Treatment of Ventricular Fibrillation Due to Ammonium Bifluoride Poisoning With Hemodialysis

• Published in: Pediatrics (Evanston) 2018-09, Vol.142 (3), p.1
• Main Authors: Farkas, Andrew N, Wolf, Michael S, Landzberg, Elizabeth, Lynch, Michael J, Woods, Kendra S
• Format: Article
• Language: English
• Subjects: Acidosis; Ammonia; Ammonium; Ammonium compounds; Ammonium paratungstate; Ammonium salts; Calcium; Cardiac arrhythmia; Care and treatment; Case reports; Children; Clinical outcomes; Coma; Diphenhydramine; Drug screening; Endoscopy; Etching; Fibrillation; Fluorides; Gas chromatography; Health aspects; Hemodialysis; Hypocalcemia; Ingestion; Kinetics; Laryngoscopy; Mass spectroscopy; Medical instruments; Metabolic acidosis; Neurological complications; Pediatrics; Poisoning; Respiratory failure; Risk factors; Sodium; Sodium bicarbonate; Toxicity; Urine; Ventricle; Ventricular fibrillation; Vomiting
• ISSN: 0031-4005; 1098-4275
• DOI: 10.1542/peds.2018-0136

Ammonium bifluoride is an inorganic, fluoride-containing compound found in glass and metal etching products, as well as wheel cleaners. Fluoride toxicity is a common cause of preventable poisoning and has been reported to cause life-threatening ventricular dysrhythmias. Here, we report a case of recurrent ventricular fibrillation secondary to ingestion of ammonium bifluoride. The patient presented with vomiting and coma. She was intubated for altered mental status and respiratory failure and subsequently had 5 episodes of ventricular fibrillation, each resolving with a single defibrillation. She developed metabolic acidosis and hypocalcemia, which were treated with sodium bicarbonate and calcium gluconate, respectively. During transfer to a tertiary care children's hospital, ventricular fibrillation recurred despite electrolyte correction. Hemodialysis (HD) was initiated emergently. No further dysrhythmia occurred after initiation of HD. The result of a basic urine drug screen was negative, and a comprehensive drug screen (gas chromatography and mass spectroscopy) revealed only a nonsignificant peak for diphenhydramine. Subsequent laboratory evaluation revealed an elevated serum fluoride level. Diagnostic laryngoscopy and upper endoscopy did not reveal evidence of caustic injury. She was successfully extubated on hospital day 2 and discharged from the hospital on day 4 with no neurologic sequelae. With this example, we demonstrate a potential therapeutic approach to this potentially lethal poisoning. Fluoride toxicity is typically treated with calcium. However, dysrhythmia may result from calcium-independent direct myocardial toxicity. The kinetics of fluoride are amenable to HD, and renal clearance is slow. The potential use of HD in cases of fluoride poisoning refractory to other therapies warrants further study.