycin) and consult infectious diseases.
Oral cephalexin is the antimicrobial of choice when antibiotics are warranted.
By pathogen / setting
TargetDrug & doseNotes
MSSA / GAS — oral, first‑lineCephalexin 25 mg/kg/dose (max 1 g) PO QID; high‑dose TID for moderate cellulitisDrug of choice. Covers MSSA and GAS. High‑dose enables outpatient 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; 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 BIDPreferred oral MRSA agent — also covers GAS. Use when colonized or MRSA strongly suspected.
MRSA — alternativeClindamycin 10 mg/kg/dose PO/IV q8hOnly where local clindamycin susceptibility is high. Anti‑toxin role in severe disease.
MRSA — IV (severe)Vancomycin 15 mg/kg/dose IV q6hAdd when MRSA suspected in toxic/deep infection; stop once MRSA excluded. K. kingae is resistant to vancomycin and clindamycin and shows reduced susceptibility (high MICs) to cloxacillin — so cefazolin/cephalosporins, which cover it, are preferred empirically 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.
  • Discharge — localized, well child on oral antibiotics with review.
  • Refer — 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 / post‑auricular > 0.5 cm).
  • A supraclavicular node is never normal — it is the single highest‑risk site for malignancy (up to ~75%). 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 splenomegalySupportive, 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, toxoplasmaDon'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 independent predictors (2024 cohort): a larger node — each extra centimetre roughly doubles the odds, a node > 3 cm ≈ 12% malignant — and older age (> 12 yr ≈ 20% vs ≤ 2.5 yr < 1%); firm consistency, weight loss, and an abnormal chest X‑ray 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 25–50 mg/kg/day ÷ 3–4 OR amoxicillin‑clavulanateReview at 48 h; most settle within days. Add source control if an abscess forms.
MRSA risk / penicillin allergyClindamycin 20–40 mg/kg/day ÷ 3–4Also 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.
  • Discharge — the well child with a small, mobile, reactive node → safety‑net and review in 2–4 weeks.
  • Refer — surgery / ENT for excision (NTM, abscess, biopsy); hematology‑oncology for a red‑flag node; infectious diseases for TB or atypical infection.
Source
Pediatric cervical lymphadenopathy: an evidence‑based approach for GPs (Br J Gen Pract 2026;76(764):137); Refining indications for pediatric cervical lymph‑node biopsy (Eur J Pediatr 2026); Risk factors for malignancy in subacute/chronic focal craniocervical lymphadenopathy (Front Pediatr 2024); AAFP — Management of Cervical Lymphadenitis in Children (Am Fam Physician 2008); AAP Red Book 2024 (nontuberculous mycobacteria, cat‑scratch disease).

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 — IV15 mg/kg/dose every 6 h< 50 kg: max 15 mg/kg (750 mg/dose); ≥ 50 kg: 1 g/dose. ≤ 75 mg/kg/day.
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, renal impairment, active GI bleeding / ulcer disease, or any poorly hydrated child.
⚠ Use antipyretics for comfort, not the thermometer
  • Give only while the child is uncomfortable.
  • Combining or alternating the two clears fever faster and gives more fever‑free time (PITCH trial), but does 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 palms, soles, conjunctivae and mucosa, 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 are absent in roughly 40–50% of neonatal HSV with CNS or disseminated disease — 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, or high‑risk labs (CRP > 120 mg/L, WBC > 20,000/µL).
  • 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.
  • Discharge — mild preseptal in a well child on oral antibiotics with 24 h review.
  • Refer — 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 or clindamycin.
Atraumatic preseptal (from sinusitis)PO cephalexin
IV cefazolin
Doses as above. Escalate to / add amoxicillin‑clavulanate (co‑amoxiclav 30 mg/kg [amoxicillin] 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
  • 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 given community‑associated MRSA prevalence higher than North America; ceftriaxone covers sinusitis streptococci with good tissue/CNS penetration; metronidazole covers anaerobes / intracranial spread.
  • Always tailor to immunization status, prior antibiotics, and the local antibiogram.
ConditionDuration
Preseptal cellulitis5–7 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) and events recurred in roughly 7% discharged from the ED and 11% discharged from hospital.
  • 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.
  • Discharge — lower‑risk BRUE with education, CPR resources, and follow‑up.
  • Refer — 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.
  • Amenorrhea: investigate primary amenorrhea if no menarche by age 15 with normal secondary sexual characteristics (or by 13 with none); in secondary amenorrhea, exclude pregnancy first.
DrugDoseRoute & notes
Tranexamic acid15–25 mg/kg/dose (max 1.5 g) every 8 hAcute heavy menstrual bleeding; PO or IV
Combined oral contraceptive / oral progestogenper gynecology protocolHormonal control of acute bleeding or refractory dysmenorrhea
NSAID (ibuprofen / mefenamic acid)ibuprofen 10 mg/kg/dose; 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 offence.
  • 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) mis‑estimate weight in obesity — verify actual weight.
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; 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).
Cefazolin · succinyl­choline · antineoplasticsTotal body weight (TBW)TBW is the correct scalar for these.
Amino­glycosides · hydrophilic drugsAdjusted or lean body weightVolume of distribution altered; use adjusted body weight.
◈ 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 disproportionately common in adolescents with obesity and T2DM.
  • 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 — the same CYP2D6/respiratory risk applies.

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/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, stacked breaths)
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 tunnelled 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?

▸
◢ 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, the stoma is the priority (it is the airway in most tracheostomy patients), moving to the face if the stoma is not the effective route. 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 a set depth — just past the tube tip, no deeper. Routine humidification (HME / “Swedish nose”) prevents the mucus plugs behind most obstructions.
  • 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 often relieves 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 mucus plug is the commonest cause; if it will not clear, 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) — 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.
when trained help arrives
⑤ Re‑establish the airway
  • Re‑cannulate with the same‑size tube; if it will not pass, use one size smaller. If it still will not pass, do not force — stop and keep ventilating until expert airway support arrives, or orally intubate (an uncut / longer ETT, cuff sited beyond the stoma)
  • Confirm with capnography. A neck roll (shoulder roll, neck extended) increases the likelihood of successful insertion.
◣ DOPE — 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)
✦ 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 — reinsertion is difficult or impossible without it.
⚠ No upper airway? (laryngectomy / fixed obstruction)
  • If the child cannot be ventilated from above (laryngectomy, severe subglottic stenosis), the stoma is the only airway — do not waste time on face‑mask ventilation; oxygenate and re‑cannulate or intubate the stoma.
  • 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 (high risk in neurologically impaired children).
  • 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 (~85% effective); 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; cover S. aureus (including MRSA) and Pseudomonas per 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). Otherwise keep the current tube, oxygenate, and get expert help.
Elective tube change (routine)
  • Two people.
  • Supine with a shoulder roll, neck extended; pre‑oxygenate and suction.
  • Load the obturator, lubricate, deflate the cuff.
  • Remove the old tube along its curve; insert the new one on the obturator (tip toward the posterior wall, then rotate downward) on expiration — 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) — prefer oral intubation and avoid blind reinsertion.
  • An established stoma can still narrow > 50% within ~12 h of decannulation, so if decannulated > ~8 h and the child is stable, call ENT before repeated attempts (dilation may be needed).
Source
National Tracheostomy Safety Project (NTSP) pediatric emergency algorithm; Care of Infants and Children with Tracheostomies — American Thoracic Society Clinical Practice Guideline (Am J Respir Crit Care Med 2025;211(11):2001–2020).
◣ Admit · Discharge · Refer
  • Admit — any airway compromise → ED/PICU.
  • Discharge — after the tube is secure and patent and the caregiver is confident.
  • Refer — 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.Silicone is MRI‑conditional — wire‑reinforced / metal variants may not be; check. 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 / NASPGHAN it can close within ~6 h, usually lost by 24 h. 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: a first PEG, or poor wound healing (malnutrition, chemotherapy), may mature more slowly — up to ~3 months; 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.
  • 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) — beware a false pH on proton‑pump inhibitors.
  • After any difficult or uncertain replacement, confirm with a water‑soluble contrast study — the ESPGHAN standard before first use of a replaced balloon tube. 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
  • Peritonitis or systemic infection
  • buried bumper syndrome
  • uncertain or difficult placement
  • concern of a false passage
  • any immature‑tract dislodgement
  • tube out > 24 h → see surgery / gastroenterology.
◣ Admit · Discharge · Refer
  • Admit — peritonitis, a dislodged tube with a lost tract, or inability to replace it.
  • Discharge — a replaced, patent tube with feeds tolerated.
  • Refer — surgery/gastroenterology for tract problems or early dislodgement (< 4 weeks).
◎ 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 favours neither. 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. 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.
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 labelled 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: up to about ⅓ have some neurodevelopmental impairment 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
  • Escalate — refractory cardiac or respiratory failure with a reversible cause → PICU / ECMO center now.
  • Discuss early — call before the child is in extremis; deterioration is often rapid.
Source
  • Extracorporeal Life Support Organization (ELSO) general and pediatric / neonatal guidelines.
  • Candidacy, thresholds, and timing are set by the PICU / ECMO center.

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: at PICU discharge up to ~60% of parents are at risk of PTSD and ~75% of depression, alongside anxiety, exhaustion, 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 immunizations; 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 — neurodevelopment / rehabilitation, psychology / psychiatry, and the relevant specialty for persistent domain‑specific problems; social work for family support.
  • Escalate — new severe mental‑health symptoms (e.g., self‑harm risk) or acute physical deterioration.
Source
  • 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; pediatric PICS reviews.

Aeromedical Transport — Pediatric & Neonatal

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 ~60–65 mmHg (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 ~35% 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: defer non‑urgent flying for roughly the first 7 days (ideally to ~40 weeks corrected) to confirm feeding, thermoregulation, and no undiagnosed cardiorespiratory problem or silent pneumothorax.
  • 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 (~70% desaturate on hypoxic challenge).
  • 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 expectedStable 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). In children, substitute an age‑appropriate PEWS (NEWS2 is validated only ≥ 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.
  • Endotracheal / tracheostomy cuff gas expands ~⅓ as cabin pressure falls — check for a leak and adjust the cuff volume as needed; monitor cuff pressure during ascent and descent.
  • 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 — the MOH Directorate of Treatment Abroad (DTA) decides transport type; involve the relevant clinical council for team and equipment.
Source
  • State of Kuwait — MOH Aeromedical Evacuation & Transport Policy A‑ADM‑014 (effective Oct 2025; review 2027) — the transport forms and checklists are in the policy on the MOH website.
  • Pre‑flight assessment thresholds align with the British Thoracic Society clinical statement and pediatric air‑travel evidence. Neonatal/infant guidance: BTS air‑travel recommendations (Thorax 2011); Fitness to fly in the paediatric population (Eur J Pediatr 2018); Khanna et al., in‑flight hypoxia in healthy infants (Thorax 2013).
06

Endocrine & Metabolic

Diabetic Ketoacidosis

HOURSISPAD 2022 · TREKK/CPEG 2023

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

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Diabetic Ketoacidosis — bedside algorithmAdapted from TREKK; aligned with the Kuwait PICU Task Force · ISPAD 2022.
Pediatric DKA algorithm flowchart
◈ 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 are admitted, but the level of care follows severity: mild DKA can be managed on a general pediatric ward with hourly monitoring; moderate/severe, young age (< 5 y), reduced consciousness, or high‑risk features → high‑dependency/PICU.
  • Discharge — not from DKA; transition to subcutaneous insulin with diabetes‑team education.
  • Refer — 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.

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◣ Define (differs from DKA)
  • Glucose > 33 mmol/L (600 mg/dL), serum osmolality > 320 mOsm/kg, pH > 7.3 and bicarbonate > 15, 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.
  • 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; restore circulation, then replace deficit steadilyAim 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.

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◣ 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 bolus, repeat; 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%20 mL/kgIV bolus, repeat
Dextrose 10%5 mL/kgIV, for low glucose
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.
  • Discharge — only after stabilization, endocrine review, and stress‑dosing/emergency‑injection education.
  • Refer — pediatric endocrinology.

Hypoglycemia (Beyond the Newborn)

MINUTESPES 2015

Plasma glucose < 3.9 mmol/L (70 mg/dL) — treat now; 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/IV/SC (or 0.03 mg/kg, max 1 mg) when there is no IV access or hyperinsulinism is suspected — 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.
  • Discharge — only after a documented safe fast and a sick‑day/emergency plan (home glucagon where indicated).
  • Refer — 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.

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◢ Hyperkalemia — get an ECG first
  • Hyperkalemia = serum K⁺ > 5.5 mmol/L (mild 5.5–6.0 · moderate 6.0–6.5 · severe > 6.5 or ECG changes); 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)2.5–5 mg (high dose 10–20 mg)Additive 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 in hypernatremic dehydration).
ProblemTreatmentNotes
Hyponatremia with seizures / encephalo­pathy3% saline 2–5 mL/kg (≈ 1–2.5 mmol/kg) IV over ~20 min; may repeatAim to raise sodium by 4–6 mmol/L to stop the seizures — that is usually enough
Hyponatremia (no severe symptoms)Treat the cause; correct slowlyDo not exceed 8 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% 0.5–1 mL/kg slow IV, cardiac monitor; then infusionTetany, seizures, prolonged QT, Chvostek / Trousseau signs. Avoid extravasation (tissue necrosis)
Refractory hypocalcemia or hypokalemiaCheck and replace magnesiumLow magnesium blocks correction of both — replace it first
⚠ 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.
  • Discharge — mild, asymptomatic, correctable causes, with a follow‑up recheck.
  • Refer — 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.

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◣ 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/day IV (max 4 mg); 4 mg/5 mL vial, dilute 1:20 in 0.9% saline, infuse over 15 minPreferred bisphosphonate for high bone turnover (malignancy, immobilization) — higher response rate (complete response ~88% vs ~70%) and a much shorter infusion (15 min vs 2–4 h) than pamidronate (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 hAlternative where zoledronic acid is unavailable; same indications; 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.
  • Discharge — mild & asymptomatic with an outpatient workup and offending agents stopped.
  • Refer — pediatric endocrinology ± oncology/nephrology; 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 fuelling 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 q6h
or 0.01–0.05 mg/kg IV (max 1 mg/dose)
Controls heart rate, tremor and agitation; slows peripheral T4→T3. Caution in heart failure — treat failure alongside
2 · Methi­mazole (thionamide)0.5–1 mg/kg/day PO/NG/PR divided q8h (max 30 mg/day)Blocks new hormone synthesis; give the thionamide before iodine. Carbimazole is the equivalent prodrug
2 · PTU (thionamide — alternative)5–10 mg/kg/day PO/NG divided q8hAlso blocks peripheral T4→T3. Either thionamide is acceptable — no difference in mortality (Lee, JAMA Netw Open 2023); ATA 2016 has historically listed PTU first in storm
3 · Potassium iodide (strong iodine solution)1–5 drops PO/NG q8hBlocks hormone release; give ≥ 1 h after the thionamide
4 · Hydro­corti­sone1–2 mg/kg/dose IV q6h
(or 50–100 mg/m²/day)
Reduces 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."

