Pediatrics
Final Professional MBBS — Pediatrics. Complete question bank: Long Questions (10 marks) and Short Notes (5 marks) across all 15 systems, with clinical pearls, drug doses, staging tables, mnemonics and key-point recaps.
DEFINITION
Shock is a state of acute circulatory failure in which oxygen and nutrient delivery is inadequate to meet tissue metabolic demands, leading to cellular dysfunction. It is a life-threatening emergency requiring immediate recognition and treatment.
TYPES OF SHOCK
Type Mechanism / causes Hypovolaemic (commonest) Fluid loss — diarrhoea/dehydration, haemorrhage, burns Distributive Vasodilatation — septic (commonest cause of septic shock), anaphylactic, neurogenic Cardiogenic Pump failure — myocarditis, arrhythmia, congenital heart disease Obstructive Obstruction to flow — cardiac tamponade, tension pneumothorax STAGES
- Compensated — blood pressure maintained by tachycardia and vasoconstriction (cool peripheries, prolonged capillary refill); the crucial stage to catch.
- Decompensated (hypotensive) — hypotension is a LATE sign in children; signals imminent collapse.
- Irreversible — multi-organ failure.
CLINICAL FEATURES
- Tachycardia, prolonged capillary refill (> 3 s), cool/mottled extremities and weak peripheral pulses.
- Altered sensorium (irritability → lethargy), reduced urine output, tachypnoea.
- Hypotension is a late, ominous finding — do not wait for it to diagnose shock.
MANAGEMENT
- ABC — secure the airway, give high-flow oxygen, obtain IV/intraosseous access quickly.
- Fluid resuscitation — isotonic crystalloid boluses, reassessing after each (cautious, smaller aliquots in cardiogenic shock and severe malnutrition).
- Vasoactive drugs/inotropes (adrenaline/noradrenaline/dopamine) for fluid-refractory shock.
- Treat the cause — early antibiotics for sepsis, blood for haemorrhage, adrenaline for anaphylaxis.
- Correct hypoglycaemia/electrolytes; monitor and admit to intensive care.
PATHOPHYSIOLOGY
Reduced oxygen delivery to tissues → Compensation — tachycardia, vasoconstriction (BP maintained) → Anaerobic metabolism → lactic acidosis → Decompensation — hypotension, organ dysfunction
INVESTIGATIONS
- Blood glucose, electrolytes, blood gas/lactate, renal/liver function.
- Blood cultures and CBC/CRP (sepsis); coagulation; imaging as indicated by the cause.
MONITORING
- Heart rate, capillary refill, blood pressure, urine output (aim > 1 mL/kg/h), sensorium, and lactate clearance.
- Frequent reassessment after each intervention.
WARM vs COLD SHOCK
Feature Cold shock Warm shock Peripheries Cool, mottled Warm, flushed Pulses Weak, narrow pulse pressure Bounding, wide pulse pressure Capillary refill Prolonged Flash (brisk) First-line inotrope Adrenaline Noradrenaline GOALS OF RESUSCITATION
- Restore normal heart rate, capillary refill < 2 s, normal blood pressure and mentation.
- Urine output > 1 mL/kg/h and falling lactate indicate improving perfusion.
KEY EXAM POINT
The single most important lesson is that children compensate until they suddenly decompensate — recognise compensated shock by perfusion signs (tachycardia, prolonged capillary refill, cool peripheries) and resuscitate promptly with oxygen, IV/IO access and titrated fluid boluses, before hypotension appears.
SUMMARY
Shock is common and treatable if caught early; the priorities are rapid recognition of compensated shock, aggressive but titrated fluid resuscitation, timely inotropes, and treatment of the underlying cause (especially early antibiotics in sepsis).
💊KEY DRUG DOSES (viva)- Crystalloid bolus 10–20 mL/kg (0.9% saline / Ringer lactate), reassess and repeat as needed (10–20 mL/kg in severe malnutrition/cardiogenic — with great caution).
- Adrenaline infusion 0.05–0.3 µg/kg/min (cold shock); noradrenaline for warm/vasodilated shock.
- Septic shock — broad-spectrum antibiotics within the first hour.
- Correct hypoglycaemia — IV 10% dextrose 2–5 mL/kg.
⚠️DANGER / REMEMBER: Hypotension is a late sign in children — they compensate well and then crash suddenly. Recognise compensated shock (tachycardia, cool peripheries, prolonged capillary refill) and act before the blood pressure falls.📝CLINICAL / APPLIED POINTS- Diagnose shock clinically (perfusion) — never wait for hypotension, which is a pre-terminal sign in children.
- Get IV/IO access fast; if IV fails, use the intraosseous route without delay.
- Give fluid in boluses and reassess after each — titrate to response, and be cautious in cardiogenic shock/severe malnutrition.
- In septic shock, antibiotics within the first hour save lives.
- Start inotropes early if shock persists after adequate fluids.
🔑KEY POINTS TO REMEMBER- Acute circulatory failure → inadequate tissue perfusion; an emergency.
- Types: hypovolaemic (commonest), distributive (septic), cardiogenic, obstructive.
- Compensated (tachycardia, cool peripheries, prolonged CRT) → hypotension is LATE.
- ABC + O2 + IV/IO; crystalloid boluses 10–20 mL/kg with reassessment; inotropes if refractory.
