Pediatrics

Organophosphate Poisoning

Pathophysiology: organophosphate compounds irreversibly inhibit acetylcholinesterase, causing acetylcholine accumulation at muscarinic and nicotinic synapses, producing a characteristic cholinergic toxidrome.

Clinical features (mnemonics SLUDGE/DUMBELS): Salivation, Lacrimation, Urination, Defecation, GI distress, Emesis; or Diarrhea, Urination, Miosis, Bradycardia/Bronchorrhea/Bronchospasm, Emesis, Lacrimation, Salivation — bronchorrhea and bronchospasm being the most immediately life-threatening muscarinic manifestations. Nicotinic effects: fasciculations, weakness, and, in severe cases, respiratory muscle paralysis. CNS: confusion, seizures, coma.

Antidote protocol:

• Atropine — competitive muscarinic antagonist, titrated aggressively to effect (drying of secretions/resolution of bronchorrhea, not a fixed heart rate/pupil size target); initial dose 0.02–0.05 mg/kg IV, doubled and repeated every 5–10 minutes until adequate atropinization — addresses only muscarinic effects, no effect on nicotinic toxicity
• Pralidoxime (2-PAM) — reactivates acetylcholinesterase by displacing the organophosphate, effective only before “aging” occurs (permanent enzyme-bond stabilization within hours) — give as early as possible, ideally alongside atropine. Addresses both muscarinic and nicotinic toxicity, a genuinely complementary addition to atropine
• Supportive care: aggressive airway management/suction, mechanical ventilation for respiratory failure, benzodiazepines for seizures, thorough decontamination (clothing removal, skin washing) to prevent ongoing absorption and protect healthcare workers

Paracetamol (Acetaminophen) Overdose

Pathophysiology: at therapeutic doses, paracetamol is metabolized via glucuronidation/sulfation; a small fraction via CYP450 to toxic NAPQI, normally detoxified by glutathione conjugation. In overdose, glucuronidation/sulfation saturate, diverting more through CYP450, generating NAPQI faster than glutathione can detoxify — causing centrilobular hepatocellular necrosis.

Rumack-Matthew Nomogram: plasma paracetamol concentration vs time since ingestion (starting from 4 hours post-ingestion), used to determine need for NAC after a single acute overdose of known timing. Not valid for staggered/chronic ingestion, modified-release formulations, or unknown ingestion timing — a lower threshold for empirical NAC applies in these scenarios.

Antidote — N-Acetylcysteine (NAC): replenishes hepatic glutathione stores, restoring NAPQI detoxification capacity, plus direct antioxidant/hepatoprotective properties. Efficacy is highest, hepatotoxicity risk essentially eliminated, when given within 8–10 hours of ingestion. Still beneficial (reduced efficacy) when started later, and given in established hepatotoxicity/fulminant hepatic failure given benefit even at this late stage. May be given via traditional IV three-bag protocol or an oral/enteral regimen — IV generally preferred with significant vomiting, altered mental status, or established hepatic failure.

Recognition and Initiation

Pediatric cardiac arrest is most commonly the end result of progressive respiratory failure or shock, rather than a primary sudden cardiac (arrhythmic) event as more typical in adults — underlying the pediatric-specific emphasis on early recognition and aggressive treatment of respiratory failure/shock to prevent progression to arrest, since outcomes from established cardiac arrest remain poor. Upon recognizing arrest (unresponsive, not breathing normally, no palpable pulse within 10 seconds, or uncertainty), high-quality CPR is initiated immediately.

High-Quality CPR — Core Components

• Compression rate: 100–120 per minute
• Compression depth: at least one-third of the AP chest diameter (~4 cm in infants, ~5 cm in children)
• Allow full chest recoil between compressions, minimizing interruptions
• Compression-to-ventilation ratio: 30:2 for a single rescuer; 15:2 for two rescuers — a pediatric-specific ratio distinguishing team-based pediatric CPR from the universal 30:2 used in adult resuscitation, reflecting the predominantly respiratory/asphyxial etiology
• Once an advanced airway is in place, compressions become continuous (asynchronous), with ventilation ~1 breath every 2–3 seconds (20–30 breaths/minute)
• Rotate compressors approximately every 2 minutes to prevent fatigue-related decline in quality

The Shockable vs Non-Shockable Rhythm Branch Point

Non-shockable rhythms (Asystole/PEA) — the more common pediatric presentation:

• Continue high-quality CPR
• Epinephrine as soon as possible, repeated every 3–5 minutes — dose 0.01 mg/kg IV/IO of the 1:10,000 concentration (0.1 mL/kg)
• IO access is now explicitly preferred over prolonged peripheral IV attempts if IV is not rapidly obtainable
• Search for and treat reversible causes throughout (“H's and T's” — Hypoxia, Hypovolemia, Hydrogen ion/acidosis, Hypo-/Hyperkalemia, Hypothermia, Hypoglycemia; Tension pneumothorax, Tamponade, Toxins, Thrombosis)
• Reassess rhythm approximately every 2 minutes

Shockable rhythms (VF/pulseless VT):

• Immediate defibrillation — 2 J/kg for the first shock, escalating to 4 J/kg for subsequent shocks (up to a maximum of 10 J/kg or the adult dose, whichever is lower)
• Immediately resume high-quality CPR after each shock (no pause to reassess rhythm/pulse post-shock), continuing 2 minutes before next rhythm check
• Epinephrine as above; for refractory shockable rhythms (persisting after 2nd–3rd shock), consider Amiodarone (5 mg/kg IV/IO bolus) or Lidocaine (1 mg/kg IV/IO)
• Continue the cycle of shock–CPR–rhythm check

Airway Management During Arrest

Bag-mask ventilation with 100% oxygen is the initial approach; advanced airway (supraglottic device or ETT) pursued when feasible without significantly interrupting compressions. Waveform capnography, once an advanced airway is placed, confirms tube placement and serves as a real-time indicator of CPR quality/effectiveness and, during sustained resuscitation, a prognostic clue (though used as one component of overall judgment).

Intraosseous Access — A Reinforced, Current-Guideline Priority

IO access is explicitly recommended as an acceptable, and in many circumstances preferred, alternative to IV when IV cannot be rapidly established — virtually all resuscitation medications and fluids can be safely and effectively administered via IO.

Post-Cardiac Arrest Care

• Avoid both hyperoxia and hypoxia — titrate FiO₂ to target normal saturation
• Avoid hyperventilation — target normocapnia
• Hemodynamic optimization — vasoactive support as needed given post-arrest myocardial dysfunction/vasoplegia
• Targeted temperature management — either strict normothermia (36–37.5°C) or therapeutic hypothermia (32–34°C) for comatose children post-ROSC, per THAPCA trial evidence showing no significant neurological outcome difference between the two — aggressive avoidance of fever is the one universally agreed non-negotiable component
• Glucose monitoring and control, avoiding hypoglycemia and significant hyperglycemia
• Seizure monitoring (continuous EEG where feasible) and prompt treatment
• Neuroprognostication approached cautiously, generally deferred beyond the immediate post-arrest period, incorporating multiple modalities rather than any single early data point

Neurotoxic vs Vasculotoxic (Hemotoxic) Envenomation

Neurotoxic (classically elapids — cobra, krait): progressive descending flaccid paralysis — early ptosis and ophthalmoplegia, progressing to bulbar palsy (dysphagia, dysarthria), neck muscle weakness, and ultimately respiratory muscle paralysis, the primary life-threatening concern. Krait bites are notable for being relatively painless with minimal local signs (potentially delaying recognition) and a characteristic nocturnal bite pattern with symptom onset sometimes delayed by several hours.

Vasculotoxic (Hemotoxic) (classically viperids — Russell's viper, saw-scaled viper): local tissue effects (pain, swelling, blistering, necrosis) and systemic coagulopathy (spontaneous bleeding — gum bleeding, hematuria, hematemesis), progressing to DIC, acute kidney injury (particularly characteristic of Russell's viper), and severe cases hypotension/shock.

Clinical Grading

Severity grading (mild/moderate/severe) based on extent of local swelling, systemic signs, and laboratory parameters, most notably the 20-minute whole blood clotting test (20WBCT) — a bedside test placing a blood sample in a clean, dry glass tube and observing clot formation at 20 minutes; failure to clot indicates significant coagulopathy and is used in resource-limited settings as a practical indication for ASV.