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◣ 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; little or no acidosisMaple‑syrup odor (urine/cerumen); high plasma leucine
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 and 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 / rising / coma
Urgent hemodialysis or CRRT. Transfer to a metabolic center.
Drug / measureDoseRoute & notes
Dextrose 10%1.5× maintenance; glucose infusion rate 8–10 (up to 15–20) mg/kg/minIV — reverses catabolism
Sodium benzoate + sodium phenylacetate250 mg/kg load over 90–120 min, then 250 mg/kg/dayIV; central line preferred, peripheral acceptable 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 hydrochloride200–600 mg/kgIV load then per day; 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 ammoniaOral/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.
  • Discharge — not acutely; under the metabolic team with an emergency regimen.
  • Refer — 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, copious irrigation with saline (or clean water) for ≥ 15–30 min BEFORE examination or imaging; evert the lids, sweep out particulate matter, recheck pH until neutral (≈ 7.0–7.5). 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.
  • 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.
  • 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.
⚠ 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
  • 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.

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◣ 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 ~10 s in cold milk or saline, reinsert, have the child bite on gauze.
  • If reimplantation isn't possible, transport the tooth in Hank's solution or cold milk — never water.
  • 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 — 15–20 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 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
  • Dental / maxillofacial urgently — avulsion, fractures with pulp exposure, facial fractures, or a facial‑space infection; refer an intruded tooth to a pediatric dentist; for any airway threat call anesthesia, oral & maxillofacial surgery, ENT, or pediatric surgery — all are equipped to manage these cases.

Dermatologic Emergencies

HOURSCAN'T‑MISS

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

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⚠ 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.
  • 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 etanercept (anti‑TNF) carry the most promising (still low‑certainty) mortality signals; corticosteroids are controversial; IVIG monotherapy is not supported (used, if at all, combined with corticosteroids). 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; European S3 guideline 2024; 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 1 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 5–10 mg/kg/dose q8h (dose by ideal body weight; 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 0.5–1 mg/kg/day (max 60 mg/day) with a slow taper over weeks–months 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 for up to 2 years. 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) q6–8h (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 as an adjuvant in selected cases (streptococcal toxic shock). 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
  • 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.

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⚠ 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
  • 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.

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⚠ 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
  • 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.

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◣ 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, fibrinogenCoagulopathyCorrect before/with endoscopy; 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. Protect the airway in brisk hematemesis.
Hemodynamically unstable?
UNSTABLE / MASSIVE
Resuscitate to hemodynamics and activate the massive transfusion protocol — not a fixed Hb target. PICU; urgent endoscopy once stabilized.
STABLE
Restrictive transfusion — transfuse at Hb < 7 g/dL, target 7–9 g/dL. 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. Urgent endoscopy — band ligation/sclerotherapy.
NON‑VARICEAL
High‑dose IV proton pump inhibitor. Endoscopy for hemostasis — injection + cautery/clips (± haemostatic powder) — early (≤ 24 h) once resuscitated; emergent/urgent (≤ 6–12 h) endoscopy only if still unstable despite resuscitation.
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 (titrate up to ~5 mcg/kg/h if bleeding continues)IV; variceal bleeding. Once bleeding stops, wean gradually (rebound risk); monitor glucose
Pantoprazole / omeprazole1–2 mg/kg (max 40 mg) IV bolus, then 0.1–0.2 mg/kg/h infusion (max 8 mg/h) for severe bleeding, or intermittent high‑dose IVNon‑variceal; also stress‑ulcer prophylaxis
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; transfuse promptly for hemodynamic instability or ongoing massive bleeding regardless of Hb
⚠ At the bedside
Do not routinely place a nasogastric tube — it does not improve outcomes, is complicated in about a third of patients, and endoscopy is the diagnostic and therapeutic tool. 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. Protect the airway in brisk hematemesis; do not over‑transfuse a stable variceal bleed.
◣ Admit · Discharge · Refer
  • Admit — all significant bleeds → resuscitation and endoscopy.
  • Discharge — a minor self‑limited bleed after observation, with follow‑up.
  • Refer — 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 sign; free airIntussusception; NEC / perforation
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.
  • Discharge — a well child with a minor self‑limited cause (fissure, small polyp bleed) and follow‑up.
  • Refer — pediatric surgery for intussusception/volvulus/Meckel/NEC; gastroenterology for endoscopy, 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)
  • 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.
  • Consider adding acyclovir in a neonate with suspected HSV infection, and N‑acetylcysteine if acetaminophen toxicity is suspected.
DrugDoseRoute & notes
10% dextrose infusionglucose infusion rate 6–8 mg/kg/min, titrateKeep glucose normal; check frequently
Vitamin Ksingle parenteral doseTo exclude vitamin K–responsive coagulopathy
N‑acetyl­cysteineper acetaminophen protocolAcetaminophen toxicity; not routine in non‑acetaminophen disease — the pediatric RCT showed no survival benefit, so any use is a transplant‑center/hepatology decision
Acyclovirconsider in a neonate/infant with suspected HSVHSV 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.
  • Discharge — not acutely.
  • Refer — 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, bilirubin, GGT ± triglyceridesRaised 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 diseaseMost 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 with suspected obstruction: MRCP first (first‑line and prerequisite), then ERCP for stone clearance if obstruction is confirmed; involve surgery and GI.
◣ Admit · Discharge · Refer
  • Admit — essentially all confirmed cases — for IV fluids, analgesia, and monitoring; ICU for organ dysfunction or predicted severe disease.
  • Discharge — mild disease once pain is controlled, feeding is re‑established, and the cause is being addressed.
  • Refer — 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.
  • Discharge — well child with stable or improving enzymes, normal INR, tolerating oral intake, with follow‑up.
  • Refer — urgent transplant‑center/hepatology referral if it evolves to acute liver failure (rising INR, encephalo­pathy).

Neonatal Cholestasis

ASSESSNASPGHAN/ESPGHAN 2025

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

▸
◣ The rule
  • Any infant still jaundiced at 2 weeks (3 weeks if breastfed and well) needs a fractionated (total and direct) bilirubin — 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 signClue 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
  • Kasai portoenterostomy works best within the first 60 days of life — outcomes fall sharply after.
  • 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.
  • Discharge — a stable infant with an expedited outpatient workup.
  • Refer — pediatric hepatology urgently (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 lateral CXR locates and characterises an esophageal object and shows the button‑battery double‑ring / halo sign (vs a coin); the abdominal film tracks an object that has passed into the stomach or bowel.
  • Radiolucent objects (most plastic, wood, glass, thin aluminium, 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 (any level); 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, or magnets, sitting in the stomach or duodenum. Object ≥ 2.5 cm (25 mm, ~1 inch) wide or ≥ 5–6 cm (~2 inches) long — too big to pass the pylorus or duodenum.
Observe
at home, elective
A single blunt object (e.g., a coin) already past the esophagus into the stomach, < 2.5 cm wide and < 5 cm long, with no battery or magnet. 80–90% pass within 1–2 weeks. Re‑image only if symptoms appear; remove if it is still in the stomach at ~ 2–4 weeks.
Water beads
admit & observe; surgery, not endoscopy
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. Endoscopy rarely retrieves them and is not the pathway. Involve pediatric surgery early for large ingestions or any sign of obstruction — most symptomatic children need an operation.
⚠ Red lines
  • Batteries and magnets are never simply observed — an esophageal battery or two or more magnets is an emergency at any level (see Button Battery Ingestion).
  • 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).
  • Discharge — asymptomatic gastric blunt object with return advice.
  • Refer — 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.
Battery in the esophagus?
YES — ESOPHAGEAL
Endoscopic removal within 2 hours. See mitigation doses below — do not let them delay removal.
PAST ESOPHAGUS, asymptomatic
Often expectant with follow‑up imaging; remove if symptomatic, co‑ingested magnet, or fails to progress.
MitigationDoseRoute & notes
Honey10 mL every 10 min, up to 6 dosesOral; within 12 h. 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
⚠ After removal
Injury continues — watch for delayed strictures and tracheo-/aorto‑esophageal fistula.
◣ Admit · Discharge · Refer
  • Admit — all esophageal batteries → emergency.
  • Discharge — after confirmed passage past the esophagus in an asymptomatic child, per protocol.
  • Refer — 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.
MaintenancePEG 0.4–1.5 g/kg once daily (start ~0.4 g/kg, titrate up to ~1.5 g/kg/day as needed)First‑line and superior to lactulose. Titrate to the goal above; reassess at 2 weeks if inadequate.
Add‑on / alternativeStimulant (senna or bisacodyl, age‑appropriate); lactulose if PEG unavailableSecond‑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 nappy‑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 or unlicensed.
  • General — titrate to one soft, painless stool daily; do not stop abruptly (relapse); recheck adherence and dose before escalating.
◈ Infants < 1 year
  • PEG is effective and first‑line; lactulose is the alternative where PEG is unavailable or unlicensed.
  • 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.
  • Prucalopride, lubiprostone and linaclotide are not established in children — specialist use only.
✦ Diet, behavior & counselling
  • Normal fiber and fluid; fiber supplements, extra fluid, and probiotics are not proven and do not replace 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.
  • Discharge — most, with disimpaction, maintenance laxatives, and education.
  • Refer — 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.
  • Discharge — uncomplicated reflux with reassurance and feeding advice.
  • Refer — 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. PUCAI in ulcerative colitis).
  • Toxic megacolon — colonic dilatation with systemic toxicity (fever, tachycardia, tenderness/distension); a surgical emergency.
⚠ What makes it worse
  • Avoid antimotility agents, opioids and anticholinergics — they can precipitate toxic megacolon.
  • 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 corticosteroids for severe colitisGastroenterology‑directed; escalate to infliximab or cyclosporine by day 5 if inadequate response; pharmacologic VTE prophylaxis for all hospitalized
Toxic megacolonBowel rest, decompression, urgent surgical reviewColectomy if deteriorating/perforation
◣ Admit · Refer
  • Admit all acute severe colitis.
  • Call/Refer — 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).
Empiric broad‑spectrum antibiotics within 1 hour — 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, perianal, line site)
  • 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; 2 g/dose if CNS/severe)IV; for penicillin / β-lactam allergy; 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.
◣ Admit · Discharge · Refer
  • Admit — high‑risk febrile neutropenia (oncology/chemotherapy) → immediate empiric antibiotics.
  • Discharge — selected low‑risk after risk assessment with close follow‑up (the well‑appearing non‑oncologic child).
  • Refer — 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 ethnicity (benign ethnic neutropenia).
  • Fever (neutropenic definition): single oral temp ≥ 38.3 °C, or ≥ 38 °C sustained > 1 h, or twice > 38 °C in 12 h. 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)
  • Well‑appearing, immunocompetent, clear viral context, no features of sepsis or primary immunodeficiency.
  • 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)Canadian guidance leans toward routine culture. Don’t rely on urinalysis — pyuria is often absent in neutropenia.
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.
  • Discharge — well child — expectant management with a scheduled recheck of counts.
  • Refer — hematology for persistent (> 6 weeks), profound (< 500 consistently), or recurrent neutropenia.

Tumor Lysis Syndrome

MINUTES

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
  • Vigorous IV fluids (up to ~3–4 L/m²/day per renal status; if body surface area unknown or unmeasurable, use weight‑based hydration — 4‑2‑1 rule at 1.5× maintenance). No potassium in fluids.
  • Routine urinary alkalinization not recommended.
Risk level?
INTERMEDIATE
Allopurinol + hydration.
HIGH / ESTABLISHED
Rasburicase + hydration. Do not give allopurinol on a rasburicase day. High risk includes (not limited to) white cell count > 50,000, elevated or rapidly rising uric acid, or suspected lymphoma with bulky disease (mediastinal mass, multiple significantly enlarged nodes).
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).
DrugDoseRoute & notes
Allopurinol10 mg/kg/day PO divided every 8 h (max 800 mg/day)PO; start before chemotherapy; prevents new urate
RasburicaseFixed by weight, 1 dose/24 h:
< 15 kg → 1.5 mg
15–25 kg → 3 mg
26–35 kg → 4.5 mg
> 35 kg → 6 mg (max)
IV over 30 min; breaks down existing urate. Reassess daily by uric acid — often 1 dose is adequate. Do NOT give in known G6PD deficiency.
⚠ Rasburicase + G6PD deficiency
  • Rasburicase is contraindicated in glucose‑6‑phosphate dehydrogenase deficiency (causes hemolysis and methemoglobinemia) — screen before giving — quantitative 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).
  • Discharge — after resolution of TLS and confirmed stability; not acutely; after resolution.
  • Refer — 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.
HydrationMaintenance fluids (0.75× maintenance if concern for acute chest syndrome)Avoid over‑hydration (acute chest risk)
Oxygen + warmthIf SpO₂ < 95% or below baselineKeep 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 (10 breaths every 2 h while awake).
  • Escalation: early hematology/PICU discussion for simple vs exchange transfusion if severe hypoxia or falling hemoglobin.
⚠ Splenic sequestration
  • Rapidly enlarging spleen + falling hemoglobin and/or platelet count → hypovolemic shock. Give fluids for shock and consult hematology immediately.
  • Transfuse cautiously (~5 mL/kg toward partial correction) — over‑transfusion causes rebound hyperviscosity as the spleen releases trapped cells.
⚠ Acute stroke
  • Sudden focal deficit, seizure, or new altered consciousness → urgent neuroimaging with immediate hematology and neurology involvement.
  • Ischemic stroke — transfuse urgently, do not delay. Exchange transfusion is the definitive treatment (goal HbS < 30%; keep total Hb ≤ 10 g/dL to avoid hyperviscosity), under hematology and neurology. If the child is significantly anemic (Hb < 9 g/dL) or exchange is not immediately available, give a simple (top‑up) transfusion as an immediate bridge — but do not raise Hb above ~10 g/dL. Aim to start exchange within 6 h.
  • 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 — give prompt empiric antibiotics — ceftriaxone is the agent of choice (once‑daily; enables outpatient management of low‑risk cases). 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.
  • Discharge — pain controlled on oral analgesia, well and hydrated, with follow‑up.
  • Refer — 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/kgIV; aim 80–100%
Mild hemophilia ADesmopressin (DDAVP)Only if a documented prior response; not for major bleeds
Known inhibitor — life/limb threatrFVIIa 90 mcg/kg, or FEIBA 75–100 units/kgIV; bypassing agents — call hematology urgently for use and guidance
Tranexamic acid (mucosal / oral bleeds)25 mg/kg/dose PO every 8 h, or 10 mg/kg/dose IV 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.
  • If weight unknown, give roughly three times the usual joint‑bleed dose.
  • Contact the on‑call hematologist.
  • Do not hesitate to give factor; use the Breslow tape to estimate weight if unknown.
◣ Admit · Discharge · Refer
  • Admit — major or life‑threatening bleeds (head, neck, gut, compartment).
  • Discharge — minor bleeds controlled after factor, with a home plan.
  • Refer — 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 — reserve for atypical features (other cytopenias, organomegaly, constitutional symptoms) or before splenectomy.
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 onceIV; only if Rh(D)-positive, non‑splenectomized, no autoimmune hemolysis — watch for hemolysis
Tranexamic acid10–15 mg/kg/dose (max 1000 mg) every 8 hPO/IV; adjunct for mucosal bleeding — avoid in hematuria
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 + tranexamic acid together, and call hematology/critical care.
  • Avoid IM injections, aspirin/NSAIDs and contact sport while counts are low.
◣ Admit · Refer
  • Admit — wet purpura, severe bleeding, or any diagnostic doubt.
  • Refer/Call — hematology for all new severe thrombocytopenia; urgently if red flags for malignancy — do not hesitate to reach out for guidance.