- Treat the cause (antibiotics within 1 h for sepsis); correct glucose.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; PALS guidelines.INTRODUCTION
Acute poisoning is common in young children (accidental) and adolescents (intentional). Management follows a structured approach — stabilise first, then decontaminate, give antidotes where available, and provide supportive care.
STEP 1 — RESUSCITATION & STABILISATION
- ABC — airway, breathing, circulation; oxygen and IV access.
- Check and treat hypoglycaemia; manage seizures and arrhythmias.
- Assess the level of consciousness.
STEP 2 — HISTORY & TOXIDROME RECOGNITION
- Identify the agent, amount and time of exposure; look for the container/tablets.
- Recognise toxidromes — cholinergic (organophosphate), anticholinergic, opioid, sympathomimetic.
STEP 3 — DECONTAMINATION
- Skin/eye — remove clothing, wash thoroughly.
- Gastrointestinal — activated charcoal (most useful within 1 hour, if the toxin binds and the airway is protected); gastric lavage only early and in selected serious cases.
- Do NOT induce vomiting (ineffective/harmful), and avoid lavage/charcoal for corrosives and hydrocarbons (aspiration risk).
STEP 4 — ENHANCED ELIMINATION & ANTIDOTES
- Enhanced elimination in specific poisonings — urinary alkalinisation (salicylates), haemodialysis (methanol, salicylates, lithium).
- Give the specific antidote where one exists (see table).
COMMON ANTIDOTES
Poison Antidote Organophosphate Atropine + pralidoxime Paracetamol N-acetylcysteine Opioids Naloxone Iron Desferrioxamine Benzodiazepine Flumazenil Methanol/ethylene glycol Ethanol / fomepizole STEP 5 — SUPPORTIVE CARE & PREVENTION
- Meticulous supportive care is the mainstay for most poisonings; monitor and treat complications.
- Prevention — safe storage of chemicals/medicines out of reach, child-resistant containers, and parental education.
TOXIDROMES (recognition aids)
Toxidrome Features Example Cholinergic Salivation, miosis, bronchorrhoea, bradycardia Organophosphate Anticholinergic Dry, flushed, dilated pupils, delirium, tachycardia Atropine, antihistamine Opioid Pinpoint pupils, respiratory depression, coma Opioids Sympathomimetic Agitation, dilated pupils, hypertension, tachycardia Amphetamine COMMON CHILDHOOD POISONS (India)
- Kerosene/hydrocarbons, organophosphates, corrosives, paracetamol, iron, rodenticides, and plant poisons.
- Age pattern — accidental in toddlers, intentional in adolescents.
GASTRIC LAVAGE — LIMITED ROLE
Gastric lavage is considered only for a recent (within ~1 hour), potentially life-threatening ingestion with a protected airway; it is contraindicated for corrosives and hydrocarbons. Forced emesis (ipecac) is no longer used.
PREVENTION (a key public-health message)
- Store medicines and chemicals in original, labelled, child-resistant containers out of reach.
- Never store kerosene/pesticides in drink bottles; supervise young children; parental education.
KEY EXAM POINT
The mantra is 'treat the patient, not the poison' — stabilise ABC and glucose first; then decontaminate appropriately (activated charcoal early, no forced emesis, no GI measures for corrosives/hydrocarbons), give a specific antidote if one exists, and provide meticulous supportive care.
SPECIFIC POISONS — QUICK NOTES
- Iron — vomiting/GI bleeding, metabolic acidosis, shock; desferrioxamine.
- Corrosives — oral/oesophageal burns; do NOT lavage/neutralise; endoscopy.
- Datura/plant — anticholinergic features; supportive care.
DISPOSITION
- Observe asymptomatic children for the expected toxic window of the agent.
- Admit symptomatic/serious ingestions; involve a poison-information centre where available.
STRUCTURED SUMMARY OF THE APPROACH
Resuscitate (ABC + glucose) → Identify agent/amount/time + toxidrome → Decontaminate appropriately → Antidote (if available) + enhanced elimination → Supportive care + observe + prevent recurrence
📝CLINICAL / APPLIED POINTS- Resuscitate first — a poisoned child's airway/breathing/circulation and glucose take priority over identifying the toxin.
- Activated charcoal helps only early (within ~1 h) and only for adsorbable toxins with a protected airway.
- Never induce vomiting; avoid gastric measures in corrosive and hydrocarbon ingestion.
- Learn the common antidotes — they are frequently examined.
- Most poisonings are managed with supportive care; specific antidotes exist for only a few.
🔑KEY POINTS TO REMEMBER- Stabilise (ABC, glucose) → history/toxidrome → decontamination → antidote → supportive care.
- Activated charcoal within ~1 h (protected airway); no forced emesis; avoid GI measures in corrosives/hydrocarbons.
- Know antidotes: OP → atropine + pralidoxime; paracetamol → NAC; opioids → naloxone; iron → desferrioxamine.
- Enhanced elimination (alkalinisation, dialysis) for specific poisons.
- Supportive care is the mainstay; prevent with safe storage.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Snakebite envenomation is a medical emergency. In India, the medically important venomous snakes are the 'Big Four' — cobra, krait, Russell's viper and saw-scaled viper.
TYPES OF VENOM & EFFECTS
Venom type Snakes Effects Neurotoxic Cobra, krait Ptosis, ophthalmoplegia, bulbar & descending paralysis, respiratory failure Vasculotoxic/haemotoxic Russell's viper, saw-scaled viper Local swelling/necrosis, coagulopathy/bleeding, AKI, DIC CLINICAL FEATURES
- Local — fang marks, pain, swelling, blistering, necrosis (vasculotoxic).
