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Iron, Caustic, Hydrocarbon & Button-Battery Ingestions

Name: Iron, Caustic, Hydrocarbon & Button-Battery Ingestions
Creator: Veli Bakalov, MD

Four ingestions where routine decontamination does harm

Emergency & Critical Care·Toxicology·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Iron poisoning stages: GI vomiting and hematemesis (0–6 h) → deceptive latent phase → shock with anion-gap acidosis → hepatic necrosis → gastric outlet stricture weeks later.
Iron toxicity is dosed by elemental iron (>60 mg/kg serious); X-ray shows radiopaque pills and serum iron is drawn at 4–6 h.
Activated charcoal does not bind iron: use whole-bowel irrigation and IV deferoxamine for systemic toxicity (vin rosé urine, hypotension if fast, Yersinia sepsis).
Alkali causes deep liquefactive esophageal necrosis; acid causes coagulative necrosis that mainly injures the stomach.
Caustic ingestion: no emesis, neutralization, charcoal, or blind NG tube; secure the airway if stridor or drooling, then endoscopy within 12–24 h even without oral burns.
Caustic survivors develop esophageal strictures and, decades later, squamous cell carcinoma.
Hydrocarbon ingestion is a lung injury (aspiration pneumonitis): no emesis or lavage, observe 6 h with a chest X-ray.
Huffed halogenated solvents sensitize the heart to catecholamines (sudden sniffing death); treat ventricular arrhythmias with a β-blocker.
Esophageal button battery (double-ring sign) needs emergent endoscopic removal, with honey or sucralfate en route if over 1 year; multiple magnets need surgical or GI consultation.

Iron poisoning

Why it matters. Iron tablets and prenatal vitamins are within reach in many homes, and iron was historically a leading cause of fatal poisoning in toddlers. Toxicity depends on the elemental iron swallowed: ferrous sulfate is 20% elemental iron. Less than 20 mg/kg rarely causes more than mild GI upset, whereas more than 60 mg/kg risks severe systemic toxicity.

Mechanism. Iron corrodes the gastric and intestinal mucosa directly. Once transferrin is saturated, free iron disrupts mitochondrial oxidative phosphorylation, producing lactic acidosis and shock, and portal delivery concentrates it in the liver.

GI stage (0–6 h)Vomiting, diarrhea, abdominal pain, hematemesis, and bloody stools.
Latent stage (6–24 h)Symptoms seem to resolve while cellular injury continues; a deceptive calm.
Shock stage (6–72 h)Hypovolemic and cardiogenic shock, anion-gap metabolic acidosis, coagulopathy.
Hepatic stage (12–96 h)Hepatocellular necrosis and liver failure.
Stricture stage (2–8 weeks)Scarring causes gastric outlet or bowel obstruction.

Clinical stages of iron poisoning

Diagnosis. An abdominal X-ray shows radiopaque tablets, but chewable and liquid preparations may not appear, so a negative film does not exclude ingestion. Serum iron peaks 4–6 hours after ingestion; a level above 500 μg/dL signals serious toxicity. Total iron-binding capacity is not useful. An anion-gap metabolic acidosis marks systemic poisoning.

Treatment. Give IV fluids for GI losses. Activated charcoal does not bind iron (nor lithium, other metals, alcohols, caustics, or hydrocarbons), so decontaminate with whole-bowel irrigation using polyethylene glycol when pills are visible; induced emesis and routine lavage add risk. Give IV deferoxamine for systemic toxicity: shock, metabolic acidosis, altered mental status, serum iron above 500 μg/dL, or many pills on X-ray. Deferoxamine binds free iron as ferrioxamine, which is renally excreted and can turn the urine reddish (vin rosé), though the color change is too inconsistent to guide therapy.

Deferoxamine given too fast causes hypotension, infusions beyond about 24 hours are linked to ARDS, and Yersinia enterocolitica uses ferrioxamine as a siderophore, so iron chelation predisposes to Yersinia sepsis.