New‑Diagnosis Oncologic Emergencies

MINUTESCOG · AAP 2026

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 (2–3× maintenance), 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 identified, All‑Trans Retinoic Acid (ATRA) is life‑saving and given without delay — under hematology/oncology guidance after hematopathology confirmation.
◣ 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.
  • 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.
◣ 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 + supine chest X‑ray, CT chest and echocardiogram; 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.
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
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 hIV/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.
IV fluids (leukostasis / TLS)2–3× maintenance, 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
  • 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.
apnea / gasping / HR < 100
Golden minute Start PPV within 60 s. Term 21% oxygen; preterm 21–30%. 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.
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.
  • Discharge — a passed screen with a normal exam.
  • Refer — 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, noradrenaline, 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
Noradrenalinespecialist‑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.
  • Discharge — not acutely; after weaning support, with follow‑up.
  • Refer — 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 dextrosehold > 2.6 mmol/L (47 mg/dL)Suspect a disorder if glucose cannot be held > 2.6 mmol/L on GIR 5–8 mg/kg/min.
First 72 h — symptomatic (any level), or asymptomatic glucose < 2.6 mmol/L (47 mg/dL)?
SYMPTOMATIC, or < 1.8 mmol/L (32 mg/dL)
IV D10 mini‑bolus 2 mL/kg, then infusion at GIR 5–8 mg/kg/min. Recheck in 20–30 min; escalate GIR in 2 mg/kg/min steps. 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 mgIM/IV as a bridge when IV access is not yet available; less effective in hyperinsulinism; watch for hyponatremia.
Diazoxide1.7–5 mg/kg/dose PO q8hEndocrinology‑led, for confirmed hyperinsulinism; usually with chlorothiazide. Pre‑treatment echo (fluid retention, pulmonary hypertension risk).
⚠ 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 at glucose < 2.6–2.8 mmol/L (best < 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.
  • 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.
  • Discharge — transient, resolved, feeding well with stable pre‑feed glucose.
  • Refer — 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: gestation < 38 weeks, 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 — these lower the threshold.
  • 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 2 mg/dL (30 µmol/L) of the exchange line — 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 2–7, 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 the 35–37‑week lines rise by ≤ 20 µmol/L and the ≥ 38‑week lines 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.
  • Discharge — below threshold, feeding well, with a bilirubin‑recheck plan.
  • Refer — hematology for hemolysis; an exchange‑capable unit near exchange thresholds; 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 ± CSF/urine, blood count, CRP), check glucose. 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 usually nosocomial (coagulase‑negative staphylococci, S. aureus, Gram‑negatives) and needs different empiric cover per your unit protocol.
DrugDoseRoute & notes
Ampicillin50 mg/kg/dose (meningitis 100 mg/kg/dose)IV; interval by postnatal age. Use the meningitic dose if CSF not obtained or CNS involvement.
Gentamicin4–5 mg/kgIV (interval by gestation/age)
Cefotaxime50 mg/kgIV, add if meningitis suspected
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 — all with risk factors or clinical signs → empiric antibiotics after cultures.
  • Discharge — not until sepsis is excluded/treated; a reassuring 36–48 h course with negative cultures may stop antibiotics.
  • Refer — 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 (~1 in 1000) 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 — doses shown are general pediatric (per dose · interval); adjust for neonates by gestational/postnatal age and for hepatic/renal impairment; confirm against the local formulary and antibiogram
DrugDose (per dose · interval)Role
Cefotaxime50 mg/kg/dose q6hGram‑negative cover
+ Cefazolin33–50 mg/kg/dose q8hGram‑positive (MSSA) — use vancomycin where MRSA is prevalent
± Metronidazole7.5–10 mg/kg/dose q6–8hAdd for anaerobes — foul discharge or maternal chorioamnionitis
Meropenem40 mg/kg/dose q8hOR (severe cases) — alternative for necrotizing fasciitis (with vancomycin + clindamycin)
± Vancomycin15 mg/kg/dose q6h (max 1 g/dose)Where MRSA is prevalent; monitor levels
± Clindamycin5–10 mg/kg/dose q6–8hNecrotizing fasciitis (antitoxin effect)
◈ 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.
  • 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).
  • Discharge — not acutely; complete the IV course — older infants may step down to oral.
  • Refer — pediatric surgery for necrotizing fasciitis or 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 ileusNPO + 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)NPO + NG ~7–10 days; antibiotics 7–10 days
III — AdvancedCritically ill: shock, acidosis, DIC, peritonitis. IIIA bowel intact; IIIB perforated (pneumoperitoneum)NPO + NG ~14 days; antibiotics 14 days; surgery
Treat
  • Stop enteral feeds (NPO), nasogastric tube on free drainage, IV fluids and parenteral nutrition.
  • Broad‑spectrum 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.
  • 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.
✦ 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 anaerobe‑covering antibiotics (~7 days) plus drainage or laparotomy.
◣ Admit · Discharge · Refer
  • Admit — all → NICU, nil by mouth, gut decompression, antibiotics.
  • Discharge — not acutely; after recovery, with feeding advice.
  • Refer — 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.
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). Use the shortest course; discontinue early once acute provoked seizures are controlled.
Levetiracetam40–60 mg/kg (max 4.5 g)IV; second‑line — preferred when there is cardiac disease.
Phenytoin / fosphenytoin20 mg/kg (PE)IV; second‑line; favored for suspected sodium‑channelopathy (e.g. KCNQ2, SCN2A).
Midazolam infusion0.05–0.4 mg/kg/h (after 0.2 mg/kg load)IV; refractory seizures.
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 ÷ dosesIf 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 and stop early once acute provoked seizures are controlled — often before discharge.
  • 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.
  • Discharge — not acutely; under neurology with a plan.
  • Refer — 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 enzyme‑inducing drugs (anticonvulsants, rifampicin, warfarin).
  • Classic (day 2–7) — bruising, GI or umbilical bleeding in a baby who missed prophylaxis.
  • Late (2–12 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 (0.5 mg if < 1500 g)IM — single dose; the reliable route
Active bleedingVitamin K₁ 1–2 mg slow IVPlus FFP or prothrombin complex concentrate for serious/intracranial bleeding
◈ Counselling
  • 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 — 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.
✦ 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/observe for scoring; escalate if seizures or failure of supportive care.
  • Refer — neonatology, social work and safeguarding as indicated.

Neonatal Dosing by Corrected Age (PMA)

DOSINGNeoFax / Lexicomp / BNFc · confirm against unit formulary

The dose per kg barely changes — corrected age changes 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 — draw a trough just before the next dose and do not give it until the level is acceptable. 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). NeoFax · AAP Red Book
✦ 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 / FDA label
◈ Sources
  • NeoFax / Micromedex (gentamicin, amikacin, vancomycin, β-lactams); vancomycin AUC target — ASHP/IDSA/PIDS consensus 2020; ANMF Neonatal Medicines consensus 2024; AAP Red Book (empiric regimens); CAP trial (Schmidt, NEJM 2006) and FDA Cafcit label (caffeine).
  • Neonatal dosing varies by unit and drug‑monitoring protocol — this is a starting point, not a substitute for your local formulary.
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 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 (preferred — fewer side effects and easy administration), 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/buccal/intranasal (max 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 for safety
Valproate40 mg/kg (max 3 g)IV; avoid if metabolic/mitochondrial disease or liver failure suspected. Avoid in suspected mitochondrial/POLG disease, significant liver disease, or thrombocytopenia/coagulopathy
Fosphenytoin20 mg PE/kg (max 1.5 g)IV (PE = phenytoin equivalents)
Phenytoin20 mg/kg (max 1.5 g)IV slow, cardiac monitoring — 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/hIV; 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.
  • Discharge — not from the acute episode; a first seizure that stops may go home after workup, neurology follow‑up.
  • Refer — 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, then move to second‑line — don't keep repeating.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/buccal/intranasal midazolam 0.2 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 > 6 years, 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 labelling 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.
  • Discharge — simple febrile seizure, well child, normal exam, reliable carers with safety‑net advice.
  • Refer — 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.

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◣ 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).
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 (AUC/MIC‑guided) for CNS infection (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)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; within 4 h of the first antibiotic — see steroid note. Not in neonates.
Acyclovir≤ 4 mo: use neonatal HSV dosing (20 mg/kg/dose every 8 h). > 4 mo–< 12 y: 15–20 mg/kg/dose every 8 h (Red Book target 20; balance against nephrotoxicity). ≥ 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 and H. influenzae 7 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: S. pneumoniae 10–14 d
  • Hib 7–10 d
  • N. meningitidis 5–7 d
  • GBS 14–21 d (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 at the end of therapy for confirmed HSV encephalitis.
  • Arrange chemoprophylaxis for close contacts of meningococcal (and Hib per criteria) via public health.
⚠ Defer the LP (but never the antibiotics) if
  • reduced or fluctuating consciousness, focal signs, signs of raised ICP, coagulopathy, or skin infection over the site (stabilize a cardiorespiratorily unstable child before any imaging) — image (contrast CT and/or MRI) 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.
  • Discharge — not from the acute illness; complete the course with audiology and neurodevelopmental follow‑up.
  • Refer — 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.

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◣ 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 brain and whole spine with contrast is the test of choice (spine imaging stages leptomeningeal / “drop” metastases); contrast CT if MRI is not immediately available or to exclude acute hydrocephalus / hemorrhage.
  • 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/dose, and for severe edema or impending herniation a 1–2 mg/kg IV load then 1–1.5 mg/kg/day divided q6h (max 16 mg/day). Add a PPI (e.g., omeprazole) for gastric protection.
  • 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.
  • Discharge — not during the acute presentation; expedite imaging and specialist review.
  • Refer — 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 + vancomycin. Covers the Streptococcus anginosus (milleri) group and anaerobes.
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 ≈ 4–8 weeks, 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.
  • Discharge — after prolonged IV therapy and imaging response, with follow‑up.
  • Refer — 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.

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◣ 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.
DrugDoseRoute & notes
Hypertonic saline 3%3–5 mL/kg over 10–15 minIV; for raised ICP / herniation
Mannitol0.5–1 g/kg over 10–15 minIV; alternative (caution if hypovolemic/hypotensive)
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. 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.
  • Discharge — not from the acute episode.
  • Refer — 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. 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 (and NIF/MIP) every 4–6 h in the progressive phase, plus bulbar assessment; act on the “20/30/40” thresholds (FVC < 20 mL/kg, MIP < 30, MEP < 40 cmH₂O) or a > 30% fall from baseline — these predict the need for ventilation.
  • 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.
  • 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.
TreatmentDoseNotes
IV immunoglobulin2 g/kg total, over 2–5 daysFirst‑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.

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◣ 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.
  • Check ionized K⁺, ECG and CK after any procedure.
⚠ 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).
◣ 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 drives catabolism, hypoglycemia and rhabdomyolysis.
◣ 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≈ triple the maintenance steroid dose during the illnessPO; for the child on chronic steroids (Duchenne)
Stress steroids — unwell / vomiting / shockHydro­corti­sone ≈ 2 mg/kg (or 50 mg/m²) IV, then continuedIV/IM; treat as adrenal crisis — do not wait
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.
  • 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; 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. Delay antibiotics until a joint aspirate is obtained whenever clinically feasible.
  • Discharge — not acutely; step down to oral with monitoring and orthopedic follow‑up.
  • Refer — 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. Hip and shoulder are especially time‑critical (avascular‑necrosis risk). Send synovial fluid for cell count, Gram stain, culture (blood‑culture bottle) + PCR.
Empiric therapy after cultures: IV cefazolin — covers MSSA and K. kingae.
Antibiotic therapy
ScenarioDrug & doseNotes
Empiric — first‑line IVCefazolin 37.5–50 mg/kg/dose IV q6–8h (max 2 g/dose)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, clindamycin & cloxacillin.
Oral step‑down — MSSA / culture‑negCephalexin 40–50 mg/kg/dose PO TID (max 6 g/day)First‑line oral. Cloxacillin 25 mg/kg/dose QID is an alternative (poor taste).
Oral step‑down — MRSAClindamycin, TMP‑SMX, or linezolidPer susceptibilities, with infectious‑diseases input; MRSA usually needs longer before switching.
◈ IV → oral switch & duration
  • Switch to oral when clinically improved (afebrile, using the limb) and CRP falling (≈ 50% drop, often < 20–30 mg/L) with assured adherence — even after prior bacteremia. Duration (CRP‑guided): AHO 3–4 weeks
  • isolated SA 2–3 weeks
  • SA with adjacent osteomyelitis 4 weeks
  • hip/shoulder SA 4–6 weeks.
  • 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.
  • Discharge — transient synovitis in a well child with safety‑net advice and review.
  • Refer — orthopedics for red flags; 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 — self‑limiting, usually post‑viral hip inflammation and the commonest cause of an atraumatic limp (3–8 years); symptoms usually resolve within 7–10 days. 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; 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.
✦ 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.
  • Discharge — transient synovitis, afebrile, mobilizing, with review.
  • Refer — 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 meta‑analysis shows it is more effective and less painful than supination‑flexion — 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.
  • Discharge — after successful reduction and return of normal arm use.
  • Refer — 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 a stable slip; for an unstable slip avoid forced frog‑leg positioning and use AP + cross‑table lateral to prevent further displacement. Klein's line fails to intersect the epiphysis on the affected side. The frog‑leg view is most sensitive.
⚠ 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.
  • Consider prophylactic contralateral fixation in high‑risk patients (young age, obesity, endocrinopathy).
✦ 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.
  • Discharge — post‑operative.
  • Refer — orthopedics urgently (surgical fixation); 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), greenstick, and toddler's fracture (spiral distal tibia in an ambulant toddler).
  • Physeal (Salter‑Harris) fractures cross the growth plate (SH‑II commonest) and risk growth arrest — always classify and follow up.
  • Radiograph the joint above and below; obtain comparison views when needed.
  • 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 — appearing on average ~7 hours before any neurovascular change.
  • 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.
  • Discharge — post‑operative.
  • Refer — 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.
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.
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.
  • Discharge — not acutely; post‑operative/reduction.
  • Refer — 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 colour, 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
  • Splint in the position of deformity in the emergency 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.
  • Discharge — only after definitive management and consultant confirmation that perfusion is restored.
  • Refer — 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 theatre 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.
  • Discharge — selected uncomplicated injuries after stable reduction, satisfactory imaging, normal neurovascular findings, and arranged follow‑up; advise return for increasing pain, swelling, or numbness.
  • Refer — 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.
  • Discharge — only after definitive stabilization, mobility, and a follow‑up plan.
  • Refer — 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.
  • Do not give high‑dose methylprednisolone routinely for traumatic spinal cord injury.
◣ Admit · Discharge · Refer
  • Admit — all; PICU for cord injury, neurogenic shock, or respiratory compromise.
  • Discharge — not acutely.
  • Refer — 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. Hypoxia is the commonest cause of traumatic arrest.
<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 then finger thoracostomy). Both decompression sites are correct: 4th–5th intercostal space anterior to the mid‑axillary line (ATLS), or the 2nd intercostal space, mid‑clavicular line (PALS) — prefer the 2nd space, mid‑clavicular line in younger children and infants
  • 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; consider tranexamic acid within 3 h. 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 eachFirst‑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)
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; > 40 kg → 1 g then 1 g over 8 hWithin 3 h of injury
◈ Resuscitation reasoning
  • Estimated blood volume ~70 mL/kg in a child (80–90 in an infant), so small losses matter.
  • Move to blood early and limit crystalloid; transfuse to a hemoglobin goal of 7 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
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
Not low‑risk — image (CT if stable) and involve surgery. 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 repeatedly spring the pelvis. (The binder is applied in the primary survey.)
C‑spine
  • Clear with the PECARN 3‑tier rule (clinical clearance / radiograph / CT).
  • 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). 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 bolus (impending herniation)First‑line hyperosmolar bridge; infusion regimens are intensive‑care therapy
Mannitol0.5–1 g/kg over 15–20 minAlternative; caution if hypovolemic or hypotensive
Levetiracetam20–55 mg/kg IV (max 4.5 g), then 10 mg/kg BIDProphylaxis 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.
  • Discharge — minor head injury meeting a validated low‑risk rule, observed, with head‑injury advice.
  • Refer — neurosurgery for surgical lesions or deterioration; safeguarding if abuse is suspected.