- Neurotoxic — ptosis (early), diplopia, dysphagia, and descending respiratory-muscle paralysis.
- Haemotoxic — spontaneous bleeding, incoagulable blood, and acute kidney injury.
- 20-minute whole-blood clotting test (20WBCT) — a simple bedside test for coagulopathy (viper bites).
FIRST AID
- Reassure, keep the patient still, and immobilise the bitten limb (splint) at heart level.
- Remove tight items (rings/bangles); transport urgently to hospital.
- Avoid tourniquets, incision, suction and traditional remedies (harmful).
HOSPITAL MANAGEMENT
- Anti-snake venom (polyvalent ASV) for signs of systemic envenomation or severe local envenomation.
- Neurotoxic envenomation — atropine + neostigmine (anticholinesterase) and airway/ventilatory support.
- Haemotoxic — repeat ASV guided by the 20WBCT, manage bleeding and AKI (dialysis if needed).
- Monitor for ASV reactions (have adrenaline ready); wound care and tetanus prophylaxis.
DIFFERENTIATING BITES
- Dry bite — no envenomation (no local/systemic signs); observe.
- Local envenomation — pain, swelling, necrosis; systemic — neurotoxic or haemotoxic features (need ASV).
ASV REACTIONS
- Anaphylactic reactions to ASV are common — monitor closely and keep adrenaline ready.
- Pyrogenic and late serum-sickness reactions can also occur.
COMPLICATIONS & PROGNOSIS
- Respiratory failure (neurotoxic), acute kidney injury and bleeding (haemotoxic), local necrosis/compartment syndrome.
- Early ASV and good supportive/ventilatory care greatly improve outcome.
INVESTIGATIONS
- 20-minute whole-blood clotting test at the bedside; coagulation profile, platelets.
- Renal function and urine output (AKI), CBC, and monitoring of neurological/respiratory status.
SUPPORTIVE CARE
- Airway/ventilation for neurotoxic paralysis; blood products for significant bleeding; dialysis for AKI.
- Wound care, tetanus prophylaxis, and treatment of secondary infection.
KEY EXAM POINT
Immobilise and transport quickly (no tourniquet/incision/suction); give polyvalent ASV for systemic envenomation with adrenaline ready for reactions; add neostigmine/atropine and ventilation for neurotoxic bites, and use the 20-minute whole-blood clotting test to guide viper management.
PREVENTION & COMMUNITY MEASURES
- Wear footwear in fields/at night; use a torch; keep surroundings clear of rodents/debris.
- Community awareness, prompt transport to a facility with ASV, and training of health workers reduce mortality.
PROGNOSIS
With early anti-snake venom, airway/ventilatory support for neurotoxic bites, and management of coagulopathy and AKI for viper bites, most patients recover; delay is the main determinant of death and disability.
SUMMARY OF MANAGEMENT
First aid — reassure, immobilise limb, transport → Assess envenomation (local/neurotoxic/haemotoxic; 20WBCT) → ASV for systemic/severe local envenomation → Neostigmine+atropine + ventilation (neurotoxic); manage bleeding/AKI (haemotoxic) → Monitor for ASV reactions; wound/tetanus care
💊KEY DRUG DOSES (viva)- Polyvalent ASV — initial ~8–10 vials (per severity/protocol), repeated for persistent coagulopathy/neurotoxicity.
- Neostigmine 0.04 mg/kg IV with atropine 0.05 mg/kg (neurotoxic bites).
- Keep adrenaline 0.01 mg/kg IM ready for ASV anaphylaxis.
📝CLINICAL / APPLIED POINTS- Immobilise the limb and transport quickly — avoid tourniquets, cutting and suction.
- The 20-minute whole-blood clotting test is a cheap, powerful bedside test for viper coagulopathy.
- Give ASV for systemic envenomation; be prepared to treat an anaphylactic ASV reaction.
- Neurotoxic bites need neostigmine/atropine and, crucially, airway and ventilatory support.
- Reassess and repeat ASV guided by clotting/neurology; manage AKI.
🔑KEY POINTS TO REMEMBER- India's 'Big Four': cobra, krait (neurotoxic); Russell's & saw-scaled viper (vasculotoxic).
- Neurotoxic — ptosis, descending paralysis, respiratory failure; haemotoxic — bleeding, coagulopathy, AKI.
- First aid: reassure, immobilise limb, transport; NO tourniquet/incision/suction.
- ASV for envenomation; neostigmine+atropine + ventilation for neurotoxic bites.
- 20WBCT guides viper management; keep adrenaline ready for ASV reactions.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; WHO/national snakebite guidelines.INTRODUCTION
Cardiopulmonary resuscitation (CPR) restores circulation and oxygenation in cardiorespiratory arrest. In children, arrest is usually the end-result of progressive hypoxia (respiratory) rather than a primary cardiac event, so airway/breathing are especially important.
BASIC LIFE SUPPORT (BLS) — sequence
- Ensure scene safety; assess responsiveness and call for help/activate emergency response.
- C-A-B — check the pulse (≤ 10 s: brachial in infants, carotid/femoral in children); if absent/< 60 with poor perfusion, start chest compressions.
- High-quality compressions — rate 100–120/min, depth about one-third of the chest AP diameter (~4 cm infant, ~5 cm child), full recoil, minimal interruptions.
