Emergency and Critical Care

Common pediatric ingestions: acetaminophen, iron, caustics, button batteries

Clinical Overview and When to Suspect

Pediatric poisoning accounts for >1 million calls to US poison control centers annually; most involve children <6 years old with exploratory ingestions.

→ Acetaminophen (APAP) — most common cause of acute liver failure in children

→ Iron — direct GI mucosal injury + systemic cellular toxicity

→ Caustics (acids & alkalis) — tissue destruction on contact

→ Button batteries — electrochemical burn within 2 hours of lodging in esophagus

Four ingestions carry uniquely high morbidity and demand rapid, specific management:

Board pearl: A well-appearing child after ingestion does NOT mean the ingestion is benign — APAP and iron both have deceptive 'latent' periods where the child looks well before catastrophic deterioration

Suspect toxic ingestion in any toddler with unexplained vomiting, altered mental status, metabolic acidosis, or hepatic dysfunction

Pediatric Assessment Triangle: appearance may be normal early; abnormal circulation to skin (pallor, diaphoresis) suggests systemic toxicity or hemorrhagic GI injury

History — Rapid Focused Assessment

→ WHAT was ingested? (exact product, concentration, formulation — sustained-release vs immediate-release)

→ HOW MUCH? (worst-case estimate: # pills missing from bottle, volume of liquid)

→ WHEN? (time since ingestion drives management decisions for APAP nomogram, iron levels)

→ Any CO-INGESTANTS? (combination products, e.g., APAP + diphenhydramine)

→ Was the ingestion INTENTIONAL? (adolescent self-harm → psychiatric evaluation mandatory)

Five critical questions for ANY ingestion:

APAP-specific: ask about extended-release formulations, repeated supratherapeutic dosing (chronic ingestion)

Iron-specific: identify product (prenatal vitamins contain 60–65 mg elemental iron/tablet vs children's vitamins with 10–18 mg)

Caustics: identify pH, concentration, liquid vs solid (liquid → oropharynx + esophagus; solid granules → mouth + proximal esophagus)

Button battery: size, type (lithium > other), time of ingestion

Clinical tip: Call Poison Control (1-800-222-1222) for every ingestion — they provide real-time, substance-specific guidance

Physical Exam — Key Findings by Ingestion

→ Phase 1 (0–6 hrs): vomiting, diarrhea, hematemesis, abdominal pain (direct GI corrosive injury)

→ Phase 2 (6–24 hrs): deceptive clinical improvement — "latent period"

→ Phase 3 (12–48 hrs): shock, metabolic acidosis, hepatic failure, coagulopathy

→ Phase 4 (days–weeks): GI scarring/strictures

APAP: early exam is often NORMAL; RUQ tenderness develops 24–72 hrs post-ingestion as hepatotoxicity evolves; jaundice and altered mental status are late signs

Iron:

Caustics: inspect lips, oral mucosa, oropharynx for burns, edema, drooling; stridor suggests laryngeal involvement; chest/abdominal pain may indicate perforation

Board pearl: Absence of oral burns does NOT exclude esophageal injury — up to 30% of children with significant esophageal burns have no visible oral lesions

Button battery: may be asymptomatic initially; drooling, dysphagia, chest pain, or refusal to eat suggest esophageal lodgment; wheezing/stridor if compressing airway

Diagnostic Workup — Acetaminophen

→ The nomogram applies ONLY to acute, single-time ingestions

→ Treatment line starts at 150 µg/mL at 4 hrs (some use lower 100 µg/mL line for added safety)

Serum APAP level drawn ≥4 hours post-ingestion — plot on Rumack-Matthew nomogram

Board pearl: If the time of ingestion is unknown, draw the level immediately — if detectable and transaminases elevated, treat with NAC

Additional labs: hepatic panel (AST, ALT), INR/PT, BMP (glucose, creatinine, electrolytes), lipase

AST/ALT are the most sensitive markers of hepatotoxicity; may lag 24–48 hrs

In chronic/repeated supratherapeutic dosing (common in children given multiple APAP-containing products): nomogram does NOT apply → treat based on elevated APAP level or rising transaminases

Clinical tip: Always check APAP level in any adolescent presenting with intentional ingestion or altered mental status, regardless of reported substance — APAP is a common co-ingestant