Child Protection & Safeguarding

ASSESSAAP · NICE NG76

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: bruising of Torso, Ears, Neck in a child ≤ 4 years, any bruising < 4 months, or of the Frenulum, Angle of jaw, Cheek, Eyelid, Sclera, or patterned marks.
  • 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 — the triad of subdural hemorrhage, retinal hemorrhages and encephalo­pathy.
  • 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 intracranial injury is found in up to 37% of high‑risk infants (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: PT, aPTT, CBC with platelets, von Willebrand antigen and activity, factor VIII and IX activity. 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; 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.
  • Call/Refer — 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 — any of
  • > 40 mL/kg of blood products in 24 h · ~1 blood volume (≈ 70–80 mL/kg) in 24 h · or > 20 mL/kg red cells in 2 h with ongoing bleeding.
  • Uncontrolled hemorrhage with instability, a high pediatric age‑adjusted shock index (SIPA), or clinical judgment — activate the protocol early, not late.
Component (aim 1:1:1)DoseNotes
Packed red cells10–20 mL/kgEmergency: uncrossmatched O‑negative until type‑specific is ready
Fresh frozen plasma10–20 mL/kgGive in a 1:1:1 ratio with red cells & platelets
Platelets10–20 mL/kg (often 10)
Cryo­precipitate5–10 mL/kgFor fibrinogen < 1.5 g/L (or give fibrinogen concentrate)
Low‑titer O whole bloodPer protocolEmerging in pediatric trauma — observational evidence
⚠ 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 after every ~30–40 mL/kg. 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 IV (max 1 g) over 10 min, then 2 mg/kg/h for 8 h (max 1 g)Give within 3 h of injury; consider in TBI with GCS < 12 before intracranial bleed is excluded
Calcium gluconate50–100 mg/kg IV (max 2–3 g)Peripheral‑safe
Calcium chloride20 mg/kg IV (max 1 g)Central line preferred — 3× the elemental calcium of gluconate
◣ Targets
  • Fibrinogen ≥ 1.5–2.0 g/L · platelets > 50 ×10⁹/L (> 100 with TBI or ongoing bleeding) · INR < 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; 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.
  • Sources: European guideline on major bleeding & coagulopathy after trauma, 6th ed. (Rossaint 2023); ATOMAC pediatric MTP; PED‑TRAX; Transfusion Ontario pediatric appendix.
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, or a rise ≥ 26.5 µmol/L (≥ 0.3 mg/dL)< 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) — 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 plus measured output; do not apply routine 4‑2‑1 (Holliday–Segar) maintenance during established AKI.
  • 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.
  • Discharge — resolving pre‑renal AKI with normalizing function and follow‑up.
  • Refer — 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 (every 3 years if < 7 years at the last dose); 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.
  • Discharge — not acutely; after hematologic and renal recovery.
  • Refer — 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% in the first 8 hours, then normalize over 24–48 hours.
  • 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
Hydralazine0.1–0.5 mg/kg/dose (max 20 mg)IV/IM every 4 h; second‑line; may cause reflex tachycardia
Sodium nitroprusside0.3–8 mcg/kg/minIV; reserve — cyanide risk with prolonged use/renal impairment
Esmolol50–300 mcg/kg/min (after load)IV; short‑acting; may cause bradycardia/bronchospasm
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.
  • Discharge — not from the emergency; controlled blood pressure with a plan.
  • Refer — nephrology/cardiology for cause and 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, oliguria; needs urgent senior/nephrology input; treat with fluid resuscitation if needed and 20% albumin plus a diuretic (avoid diuretic monotherapy). 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.
  • Discharge — 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 — Nephrology for any atypical feature (age < 1 or > 12 years, persistent hypertension, gross hematuria, low complement (C3), renal impairment), 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, ≤1 mL, 3–4 mg/kg) — success ~90–100%, complications <0.1%.
  • 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 nappy change; avoid soap and wipes (they sting).
  • Gomco / Mogen: apply petroleum jelly (or antibiotic ointment) to the glans and on the nappy 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 judgement.
⚠ 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 if detorsion occurs within ~6 hours of onset, falling sharply thereafter.
  • 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, with antibiotics only if urinalysis or urine culture shows bacterial infection (send the culture before treating — prepubertal epididymitis is usually non‑bacterial).
✦ 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.
  • Discharge — 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; prepubertal epididymitis warrants outpatient renal‑tract ultrasound (underlying urogenital anomaly in ~25–30%).
  • Refer — surgery/urology IMMEDIATELY to confirm the diagnosis (torsion → exploration within 6 h).
◈ 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.
  • Discharge — post‑operative.
  • Refer — 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 or procedural analgesia.
  • Reduce edema — sustained manual compression of the glans (± a wrap such as saline‑soaked gauze, ice, or an osmotic agent such as granulated sugar) for several minutes.
  • 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.
  • Discharge — after successful reduction with follow‑up.
  • Refer — urology for failed reduction or 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 4–6 weeks≈ 80% success; 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.
  • Discharge — most, with hygiene and topical treatment.
  • Refer — 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; short self‑limiting 'stuttering' episodes often precede a major 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)100–200 mcg/dose every 3–5 min (dilute to 100–500 mcg/mL); max ~1 mgMonitor BP and HR; use with caution — reduced dose in children.
✦ 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.
  • Discharge — after detumescence with follow‑up.
  • Refer — 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.
  • Discharge — well child with a benign cause and outpatient workup.
  • Refer — 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.
  • Antibiotics only for a current infection (e.g., active pharyngitis or impetigo) — they do not alter the nephritis and are not given for the nephritis itself.
  • 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.
◣ Admit · Discharge · Refer
  • Admit — hypertension, oliguria, edema/overload, raised creatinine or hyperkalemia.
  • Discharge — normal blood pressure and urine output; check blood pressure and urinalysis at 1–2 weeks, C3 at 6–8 weeks.
  • Refer — nephrology if creatinine keeps rising, nephrotic‑range proteinuria, C3 still low at 12 weeks (consider C3 glomerulopathy), or hematuria/proteinuria beyond 1 year — these may need a biopsy.

Rhabdomyolysis

MINUTESKDIGO · 2025 review

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.
✦ 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).
  • 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 — 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 on either: (a) acute skin or mucosal signs plus respiratory or cardiovascular compromise; or (b) sudden hypotension, bronchospasm, or laryngeal symptoms after exposure to a known / likely allergen (skin signs may be absent). Two or more organ systems involved after a likely allergen also qualifies — you do not need every feature below.
  • Skin: urticaria, flushing, angiedema, 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.
1ST LINE Intramuscular epinephrine NOW — there is no contraindication
Then
  • 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/lip 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 0.5 mg)IM, 1 mg/mL (1:1000), anterolateral thigh; repeat every 5–15 min
Epinephrine autoinjector (not stocked in Kuwait)0.1 / 0.15 / 0.3 mg0.1 (7.5–14 kg) · 0.15 (15–25 kg) · 0.3 (>25 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/minIV infusion; titrate to effect under PICU supervision with continuous cardiac monitoring
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. May use cetirizine (age‑appropriate dose) as a non‑sedating alternative
Glucagon20–30 mcg/kg (max 1 mg)IV over 5 min, only if on a beta‑blocker and refractory
⚠ Before discharge
  • Observe 4–6 hours (longer if severe, asthmatic, or biphasic risk).
  • Epinephrine for home: autoinjectors are not stocked in Kuwait — arrange supply through the allergy clinic (imported device) and document the pathway; until the child has one, teach the family recognition and to call emergency services at the first sign. Give a written action plan and refer to allergy.
  • Routine corticosteroids are no longer recommended (consider glucocorticoids for persistent bronchospasm, or severe symptoms requiring more than 2 doses of IM epinephrine or IV epinephrine).
◣ Admit · Discharge · Refer
  • Admit — more than one epinephrine dose needed, ongoing or biphasic symptoms, a severe reaction, or reactive airways — observe (typically 4–6 h, longer if severe or asthmatic).
  • Discharge — full resolution after a single epinephrine dose and an adequate observation period, sent home with a documented epinephrine plan (two autoinjectors where obtainable through the allergy clinic), a written action plan, and allergy follow‑up.
  • Refer — Allergy/Immunology for every case; PICU for refractory anaphylactic shock (cardiovascular compromise) despite repeated IM epinephrine requiring an epinephrine infusion, or airway compromise requiring definitive airway management.
Anaphylaxis — epinephrine firstRecognize (2‑system rule) → IM epinephrine now → fluids & repeat → refractory (PICU).
!IM EPINEPHRINE FIRST, ALWAYSThere is no contraindication — give it before antihistamine or steroid.TWO‑SYSTEM RULESkin/mucosa + respiratory or cardiovascular — orhypotension/bronchospasm/laryngeal signs after a likelyallergen.1recognizeIM EPINEPHRINE0.01 mg/kg (max 0.5 mg) of 1:1000 in the anterolateralthigh. Lay 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

Acute Asthma

MINUTESGINA 2026

Grade severity continuously: speech, work of breathing, SpO₂, silent chest. Doses and steps follow the Global Initiative for Asthma (GINA) 2026 strategy.

▸
◣ 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.
✦ 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 only if SpO₂ < 92%, then target 94–98% (93–95% in adolescents) — avoid routine over‑oxygenation.
  • Inhaled salbutamol every 20 min × 3 in the first hour, reassessing before each repeat.
  • Systemic corticosteroid for a moderate–severe exacerbation or inadequate response to salbutamol (oral preferred, 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. IV salbutamol or aminophylline infusion, heliox‑driven or high‑output continuous nebulization, non‑invasive ventilation, and intubation are PICU‑directed.
Bronchodilators
DrugDoseRoute & notes
Salbutamol (inhaler + spacer)≤5 yr: up to 6 puffs
>5 yr: up to 12 puffs
100 mcg/puff; every 20 min × 3 in the first hour (one puff at a time, 4–5 breaths each)
Salbutamol (nebulized)2.5–5 mgEvery 20 min × 3
Ipratropium bromide (nebulized)250 mcgEvery 20 min × 3, moderate–severe
Magnesium sulfate40–50 mg/kg (max 2 g)IV over 20 min, age ≥ 2 yr
Aminophylline5 mg/kg load, then infusionIV infusion — PICU‑directed; 3rd line, monitor levels
Salbutamol IVbolus then infusionIV — PICU‑directed; 3rd line, cardiac monitoring; watch for hypokalemia and lactic acidosis
Salbutamol — continuous (high‑output nebulizer)≈ 0.5 mg/kg/hr (commonly 10–20 mg/hr)Continuous nebulization for severe/life‑threatening; large‑volume high‑output nebulizer, O₂- or heliox‑driven; PICU‑directed, cardiac + K⁺ monitoring
Heliox (helium–oxygen ≥ 70:30)as driving / breathing gasSevere/refractory or impending respiratory failure — lowers airway resistance and improves distal aerosol delivery; a temporizing bridge. Needs low fraction of inspired oxygen (FiO₂ tolerance (effect requires ≥ 70% helium). PICU‑directed
◈ Heliox & high‑output nebulization — where they fit
  • In severe or refractory asthma (or impending respiratory failure), a heliox (helium–oxygen ≥ 70:30) driving or breathing gas reduces turbulent airway resistance and improves distal drug delivery, and a high‑output / large‑volume continuous nebulizer sustains bronchodilator delivery over hours — both are temporizing bridges and a critical‑care decision, not first‑line.
  • Benefit is seen mainly in the most severe subgroup, not routine exacerbations; heliox needs ≥ 70% helium, so it is unsuitable when a high FiO₂ is required.
Corticosteroids — choose one; oral first‑line
DrugDoseRoute & notes
Prednisolone1–2 mg/kg once daily (max 40 mg)PO, first‑line, 3–5 days
Dexa­methasone0.3–0.6 mg/kg (max 12–16 mg)PO/IV, 1–2 doses; oral alternative
Methyl­predniso­lone1–2 mg/kg load, then 0.5–1 mg/kg every 6 hIV agent when oral is not tolerated
Hydro­corti­sone4 mg/kg every 6 h (max 100 mg/dose)IV alternative when oral is not tolerated (equivalent to methylprednisolone)
◈ Steroid choice & availability
  • Oral prednisolone (or dexamethasone) is first‑line and as effective as IV; reserve IV steroid for the child who cannot take oral.
  • When IV is needed, methylprednisolone and hydrocortisone are both acceptable — evidence does not clearly favour one.
  • 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.
  • Discharge — SpO₂ ≥ 92% on room air, salbutamol stretched to ≥ every 4 h, feeding and talking, inhaler and spacer technique confirmed; discharge prescription = salbutamol via spacer (2–6 puffs every 4 h, weaning over days), the oral steroid course, and an inhaled corticosteroid controller started or stepped up (GINA: an exacerbation is a failure of controller treatment — no child ≥ 6 years leaves on salbutamol alone; preschool wheeze by phenotype); written action plan; review within 1–2 weeks.
  • Refer — Pulmonology for any PICU‑level escalation, ≥ 2 admissions per year, or diagnostic doubt; PICU for impending respiratory failure; Allergy/Immunology for difficult‑to‑control atopic disease.