- Compression:ventilation ratio — 30:2 (single rescuer), 15:2 (two rescuers) for infants/children.
- Technique — infant: two-finger or two-thumb encircling; child: one or two hands.
ADVANCED LIFE SUPPORT (PALS)
- Attach a monitor/defibrillator and classify the rhythm.
- Non-shockable (asystole/PEA) — CPR + adrenaline, and treat reversible causes.
- Shockable (VF/pulseless VT) — defibrillate 2–4 J/kg, resume CPR, adrenaline, and consider amiodarone.
- Secure the airway and vascular/intraosseous access; give drugs; reassess every 2 minutes.
REVERSIBLE CAUSES (4 Hs & 4 Ts)
- 4 Hs — Hypoxia, Hypovolaemia, Hypo/hyperkalaemia (metabolic), Hypothermia.
- 4 Ts — Tension pneumothorax, Tamponade, Toxins, Thromboembolism.
CHOKING / FOREIGN-BODY OBSTRUCTION
- Infant — alternating 5 back blows and 5 chest thrusts (no abdominal thrusts).
- Child — abdominal thrusts (Heimlich); if unconscious, start CPR.
HIGH-QUALITY CPR METRICS
- Correct rate (100–120/min) and depth (⅓ AP), full recoil, minimal interruptions, avoid over-ventilation.
- Rotate compressors every 2 minutes to prevent fatigue; use waveform capnography if available.
TEAM & AIRWAY
- Assign clear roles; establish a definitive airway and IO/IV access early.
- Reassess rhythm and pulse every 2 minutes.
SIGNS OF GOOD CPR / ROSC
- Return of a palpable pulse, spontaneous breathing, rising end-tidal CO2, and improving colour/consciousness.
- On ROSC, move immediately to structured post-resuscitation care.
DEFIBRILLATION PRACTICE
- Minimise interruptions — charge during compressions, deliver the shock, and immediately resume CPR.
- Use paediatric pads/attenuator where available; 2 J/kg first, then 4 J/kg.
DRUGS & ACCESS IN PALS
- Intraosseous access is a rapid, reliable route when IV access fails.
- Give adrenaline every 3–5 minutes; amiodarone for refractory shockable rhythms; treat reversible causes.
KEY EXAM POINT
Because paediatric arrest is usually the end-point of hypoxia, effective ventilation plus high-quality compressions (correct rate/depth, full recoil, minimal interruptions) and early adrenaline give the best chance of survival.
ETHICAL & PRACTICAL ASPECTS
- Decisions to start/stop resuscitation follow guidelines and clinical judgement; involve seniors early.
- Debrief the team and support the family after the event.
PREVENTION OF ARREST
Since paediatric arrest is usually the end-stage of respiratory or circulatory failure, early recognition and treatment of the sick child (the 'chain of survival' begins with prevention) is the most effective way to improve outcomes.
THE CHAIN OF SURVIVAL
- Prevention/early recognition → early CPR → early defibrillation (shockable) → advanced care → post-arrest care.
- Each link improves the chance of intact survival; bystander CPR is crucial.
💊KEY DRUG DOSES (viva)- Adrenaline 0.01 mg/kg (0.1 mL/kg of 1:10,000) IV/IO every 3–5 minutes.
- Defibrillation 2 J/kg (first shock) → 4 J/kg (subsequent).
- Amiodarone 5 mg/kg IV/IO for refractory VF/pulseless VT.
POST-RESUSCITATION CARE
- Optimise oxygenation/ventilation (avoid hyperoxia/hypocapnia), support circulation, control temperature, and manage the underlying cause.
- Transfer to intensive care.
📝CLINICAL / APPLIED POINTS- Paediatric arrest is usually hypoxic — prioritise oxygenation and ventilation.
- High-quality compressions (rate, depth, recoil, minimal interruptions) are the foundation of survival.
- Start compressions if the pulse is absent OR < 60/min with poor perfusion.
- Adrenaline 0.01 mg/kg is the key drug; defibrillate shockable rhythms at 2–4 J/kg.
- Always look for and correct the 4 Hs and 4 Ts.
🔑KEY POINTS TO REMEMBER- Paediatric arrest is usually hypoxic (respiratory) — airway/breathing crucial.
- BLS: C-A-B; compressions 100–120/min, depth ⅓ AP; ratio 30:2 (single)/15:2 (two rescuers).
- PALS: shockable (defib 2–4 J/kg) vs non-shockable; adrenaline 0.01 mg/kg IV/IO q3–5 min.
- Reversible causes — 4 Hs (hypoxia, hypovolaemia, metabolic, hypothermia) & 4 Ts.
- Post-arrest: optimise oxygenation/circulation/temperature; ICU care.
📚SOURCES: Ghai Essential Pediatrics; PALS/AHA guidelines.DEFINITION
Child abuse and neglect (child maltreatment) is any act of commission or omission by a caregiver that causes harm, potential harm, or threat of harm to a child. It is under-recognised and has serious lifelong consequences.
TYPES
- Physical abuse — non-accidental injury (NAI).
- Sexual abuse.
- Emotional/psychological abuse.
- Neglect — physical, medical, educational or emotional.
- Fabricated or induced illness (Munchausen syndrome by proxy).
RED FLAGS IN THE HISTORY
- A history inconsistent with the injury or with the child's developmental stage.
- Delayed presentation, a changing/vague story, or inappropriate caregiver behaviour.