Diagnostic Workup — Iron, Caustics, Button Batteries

→ Serum iron level at 4–6 hrs post-ingestion; >500 µg/dL = severe toxicity

→ TIBC is unreliable in acute overdose — do NOT use to guide treatment

→ Anion-gap metabolic acidosis (AGMA), ↑ lactate, ↑ WBC >15k, glucose >150 correlate with severe poisoning

→ Abdominal X-ray: iron tablets are radiopaque — visualize pill burden, confirm GI decontamination

→ Labs: CBC, BMP, blood gas if perforation suspected

→ CXR/AXR if concern for perforation (free air)

→ Endoscopy (EGD) within 12–24 hrs is the gold standard for grading esophageal/gastric injury; should NOT be delayed beyond 24 hrs (↑ perforation risk)

→ AP + lateral chest/abdominal X-ray STAT to locate battery

→ Battery lodged in esophagus = EMERGENCY → removal within 2 hours

→ Board pearl: On AP X-ray, button battery shows "double-density" or "halo" sign (step-off at battery edges); distinguish from coin which has uniform density

IRON:

CAUSTICS:

BUTTON BATTERY:

Management — Acetaminophen: NAC Protocol

→ Charcoal adsorbs APAP effectively; most beneficial within first hour

→ Replenishes hepatic glutathione stores, detoxifying the toxic metabolite NAPQI

→ MOST effective if started within 8 hrs of ingestion; still beneficial up to 24+ hrs

→ IV protocol (preferred in pediatrics): 150 mg/kg over 1 hr → 50 mg/kg over 4 hrs → 100 mg/kg over 16 hrs (total 21-hr protocol)

→ Oral protocol: 140 mg/kg loading → 70 mg/kg q4h × 17 additional doses (72-hr protocol)

GI decontamination: activated charcoal (1 g/kg, max 50 g) if within 1–2 hrs of ingestion AND patient is alert with protected airway

N-Acetylcysteine (NAC) — the definitive antidote:

Board pearl: Anaphylactoid reactions (flushing, urticaria, bronchospasm) can occur with IV NAC — slow the infusion rate, give antihistamines; this is NOT a true allergy and is NOT a contraindication to continuing NAC

Continue NAC until APAP level undetectable, transaminases trending down, and INR normalizing

Management — Iron Poisoning

→ <20 mg/kg: minimal toxicity expected

→ 20–60 mg/kg: moderate risk → observe, obtain levels

→ >60 mg/kg: severe toxicity likely → aggressive treatment

→ Activated charcoal does NOT bind iron — do NOT give

→ Whole bowel irrigation (WBI) with polyethylene glycol solution if large ingestion or tablets visible on X-ray

→ Indication: serum iron >500 µg/dL, significant symptoms (persistent vomiting, AGMA, shock, AMS), or ≥5 tablets on X-ray

→ Dose: 15 mg/kg/hr IV continuous infusion (max 6–8 g/day)

→ Monitor urine for "vin rosé" (pinkish-orange) color change indicating iron-deferoxamine complex excretion

→ Continue until symptoms resolve, AGMA corrects, and urine color normalizes

Risk stratification by dose of ELEMENTAL iron ingested:

GI decontamination:

Deferoxamine — the specific chelator:

Board pearl: Deferoxamine may cause hypotension with rapid infusion; pulmonary toxicity (ARDS) with prolonged use >24 hrs

Supportive care: aggressive IV fluid resuscitation for hemorrhagic shock

Management — Caustics and Button Batteries

→ Do NOT induce emesis (re-exposure of tissue to caustic agent)

→ Do NOT give activated charcoal (ineffective, obscures endoscopy view)

→ Do NOT attempt "neutralization" (exothermic reaction worsens injury)

→ Dilution with small sips of water/milk is controversial; acceptable only if no perforation or airway compromise

→ Priority: airway assessment → if stridor/edema → early intubation

→ EGD within 12–24 hrs to grade injury (Grade I = superficial; Grade IIa = non-circumferential ulcers; Grade IIb/III = circumferential/transmural → highest stricture risk)

→ Steroids are NOT routinely recommended for caustic ingestions

→ Esophageal battery: EMERGENT endoscopic removal (within 2 hrs)

→ Pre-removal: if ≥12 mm battery in esophagus and delay to removal anticipated → irrigate with honey (10 mL q10 min, age ≥12 months) to neutralize alkaline discharge

→ Board pearl: Honey is the first-line temporizing measure for esophageal button battery in children ≥1 yr — reduces tissue injury before endoscopic removal