Anti-Snake Venom (ASV) — Dosage and Administration Protocol

• Polyvalent ASV (covering the “big four” — cobra, common krait, Russell's viper, saw-scaled viper) is standard across most of India
• Indications: systemic envenomation signs (neurotoxic or hemotoxic) or a significantly abnormal 20WBCT — not indicated for purely local swelling/pain
• Dosing: standard initial dose (commonly cited 8–10 vials, varies by protocol/product) as a slow IV infusion, diluted in normal saline, over ~1 hour with close monitoring
• Dose is NOT weight-based in children — the same dose regardless of body weight, since ASV neutralizes a defined quantity of injected venom, independent of victim size
• Repeat dosing guided by clinical/laboratory response — persistent coagulopathy or progressive neurotoxicity at a defined reassessment interval (commonly 6 hours for coagulopathy, sooner for progressive neurotoxicity)

Management of Reactions to ASV

Given ASV is derived from equine serum, hypersensitivity reactions are relatively common (mild urticaria to severe anaphylactoid reactions). Pre-medication with antihistamines (± hydrocortisone) is practiced in some protocols, though current WHO guidance does not strongly endorse routine premedication. Slow infusion with close monitoring, particularly the first 10–20 minutes; if a significant reaction develops, immediate cessation and IM epinephrine (as first-line, exactly as for any anaphylaxis), followed by antihistamines/corticosteroids, with ASV cautiously restarted at a slower rate once controlled.

Supportive Care

Neurotoxic: vigilant respiratory monitoring with prompt intubation/ventilation for evolving respiratory failure; a trial of IV neostigmine with atropine may be used as an adjunct, particularly for cobra envenomation (post-synaptic blockade) in contrast to krait (predominantly pre-synaptic, generally less neostigmine-responsive).

Vasculotoxic: management of coagulopathy (ASV primary; blood product support — FFP, cryoprecipitate — adjunctive only after adequate ASV), AKI monitoring/management, and wound/local tissue care (surgical debridement for confirmed necrotic tissue; fasciotomy only for confirmed, measured compartment syndrome, since snakebite swelling frequently mimics but does not represent true compartment syndrome).

Pathophysiology — The Autonomic Storm

Scorpion venom (particularly the red scorpion, Mesobuthus tamulus, in India) contains neurotoxins causing massive, sustained catecholamine release from the adrenal medulla and sympathetic nerve terminals — an initial brief sympathetic-predominant phase (hypertension, tachycardia, sweating) is typically followed within hours by a more prolonged, dangerous phase in which the catecholamine surge itself produces acute myocardial dysfunction/toxic myocarditis, peripheral vasoconstriction followed by vasodilation, and acute pulmonary edema. The pulmonary edema reflects a combination of acute LV dysfunction (catecholamine-induced myocardial injury/stunning) and increased pulmonary capillary permeability, not a purely cardiogenic (volume overload) process.

Clinical Features

Local pain/swelling at the sting site typically prominent early. Systemic manifestations: initially hypertension, tachycardia, sweating, agitation; progressing in significant envenomation to cool extremities, hypotension, tachypnea, and, in the most severe cases, frank acute pulmonary edema with respiratory distress, cough, and pink frothy sputum.

Management

Prazosin — the specific, pathophysiologically-targeted first-line pharmacotherapy: a selective alpha-1 antagonist directly countering the vasoconstrictive/hypertensive component, shown to reduce incidence/severity of pulmonary edema and improve survival. Given orally (via NG tube if unable to swallow), with dosing repeated at defined intervals based on clinical response (resolution of cold extremities/sweating being a practical marker) — a genuinely specific, evidence-based antidotal therapy rather than merely supportive care.

• Dobutamine — preferred inotropic agent where cardiovascular support is required, given combined inotropic support with relatively less vasoconstrictive effect, complementing prazosin's vasodilatory action (avoiding agents with predominant alpha-agonist activity that would counteract prazosin)
• Careful, judicious fluid management — given the mixed cardiogenic/permeability nature of the edema, avoiding overload while ensuring adequate preload
• Oxygen supplementation and respiratory support, escalating to non-invasive/invasive ventilation as needed
• Anti-Scorpion Venom (ASV), where available, may be used as an adjunct, though its role/evidence base is less robust than prazosin
• Continuous cardiac monitoring given arrhythmia and ongoing myocardial dysfunction risk throughout the autonomic storm period

Primary and Secondary Survey in Pediatric Polytrauma

The assessment follows the same fundamental ABCDE sequence used in adult trauma, with pediatric-specific modifications: Airway (with cervical spine protection, accounting for pediatric airway anatomical differences), Breathing, Circulation (children maintain BP via compensatory vasoconstriction until very late — normotension does not exclude significant blood loss/shock), Disability (pediatric-modified GCS, pupillary response), and Exposure (attention to preventing hypothermia, given greater surface-area-to-body-mass ratio). The secondary survey — comprehensive head-to-toe examination and focused history (AMPLE framework) — searches for injuries not identified during the primary survey.

