methyl-ethyl-ketone-peroxide and Edema

Although ingestion of methyl ethyl ketone peroxide (MEKP) is rare, it carries a high risk of morbidity and mortality. This paper reports the first such case from Turkey in which a 70-year-old man unintentionally ingested MEKP in his kitchen. The patient was brought into the emergency department (ED) within 1 hour of ingestion, with the symptoms of sore throat, shortness of breath, nausea and vomiting. Visual examination of the oropharynx revealed minor burns and uvular edema. A laryngoscope examination performed in the ED showed superficial mucosal injury with edema of the oropharynx, uvula, posterior pharynx, epiglottis, arytenoids and vocal cords. Lateral cervical radiography revealed a narrowing of airway due to a thickened epiglottis. After the diagnostic evaluation was completed, the patient was admitted to the gastroenterology intensive care unit for monitoring of adverse reactions. During follow-up, the patient made an uneventful recovery. Ingestion of MEKP generally results from accidental ingestion from a container. Therefore, these containers should be kept in safe places. In addition, the priority following the ingestion of MEKP should be given to maintain open and adequate airway in the ED.

Topics: Accidents; Administration, Oral; Aged; Airway Obstruction; Burns, Chemical; Butanones; Edema; Epiglottis; Humans; Male; Oropharynx; Treatment Outcome

The plastic hardener methyl ethyl ketone peroxide (MEKP) is an unstable peroxide that releases free oxygen radicals. Ingestion of this compound induces widespread liver necrosis that is often fatal, extensive ulceration with subsequent scarring, and stenosis of the proximal digestive tract in survivors. Severe metabolic acidosis occurs due to the accumulation of formic acid and other organic acids inducing neurologic damage, such as optic nerve lesions. A 53-year-old man unintentionally ingested approximately 120 ml of a 33% solution of this compound in dimethylphtalate. The patient was treated with the free radical scavenger N-acetylcysteine to counteract free radical-mediated damage and with hemodialysis to remove accumulated organic acids. Although our patient demonstrated considerable edema and ulceration of the distal esophagus, stomach and duodenum in the acute phase, there was never any sign of liver damage or neurological damage, nor were there any demonstrable lesions in the proximal digestive tract three weeks after the event. Treatment with a combination of N-acetylcysteine and haemodialysis may be a promising therapy for this severe and potentially life-threatening intoxication.

Topics: Acetylcysteine; Acidosis; Butanones; Edema; Free Radical Scavengers; Free Radicals; Gastrointestinal Diseases; Humans; Liver; Male; Middle Aged; Phthalic Acids; Renal Dialysis