→ Battery past esophagus (in stomach/intestine) in asymptomatic child: observe with serial X-rays; most pass spontaneously

CAUSTICS:

BUTTON BATTERY:

Age-Specific Considerations — Neonates and Infants

→ APAP: neonatal liver has immature CYP2E1 → less NAPQI production → relatively more resistant to hepatotoxicity, BUT treatment threshold remains the same

→ Button battery ingestion peaks: age 6 months–3 years (oral exploratory phase)

→ Lithium 20-mm coin cells are the most dangerous — fit in esophagus of children <5 yrs

→ Iron: infant multivitamin drops rarely cause severe toxicity due to low elemental iron content

→ Caustic ingestions: household cleaners stored in lower cabinets — classic scenario

Neonates: toxic ingestions are rare; exposure occurs via breast milk (maternal medications), medication errors (10× dosing errors common), or iatrogenic IV/oral overdoses in NICU

Infants (1–12 months):

Board pearl: The most dangerous APAP formulations for small children are adult extra-strength (500 mg) tablets and concentrated "infant drops" (now discontinued but occasionally found in homes)

Weight-based dosing errors are the leading cause of iatrogenic APAP toxicity in infants

Age-Specific Considerations — Children and Adolescents

→ "Taste and spit" vs true ingestion — assess quantity carefully

→ Iron from prenatal vitamins left within reach is a classic board scenario

→ Button batteries in toys, remotes, hearing aids

→ APAP is the #1 drug used in pediatric suicide attempts

→ Often involves large quantity, delayed presentation, possible co-ingestants

→ Board pearl: Every adolescent with intentional ingestion needs psychiatric evaluation and safety planning before discharge — even if medically cleared

→ Chronic/repeated supratherapeutic APAP dosing ("stacking" doses for pain) → presents with hepatotoxicity without a single massive ingestion → nomogram does NOT apply

Toddlers (1–5 yrs): exploratory ingestions — usually small quantities, single substance

School-age (6–12 yrs): ingestions less common; consider medication errors, environmental exposure

Adolescents: INTENTIONAL ingestions (self-harm, suicide attempts)

Caustic ingestions in adolescents: consider intentional ingestion — severity tends to be worse due to larger volume consumed

Complications — Acetaminophen and Iron

→ Fulminant hepatic failure (peak AST/ALT >10,000 IU/L possible)

→ Coagulopathy (↑ INR is the most sensitive prognostic marker)

→ Hypoglycemia (liver unable to maintain gluconeogenesis)

→ Hepatic encephalopathy → cerebral edema → death

→ Renal tubular injury (direct NAPQI toxicity, hepatorenal syndrome)

→ Referral for liver transplant evaluation if: persistent AGMA, INR >6.5, creatinine >3.4, or Grade III/IV encephalopathy (King's College criteria logic)

→ Hemorrhagic gastritis and GI necrosis (Phase 1)

→ Cardiovascular collapse, lactic acidosis (Phase 3)

→ Hepatic failure with coagulopathy

→ Late GI strictures and pyloric stenosis (Phase 4 — weeks later)

APAP COMPLICATIONS:

IRON COMPLICATIONS:

Board pearl: Serum iron level alone does not determine severity — clinical picture (acidosis, shock, AMS) is more important; a child in Phase 2 ("feels better") may deteriorate rapidly

Complications — Caustics and Button Batteries: When to Escalate

→ Esophageal perforation → mediastinitis → sepsis, death

→ Gastric perforation → peritonitis

→ Esophageal strictures (Grade IIb–III burns) → develop over weeks–months → require serial dilation

→ ↑ Risk of esophageal squamous cell carcinoma decades later (lifelong surveillance)

→ Airway compromise: laryngeal edema, epiglottic swelling → emergent intubation or surgical airway

→ Esophageal burns begin within 15 minutes; full-thickness necrosis by 2 hours

→ Mechanism: hydroxide ion generation at negative pole creates alkaline tissue injury (liquefactive necrosis)

→ Tracheoesophageal fistula, esophageal perforation, mediastinitis

→ Aortoesophageal fistula → massive hemorrhage → death (most feared complication)

→ Board pearl: Delayed hemorrhage from aortoesophageal fistula can occur days to weeks after battery removal — parents must be counseled about warning signs (hematemesis, melena)

CAUSTIC COMPLICATIONS:

