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Methyl ethyl ketone peroxide ingestion: toxicity and outcome in a 6-year-old child
N Bates1, C P Driver, A Bianchi
1National Poisons Information Service, Medical Toxicology Unit, London SE14 5ER United Kingdom.
Insights
Methyl ethyl ketone peroxide (MEKP) ingestion caused severe gastrointestinal burns and systemic effects in a child. Long-term management, including surgery and dilation, was required for recovery.
Area of Science:
- Toxicology
- Pediatric Gastroenterology
- Chemical Safety
Background:
- Industrial chemicals like methyl ethyl ketone peroxide (MEKP) pose significant health risks.
- Understanding the systemic and local effects of chemical ingestion is crucial for effective treatment.
Observation:
- A 6-year-old boy experienced severe esophageal and gastric burns, respiratory distress, metabolic acidosis, and coagulopathy after MEKP ingestion.
- The patient required intensive care, followed by gastric resection and reconstruction due to stricture and fibrosis.
Findings:
- MEKP induces cellular damage through lipid peroxidation and free radical production.
- Long-term complications included gastroesophageal stricture and gastric fibrosis, necessitating surgical intervention and ongoing dilation therapy.
Implications:
- This case highlights the severe systemic and local gastrointestinal toxicity of MEKP.
- Acetylcysteine may be a potential therapeutic agent for MEKP poisoning.
- Effective long-term management strategies are essential for patients with severe chemical ingestions.
Abstract:
A 6-year-old boy developed respiratory distress, metabolic acidosis, severe esophageal and gastric burns, and a coagulopathy after ingestion of an unknown volume of methyl ethyl ketone peroxide (MEKP) in dimethyl phthalate. He was discharged from the pediatric intensive care unit 19 days postingestion but subsequently developed a stricture of the gastroesophageal junction and complete fibrosis of the middle third of the stomach, necessitating gastric resection and reconstruction. He was discharged 93 days postingestion on a program of dilation for the residual esophageal stricture. MEKP acts by initiating lipid peroxidation via free radical production that results in cellular dysfunction and death. Acetylcysteine, a glutathione precursor and possible free radical scavenger, may be of use in severe MEKP poisoning. This case demonstrates the severe effects that some industrial chemicals can have both systemically and locally at the point of contact with the gastrointestinal tract, as well as the long-term management required to ensure good quality of life.