Iron Toxicity: Pharmacy Case #57

A vomiting toddler is usually gastroenteritis, and that is exactly what her mother reasonably concluded. Two details break that reading. There is fresh blood in the vomit and a dark stool, and she is poorly perfused — heart rate 168, blood pressure 78/44, capillary refill three seconds — while remaining afebrile. Gastroenteritis does not corrode the gastric mucosa and does not usually produce that degree of circulatory compromise in three hours. Blood plus shock plus no fever is a prompt to ask what the child could have swallowed, and the answer was on the floor beside the sofa. Iron poisoning is quantified on elemental iron per kilogram rather than on tablet count, which is why the label matters: 65 mg of elemental iron per tablet, up to twenty tablets, in a 12 kg child, gives a worst-case 108 mg/kg. Below 20 mg/kg is generally nontoxic and 20 to 60 mg/kg produces moderate symptoms, but exceeding 60 mg/kg carries severe and potentially fatal toxicity, so she is well into the dangerous range on the exposure history alone. The serum concentration then confirms it. At 620 mcg/dL she is above the 500 mcg/dL threshold associated with severe systemic toxicity, and the timing of the sample is part of the interpretation — levels typically peak within two to six hours of ingestion, and hers was drawn at four, so this is a meaningful measurement rather than a possibly pre-peak underestimate. The acidosis is the third strand: pH 7.24, bicarbonate 12, anion gap 22, lactate 4.8. That is the mechanism made visible, since free iron promotes lipid peroxidation and disrupts cellular membranes, driving the systemic oxidative stress that produces metabolic acidosis in moderate-to-severe poisoning. The most important thing in this case is what has not happened yet. Her liver enzymes and clotting are entirely normal, and it would be easy to read that as evidence she is not badly poisoned. She is four hours in. The poisoning runs through five stages: gastrointestinal symptoms with haematemesis at 0.5 to 6 hours, which is where she is now; a transient asymptomatic period from 6 to 24 hours despite continued systemic absorption; then from 6 to 72 hours a return of symptoms with shock, metabolic acidosis, hepatocellular injury, coagulopathy, cardiac dysfunction and renal failure; progressive hepatic failure with rising aminotransferases and encephalopathy from 12 to 96 hours; and late gastric outlet obstruction and bowel strictures at 2 to 8 weeks. That second stage is the trap that kills children, because a child who looks better at eight hours is still absorbing. Treatment does not wait for the deterioration. She meets the indications for deferoxamine three times over — serum iron greater than 500 mcg/dL, metabolic acidosis, and shock — and it is given at 15 mg/kg/hour, up to a maximum of 35 mg/kg/hour and a maximum daily dose of 6 g. The last point belongs to the aunt rather than the child: adult iron preparations, prenatal vitamins above all, are potent enough that a handful is a life-threatening dose for a toddler.