BUTTON BATTERY COMPLICATIONS:

Escalate to PICU: hemodynamic instability, airway compromise, suspected perforation, need for emergent endoscopy

Key Differentials — Distinguishing Toxic Ingestions from Mimics

→ Ingestion clue: abrupt onset, no diarrhea (initially), no sick contacts

→ AGMA + vomiting: consider APAP (late), iron, ethylene glycol, methanol, salicylates

→ APAP toxicity (most common), Wilson disease, autoimmune hepatitis, viral hepatitis (A, B, EBV), Reye syndrome (aspirin + viral illness)

→ Board pearl: APAP level should be checked in ALL children presenting with unexplained liver failure

→ X-ray differentiates: battery has halo/step-off; coin is uniform; food is radiolucent

Unexplained vomiting in toddler: ingestion vs gastroenteritis vs intussusception vs DKA

Acute hepatic failure differential:

Hematemesis in a toddler: iron ingestion vs Mallory-Weiss tear vs peptic ulcer vs foreign body

Drooling + dysphagia: button battery vs coin vs food bolus impaction vs caustic ingestion vs peritonsillar abscess

Stridor after ingestion: caustic laryngeal burn vs anaphylaxis vs foreign body aspiration

Key Differentials — Iron vs Other Causes of Anion-Gap Metabolic Acidosis

→ Consider: methanol, uremia, DKA, iron/isoniazid, lactic acidosis, ethylene glycol, salicylates, inborn errors of metabolism

→ Direct mitochondrial toxicity → ↑ lactate

→ Hepatic failure → ↓ lactate clearance

→ Ferric iron (Fe³⁺) releases H⁺ when converted from ferrous (Fe²⁺)

→ Iron: history of ingestion, radiopaque pills on X-ray, elevated serum iron, GI hemorrhage

→ Sepsis: fever, leukocytosis with left shift, positive cultures, identifiable source

Classic mnemonic concept for AGMA in pediatrics (without using copyrighted acronyms):

Iron causes AGMA via multiple mechanisms:

Key distinction: Iron poisoning vs sepsis: both cause AGMA + shock + coagulopathy

Salicylate toxicity can mimic iron: vomiting, AGMA, tachypnea — but salicylates cause primary respiratory alkalosis BEFORE metabolic acidosis (mixed picture), tinnitus

Clinical tip: When in doubt, check levels for APAP, salicylates, iron, ethanol, and a blood gas in any pediatric ingestion with systemic symptoms

Preventive Care and Anticipatory Guidance

→ Store all medications in original child-resistant containers, up and away from children

→ Never call medicine "candy"

→ Keep Poison Control number visible: 1-800-222-1222

→ Install child safety locks on cabinets with cleaning products/caustics

→ Educate on weight-based dosing (10–15 mg/kg/dose q4–6h, max 5 doses/day)

→ Warn about multiple APAP-containing products (combination cold remedies → accidental double-dosing)

→ Maximum daily dose: 75 mg/kg/day or 4 g/day (whichever is less)

→ Secure battery compartments in devices (tape shut if no screw closure)

→ Immediately dispose of dead batteries (still cause burns)

→ Keep loose batteries out of reach

Poisoning prevention is a CORE anticipatory guidance topic at every well-child visit from 6 months onward:

Iron-specific: prenatal vitamins are the most dangerous source — counsel parents to store safely

APAP-specific:

Button battery-specific:

Board pearl: Anticipatory guidance about poisoning prevention should begin at the 6-month visit as infants develop pincer grasp and oral exploration

Screening, Follow-Up, and Disposition Decisions

→ Esophageal → emergent removal → post-removal monitoring for delayed complications (minimum 24 hrs observation)

→ Gastric → if ≥20 mm and child <5 yrs, endoscopic removal if not passed in 48 hrs

→ If passed beyond duodenum → outpatient follow-up with serial X-rays

APAP: if nomogram indicates treatment → admit for full NAC course; recheck AST/ALT, INR, APAP level at end of treatment; discharge when transaminases trending down and APAP undetectable

Iron: observe 6 hrs if asymptomatic + low-risk dose (<20 mg/kg); admit if symptomatic, serum iron >350 µg/dL, or pills visible on X-ray; recheck iron level to ensure decline

Caustics: all symptomatic ingestions → admit for EGD; Grade I → discharge with follow-up; Grade II–III → admission, NPO, serial assessments, GI/surgery follow-up for stricture monitoring