Croup

HOURS6 MO–6 YR

Barking cough, hoarse voice, inspiratory stridor; worse at night. Grade severity 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 epinephrine; observe ≥ 2–4 hours for rebound; oxygen if hypoxic.
DrugDoseRoute & notes
Dexa­methasone0.6 mg/kg (max 16 mg)PO/IM/IV, single dose, all severities
Budesonide (nebulized)2 mgIf oral steroid not tolerated
Epinephrine (nebulized)L‑epinephrine (adrenaline) 1:1000 (1 mg/mL) 0.5 mL/kg (max 5 mL) [racemic 2.25% 0.05 mL/kg, max 0.5 mL]Moderate–severe; observe for rebound
◈ L‑epinephrine vs racemic
  • Both are equally effective.
  • Racemic epinephrine 2.25% is a 50:50 mix of D- and L‑isomers and only the L‑isomer is active, so 0.5 mL of 2.25% racemic ≈ 5 mL of 1:1000 L‑epinephrine (adrenaline).
  • L‑epinephrine (the single active isomer) is cheaper and more widely available — racemic is often unavailable outside the USA.
  • Do not confuse racemic 2.25% with 1:1000 or 1:10 000 epinephrine — different formulations.
◈ Heliox in severe croup
  • In severe croup with significant distress not settling after dexamethasone and nebulized 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 epinephrine, any oxygen requirement, or a repeat epinephrine dose needed — observe ≥ 2–4 h after epinephrine for rebound before any discharge.
  • Discharge — mild croup (no stridor at rest, no distress) after a single steroid dose, feeding well, with reliable carers and safety‑netting.
  • Refer — 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?
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 (amoxicillin component) every 8 h IV (max 1.2 g/dose)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.
  • Discharge — 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 — 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, angiedema, 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.
  • Prepare: assign the team (1st + 2nd airway managers, assistant, respiratory therapist, drug nurse, circulating nurse); a time‑out to agree Plan A + B (1st / 2nd intubator and technique); 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 — only when saturation is at its best and the patient is stable. Videolaryngoscopy (first choice in an anticipated difficult airway); max 4 attempts total (DL + VL). Between attempts change operator or blade (straight / curved / hyperangulated), add a bougie or a flexible intubation scope (FIS) — via the nose, an oral bite‑block, or through a supraglottic airway — or try a smaller endotracheal tube (ETT). In infants < 5 kg a standard‑geometry (Macintosh‑style) blade often beats a hyperangulated one. 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; reverse the muscle relaxant (sugammadex if rocuronium was used) and reassess; keep apneic O2 (NC / HFNC) and treat laryngospasm. ENT available: rigid bronchoscopy ventilation or tracheostomy. ENT not available: needle cricothyrotomy (younger child), or percutaneous / “slash” surgical cricothyrotomy (older child). Call for help if it has not arrived.
✦ Confirm placement
On successful intubation, confirm the tube primarily with continuous waveform capnography (EtCO2); support with auscultation, chest rise, and a chest X‑ray.
◣ Have ready (difficult‑airway trolley)
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 (RSV): coryza → cough, fast breathing, wheeze/crackles, feeding difficulty.

▸
◣ Supportive care is the treatment
  • Nasal 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). Escalate early to a local HFNC/CPAP‑capable team or PICU if work of breathing rises, apnea recurs, or hypoxemia persists.
✦ 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, corticosteroids, antibiotics, chest physiotherapy, routine chest X‑ray or viral testing. Red flags: apnea, grunting, severe recession, SpO₂ < 90%, dehydration, age < 6–12 weeks, comorbidity.
◣ 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 < 8–12 wk, prematurity, or cardiopulmonary disease).
  • Discharge — maintaining saturations in air, feeding adequately, work of breathing settling, carers able to cope with clear safety‑netting.
  • Refer — 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.

Choking (Foreign‑Body Obstruction)

MINUTES

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

▸
Effective cough?
EFFECTIVE
Encourage coughing, stay, monitor closely.
INEFFECTIVE + CONSCIOUS
Infant: 5 back blows + 5 chest thrusts (no abdominal thrusts). Child: 5 back blows + 5 abdominal thrusts. Repeat.
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.
  • If complete obstruction persists after basic life support → call anesthesia/ENT/PICU immediately; advanced airway maneuvers (direct laryngoscopy with Magill forceps, pushing the object distally to intubate, needle cricothyroidotomy as a last resort) should be attempted only by experienced clinicians.
◣ Stable child — route by site
  • No respiratory distress and normal oxygen saturation: refer by location — above the clavicle to ENT, below the clavicle to chest surgery or pulmonology for bronchoscopy.
  • A likely bronchial foreign body (one‑sided wheeze or reduced air entry) needs rigid bronchoscopy by an experienced anesthesia and surgical team under optimal conditions, ideally within 24 hours; delay beyond 24 h increases complications.
◣ Admit · Discharge · Refer
  • Admit — after removal, observe for airway injury/aspiration; any hypoxia, stridor, or incomplete relief → ED/PICU.
  • Discharge — fully recovered, effective cough and normal exam/SpO₂.
  • Refer — 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; in children it looks like hyperactivity, not sleepiness.

▸
◣ Recognize
  • Obstructive sleep apnea (OSA) — habitual snoring (> 3 nights/week), witnessed apnea or gasping, restless sleep, mouth breathing, enuresis; by day hyperactivity, inattention and poor concentration rather than sleepiness. 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: polysomnography (PSG; the apnea‑hypopnea index, AHI, grades severity) or sleep‑clinic referral; ECG/echocardiography if cor pulmonale or pulmonary hypertension is suspected. Chronic treatment (adenotonsillectomy, CPAP, intranasal steroid, weight management) is decided in clinic, not in the emergency setting.
◣ Red flags
  • Severe OSA (AHI ≥ 10 or nadir SpO₂ < 80%), 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 — transient compromise does not necessarily require admission or overnight monitoring.
  • Higher‑risk features (age < 3 y, severe OSA on PSG, obesity, craniofacial/neuromuscular disease or Down syndrome, cor pulmonale, recent upper‑respiratory infection, or failure to thrive) lower the threshold for a monitored bed. Opioids: avoid codeine and tramadol after tonsillectomy/adenoidectomy (FDA — CYP2D6 ultra‑rapid metabolizer deaths).
  • In children with moderate‑to‑severe OSA, minimize opioids, use opioid‑sparing analgesia where possible, and monitor closely — they are at higher risk of opioid‑induced respiratory depression; reduce other opioid doses by ~50% in severe OSA (opioid hypersensitivity from chronic intermittent hypoxia) and titrate with monitoring.
  • Position ramped, keep airway adjuncts and CPAP ready.
✦ Pearl — it looks like ADHD
A snoring child who is hyperactive and inattentive may have OSA, not just a behavior problem — ask about snoring and witnessed apnea at every visit.
◣ Admit · Discharge · Refer
  • Admit — severe OSA with desaturation or cor pulmonale, and high‑risk post‑adenotonsillectomy (age < 3, severe OSA, comorbidity).
  • Discharge — mild/uncomplicated for outpatient sleep study and ENT follow‑up.
  • Refer — ENT (adenotonsillectomy) and sleep medicine; cardiology if pulmonary hypertension.

Cow's Milk Protein Allergy

ASSESSINFANT · WAO / CPS 2024

The commonest infant food allergy — IgE‑mediated (fast) or non‑IgE (delayed, cell‑mediated).

▸
◣ Recognize the two patterns
  • IgE‑mediated (minutes–2 h): urticaria, angiedema, vomiting, wheeze, anaphylaxis.
  • Non‑IgE (hours–days): eczema flare, reflux/regurgitation, colic, blood or mucus in stool, loose stools or constipation, faltering growth. Distinct from lactose intolerance (an enzymatic, non‑immune condition).
  • Diagnosis is clinical: exclude cow's milk protein from the diet; a planned reintroduction confirms non‑IgE-mediated disease. For IgE‑mediated reactions, strictly avoid cow's milk protein and use an extensively hydrolyzed (EHF) or amino acid formula (AAF).
◣ Non‑IgE subtypes — recognize the pattern
  • FPIAP (proctocolitis) — a well‑appearing infant with blood/mucus streaks in the stool, onset 2–8 wks. Most common subtype; up to 50% occur in exclusively breastfed infants.
  • FPE (enteropathy) — diarrhea, emesis, abdominal distension, failure to thrive; steatorrhea in up to 80%. Uncommon — the only subtype needing gastroscopy + biopsy (villous atrophy, crypt hyperplasia) to exclude celiac disease, infection, or cystic fibrosis.
  • FPIES (enterocolitis) — profuse repetitive vomiting ± bloody diarrhea, pallor, lethargy; ~15% develop hypovolemic shock. Rare (0.015–0.7%); the severe end of the spectrum.
  • Diagnosis is clinical in FPIAP and FPIES — symptom resolution on elimination confirms it.
Management — by feeding & subtype
SituationFirst choiceNotes
IgE‑mediated — anaphylaxisAmino acid formula (AAF)Use AAF for anaphylactic reactions to cow's milk protein.
IgE‑mediated — milder immediate reactionExtensively hydrolyzed formula (EHF)Step up to AAF if EHF fails (not tolerated or symptoms persist).
FPIAP, breastfedMaternal dairy + soy elimination, 2 wksContinue breastfeeding; dietitian; maternal calcium 500 mg BID + vitamin D. Symptoms improve within 72 h; stools normalize by 2 wks.
FPIAP, formula‑fedExtensively hydrolyzed formula (EHF)Switch to AAF only if symptoms persist 2–4 wks. Soy formula an option > 6 mo if soy is tolerated.
FPE, breastfedMaternal dairy + soy elimination, 2–4 wksIf no improvement (or formula‑fed) → AAF directly. Monitor growth and nutrition; resolution takes weeks.
FPE, formula‑fedAmino acid formula (AAF)First‑line (not EHF), given malabsorption severity.
FPIES, breastfedContinue breastfeeding / oral rehydrationRare in this group. If reacting: maternal dairy + soy elimination; if unresolved, discontinue breastfeeding → EHF.
FPIES, formula‑fedEHF first; AAF if no improvement in 2 wks10–20% need AAF from the start; AAF preferred if failing to thrive. Strictly avoid all forms (incl. heated/baked) of the trigger.
Acute FPIES with shockMedical emergencyAggressive IV fluids, steroids, ondansetron (monitor QT). Mimics sepsis — CBC, blood gas, chemistry to gauge severity.
⚠ Avoid
  • Food‑specific IgG panel testing (not evidence‑based — drives overdiagnosis). Prolonged dietary elimination beyond the resolution windows (growth impairment, cost). Goat's / sheep's milk (high cross‑reactivity) and partially hydrolyzed / “comfort” or “HA” formulas; soy formula before 6 months.
  • Overusing EHF/AAF beyond what is clinically indicated — refer to pediatric GI when the diagnosis is unclear rather than escalating formula empirically.
  • Involve a dietitian to protect calcium and growth.
✦ Natural history & re‑challenge
Most non‑IgE CMPA resolves: tolerance ~50% by age 1, > 75% by 3, > 90% by 6. FPIAP / FPE — home re‑challenge with fresh pasteurized cow's milk after age 1 (most tolerant by 1–2 yr; if not tolerant at 1 yr, defer FPE re‑challenge to ~18 mo). FPIES — physician‑supervised oral food challenge 12–18 mo after the last reaction (not a home re‑challenge); resolution 35% by 2, 70% by 3, 85% by 5.
◣ Admit · Discharge · Refer
  • Admit — acute FPIES with shock/dehydration.
  • Discharge — most, with dietary elimination and advice.
  • Refer — allergy/gastroenterology and a dietitian; anaphylaxis → allergy urgently; unclear diagnosis or FPE → pediatric GI.
Source
Canadian Pediatric Society position statement — Sathya & Fenton, Nutrition & Gastroenterology Committee (non‑IgE‑mediated CMPA), Pediatr Child Health 2024;29(6):382; WAO DRACMA 2024 (IgE‑mediated); ESPGHAN 2024.

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 (positive predictive value of skin testing only ~50%; 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 (~+13%), vancomycin‑resistant enterococci (VRE) (~+30%), longer stays, more surgical‑site infections, ICU admission, aminoglycoside‑related acute kidney injury, and a ~50‑min delay to the first ED antibiotic dose. 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 a direct oral challenge; Medium → skin test ± challenge, pick a non‑cross‑reacting 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, or a reaction history but tolerated the antibiotic since the index event; family history only.De‑label the record. Give penicillin if indicated.
LowIntolerance (GI upset, headache); non‑IgE‑mediated reaction; delayed maculopapular rash starting (≥ 3 days) into the course.De‑label the record. Give penicillin if 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 cephalosporins.
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. Avoid penicillins and cephalosporins.
⚠ When to involve an allergist
Any type‑1 (immediate / IgE‑mediated) reaction — urticaria, angiedema, 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
  • Prescribing a 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. Cefazolin has a unique side chain and is safe even after penicillin anaphylaxis. Use only for immediate / IgE histories — 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 (urticaria, angiedema, anaphylaxis) — avoid all cephalosporins and penicillins; use an alternative and refer to allergy.
  • 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.
Source
  • Kuwait Pediatric Council practice point on skin testing before antibiotic administration (Table 1 modified from Wong et al., Pediatr Child Health 2020, and Devchand & Trubiano, Aust Prescr 2019); CHOP Penicillin Drug Allergy Clinical Pathway (rev.
  • Nov 2025); BC PACE Beta‑lactam Allergy Delabeling Guideline & Toolkit (2021); De‑Labeling Penicillin Allergies in the Pediatric ED, Children 2025 (PMC12730042QR); Khan et al., Drug Allergy: 2022 Practice Parameter Update, JACI.
  • Apply to 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 Angiedema — Acute Attack

MINUTES

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

▸
◣ Recognize
  • Recurrent angiedema 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 an hereditary angioedema (HAE)‑specific agent early; earlier treatment means a milder, shorter attack.
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, age ≥ 2 yr; ready‑to‑use prefilled syringe. Not recommended < 12 kg (EMA/FDA label)
Fresh frozen plasma10 mL/kgIV; only if specific agents unavailable
◣ Admit · Discharge · Refer
  • Admit — laryngeal or severe attacks → a monitored bed.
  • Discharge — after resolution with on‑demand therapy and a written plan.
  • Refer — 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 ≥ 8 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.
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, FTTCombined / T‑cell (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) infection, or lupus‑like diseaseComplement deficiencyLow or absent CH50 / AH50 (total classical / alternative‑pathway complement activity)
⚠ 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), and specific antibody responses (vaccine titres, isohemagglutinins).
  • Add a neutrophil oxidative‑burst test (dihydrorhodamine) if a phagocyte defect is suspected. Save a pre‑treatment serum sample before giving intravenous immunoglobulin (IVIG).
⚠ 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.
  • Transfuse only irradiated, CMV‑negative, leukoreduced blood products (prevents transfusion‑associated graft‑versus‑host disease). For highly suspected SCID: isolate the infant and start Pneumocystis prophylaxis — co‑trimoxazole 5 mg/kg/dose (trimethoprim) once daily — plus antifungal prophylaxis (fluconazole 5 mg/kg/dose once daily).
  • Do not delay empiric antibiotics for fever — treat any infection promptly and aggressively; avoid non‑essential steroids/immunosuppression before a diagnosis.
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.
  • Discharge — per the acute problem, with the workup arranged.
  • Refer — immunology; avoid live vaccines and use irradiated blood products until cleared.

