Unproven ingestion: an unrecognized bias in toxicological case series.

BACKGROUND: Case series of ingestion in preschool children may include patients without significant exposure if the substance is not measured. METHODS: In order to evaluate the unproven ingestion bias, we conducted, between January 2000 and June 2004, a retrospective analysis of a poison control center-based series of children <6 years old with a history of toxic methanol or ethylene glycol ingestion. RESULTS: Over the 54 month period, 115 children were referred to obtain a level. Of these, 102 children, aged 25 +/- 10 months, actually had a level analyzed. Only 21 patients had positive levels measured a median of 90 minutes post-ingestion. CONCLUSION: Our findings suggest that a significant fraction of purported cases were not confirmed. When a study aims at determining the toxicity of the substance, measurements of the xenobiotic should be required in any case series involving preschool aged children in order to decrease the unproven ingestion bias.

Methylphenidate unintentional ingestion in preschool children.

BACKGROUND: With the rising number of prescriptions for methylphenidate has come an increase in preschool younger siblings being exposed to the risk of ingesting methylphenidate. Furthermore, the symptoms of methylphenidate ingestion in preschool children have not been previously defined. METHODS: Over a 3-year period we enrolled and followed by telephone children aged <6 years with methylphenidate ingestion, whether it was their own medication or someone else's, at time of first call to the poison control center. RESULTS: A total of 49 children aged 30+/-11 months were included. Patients ingested a median of 1 tablet (range 0.25-10) for a total median dose of 0.9 mg/kg (range 0.26-12). Twenty-one patients were referred to a health care facility, and the poison control center recommended activated charcoal for 12 of them. Patients referred to a health care facility ingested more methylphenidate: median 1.8 versus 0.7 mg/kg (P<0.001). Patients for whom activated charcoal was recommended ingested more methylphenidate: median 3.5 versus 0.8 mg/kg (P<0.001). Twenty-four patients developed symptoms: agitation or irritability in 17, somnolence in 5, vomiting in 2, and abdominal pain in 2. Two patients had tachycardia. Patients who ingested an extended-release preparation had similar rates of symptoms as those who ingested a regular preparation, 7/9 versus 17/40 (P=0.07), while having ingested similar amounts, median 1.6 versus 0.8 mg/kg (P=0.08). Patients who ingested 1 tablet or less had a similar rate of symptoms as those who ingested more than 1 tablet: 12/29 versus 10/17 (P=0.25). There was no difference in the dose ingested for those who became symptomatic compared with those who remained asymptomatic: median 1.2 (range 0.26-12) versus 0.8 mg/kg (range 0.26-3.8) (P=0.08). CONCLUSION: Preschool children ingesting less than 1 mg/kg of regular methylphenidate can be safely managed at home in spite of the fact that some will develop minor symptoms.

Status epilepticus after a massive intravenous N-acetylcysteine overdose leading to intracranial hypertension and death.

Cases of N-acetylcysteine overdose have been reported before. In some cases, these overdoses have led to death if an anaphylactoid reaction was present. A healthy 30-month-old girl allegedly ingested acetaminophen at 418 mg/kg. Because the emergency physician feared the time of ingestion might not be accurate, he decided to start the 20.5-hour intravenous N-acetylcysteine protocol 8 hours after ingestion. He mistakenly prescribed the maximum milliliter-per-kilogram volume of the dextrose 5% diluent for the milliliter-per-kilogram volume of N-acetylcysteine 20% to be administered. Five hours after the error was detected (19.5 hours postingestion), the patient started developing myoclonus on the left side of her body, with left eye deviation. This condition persisted intermittently for 3 hours despite treatment with diazepam, lorazepam, and phenytoin. A first computed tomographic scan result was normal. A few hours later, she sustained shorter recurrences of the myoclonus. At 30 hours after ingestion, she started to have irregular breathing and became unresponsive to pain. A repeated computed tomographic scan showed diffuse cerebral edema. A postmortem examination showed the presence of acute anoxic encephalopathy with marked cerebral edema and the beginning of uncal herniation that confirmed the clinical diagnosis of intracranial hypertension and brain death. A cumulative intravenous dose of 2,450 mg/kg of N -acetylcysteine was associated with status epilepticus, intracranial hypertension, and death in a child.