Button battery:

Clinical tip: All intentional ingestions require psychiatric evaluation and 1:1 safety monitoring regardless of medical severity

Poison Control follow-up call at 24–48 hrs for any ingestion managed at home

Family Counseling and Psychosocial Considerations

→ Reassure parents — exploratory ingestions are developmentally normal in toddlers

→ Avoid blame; focus on concrete prevention steps going forward

→ Reinforce safe storage, childproofing, Poison Control number

→ Assess family dynamics, mental health history, prior attempts, bullying, substance use

→ Mandatory psychiatric consultation before discharge; safety plan with lethal means restriction

→ Secure all medications in the home — including APAP, iron supplements, cleaning agents

→ Board pearl: Access to lethal means is a modifiable risk factor for completed suicide — counseling on safe medication storage is a life-saving intervention

→ Prepare for possible serial dilations, long-term GI follow-up

→ Discuss signs of delayed bleeding (hematemesis, melena) after battery removal

After accidental ingestion:

After intentional ingestion (adolescent):

Button battery/caustic families:

Address parental guilt and anxiety; connect with social work if recurrent ingestions raise concern for neglect or inadequate supervision

High-Yield Associations and Rapid-Fire Board Facts

APAP toxic metabolite = NAPQI (via CYP2E1) → depletes glutathione → hepatocellular necrosis

NAC = glutathione precursor; most effective within 8 hrs

Iron: activated charcoal is USELESS; deferoxamine is the chelator; "vin rosé" urine confirms chelation

Caustics: alkali → liquefactive necrosis (deeper, worse); acid → coagulative necrosis (surface eschar limits depth)

Board pearl: Alkali ingestion is generally MORE dangerous than acid — liquefactive necrosis penetrates deeper into tissue

Button battery: negative pole faces esophageal wall → generates hydroxide ions → alkaline burn (liquefactive necrosis, same mechanism as caustic alkali)

Honey (age ≥1 yr) is the pre-hospital temporizing agent for esophageal button battery

APAP is the most common cause of acute liver failure in US children and adolescents

King's College criteria logic for transplant: progressive coagulopathy (INR), acidosis, renal failure, encephalopathy

Iron tablets are RADIOPAQUE; APAP is radiolucent

Syrup of ipecac: NO longer recommended for ANY ingestion

Gastric lavage: rarely indicated; only within 1 hr of life-threatening ingestion with protected airway

One-Line Recap

Common pediatric ingestions are managed by substance-specific protocols: acetaminophen → APAP level on Rumack-Matthew nomogram → NAC within 8 hrs; iron → serum iron level + abdominal X-ray → deferoxamine for severe toxicity (charcoal is useless); caustics → no emesis/no charcoal/no neutralization → EGD within 12–24 hrs to grade injury; button batteries → AP/lateral X-ray to locate → emergent endoscopic removal if esophageal (honey as temporizing agent ≥1 yr) — with the unifying principle that early identification, substance-specific antidotes/interventions, avoidance of harmful decontamination (ipecac, charcoal for iron/caustics), and age-appropriate prevention counseling are the keys to reducing morbidity and mortality.

Board Question Stem Patterns

2-yr-old found with open bottle of grandmother's prenatal vitamins, vomiting blood → next step → abdominal X-ray (radiopaque tablets) + serum iron level → if >500 µg/dL or symptomatic → deferoxamine

Adolescent brought in 6 hrs after intentional APAP ingestion, feels fine → next step → draw APAP level, plot on nomogram at 6-hr mark → start NAC if above treatment line

3-yr-old with drooling, refuses to eat; X-ray shows round object in esophagus with "double ring" sign → button battery → emergent endoscopic removal

18-month-old drank liquid drain cleaner, oral burns, drooling → next step → airway assessment, NPO, EGD within 12–24 hrs; do NOT induce vomiting or give charcoal

Toddler with unexplained liver failure, ↑ AST/ALT, ↑ INR → check serum APAP level → if elevated → start NAC immediately

Child ingested iron 2 hrs ago, asymptomatic, amount estimated <20 mg/kg elemental iron → observe 6 hrs → discharge if remains well

Board pearl: If a question says "activated charcoal" for iron or caustic ingestion → that is the WRONG answer

Adolescent medically cleared after APAP overdose → next step before discharge → psychiatric evaluation

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