- Recurrent 'accidents' or injuries.
SUGGESTIVE PHYSICAL FINDINGS
- Bruises at unusual sites or in patterns (belt, hand), and injuries of different ages.
- Fractures suggestive of abuse — metaphyseal ('corner'), posterior rib, and multiple/spiral fractures in a non-ambulant child.
- Burns — cigarette burns, symmetrical immersion (glove-and-stocking) scalds.
- Abusive head trauma ('shaken baby') — the triad of subdural haemorrhage, retinal haemorrhages and encephalopathy; a torn frenulum in infants.
EVALUATION
- Detailed history and a thorough, fully documented examination (with a growth assessment).
- Skeletal survey (occult fractures), fundoscopy (retinal haemorrhages), and neuroimaging as indicated; coagulation screen to exclude bleeding disorders.
- Multidisciplinary assessment.
MANAGEMENT
- Treat the injuries and stabilise the child.
- Ensure the child's safety — admit if necessary; involve child-protection services.
- Mandatory reporting — in India, sexual abuse must be reported under the POCSO Act; follow local child-protection law.
- Psychological support and counselling; long-term follow-up and prevention.
⚠️DANGER / REMEMBER: A child's safety takes precedence — if abuse is suspected, ensure the child is protected (admit if needed) and report as legally required (POCSO for sexual abuse in India). Careful, contemporaneous documentation is essential (medico-legal).SEXUAL ABUSE — SPECIFIC POINTS
- May present with genital/anal injuries, sexually transmitted infections, pregnancy, or sexualised behaviour; often no physical signs.
- Requires sensitive, expert evaluation, forensic considerations, and mandatory reporting under POCSO.
RISK FACTORS
- Child factors (prematurity, disability, difficult temperament), caregiver factors (substance abuse, mental illness, own abuse history), and social stressors (poverty, isolation).
LONG-TERM CONSEQUENCES
- Physical injury/disability; psychological trauma — depression, anxiety, PTSD, behavioural problems.
- Impaired development and attachment; intergenerational cycle of abuse.
MUNCHAUSEN SYNDROME BY PROXY
In fabricated or induced illness, a caregiver invents or produces symptoms/signs in a child (e.g. by giving substances), leading to unnecessary investigations and harm; it requires a high index of suspicion and careful, multidisciplinary handling.
PREVENTION
- Support for at-risk families, parenting education, early identification of stressors and mental-health/substance problems.
- Home-visiting programmes and social support reduce risk.
KEY EXAM POINT
Suspect abuse when the history is inconsistent with the injury or with development, presentation is delayed, or injuries are patterned/of different ages; ensure the child's safety, document meticulously, exclude medical mimics, and report as legally mandated (POCSO for sexual abuse in India).
ROLE OF THE PAEDIATRICIAN
- Recognise, stabilise and document; exclude medical mimics (bleeding/bone disorders) without delaying protection.
- Coordinate with child-protection services, social workers and law enforcement as appropriate.
PROGNOSIS & FOLLOW-UP
Outcomes depend on the severity/chronicity of maltreatment and the support provided; early intervention, a safe environment and psychological therapy improve long-term physical and mental-health outcomes.
📝CLINICAL / APPLIED POINTS- Suspect abuse when the history doesn't fit the injury, presentation is delayed, or the story keeps changing.
- Certain fractures (metaphyseal, posterior rib) and the shaken-baby triad are strongly suggestive of abuse.
- Always exclude medical mimics (bleeding disorders, bone disease) but never let this delay protecting the child.
- Documentation is medico-legal — record findings meticulously with diagrams/photographs where permitted.
- Reporting suspected sexual abuse is mandatory under POCSO in India.
🔑KEY POINTS TO REMEMBER- Maltreatment: physical, sexual, emotional abuse; neglect; fabricated illness.
- Red flags: history inconsistent with injury, delayed presentation, changing story.
- Suggestive: patterned/different-aged bruises, metaphyseal/rib fractures, immersion burns, shaken-baby triad.
- Evaluate: documented exam + skeletal survey + fundoscopy ± neuroimaging; exclude mimics.
- Ensure safety, treat injuries, MANDATORY reporting (POCSO for sexual abuse), counselling.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; POCSO Act (India).DEFINITION
Organophosphate (OP) poisoning results from insecticides that inhibit acetylcholinesterase, causing accumulation of acetylcholine and a cholinergic crisis. It is a common and serious poisoning in India.
CLINICAL FEATURES
- Muscarinic — remembered as DUMBELS (Diarrhoea, Urination, Miosis, Bronchorrhoea/Bradycardia, Emesis, Lacrimation, Salivation); pinpoint pupils.
- Nicotinic — muscle fasciculations, weakness, and paralysis (including respiratory).
- CNS — anxiety, seizures, coma; a characteristic garlic odour.
DIAGNOSIS & MANAGEMENT
- Clinical (cholinergic toxidrome) supported by low plasma/RBC cholinesterase levels.
- Decontamination (remove clothes, wash skin) and airway/ventilatory support.
- Atropine — titrated to reverse bronchorrhoea/bronchospasm ('atropinisation').
- Pralidoxime (2-PAM) — reactivates cholinesterase (best given early, for nicotinic effects).
INTERMEDIATE & DELAYED EFFECTS
- Intermediate syndrome — proximal muscle/respiratory weakness 1–4 days after apparent recovery.
- Delayed peripheral neuropathy can follow some agents.