Caustic ingestions

Alkali vs acid

Feature	Alkali	Acid
Sources	Drain and oven cleaners, lye	Toilet bowl cleaners, battery acid, rust removers
Necrosis	Liquefactive (saponifies fat, dissolves protein)	Coagulative (eschar limits penetration)
Depth	Deep; perforation risk	Usually shallower
Main site	Esophagus	Stomach, especially the antrum
Taste	Often tasteless, so larger volumes are swallowed	Painful, so smaller volumes
Systemic effects	Rare	Occasional metabolic acidosis

Do not induce vomiting (it re-exposes the esophagus), attempt neutralization (the reaction generates heat), give activated charcoal (it does not bind and obscures endoscopy), or pass a blind nasogastric tube (perforation).

Airway first. Stridor, drooling, or hoarseness means laryngeal and pharyngeal edema that can progress quickly; intubate early under direct or fiberoptic visualization.

Endoscopy. Drooling, dysphagia, odynophagia, stridor, vomiting, and hematemesis predict significant injury, but the absence of oral burns does not exclude esophageal damage. Symptomatic patients and intentional ingestions need upper endoscopy within 12–24 hours to grade the injury and guide feeding and monitoring. Avoid endoscopy from roughly day 5 to day 15, when the healing wall is weakest. Suspected perforation (severe chest or abdominal pain, mediastinitis, peritonitis, free air) calls for CT and surgical consultation rather than endoscopy.

Late complications. Deep burns heal with esophageal strictures over weeks to months, treated with serial dilation, and acid burns can cause gastric outlet obstruction. Decades later, esophageal squamous cell carcinoma risk is markedly increased, so surveillance endoscopy begins roughly 15–20 years after the injury.

Hydrocarbons

Aspiration is the danger. Hydrocarbons with low viscosity and low surface tension, such as gasoline, kerosene, lamp oil, and furniture polish, spread easily into the airways. Even a small aspirated volume dissolves surfactant, causing alveolar collapse and chemical pneumonitis: coughing, gagging, tachypnea, hypoxemia, and often fever.

Management. Never induce emesis or perform lavage, and do not give charcoal. Observe for about 6 hours with a chest X-ray, because radiographic changes can lag behind the exposure; an asymptomatic child with a normal film at 6 hours can go home. Symptomatic patients receive oxygen and supportive care. Steroids and prophylactic antibiotics do not help, and fever alone does not mean bacterial pneumonia.

Inhalant abuse. Huffing or bagging halogenated hydrocarbons (chlorinated solvents, refrigerants, some propellants) sensitizes the myocardium to catecholamines, so a startle or sudden exertion can trigger ventricular fibrillation, called sudden sniffing death. Avoid catecholamines when possible and treat ventricular dysrhythmias with a β-blocker such as esmolol. Chronic toluene use causes a normal-gap metabolic acidosis with hypokalemia (distal RTA) and white-matter damage.

Button batteries and magnets

Mechanism. A disc battery lodged against the moist esophageal wall completes a circuit, generating hydroxide at its negative pole and burning through tissue within hours. Lithium coin cells 20 mm or larger are the most dangerous. Complications include perforation, tracheoesophageal fistula, aortoesophageal fistula with fatal hemorrhage (sometimes days to weeks later), stricture, and vocal cord paralysis.

Imaging. On the frontal X-ray a battery shows a halo or double-ring edge and on the lateral view a step-off, whereas a coin has uniform density and a flat profile. An asymptomatic esophageal coin may be observed briefly for passage but is removed if it stays; a battery is never observed there.

Battery in the esophagusEmergent endoscopic removal. En route, if the child is older than 1 year and swallowed it within 12 hours, give honey (10 mL every 10 minutes, up to 6 doses) or sucralfate; no honey under 1 year (botulism). Never delay removal.
Battery beyond the esophagus, no symptomsUsually observe, with a repeat X-ray in 7 to 14 days if passage is not seen; return for abdominal pain, vomiting, or bleeding. Consider endoscopy if the ingestion was unwitnessed or its timing is unknown (to look for esophageal injury), or for removal when a child under 5 swallowed a battery 20 mm or larger.
Multiple magnets, or a magnet plus metalUrgent GI or surgical consultation for removal.

Triage by location and object

Magnets. A single small magnet behaves like any blunt foreign body, but two or more magnets, or a magnet with metal, attract across adjacent bowel loops and pinch the walls between them, causing pressure necrosis, perforation, fistulas, and obstruction.