Introduction

Though acetaminophen overdoses are common, acetaminophen induced methemoglobinemia is rare and it is thought to be due to oxidative stress from reactive metabolites. However, few prior cases of sulfhemoglobinemia in the setting of acetaminophen overdose have been reported. We report a case of mixed methemoglobinemia and sulfhemoglobinemia in the setting of a large, isolated acetaminophen ingestion.

Case report

A 30-year-old African American male presented after intentionally ingesting 50 tablets of 500 mg acetaminophen two days prior. He was cyanotic and tachypneic. Peripheral oxygen saturation was 78 % on room air and minimally improved with high-flow oxygen. He was noted to have leukocytosis, thrombocytopenia, anion gap metabolic acidosis with lactic acidemia, acute kidney injury, transaminitis, hyperbilirubinemia, and coagulopathy. Arterial partial pressure of oxygen was normal. Methemoglobin and sulfhemoglobin concentrations were 8.5 % and 5.2 %, respectively. Along with intravenous N-acetylcysteine, methylene blue was administered without clinical improvement. Hemolytic anemia was subsequently noted. Glucose-6- phosphate dehydrogenase (G6PD) deficiency was then confirmed with a quantitative assay and genetic testing. He also received one dose of intravenous metoclopramide. The patient ultimately required eight units of packed red blood cells and several weeks of hemodialysis before discharge on hospital day 43.

Discussion

Acetaminophen is structurally related to compounds known to cause methemoglobinemia and sulfhemoglobinemia. We hypothesize that these dyshemoglobinemias were triggered by acetaminophen-induced oxidative stress. The role of G6PD deficiency in the formation of sulfhemoglobinemia is unclear. Acetaminophen overdoses presenting with methemoglobinemia should prompt concern for underlying G6PD deficiency. Coincidental sulfhemoglobinemia should be considered if the clinical presentation is more severe than the methemoglobin concentration alone would suggest. Use of methylene blue in this case, despite the low measured methemoglobin percentage, which likely triggered hemolytic anemia; methylene blue use in a similar circumstance should be weighed carefully against the risk of harm.

Introduction

Pediatric organophosphate insecticide poisonings are rare in the United States, and life-threatening toxicity is rarely seen. We report 2 accidental ingestions of the organophosphate insecticide coumaphos that resulted in life-threatening symptoms.

Case reports

A 7-year-old boy and 10-year-old girl both presented from home after accidental ingestion of 1 "spoonful" of coumaphos 20% liquid (Asuntol; Bayer de Mexico, S.A. de C.V., Mexico D.F., Mexico). There were no other known ingestions. Both became rapidly symptomatic, with the boy developing dyspnea, vomiting, and depressed mental status and the girl developing headache and nausea. Soon afterward, the boy had witnessed cardiopulmonary arrest and the girl developed altered mental status and flaccid paralysis. Both were treated initially with atropine, but required no additional doses. On arrival to the pediatric intensive care unit (ICU), both patients received pralidoxime with subsequent plasma exchange and continuous venovenous hemodiafiltration (CVVHDF). Transient anemia, coagulopathy, transaminitis, and hyperglycemia developed in both patients. The girl was extubated on hospital day 6 and the boy on hospital day 11. The girl's course was complicated by aspiration pneumonia and an isolated seizure. The boy's course was complicated mainly by anoxic brain injury, associated seizures, neuroagitation, spasticity, and autonomic instability. The girl was discharged on hospital day 16 and remains asymptomatic 32 days after ingestion. As of 90 days after ingestion, the boy remains admitted to inpatient rehabilitation.

Discussion

The clinical benefit of pralidoxime, plasma exchange, and CVVHDF is uncertain in these cases. The optimal treatment regimen for organophosphate insecticide toxicity remains poorly defined.