KEY EXAM POINT
Titrate atropine to drying of secretions and clear chest ('atropinisation') rather than to a fixed dose, and give pralidoxime early to reactivate the enzyme before it 'ages'.
DECONTAMINATION DETAIL
- Remove contaminated clothing and wash the skin/hair thoroughly (staff should protect themselves).
- Airway protection is critical — bronchorrhoea and weakness can cause respiratory failure.
KEY POINTS RECAP
- OP inhibits acetylcholinesterase → cholinergic crisis (muscarinic + nicotinic + CNS).
- Atropine to atropinisation + early pralidoxime + airway/ventilatory support; beware the intermediate syndrome.
SUMMARY
This is a high-yield paediatric emergency — remember the mechanism, the key clinical clue, the specific antidote/first-line treatment and its dose, and the main danger to anticipate.
💊KEY DRUG DOSES (viva)- Atropine 0.05 mg/kg IV, repeated/doubled every few minutes until secretions dry (atropinisation), then an infusion.
- Pralidoxime (2-PAM) 25–50 mg/kg IV, then infusion (give early).
🔑KEY POINTS TO REMEMBER- OP insecticides inhibit acetylcholinesterase → cholinergic crisis.
- Muscarinic (DUMBELS, miosis, bronchorrhoea) + nicotinic (fasciculations, paralysis) + CNS.
- Low cholinesterase; garlic odour.
- Decontaminate + airway support + atropine (to atropinisation) + pralidoxime (early).
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Kerosene (hydrocarbon) poisoning is a common accidental childhood poisoning. Because kerosene has low viscosity and high volatility, its main danger is aspiration causing chemical pneumonitis, not systemic absorption.
CLINICAL FEATURES
- Respiratory (from aspiration) — coughing, choking, tachypnoea, respiratory distress and fever (chemical pneumonitis).
- CNS depression (drowsiness) and gastrointestinal irritation may occur.
MANAGEMENT
- Do NOT induce vomiting or perform gastric lavage — this greatly increases the risk of aspiration.
- Supportive care — oxygen, respiratory support, and management of pneumonitis.
- Routine prophylactic antibiotics and corticosteroids are not recommended; antibiotics only if secondary infection develops.
- Observe for delayed respiratory deterioration.
WHY GASTRIC MEASURES ARE HARMFUL
Hydrocarbons are poorly absorbed from the gut but readily aspirated; inducing vomiting or lavage risks pushing kerosene into the lungs, worsening chemical pneumonitis — hence supportive care is preferred.
KEY EXAM POINT
A child who has swallowed kerosene and is coughing has likely aspirated; manage the airway/lungs and observe, but do NOT induce emesis or lavage.
COMPLICATIONS
- Chemical pneumonitis with hypoxia; rarely secondary bacterial pneumonia, pneumatocele, or effusion.
- CNS depression and, uncommonly, systemic effects.
KEY EXAM POINT
Kerosene's danger is the lung, not the gut — a coughing child has probably aspirated; provide oxygen and respiratory support and observe, but never induce vomiting or perform gastric lavage.
PROGNOSIS
Most children recover with supportive care; the course is determined by the severity of the chemical pneumonitis.
SUMMARY
This is a high-yield paediatric emergency — remember the mechanism, the key clinical clue, the specific antidote/first-line treatment and its dose, and the main danger to anticipate.
PREVENTION
Many paediatric emergencies are preventable — safe storage of poisons/medicines, supervision, protective measures and prompt first aid substantially reduce serious harm and mortality.
🔑KEY POINTS TO REMEMBER- Low-viscosity hydrocarbon → main danger is aspiration → chemical pneumonitis.
- Cough, respiratory distress, fever; ± CNS depression.
- Do NOT induce vomiting or lavage (aspiration risk); supportive care + oxygen.
- No routine prophylactic antibiotics/steroids; treat secondary infection if it occurs.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Paracetamol (acetaminophen) poisoning causes dose-dependent hepatotoxicity. In overdose, the toxic metabolite NAPQI depletes hepatic glutathione and injures hepatocytes.
CLINICAL PHASES
Phase Time Features I 0–24 h Nausea, vomiting, malaise (or asymptomatic) II 24–72 h Right upper quadrant pain, rising transaminases III 72–96 h Peak hepatotoxicity — hepatic failure, encephalopathy IV 4 days–2 weeks Recovery or death MANAGEMENT
- Assess the dose/time; use the paracetamol treatment nomogram where timing is known.
- Activated charcoal if presenting early (within ~1 hour).
- N-acetylcysteine (NAC) — the antidote (replenishes glutathione); highly effective when given early.
- Supportive care and monitoring of liver function/coagulation.
RISK ASSESSMENT
The paracetamol treatment nomogram plots the plasma level against the time since ingestion to decide on NAC; it applies to a single acute ingestion with a known time, and errs toward treating when in doubt.
KEY EXAM POINT
N-acetylcysteine is highly effective if started within 8 hours of ingestion, so do not delay it awaiting levels in a significant overdose; it replenishes glutathione and prevents hepatic necrosis.
KEY POINTS RECAP
- Overdose → NAPQI → glutathione depletion → hepatocyte necrosis.
- Four clinical phases; use the nomogram; NAC is the antidote (best within 8 h).
SUMMARY
This is a high-yield paediatric emergency — remember the mechanism, the key clinical clue, the specific antidote/first-line treatment and its dose, and the main danger to anticipate.