PECARN Criteria for Head CT in Pediatric Head Injury

A well-validated, widely-applied tool identifying children at very low risk of clinically important TBI who can safely avoid CT (and its radiation exposure), age-stratified given differences in presentation between younger and older children.

If none of the listed findings are present, the risk of clinically important TBI is very low and CT can generally be safely avoided. The rules explicitly incorporate an “observation versus immediate CT” intermediate risk category, allowing appropriately selected children with isolated, lower-risk findings to be safely observed clinically rather than reflexively imaged.

ICP Monitoring in Severe TBI

For children with severe TBI (GCS ≤8) and an abnormal CT (or specific additional risk factors even with normal CT, per some protocols), invasive ICP monitoring is recommended, following the principles detailed in Q29 — maintaining ICP below a defined threshold (generally <20 mmHg, age-adjusted) and ensuring adequate cerebral perfusion pressure.

Etiologies of Cardiogenic Shock in Children (by age-related pattern)

• Neonates/young infants: critical congenital heart disease presenting as ductal-dependent lesions decompensating with ductal closure, severe left-sided obstructive lesions (critical aortic stenosis, coarctation, hypoplastic left heart syndrome), and myocarditis
• Older infants/children: myocarditis (viral — Coxsackievirus, Adenovirus, Parvovirus B19), dilated cardiomyopathy (idiopathic, genetic, or post-myocarditis), arrhythmia-induced cardiomyopathy (prolonged unrecognized SVT), Kawasaki disease with coronary involvement/MI, sepsis-associated myocardial depression, and toxin/drug-induced cardiomyopathy

Inotropic Support

Dobutamine (beta-1 predominant, relatively favorable myocardial oxygen demand effects, often preferred for isolated cardiogenic shock without significant concurrent vasodilation/hypotension), Epinephrine (combined inotropic and vasopressor effects, for more severe shock with hypotension), and Dopamine (dose-dependent effects, increasingly used less as first-line).

Lusitropic Agents

Milrinone, a PDE-3 inhibitor, provides both inotropic support and lusitropic effect (improved diastolic relaxation/compliance) alongside significant vasodilation (afterload reduction) — particularly useful where elevated SVR/afterload contributes to poor forward output, though vasodilatory effect requires caution with significant hypotension.

Vasodilators

Used to reduce afterload and improve forward output where BP permits (not with significant hypotension) — sodium nitroprusside, nitroglycerin, and milrinone's inherent vasodilatory properties. Goal: reduce resistance against which the failing ventricle ejects, improving stroke volume without the same myocardial oxygen demand increase as pure inotropic augmentation.

Mechanical Circulatory Support

VA-ECMO provides both respiratory and full cardiac output support, considered for refractory cardiogenic shock, serving as a bridge to myocardial recovery (particularly fulminant myocarditis, with genuine potential for complete recovery) or a bridge to more definitive therapy (VAD placement, or cardiac transplantation for irreversible myocardial failure). Ventricular assist devices (VADs), as a bridge to transplantation and increasingly as destination therapy in select circumstances, offer advantages over ECMO for longer-duration support including improved mobility and reduced bleeding/thrombotic complications in appropriately selected patients.

Arterial Line Placement

Provides continuous, beat-to-beat blood pressure monitoring (more accurate/responsive than intermittent non-invasive cuff measurement, valuable in hemodynamically unstable patients requiring vasoactive infusion titration) and enables frequent arterial blood gas sampling without repeated venipuncture. Common sites: radial artery (most common, given accessibility and lower complication risk), femoral artery, and in neonates, the umbilical artery. Complications: distal ischemia, infection, thrombosis.

Central Venous Pressure (CVP) Monitoring

Reflects right atrial pressure, an estimate of RV preload, used to guide fluid management — with recognized limitations (influenced by venous tone, intrathoracic pressure/ventilator settings, RV compliance/function beyond volume status alone). Trend in response to a fluid challenge is generally more informative than any single absolute value. Central venous access also provides a route for vasoactive medications requiring central delivery and blood sampling.