Tension Pneumothorax & Needle Decompression

MINUTESAPLS/ATLS · NAEMSP 2024

Sudden distress, absent breath sounds and shock — treat before the chest X‑ray.

▸
◣ Recognize (clinical)
  • Rapidly worsening respiratory distress and hypoxia with hypotension, unilateral absent/reduced breath sounds, hyper‑resonance, distended neck veins, and (late) tracheal deviation — often after trauma, asthma, positive‑pressure ventilation, or in a ventilated neonate.
⚠ Decompress now
  • Tension pneumothorax is a clinical diagnosis — if the child is peri‑arrest, do not wait for a chest X‑ray.
  • Perform immediate needle (or finger) decompression, then place a chest drain.
  • In a ventilated patient who suddenly desaturates and drops their pressure, think of it first.
◣ Workup
  • Clinical diagnosis — do not wait for imaging. Decompress first.
  • Confirm after decompression with chest X‑ray or bedside lung ultrasound (eFAST — extended Focused Assessment with Sonography for Trauma, adding lung views); definitive chest drain follows.
StepLandmarkNotes
Needle decompression2nd intercostal space, mid‑clavicular line — or 4th/5th intercostal space anterior axillary lineOver the top of the rib; use a cannula long enough for chest‑wall thickness
DefinitiveChest tube (tube thoracostomy)Follows decompression; size for age
✦ Neonatal clue
In a ventilated or term neonate, sudden deterioration with a shift of the apex and unilateral hyper‑resonance suggests tension pneumothorax; transillumination can help at the cot‑side while you prepare to decompress.
◣ Admit · Refer
  • Admit — all pneumothoraces needing drainage; PICU/NICU.
  • Call critical care ± surgery.
16

Rheumatologic

Cytokine storm (HLH/MAS) & Kawasaki vasculitis

Cytokine Storm — HLH / MAS

HOURS

Hyperinflammation: unrelenting fever that looks like sepsis but does not respond.

▸
◣ Recognize (treat on suspicion — don't wait for all criteria; immunosuppressive dosing is hematology/rheumatology/PICU‑directed)
  • Persistent high fever, cytopenias (≥2 lines), hepatosplenomegaly, very high ferritin, high triglycerides, low fibrinogen, high lactate dehydrogenase. In MAS complicating sJIA, a falling or normal ESR alongside a rising CRP/ferritin (consumptive hypofibrinogenemia) is an early clue,.
  • Macrophage activation syndrome is the same process complicating systemic juvenile idiopathic arthritis, lupus, or infection. Overlaps with multisystem inflammatory syndrome (post‑viral hyperinflammation,).
Act Send ferritin (the key clue) + CBC, ESR, CRP, fibrinogen, triglycerides, renal & liver function (full panel). Phone hematology/rheumatology urgently. Supportive care for organ failure; PICU.
Immunosuppression — specialist‑directed
  • Corticosteroid (pulse methylprednisolone) is the accessible first step.
  • Anakinra (interleukin‑1 antagonist) is increasingly used early, especially in MAS.
  • Etoposide + dexamethasone (HLH protocol) for primary or severe HLH.
  • Emapalumab (anti‑interferon-γ) — FDA‑approved for MAS in Still's disease refractory to glucocorticoids, and for primary HLH.
DrugDoseRoute & notes
Methyl­predniso­lonePulse 30 mg/kg/dose IV once daily (max 1 g) × 3–5 days, then 2 mg/kg/day ÷ q6h–BID if neededIV; accessible first‑line
Anakinra2–10 mg/kg/day (higher in refractory)IV/subcut; interleukin‑1 receptor antagonist
Etoposide + dexamethasoneHLH‑2004 protocolSpecialist (hematology)-directed for primary/severe HLH
Second‑line (MAS)Tocilizumab, cyclosporine, or PLEX (plasma exchange)Specialist (rheumatology)-directed for MAS or HLH secondary to a rheumatic cause.
EmapalumabPrimary HLH: 1 mg/kg/dose IV twice weekly (with dexamethasone). HLH/MAS in Still’s / sJIA: 6 mg/kg once, then 3 mg/kg/dose IV every 3 days through day 16, then 3 mg/kg/dose IV twice weekly. Titrate to max 10 mg/kg/dose.Anti–interferon-γ antibody; specialist‑directed. FDA‑approved for primary HLH and for HLH/MAS in Still’s disease (inadequate glucocorticoid response or recurrent MAS). Screen and monitor for infection (TB, CMV, other).
◣ Admit · Discharge · Refer
  • Admit — all → high‑dependency/PICU.
  • Discharge — not acutely; under hematology/rheumatology.
  • Refer — hematology/rheumatology urgently (immunosuppression) and PICU.

Kawasaki Disease

HOURS

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

▸
◣ Recognize
  • Fever ≥ 5 days + ≥ 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.
  • 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 < 6 months with ≥ 5 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 2017 pathway: fever ≥ 5 days + 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 after day 7, albumin ≤ 3 g/dL, raised ALT, WBC ≥ 15 ×10⁹/L, sterile pyuria) or a positive echocardiogram → treat.
Treat within 10 days of fever onset to protect the coronaries
First‑line
  • Single high‑dose IVIG + aspirin; 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 → second IVIG 2 g/kg, or corticosteroids, or a biologic (infliximab, now dosed 10 mg/kg IV over 2 h)
AspirinLow‑dose 3–5 mg/kg/day once daily; or moderate‑to‑high dose 30–50 up to 80–100 mg/kg/day until afebrile, then low‑dosePO. AHA guidance continues to recommend moderate‑to‑high‑dose aspirin in the acute phase (until afebrile), then low‑dose antiplatelet dosing. RCTs and meta‑analyses show low‑dose 3–5 mg/kg/day from diagnosis gives equivalent coronary outcomes and IVIG resistance with fewer adverse effects, and many centers use it from the outset — either regimen is acceptable,. Continue low‑dose to 6–8 weeks / until echo normal
Methyl­predniso­lone → prednisolone (high‑risk)2 mg/kg/day, IV then oral, tapered over 2–3 weeksAdjunct 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).
⚠ 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.
  • Discharge — after defervescence and echo, with a plan for repeat echo (at ~1 week and 4–6 weeks) and aspirin.
  • Refer — cardiology (echo) and rheumatology; IVIG‑resistant cases urgently.

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 (weekly early, then spacing out to ~6–12 months) 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
◣ Admit · Refer
  • Admit — severe abdominal pain, GI bleeding, suspected intussusception, scrotal involvement, hypertension or acute kidney injury.
  • Refer — nephrology for persistent proteinuria/hypertension; surgery if intussusception.

MIS‑C (Multisystem Inflammatory Syndrome)

MINUTESACR 2022 · CDC

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

▸
◣ Recognize (criteria)
  • Fever ≥ 3 days in a child/adolescent, plus ≥ 2 systems involved (rash/conjunctivitis, hypotension/shock, cardiac dysfunction, coagulopathy, prominent GI symptoms), raised inflammatory markers (CRP, ferritin, D‑dimer), evidence of SARS‑CoV‑2 or recent exposure, and no alternative diagnosis,.
⚠ 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.
◣ 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.
TreatmentDoseNotes
IV immunoglobulin2 g/kgCornerstone; assess cardiac function before large‑volume infusion
Cortico­steroidsMethylprednisolone per protocol (moderate–high dose for severe)With IVIG in moderate/severe disease
Aspirin / thrombo­prophylaxisPer Kawasaki/coronary protocolCardiology‑guided
◣ Admit · Refer
  • Admit all; PICU for shock or cardiac involvement.
  • Call pediatric rheumatology/infectious diseases and cardiology; 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.
  • Discharge — not acutely; post‑operative.
  • Refer — 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.
  • Discharge — after successful reduction and an observation period without recurrence.
  • Refer — 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.
  • Discharge — post‑operative, feeding established.
  • Refer — 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 Score) + ultrasound first‑line; CT or MRI selectively.
Manage Nil by mouth · IV fluids · analgesia for pain · urgent surgical evaluation → appendectomy.
⚠ Mimics
Examine the testes (torsion), consider DKA (see Diabetic Ketoacidosis), lower‑lobe pneumonia, UTI, ovarian torsion.
⚠ Do not bypass surgical evaluation
  • Antibiotics — not for suspected appendicitis before surgical assessment; started before diagnosis is confirmed, they partially treat and mask it (blunted WBC/neutrophils, softer signs, more perforation).
  • 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); reserve opioids for severe pain as a single titrated dose, with no repeat opioid until the surgeon has assessed.
  • 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 6–8 h (max 4 g/dose)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, up to 24 h.
  • 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 trial).
◣ Admit · Discharge · Refer
  • Admit — all → for surgery and IV antibiotics.
  • Discharge — post‑operative per pathway.
  • Refer — 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.
  • Discharge — after successful reduction, for early elective repair.
  • Refer — 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: activated charcoal 1 g/kg (max 50 g) only if airway protected and within ~1 h — not for hydrocarbons, caustics, alcohols, iron, or lithium.
  • Call KPCC 1804774; give the specific antidote below; observe for delayed toxicity.
PoisonAntidote / treatmentNotes
Acetaminophen (acetaminophen)N‑acetylcysteine — per Rumack‑Matthew nomogramIV: 150 mg/kg over 1 h → 50 mg/kg over 4 h → 100 mg/kg over 16 h
OpioidsNaloxone 0.1 mg/kg (max 2 mg)IV/IM/IN, repeat; infusion if needed
Tricyclic antidepressantSodium bicarbonate 1–2 mEq/kgIV for QRS > 100 ms or arrhythmia
Beta‑blockerGlucagon + high‑dose insulin/euglycemia+ vasopressors
Calcium‑channel blockerCalcium + high‑dose insulin/euglycemia+ vasopressors
IronDeferoxamineIV for severe toxicity
Organo­phosphate / carbamateAtropine + pralidoximeTitrate atropine to drying of secretions
SulfonylureaOctreotide + dextroseFor recurrent hypoglycemia
Methanol / ethylene glycolFomepizole+ urgent dialysis
Carbon monoxide100% oxygen ± hyperbaricHigh suspicion with heaters/fires
Cyanide (smoke inhalation, nitroprusside)Hydroxocobalamin 70 mg/kg IV/IO (max 5 g), may repeat once; ± sodium thiosulfate 0.25 g/kg IV (max 12.5 g); do not delay oxygenation, airway control, or burn/PICU transfer while arranging the antidoteFirst‑line; give early in fire victims (lactate ≥ 8 mmol/L). Do not co‑infuse hydroxocobalamin and thiosulfate in the same line
Methemo­globinemiaMethylene blue 1–2 mg/kgIV
Local anesthetic toxicity (LAST)Lipid emulsion 20% — <70 kg: 1.5 mL/kg bolus over 2–3 min, then 0.25 mL/kg/min; ≥70 kg: 100 mL bolus, then 200–250 mL over 15–20 minCall resuscitation/PICU early and keep 20% lipid emulsion immediately available wherever regional anesthesia is used. Repeat bolus and/or double infusion if unstable; max ~12 mL/kg. Avoid vasopressin and calcium‑channel/beta‑blockers; epinephrine boluses ≤1 mcg/kg only
⚠ Avoid
  • Routine gastric lavage and ipecac; flumazenil (seizure risk) is generally avoided.
  • 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).
  • Discharge — asymptomatic after the appropriate observation window with a non‑toxic exposure.
  • Refer — the poison center/toxicology; psychiatry for intentional ingestion; safeguarding as needed.

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), start IV fluids and consult pediatric surgery immediately. Contact poison control.
◈ Endoscopy
  • Upper endoscopy within 12–24 h, once airway secure, grades the injury — earlier may miss it, later than 48 h raises perforation risk.
  • Watch for delayed strictures over the following weeks.
  • A swallowed button battery is a separate emergency — see Button (Lithium) Battery Ingestion.
◣ Admit · Discharge · Refer
  • Admit — all symptomatic or significant exposures → nil by mouth, plan imaging/endoscopy.
  • Discharge — asymptomatic minor exposure after observation.
  • Refer — ENT/GI/surgery (endoscopy) and PICU; do not blind‑pass a nasogastric tube.

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 chart (the child's palm including fingers ≈ 1%); assess depth and mechanism.
  • Suspect inhalation injury (facial burns, soot, hoarseness/stridor, enclosed‑space fire) → early airway/anesthetic involvement (see Smoke Inhalation & Carbon Monoxide Poisoning).
First aid Stop the burning; cool with running water for 20 min (not ice); remove clothing/jewelry; cover; analgesia.
Fluids (TBSA > 10%)
  • Modified Parkland — Lactated Ringer's 3–4 mL/kg × %TBSA over 24 h, ½ in the first 8 h from the time of burn, plus maintenance (4‑2‑1, with dextrose in young children)
  • 20 mL/kg bolus if shocked.
  • Titrate to urine output 0.5–1 mL/kg/h.
Refer to a burns center > 10% TBSA, full‑thickness, face/hands/feet/perineum/joints, electrical or chemical, inhalation injury, or suspected inflicted injury.
⚠ 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 (up to ~1 in 5 in burns‑unit series).
  • 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); 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.
  • Discharge — small superficial burns with dressing and review.
  • Refer — 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.
  • 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). Cold‑water immersion preferred if feasible (best for exertional heat stroke). Otherwise evaporative cooling — remove clothing, spray/mist tepid 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 core 38–39°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
  • 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.
  • Discharge — mild heat exhaustion, resolved and hydrated with normal mentation.
  • Refer — 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. In the ED, check the rhythm and give electrical therapy with a manual defibrillator if the rhythm is shockable (an AED is a prehospital substitute).
  • 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 — 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 — reserve for symptomatic or hypoxic children.
STAYS WELL
Asymptomatic with a normal exam, normal vitals, and normal SpO₂ on room air at 6–8 h → discharge with return precautions (cough, breathing difficulty, vomiting, fever, or lethargy).
SYMPTOMS / HYPOXIA
Any respiratory symptoms, an oxygen requirement, or altered mental status → admit; give oxygen and support and obtain a chest X‑ray / blood gas as indicated.
⚠ Admit
  • Respiratory distress or increased work of breathing
  • persistent or worsening symptoms
  • altered mental status
  • need for supplemental oxygen or ventilatory support.
◈ Not recommended
  • Heimlich maneuver
  • postural drainage
  • routine chest X‑ray for discharge decisions
  • glucocorticoids
  • routine antibiotics
  • routine cervical‑spine immobilization unless trauma (e.g., a diving injury) is suspected.
◣ Admit · Discharge · Refer
  • Admit — any symptomatic patient, or asymptomatic with risk features → observe.
  • Discharge — asymptomatic with a normal exam and SpO₂ on room air after 6–8 h observation, with return precautions.
  • Refer — PICU for respiratory compromise; safeguarding as needed.