PREVENTION
Many paediatric emergencies are preventable — safe storage of poisons/medicines, supervision, protective measures and prompt first aid substantially reduce serious harm and mortality.
💊KEY DRUG DOSES (viva)- N-acetylcysteine — per standard IV/oral regimen (dosed by weight and protocol); most effective within 8 hours of ingestion.
- Activated charcoal 1 g/kg if early.
🔑KEY POINTS TO REMEMBER- Overdose → toxic NAPQI depletes glutathione → hepatotoxicity.
- Phases: I (nausea) → II (RUQ pain, rising LFTs) → III (hepatic failure) → IV (recovery/death).
- Use the treatment nomogram; activated charcoal if early.
- N-acetylcysteine is the antidote — most effective given early.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Scorpion sting envenomation (notably the Indian red scorpion) causes an autonomic storm from massive catecholamine release, and can be life-threatening in children.
CLINICAL FEATURES
- Severe local pain at the sting site.
- Autonomic overactivity — sweating, hypertension, tachycardia, cool extremities, priapism, vomiting, hypersalivation.
- Life-threatening — myocarditis and pulmonary oedema (with respiratory distress).
MANAGEMENT
- Prazosin (an alpha-blocker) — the drug of choice (counters the autonomic storm and reduces pulmonary oedema).
- Scorpion antivenom (where available/indicated); analgesia for local pain.
- Manage pulmonary oedema/heart failure; supportive/intensive care as needed.
DANGER — CARDIOPULMONARY EFFECTS
The most feared complications are myocarditis and pulmonary oedema, which can cause rapid deterioration; prazosin reduces afterload/preload and counteracts the catecholamine surge, improving outcomes.
KEY EXAM POINT
Prazosin is the drug of choice for red-scorpion envenomation; watch closely for pulmonary oedema/myocarditis and manage in a monitored setting.
GRADING & MONITORING
- Severity ranges from local pain only to a full autonomic storm with cardiopulmonary involvement.
- Monitor blood pressure, heart rate, respiration and oxygenation in a facility able to manage pulmonary oedema.
KEY EXAM POINT
Red-scorpion envenomation is essentially an autonomic storm — prazosin is the drug of choice, and the child must be monitored for myocarditis and pulmonary oedema, which are the causes of death.
SUMMARY
This is a high-yield paediatric emergency — remember the mechanism, the key clinical clue, the specific antidote/first-line treatment and its dose, and the main danger to anticipate.
PREVENTION
Many paediatric emergencies are preventable — safe storage of poisons/medicines, supervision, protective measures and prompt first aid substantially reduce serious harm and mortality.
💊KEY DRUG DOSES (viva)- Prazosin — oral, per weight/protocol, repeated as needed (drug of choice).
- Scorpion antivenom as per local protocol; supportive management of pulmonary oedema.
🔑KEY POINTS TO REMEMBER- Red scorpion venom → autonomic storm (catecholamine surge).
- Severe local pain + autonomic features; danger = myocarditis, pulmonary oedema.
- Prazosin (alpha-blocker) is the drug of choice; antivenom where indicated.
- Manage pulmonary oedema; supportive/intensive care.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Drowning is the process of respiratory impairment from submersion/immersion in a liquid. The outcome is determined chiefly by the duration and severity of hypoxia.
PATHOPHYSIOLOGY & FEATURES
- Submersion → breath-holding → laryngospasm → hypoxia → cardiac arrest if prolonged.
- Consequences — hypoxic-ischaemic brain injury, aspiration and delayed pulmonary oedema/ARDS, hypothermia, arrhythmias.
MANAGEMENT
- Rescue and immediate CPR with an emphasis on oxygenation/ventilation (arrest is hypoxic).
- Oxygen, ventilatory support, rewarming, and correction of acidosis/electrolytes.
- Observe for delayed respiratory deterioration (ARDS) even if initially well.
- Neuroprotective supportive care after resuscitation.
PREVENTION
Most drownings are preventable — constant adult supervision, fencing of water bodies/pools, and safe practices are the key measures.
'DRY' vs 'WET' & TEMPERATURE
Outcome depends on hypoxia duration, not the water type; cold-water submersion can occasionally be protective (the diving reflex/hypothermia), so resuscitation is continued in hypothermic drowning ('not dead until warm and dead').
KEY EXAM POINT
Every rescued child, even if apparently well, should be observed for delayed respiratory deterioration (secondary drowning/ARDS); prevention through supervision and fencing is paramount.
COMPLICATIONS
- Hypoxic-ischaemic encephalopathy (the main determinant of long-term outcome), ARDS, arrhythmias and hypothermia.
- Aspiration pneumonia and electrolyte disturbance.
MANAGEMENT SUMMARY
- Prompt rescue and CPR (oxygenation-focused), oxygen/ventilation, rewarming, and correction of metabolic derangements.
- Admit and observe for delayed pulmonary complications; neuroprotective care after resuscitation.
KEY EXAM POINT
Continue resuscitation in a hypothermic drowned child until re-warmed ('not dead until warm and dead'), and observe every rescued child for delayed respiratory deterioration.
SUMMARY
This is a high-yield paediatric emergency — remember the mechanism, the key clinical clue, the specific antidote/first-line treatment and its dose, and the main danger to anticipate.
🔑KEY POINTS TO REMEMBER- Respiratory impairment from submersion; outcome depends on hypoxia duration.