ScvO2 (Central Venous Oxygen Saturation) Monitoring

Measures central venous blood oxygen saturation, a surrogate for the balance between systemic oxygen delivery and consumption — a low ScvO2 suggests inadequate delivery relative to demand (low cardiac output, anemia, hypoxemia), prompting interventions (fluid, inotropic support, transfusion, improved oxygenation). While historically prominent in ScvO2-targeted goal-directed sepsis resuscitation, more recent evidence has tempered the strength of this specific numerical target-driven approach in favor of broader multi-parameter assessment; ScvO2 trending remains a useful adjunctive tool.

Point-of-Care Ultrasound (POCUS) Applications

• Cardiac POCUS — rapid assessment of ventricular contractility/function, pericardial effusion, and gross volume status
• IVC assessment — diameter and respiratory variability as a non-invasive surrogate for volume status/fluid responsiveness
• Lung ultrasound — rapid bedside assessment for pneumothorax, pleural effusion, pulmonary edema/consolidation patterns
• Vascular access guidance — ultrasound-guided central/peripheral line placement, now standard practice given improved first-pass success and reduced mechanical complications vs landmark-based techniques

Pathophysiology — Moving Beyond “Dry” vs “Wet” Drowning Terminology

Historically classified into “wet drowning” (aspiration of water, more common) and “dry drowning” (laryngospasm preventing aspiration) — contemporary consensus terminology (2002 World Congress on Drowning, widely adopted) has largely abandoned this distinction as clinically unhelpful and likely based on overestimated understanding of true “dry” drowning frequency. Current terminology defines drowning simply as “the process of experiencing respiratory impairment from submersion/immersion in liquid,” with outcomes classified as death, morbidity, or no morbidity. Regardless of terminology, the fundamental endpoint is hypoxemia — from aspirated fluid causing surfactant washout/dysfunction and pulmonary edema, or laryngospasm-mediated airway obstruction — both converging on tissue hypoxia, particularly hypoxic-ischemic brain injury.

Hypothermia

Drowning frequently occurs in cold water. Hypothermia has dual significance: it is itself a serious insult requiring active rewarming and careful management (arrhythmia, coagulopathy risk), but hypothermia occurring rapidly before significant hypoxic injury accumulates may confer some neuroprotection by reducing cerebral metabolic demand — the physiological basis for remarkable neurological recovery in some cold-water drowning victims despite prolonged submersion. This underlies the clinical teaching that resuscitation efforts should generally be continued longer, and prognosis approached with greater caution/optimism, in cold-water drowning compared to warm-water drowning with comparable submersion duration.

Neurological Protection Strategies

Overlaps substantially with general post-cardiac arrest/hypoxic-ischemic brain injury care (see Q31): avoiding hyperthermia (fever actively treated, though deliberately inducing therapeutic hypothermia beyond simply avoiding fever lacks strong drowning-specific evidence), maintaining adequate oxygenation and normocapnia, adequate cerebral perfusion pressure (avoiding hypotension), glucose control, and seizure monitoring/management.

Pulmonary Management

Aspiration causes surfactant dysfunction/washout and alveolar-capillary membrane disruption, producing an ARDS-like picture requiring lung-protective ventilation strategies (see Q24) where mechanical ventilation is required, along with supplemental oxygen or non-invasive support in less severe cases. Empirical antibiotics are not routinely recommended unless specific evidence of infection or aspiration of grossly contaminated water. Bronchospasm, where present, is managed with standard bronchodilator therapy.

Assessment Scales

RASS (Richmond Agitation-Sedation Scale), adapted for pediatric use, targets and titrates sedation to a specific, individualized goal rather than empirical/excessive sedation — reflecting the principle that excessive, untargeted sedation is independently associated with worse outcomes (prolonged ventilation, increased delirium risk, longer stay). The COMFORT Scale (and COMFORT-B variant, omitting BP/HR parameters where less reliable, e.g. with vasoactive infusions) is a validated pediatric-specific behavioral scale (alertness, calmness, respiratory response/crying, physical movement, muscle tone, facial tension) guiding sedation and analgesia titration, including in preverbal infants.