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: COHb > 25% (> 20% in pregnancy), loss of consciousness/syncope, neurologic signs, cardiac ischemia, severe metabolic acidosis, or pregnancy — ideally within 6 h.
  • 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 (under‑16s excluded from the pivotal RCT); 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 ≥ 8–10 mmol/L).
  • 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 asymptomatic and COHb normal.
Hydroxo­cobalamin (suspected cyanide)70 mg/kg/dose IV (max 5 g)Empiric in smoke inhalation with shock or lactate ≥ 10 mmol/L; repeat once if needed.
HBO (severe CO)2.5–3.0 ATA, per protocolRefer to the hyperbaric unit for the criteria above.
◣ 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.
  • Discharge — asymptomatic with normal levels after observation.
  • Refer — hyperbaric/PICU for severe CO; burns/ENT for airway injury.

Envenomation — Scorpion Sting & Snakebite

MINUTESWHO 2016 · regional

Two regional bites: scorpion = an autonomic storm; snake = local tissue injury and coagulopathy.

▸
◣ Scorpion sting
  • Severe local pain, then an autonomic storm: sweating, salivation, vomiting, hypertension and tachycardia, agitation, and in severe cases pulmonary edema, myocarditis and shock (young children at highest risk).
  • Supportive care and analgesia; prazosin for autonomic/cardiovascular toxicity; benzodiazepines for agitation. Give antivenom for systemic envenomation per local protocol.
◣ 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 the limb at heart level, remove constrictions, and move to hospital. Give species‑appropriate antivenom for systemic envenomation and 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 Use the antivenom stocked for the species in your region and follow the national/Poison‑Control protocol; contact the Poison Control Center early for identification and 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, ECG, troponin + echocardiogram if cardiac signs, glucose, electrolytes, blood gas (pulmonary edema).
◣ Admit · Refer
  • Admit/observe all systemic envenomation and any child with progressing local signs.
  • 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 2020Chemo‑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 infantAny under 28 days; 29–90 days unless low‑risk on screening; ill‑appearing at any age.
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 epinephrine; hypoxia, exhaustion, or toxic appearance.
AsthmaIncomplete response to bronchodilators; ongoing oxygen need; needing bronchodilator more often than 1–2 hourly; silent chest, exhaustion, or altered consciousness (→ critical care).
PneumoniaSpO₂ under 92%; moderate to severe distress; under 3–6 months; not tolerating oral; dehydration; 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 on days 0, 3, 7, 14 (add day 28 if immunocompromised); 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 as possible into and around the wound, give any remainder IM at a site distant from the vaccine.
  • 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 early switch is as effective as completing the IV course.
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 + 4) × 2 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)systolic BP < 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 hypoxaemia 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 (5–15 L/min) gives up to ~80–90% FiO₂. 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 = litres 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 litres 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: E cylinder, 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).

▸
AgeHeart rate /minRespiratory rate /minSystolic BP mmHg
Newborn100–18040–6060–90
Infant < 1 yr100–16030–5372–104
1–2 yr90–15022–3786–106
3–5 yr80–14020–2889–112
6–11 yr70–12018–2597–120
12+ yr60–10012–20110–131
◈ 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 5.5 mmol/L (100 mg/dL) glucose above 5.5 mmol/L (Hillier; the older 1.6 factor underestimates at high glucose)
Corrected Cameasured + 0.02 × (40 − albumin g/L) mmol/L
Anion gapNa − (Cl + HCO₃); normal 8–12 mmol/L
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)QT ÷ √RR (s); prolonged > 0.46 s
eGFR (Schwartz)36.2 × height (cm) ÷ creatinine (µmol/L)
Glucose infusion ratemg/kg/min = dextrose% × rate (mL/h) ÷ (6 × weight kg)
Names & synonyms
Generic (US)Also known as
Epinephrineepinephrine
Norepinephrinenorepinephrine
Albuterolsalbutamol
Acetaminophenacetaminophen
Furosemidefrusemide
Lidocainelignocaine
Acycloviracyclovir
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.

▸
◈ Non‑emergent neonatal intubation — premedicate
  • Analgesic/vagolytic premedication is standard of care (not optional) for all non‑emergent neonatal intubations; the only exception is delivery‑room resuscitation or a life‑threatening airway without IV access.
  • Use a vagolytic + fast‑acting opioid + short‑acting relaxant: atropine 0.01–0.02 mg/kg + fentanyl 2 mcg/kg slow over 2–5 min + succinylcholine 2 mg/kg (avoid succinylcholine in hyperkalemia, malignant‑hyperthermia risk, or neuromuscular disease) — CPS.
Analgesia
DrugDoseRoute & notes
Acetaminophen15 mg/kg/dose (max 1 g/dose)PO/PR/IV; mild–moderate pain
Ibuprofen10 mg/kg/dose (max 400 mg/dose)PO; 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
Midazolam0.05–0.1 mg/kg IV; 0.3–0.5 mg/kg buccal/intranasalAnxiolysis; respiratory depression with opioids
Rapid sequence intubation
StepDoseRoute & notes
InductionKetamine 1–2 mg/kg, propofol 2–3 mg/kg, etomidate 0.3 mg/kg, or midazolam 0.1–0.3 mg/kg (± fentanyl 1–2 mcg/kg as pre‑treatment)Choose by hemodynamics
ParalyticRocuronium 1–1.2 mg/kg, or succinylcholine 1–2 mg/kgIV
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 at a Glance

MINUTES

Weight‑based resuscitation doses — use measured weight or a length‑based tape when possible (formulas are estimates); cross‑check weight, concentration, and local resuscitation chart before every dose.

▸
Drug · indicationDoseNotes
Epinephrine — cardiac arrest0.01 mg/kg (0.1 mL/kg of 1:10 000) IV/IORepeat every 3–5 min; max 1 mg/dose. Endotracheal: 0.1 mg/kg (0.1 mL/kg of 1:1000)
Epinephrine — anaphylaxis0.01 mg/kg (0.01 mL/kg of 1:1000) IMMax 0.5 mg; anterolateral thigh; repeat every 5–15 min
Amiodarone — VF / pulseless VT5 mg/kg IV/IO bolusMay repeat up to twice; max 300 mg/dose. Perfusing tachycardia: give over 20–60 min
Adenosine — SVT0.1 mg/kg rapid push (max 6 mg), then 0.2 mg/kg (max 12 mg)Immediate saline flush; use line closest to the heart
Atropine — bradycardia0.02 mg/kg IV/IOMin 0.1 mg; max 0.5 mg/dose; may repeat once
Calcium chloride 10% — hyperkalemia, Ca‑blocker toxicity, hypocalcemia20 mg/kg (0.2 mL/kg) IV/IOcentral line preferred (calcium chloride is sclerosing — high extravasation risk); calcium gluconate 10% 60 mg/kg (0.6 mL/kg) is preferred for peripheral IV
Dextrose — hypoglycemia0.25–0.5 g/kgD10W 2.5–5 mL/kg (neonate/infant); recheck glucose
Magnesium sulfate — torsades, severe asthma25–50 mg/kg IV/IO (max 2 g)Rapid in torsades; over 15–20 min in asthma
Naloxone — opioid toxicity0.1 mg/kg IV/IM/IN (max 2 mg)Titrate to breathing; re‑dose (short half‑life)
Sodium bicarbonate1 mEq/kg IV/IOTCA toxicity (QRS > 100 ms), severe acidosis, hyperkalemia
Lidocaine — VF/pVT (alternative to amiodarone)1 mg/kg IV/IOThen infusion 20–50 mcg/kg/min
Isotonic fluid bolus — shock20 mL/kg10 mL/kg in neonates, cardiac disease, DKA, or severe malnutrition; reassess after each
Defibrillation — VF/pVT2 J/kg → 4 J/kg → ≥ 4 J/kgMax 10 J/kg or adult dose (≈ 200 J biphasic / 360 J monophasic)
Synchronized cardioversion — unstable SVT/VT0.5–1 J/kg → 2 J/kgSedate if conscious and time permits
Concentrations & pitfalls
  • Epinephrine 1:10 000 = 0.1 mg/mL (IV/IO) versus 1:1000 = 1 mg/mL (IM/endotracheal) — confirm the ampoule before every dose.
  • Amiodarone is 150 mg/3 mL.
  • Use a length‑based (Broselow) tape when weight is unknown.
  • Source: American Heart Association / AAP Pediatric Advanced Life Support (PALS), 2025.

Resuscitation Dose Calculator

MINUTESPALS 2025

Enter the weight — doses compute live and cap at the maximum per dose (works in app and web version).

▸
Drug · indicationRule (per kg · max)Dose for this child
Epinephrine — arrest (IV/IO)0.01 mg/kg · max 1 mg—
Epinephrine — anaphylaxis (IM)0.01 mg/kg · max 0.5 mg—
Amiodarone — VF/pVT5 mg/kg · max 300 mg—
Adenosine — 1st dose0.1 mg/kg · max 6 mg—
Adenosine — 2nd dose0.2 mg/kg · max 12 mg—
Atropine — bradycardia0.02 mg/kg · min 0.1, max 0.5 mg—
Calcium gluconate 10%60 mg/kg (0.6 mL/kg) · max 2 g—
Dextrose 10% — hypoglycemia2.5–5 mL/kg (0.25–0.5 g/kg)—
Magnesium sulfate25–50 mg/kg · max 2 g—
Naloxone — opioid0.1 mg/kg · max 2 mg—
Sodium bicarbonate 8.4%1 mEq/kg (1 mL/kg)—
Lidocaine — VF/pVT alt1 mg/kg · max 100 mg—
Isotonic fluid bolus — shock10–20 mL/kg—
Defibrillation — VF/pVT2 → 4 J/kg · max ≈ 200 J—
Synchronized cardioversion0.5–1 → 2 J/kg—
◈ RSI — rapid sequence intubation
Drug · roleRule (per kg)Dose for this child
Fentanyl — premed/analgesia1–2 mcg/kg (slow IV)—
Ketamine — induction1–2 mg/kg IV (4–5 IM)—
Etomidate — induction0.3 mg/kg IV—
Propofol — induction2–3 mg/kg IV—
Midazolam — induction alt0.1–0.3 mg/kg IV—
Rocuronium — paralytic1–1.2 mg/kg IV—
Succinyl­choline — paralytic1–2 mg/kg IV—

Choose one induction agent (by hemodynamics) + one paralytic. Atropine premed (0.02 mg/kg, max 0.5 mg) is in the table above — no minimum dose when used as intubation premedication (the paradoxical‑bradycardia rationale for a 0.1 mg floor has been debunked). Credentialed clinicians only — airway rescue ready.

◣ Vasoactive infusions — weight‑based prep (verify locally)
InfusionMake up to 50 mLRate → dose
Epinephrine / Norepinephrine—1 mL/h = 0.1 mcg/kg/min · usual 0.05–1 mcg/kg/min (0.5–10 mL/h)
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; for larger children use your unit’s standard fixed‑concentration chart.

⚠ 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.
  • Static PDF / Word / EPUB copies show the rules and maxima but do not calculate; use the app or web (HTML) file for live values.

Resuscitation Doses by Weight

MINUTESPALS 2025

Pre‑computed arrest doses — pick the column nearest the weight. Works in every format, including print.

▸
Drug · rule (per dose)  · kg▸510203050
Epinephrine (adrenaline) 0.01 mg/kg IV/IO — mg (mL 1:10 000)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% 0.6 mL/kg (max 20) — mL36121820
Dextrose 10% 2 mL/kg — mL10204060100
Fluid bolus 20 mL/kg (10 if neonate/cardiac/DKA) — mL1002004006001000
Defibrillation 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; for an exact figure use the interactive Resuscitation Dose Calculator above (app / web).

Anticoagulation — VTE Prophylaxis & Treatment

ASSESS

Enoxaparin dosing and anti‑Xa targets in children.

▸
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
Before starting
  • Baseline complete blood count, renal function, and coagulation screen.
  • Avoid with active bleeding, platelets < 50 × 10⁽/L, or within 24 h of major surgery or a neuraxial procedure.
  • Reduce dose if creatinine clearance < 30 mL/min.
Reversal & alternatives
  • Protamine partially reverses enoxaparin (about 1 mg per 1 mg given in the prior 8 h; max 50 mg) — anti‑Xa activity is only partly neutralized.
  • Consider unfractionated heparin when rapid reversibility or severe renal impairment is needed.
  • Source: ASH 2018 and CHEST pediatric antithrombotic guidelines.

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 (plain)4.5 mg/kg (max 300 mg)Onset fast; ~30–60 min duration
Lidocaine + epinephrine7 mg/kg (max 500 mg)Longer duration; caution on end‑arteries (digits, pinna, penis)
Bupivacaine ± epinephrine2.5 mg/kg (single‑shot; epinephrine does not raise the pediatric ceiling)Most cardiotoxic; never IV or Bier block; avoid in young infants
Levo­bupivacaine2.5 mg/kgLess cardiotoxic than bupivacaine
Ropivacaine2 mg/kgLower cardiotoxicity; useful for infusions
Mepivacaine4.4 mg/kg (max ~300 mg)Duration between lidocaine and bupivacaine
Continuous infusion caps

Bupivacaine, levobupivacaine, ropivacaine: 0.2 mg/kg/h (< 3 mo), 0.3 mg/kg/h (3 mo–1 yr), up to 0.4 mg/kg/h (> 1 yr).