- Laryngospasm/hypoxia → arrest; watch for delayed pulmonary oedema/ARDS and hypothermia.
- Rescue + CPR focused on oxygenation/ventilation; rewarm; observe.
- Highly preventable — supervision and fencing.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Burns are tissue injury from heat, chemicals, electricity or radiation; scalds (hot liquids) are the commonest in children. Assessment of extent and depth guides management.
ASSESSMENT
- Extent — % total body surface area (TBSA) using a paediatric-modified rule of nines or the Lund-Browder chart (children have a relatively larger head).
- Depth — superficial, partial-thickness, full-thickness.
- Assess for inhalation/airway injury (facial burns, soot, stridor).
MANAGEMENT
- Stop the burning and cool with running water; secure the airway (early intubation if inhalation injury).
- Fluid resuscitation for significant burns using the Parkland formula, titrated to urine output.
- Analgesia, wound care, infection prevention, tetanus prophylaxis, and nutritional support.
- Refer major/complex burns to a burns unit.
CRITERIA FOR REFERRAL / ADMISSION
- Large %TBSA, full-thickness or circumferential burns, burns of face/hands/perineum, inhalation injury, electrical/chemical burns.
- Suspected non-accidental injury (pattern/immersion burns) — assess for abuse.
KEY EXAM POINT
Estimate %TBSA (paediatric-modified rule of nines/Lund-Browder), secure the airway if inhalation injury, and use the Parkland formula plus maintenance fluids titrated to urine output.
PATHOPHYSIOLOGY OF BURN SHOCK
Large burns cause massive fluid shifts and plasma loss into the burnt/injured tissues, producing hypovolaemia ('burn shock') — the reason for formula-guided fluid resuscitation titrated to urine output.
SUMMARY
This is a high-yield paediatric emergency — remember the mechanism, the key clinical clue, the specific antidote/first-line treatment and its dose, and the main danger to anticipate.
PREVENTION
Many paediatric emergencies are preventable — safe storage of poisons/medicines, supervision, protective measures and prompt first aid substantially reduce serious harm and mortality.
💊KEY DRUG DOSES (viva)- Parkland formula — 4 mL/kg × %TBSA of Ringer lactate over 24 h (half in the first 8 h), plus maintenance fluids in children; titrate to urine output.
- Analgesia (opioid) titrated to pain.
🔑KEY POINTS TO REMEMBER- Scalds commonest; assess % TBSA (paediatric rule of nines/Lund-Browder) and depth.
- Check for inhalation/airway injury (facial burns, soot, stridor).
- Stop burning + cool; airway; Parkland fluid (4 mL/kg/%TBSA) + maintenance, titrate to urine output.
- Analgesia, wound care, infection/tetanus prevention, nutrition; refer major burns.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics.DEFINITION
Anaphylaxis is a severe, potentially fatal, systemic hypersensitivity reaction (usually IgE-mediated) with rapid onset after exposure to an allergen (foods, drugs, insect stings, latex).
CLINICAL FEATURES
- Skin/mucosa — urticaria, flushing, angioedema (lips/face).
- Respiratory — stridor, bronchospasm/wheeze, respiratory distress.
- Cardiovascular — hypotension/shock, tachycardia.
- Gastrointestinal — vomiting, abdominal pain; rapid progression is typical.
MANAGEMENT
- Intramuscular adrenaline is the first-line, life-saving treatment — give immediately.
- Remove the trigger; position (supine, legs up; upright if breathing difficulty); high-flow oxygen.
- IV fluids for hypotension; bronchodilators for wheeze.
- Adjuncts (antihistamine, corticosteroid) are secondary; observe for a biphasic reaction.
- Provide an adrenaline auto-injector and allergen-avoidance advice on discharge.
COMMON TRIGGERS & BIPHASIC RISK
- Foods (nuts, egg, milk, seafood), drugs (antibiotics, NSAIDs), insect stings and latex.
- A biphasic reaction (recurrence hours later) means patients must be observed after initial recovery.
KEY EXAM POINT
The single most important action is prompt IM adrenaline into the anterolateral thigh — do not delay for antihistamines/steroids, which are only adjuncts; provide an auto-injector on discharge.
PATHOPHYSIOLOGY
Mast-cell/basophil degranulation releases histamine and other mediators, causing vasodilatation (hypotension), increased vascular permeability (angioedema), and bronchoconstriction — which adrenaline directly reverses.
SUMMARY
This is a high-yield paediatric emergency — remember the mechanism, the key clinical clue, the specific antidote/first-line treatment and its dose, and the main danger to anticipate.
💊KEY DRUG DOSES (viva)- Adrenaline 0.01 mg/kg of 1:1000 IM (max 0.5 mg), anterolateral thigh; repeat every 5–15 min as needed.
- IV fluids 10–20 mL/kg for hypotension; salbutamol nebs for bronchospasm.
🔑KEY POINTS TO REMEMBER- Severe IgE-mediated systemic hypersensitivity; rapid onset after an allergen.
- Skin (urticaria/angioedema) + respiratory (stridor/wheeze) + cardiovascular (shock) + GI.
- IM adrenaline 0.01 mg/kg (1:1000) is first-line and life-saving — give immediately.
- Oxygen, fluids, bronchodilators; antihistamine/steroid are adjuncts; watch for biphasic reaction.
📚SOURCES: Ghai Essential Pediatrics; Nelson Textbook of Pediatrics; resuscitation council guidelines.