Pharmacology of Sedatives and Analgesics

• Opioids (fentanyl, morphine) remain mainstay for analgesia — fentanyl often preferred for hemodynamic stability and rapid onset/offset (useful around procedures); morphine's longer duration advantageous for sustained background analgesia
• Benzodiazepines (midazolam) provide sedation/anxiolysis but carry tolerance, withdrawal, and delirium risks
• Dexmedetomidine — alpha-2 agonist with sedation and relatively preserved respiratory drive, more favorable delirium profile than benzodiazepines, increasingly favored for lighter sedation targets and opioid/benzodiazepine-sparing effect
• Ketamine — combined analgesia and dissociative sedation with relative hemodynamic stability, useful for procedural sedation and hemodynamically unstable patients (sympathomimetic properties supporting BP)

Withdrawal Syndrome

Prolonged (typically >several days) continuous infusion of opioids/benzodiazepines predisposes to iatrogenic physical dependence — abrupt discontinuation or rapid dose reduction precipitates withdrawal: autonomic instability (tachycardia, hypertension, sweating, fever), GI symptoms (vomiting, diarrhea), neurological symptoms (irritability, tremor, seizures in severe cases). Validated scoring tools (e.g., WAT-1) systematically assess withdrawal, guiding structured, gradual weaning (not abrupt cessation) as the primary evidence-based prevention strategy for any child who has received more than a few days of continuous infusion.

Delirium

ICU delirium — an acute, fluctuating disturbance of attention/awareness — is increasingly recognized as common in critically ill children and independently associated with worse outcomes (prolonged ICU stay, increased mortality in some studies, longer-term neurocognitive impact). Risk factors: benzodiazepine exposure, mechanical ventilation, immobilization, sleep disruption. Validated screening tools (e.g., Cornell Assessment of Pediatric Delirium, CAPD) are increasingly used routinely. Prevention/management: minimizing benzodiazepine use (favoring dexmedetomidine or alternatives), early mobilization, maintaining day-night cycling, family presence/involvement, and prompt treatment of reversible contributing causes.

Parkland Formula

The traditional formula for fluid resuscitation in burns of significant size (generally >10–15% TBSA): 4 mL × body weight (kg) × %TBSA burned, with half given over the first 8 hours from the time of burn injury (not from presentation) and the remaining half over the subsequent 16 hours, using a balanced crystalloid (Ringer's lactate traditionally preferred). This provides an initial estimate only, with ongoing administration titrated based on clinical response, particularly urine output (targeting ~0.5–1 mL/kg/hour in children; some pediatric-specific protocols target 1–2 mL/kg/hour, particularly in younger children).

Galveston Formula — A Pediatric-Specific Adaptation

Recognizing children have proportionally greater maintenance fluid requirements relative to body surface area than adults, this formula calculates total 24-hour fluid requirement based on TBSA rather than weight alone, combining burn resuscitation and maintenance needs: 5000 mL/m² burned TBSA + 2000 mL/m² total TBSA, again half over the first 8 hours and half over the subsequent 16 hours — better accounting for the disproportionately higher fluid requirements of smaller children.

Wound Care

Initial cooling of the burn wound (clean, cool — not ice-cold, given hypothermia risk in extensive burns — water or saline, limited duration), followed by cleaning/debridement of clearly non-viable tissue, and appropriate wound dressing selection (simple non-adherent dressings for superficial burns to specialized dressings/topical antimicrobials such as silver sulfadiazine for deeper/more extensive burns), with early surgical referral for excision and grafting of full-thickness/deep partial-thickness burns.

Airway Involvement

Suspected with enclosed-space burns, facial burns, singed nasal/facial hair, carbonaceous sputum, or hoarseness/stridor — any should prompt a low threshold for early, elective, controlled intubation, given that progressive airway edema over subsequent hours can convert a manageable airway into a difficult/impossible one; early controlled securing is far preferable to a delayed emergency attempt.

Nutritional Support

Burns produce a profound hypermetabolic, hypercatabolic state with significantly elevated caloric/protein requirements persisting during wound healing. Early enteral nutrition (generally preferred over parenteral where the gut is functional — reduced infectious complications, better gut mucosal integrity preservation) with individualized, elevated caloric targets (using burn-specific formulas incorporating %TBSA burned) is core to comprehensive burn management, alongside ongoing wound care, infection surveillance, and pain management.