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.
  • Source: ESRA/ASRA 2018 pediatric recommendations; ASRA 2020 LAST advisory.
Vital signs — normal vs red zone by ageThe escalation threshold, not just the normal range. Ranges: PALS/APLS.
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 >20530–60>60<601–12 months100–190<100 or >19030–53>60<701–2 years98–140<90 or >14022–37>40<70+(2×age)2–5 years80–120<80 or >12020–28>34<70+(2×age)5–12 years75–118<60 or >12018–30>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.Ranges: PALS/AHA and APLS. 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.
✦ 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.
◈ Source
  • Ministry of Health, State of Kuwait — Kuwait Childhood Immunization Schedule 2025 (Public Health Sector).
  • Transcribed from the official MOH schedule.

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 (population studies report roughly half of unions, first‑cousin predominant). 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.
◈ Local programmes & sources
  • Kuwait runs premarital screening and expanded newborn screening; a family history of consanguinity or an affected sibling is itself a red flag.
  • Sources: autosomal‑recessive disorders in Kuwait (Teebi/Al‑Awadi series); IEM & consanguinity reviews. [Verify local screening panel].

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 (≈ 0.5 mmol/L/h) to avoid osmotic demyelination. Acute symptomatic (seizing): 3% saline 2–5 mL/kg (max ~100–150 mL) to raise Na ~4–6 mmol/L and stop the seizure.
  • 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 ≤ 40–60 mmol/L; ward rate 0.25–0.5 mmol/kg/h (max 10 mmol/h); PICU up to 1 mmol/kg/h with continuous ECG. Never IV push.
✦ 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).
◈ Source
  • ISMP High‑Alert Medications (Acute Care 2024); AAP maintenance IV fluids (Feld et al., Pediatrics 2018); CJASN hyponatremia 2024; pediatric potassium administration guidance; J Infusion Nursing 2020.
  • Confirm concentration/rate ceilings against local protocol.

Decision‑Rules Engine — Cutoff → Action

REFERENCEValidated pediatric rules

The rules you already trust, each with its exact operating point and what to do next — in one place.

▸
RuleOperating point → action
PECARN head — < 2 yGCS ≤14 / AMS / palpable skull fracture → CT. Occipital‑parietal‑temporal hematoma, LOC ≥5 s, severe mechanism, or not acting normally → observe vs CT. None → no CT.
PECARN head — ≥ 2 yGCS ≤14 / AMS / basilar skull‑fracture signs → CT. LOC, vomiting, severe mechanism, or severe headache → observe vs CT. None → no CT.
PECARN c‑spine (2024)GCS 3–8 / abnormal ABC / focal deficit → CT. AMS, substantial head/torso injury, midline neck pain or tenderness → radiographs. None → clinical clearance.
Kocher (septic hip)Non‑weight‑bearing · fever >38.5 · ESR >40 · WBC >12k. Probability by count: 1≈3% · 2≈40% · 3≈93% · 4≈99%. ≥3 → aspirate / ortho; 2 → strongly consider.
Pediatric Appendicitis Score (/10)≤3 (or ≤5) low → observe/discharge; 4–6 equivocal → imaging/observe; ≥7 high → surgical consult.
Westley croup (/17)≤2 mild → dexamethasone, home; 3–7 moderate → dexamethasone ± nebulized epinephrine, observe; 8–11 severe → epinephrine + steroid, admit; ≥12 → airway / ICU.
PRAM asthma (/12)0–4 mild · 5–8 moderate · 9–12 severe → escalates bronchodilator frequency, systemic steroid, and admission/ICU.
PASS asthmaPediatric Asthma Severity Score — grades work of breathing, wheezing / air entry, and SpO2 / ability to speak or feed; higher = more severe. An alternative to PRAM to guide bronchodilator frequency, systemic steroid, and admission; reassess after each step.
Bacterial Meningitis Score1 pt each: CSF Gram+ · CSF ANC ≥1000 · CSF protein ≥80 · blood ANC ≥10k · seizure. Score 0 = very low risk (NPV ~100%). Excludes <2 mo, prior antibiotics, purpura, immunosuppression, shunt.
Febrile infant ≤ 60–90 dStep‑by‑Step low risk = well · >21 d · normal UA · PCT <0.5 · CRP ≤20 · ANC ≤10k → discharge with follow‑up. PECARN ≤60 d: negative UA + ANC ≤4090 + PCT ≤1.71 → may forgo LP/antibiotics.
Gorelick dehydration (/10)≥3 signs → ≥5% dehydration; ≥7 → ≥10%. (4‑sign subset: cap refill, tears, mucous membranes, ill appearance.)
Glasgow‑Blatchford (UGI bleed)Score 0 → low risk, outpatient. Caveat: adult‑derived, not validated in children — adjunct only.
◈ Sources
  • PECARN head (Kuppermann, Lancet 2009) & c‑spine (2024); Kocher 1999 (Caird CRP modification); Samuel PAS 2002; Westley 1978; PRAM; Nigrovic BMS 2007; Step‑by‑Step (Gomez/Mintegi 2016) & PECARN febrile (Kuppermann 2019); Gorelick 1997; Glasgow‑Blatchford 2000.
  • Cross‑link each row to its card on insertion.

How This Guide Is Maintained

GOVERNANCEIssued June 2026 · review June 2028

A reference is only trusted if it shows its currency, its reviewers, and a way to correct it.

▸
◣ Currency & review
  • Issued June 2026 · scheduled review June 2028, or sooner if a major guideline changes. Each clinical section carries a “reviewed / next review” stamp so the reader can see the section’s currency at a glance.
  • Content is written to the most recent high‑impact guideline for each topic; the guideline body and year appear on every card.
◣ Reviewers & governance
  • Prepared for the Kuwait Pediatric Council and reviewed by its named faculty panel (see the Reviewers page). Section leads sign off their section before release.
⚠ 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.
  • Use the feedback channel on the Reviewers page (a QR / email link is placed here in the published edition).
  • Every erratum is dated and credited in the change log below.
◣ Change log — this edition
  • New clinical cards — immune thrombocytopenia, IgA vasculitis, pertussis, Guillain–Barré / acute flaccid paralysis, new‑diagnosis oncologic emergencies, hyperglycemic hyperosmolar state, vitamin K deficiency bleeding, envenomation, MIS‑C, tension pneumothorax, child protection, neonatal abstinence, thyroid storm, rhabdomyolysis, toxic megacolon, neuromuscular disease, massive transfusion.
  • New reference tools — Kuwait 2025 immunization schedule, high‑alert drug & fluid safety, decision‑rules engine, symptom front‑door navigator; bilirubin nomogram + calculator and age‑banded vital‑sign red zones.
  • Corrections — US spelling & drug nomenclature throughout; bilirubin escalation defined as within 2 mg/dL of the exchange line (AAP 2022); immunization schedule updated to the MOH 2025 decree.
  • Editorial — clickable Contents restored in every PDF; workup block standardized; version label removed from published copies.
◈ How to cite
  • Kuwait Pediatric Council. Pediatric & Neonatal Common & Emergency Care Guide. Issued June 2026.
  • Decision support only — confirm against Ministry of Health protocols and specialist advice.

Shortest Antibiotic Durations

STEWARDSHIPShort‑course RCTs

An improving, immunocompetent child — how few days is actually enough.

▸
⚠ These durations assume
  • An immunocompetent child who is improving (afebrile / clearly better by 48–72 h), with source control and no bacteremia, abscess, or foreign material.
  • Confirm organism and susceptibility; extend if not improving.
InfectionShortest courseCondition
Community‑acquired pneumonia (outpatient, non‑severe) (card)5 daysImproving by day 3–4 (SCOUT‑CAP). 3 days is emerging for mild disease, not yet standard.
Acute otitis media (card)< 2 y: 10 days · ≥ 2 y: 5–7 daysA 5‑day course was inferior in under‑2s; full 10 days for < 2 y and for severe/perforated.
GAS pharyngitis (card)10 days (penicillin/amoxicillin)Unchanged — needed for eradication and rheumatic‑fever prevention.
Cystitis (afebrile, lower UTI) (card)3–5 daysAfebrile lower‑tract infection.
Febrile UTI / pyelonephritis7–10 days (5 only if clearly improving)Evidence conflicts — STOP trial: 5 d non‑inferior; SCOUT‑UTI: more failures at 5 d. Shared decision‑making.
Cellulitis / soft‑tissue (uncomplicated) (card)5 daysExtend only if not improving at day 5.
Acute osteomyelitis (card)~3 weeks total; IV→oral at 2–4 daysNon‑MRSA, good response, falling CRP before the oral switch (Peltola).
Septic arthritis10 days total; early oral switchUncomplicated, non‑MRSA/non‑Salmonella, CRP normalizing (Peltola).
Bacterial meningitis (card)Meningococcus 5–7 d · Hib 7–10 d · pneumococcus 10–14 dBy organism (GBS 14–21 d; gram‑negative/Listeria 21 d).
Perforated appendicitis (post‑op) (card)Often 3–5 daysAdequate source control; stop when afebrile ~24 h and tolerating diet.
Neonatal culture‑negative "rule‑out" (card)Stop at 36–48 hBlood culture negative and infant well — most pathogens grow by 36 h.
✦ The stewardship habit
  • Set a stop or review date when you start.
  • For most improving outpatient infections, shorter is now standard — the exceptions are the under‑2 ear, the strep throat, and febrile UTI, where the longer course still holds.
◈ Sources
  • SCOUT‑CAP (JAMA Peds 2022) & CAP‑IT (2021); AAP AOM 2013; IDSA GAS 2012 / CDC; STOP (Pediatrics 2024) & SCOUT‑UTI (JAMA Peds 2023); IDSA SSTI 2014; Peltola osteomyelitis (PIDJ 2010) & septic arthritis (CID 2009); AAP Red Book (meningitis durations); pediatric appendicitis pathways.
  • Confirm against your current Red Book / local antibiogram.
Emergency Dose Calculator — enter the actual weight
Exact per‑kg doses with max caps (AHA PALS). The color table below prints; this calculator is the accurate bedside tool. Verify before giving.
doses compute live
⚠ Epinephrine in arrest is 1:10,000 (0.1 mg/mL), 0.1 mL/kg — never 1:1,000 IV. ETT size is a starting estimate — confirm by length tape, ETCO₂ and auscultation; keep ±0.5 mm ready.
Bolus 20 mL/kg (septic/hypovolemic); 10 mL/kg in trauma, DKA, neonates; 5 mL/kg in cardiogenic shock. Defib 2→4 J/kg; cardioversion 1→2 J/kg. Dextrose 5 mL/kg of 10% = 0.5 g/kg. Not a substitute for judgment or your formulary.
Weight ruler — Broselow–Luten color zonesFind the weight → color zone → read across. Doses are per‑kg (AHA PALS); ETT sizes are the standardized zone values. Confirm with a length‑based tape and your formulary.
Broselow-Luten weight ruler
✚

Bedside Calculators

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

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 × weight (kg) ÷ concentration (mcg/mL), with dose in mcg/kg/hr (× 60 if per‑minute; × 1000 if mg/kg/hr). Concentrations are never assumed — presets are common preparations you can edit, or type your own. Dose ranges are titrated to response. Source: AHA/AAP PALS 2025; pediatric Surviving Sepsis Campaign (Weiss, 2020).

Maintenance fluids & bolus

▸
Enter weight.
Maintenance — Holliday–Segar: 4‑2‑1 mL/kg/hr (100‑50‑20 mL/kg/day) for the first 10 / next 10 / each further kg. Use an isotonic fluid with glucose (AAP 2018). Bolus 10–20 mL/kg balanced crystalloid; reassess after each. Source: Holliday & Segar 1957; AAP Clinical Practice Guideline 2018; PALS 2025.

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 2–5 more days with daily scoring; < 35 → responding. Source: Turner 2007 (Gastroenterology); ESPGHAN/ECCO acute severe colitis guideline 2025 (Assa et al., JPGN).

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). Factors (L/psi): D 0.16 · E 0.28 · M 1.56 · G 2.41 · H/K 3.14 (US/CGA; metric cylinders vary — check the label). Source: Egan's Fundamentals of Respiratory Care 12e; AARC; BOC cylinder data.

Electrolyte & lab corrections

▸
Corrected sodium (for hyperglycemia)
—
Anion gap
—
Corrected calcium
—
Serum osmolality (calculated)
—
Corrected Na = measured + 2.4 × (glucose − 5.5) ÷ 5.5 (Hillier 1999). Anion gap = Na − (Cl + HCO₃), ref 8–16; albumin‑corrected + 2.5 × (40 − albumin g/L) ÷ 10. Corrected Ca (mmol/L) = measured + 0.02 × (40 − albumin g/L). Osmolality = 2 × Na + glucose + urea (mmol/L). Source: Hillier, Am J Med 1999; Payne 1973; standard SI formulae.

QTc (corrected QT)

▸
Enter QT (ms) and heart rate.
Bazett: QTc = QT ÷ √RR. Fridericia: QTc = QT ÷ RR^⅓, where RR (s) = 60 ÷ HR. Prolonged > 450 ms (> 460 ms in females/infants); > 500 ms = high risk of torsades. Bazett over‑corrects at extremes of rate. Source: Bazett 1920; Rautaharju/AHA 2009.

Glasgow Coma Scale

▸
—
Pediatric verbal responses shown for pre‑verbal children. GCS ≤ 8 signals a threatened airway → involve PICU/anesthesia. Source: Teasdale & Jennett 1974; pediatric modification (James 1986).

Westley croup score

▸
—
≤ 2 mild · 3–5 moderate · 6–11 severe · ≥ 12 impending respiratory failure. Give dexamethasone 0.15–0.6 mg/kg for all; nebulized epinephrine for moderate–severe. Source: Westley 1978.

APGAR

▸
—
Scored at 1 and 5 min (continue every 5 min to 20 if < 7). APGAR does not guide resuscitation — do not delay NRP steps to assign it. Source: Apgar 1953; NRP 8th ed / AHA‑AAP 2025.

Endotracheal tube — size & depth

▸
Enter age (≥ 1 year). For neonates use weight‑based sizing.
Cuffed ID (mm) = age ÷ 4 + 3.5; uncuffed = age ÷ 4 + 4 (≥ 1 yr). Depth at lip (cm) = age ÷ 2 + 12, or 3 × tube ID. Confirm with capnography and CXR. Neonate: ID ≈ 2.5–3.5 by weight; depth ≈ weight (kg) + 6 cm. Source: APLS; AHA/AAP PALS 2025.
§

References

Primary guidelines & landmark trials (Vancouver)

Sources

Tap to view the full reference list.

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  3. 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
  4. AHA & AAP. Part 5: Neonatal Resuscitation: 2025 Guidelines for CPR and ECC. Circulation. 2025. doi:10.1161/CIR.0000000000001367
  5. 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
  6. Weiss SL, Peters MJ, Alhazzani W, et al. Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis‑Associated Organ Dysfunction in Children. Pediatr Crit Care Med. 2020;21(2):e52–e106. doi:10.1097/PCC.0000000000002198
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