Treatment of Ventricular Fibrillation Due to Ammonium Bifluoride Poisoning with Hemodialysis Andrew N

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Treatment of Ventricular Fibrillation Due to Ammonium Bifluoride Poisoning with Hemodialysis Andrew N Treatment of Ventricular Fibrillation DueAndrew N. Farkas, to MD, Ammonium a Michael S. Wolf, MD, b Elizabeth Landzberg, Bifluoride MD, c Michael J. Lynch, MD, a Kendra S. Woods, MDb Poisoning With Hemodialysisabstract 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 Divisions of aMedical Toxicology and bPediatric Critical bifluoride.‍ The patient presented with vomiting and coma.‍ She was Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania; and cDepartment of Pediatrics, intubated for altered mental status and respiratory failure and subsequently Children’s Hospital of Pittsburgh of University of Pittsburgh had 5 episodes of ventricular fibrillation, each resolving with a single Medical Center, Pittsburgh, Pennsylvania defibrillation.‍ She developed metabolic acidosis and hypocalcemia, which ’ Dr Farkas drafted the initial manuscript; were treated with sodium bicarbonate and calcium gluconate, respectively.‍ Dr Landzberg prepared the figure; all authors During transfer to a tertiary care children s hospital, ventricular fibrillation reviewed and revised the original manuscript and participated equally in conceptualizing and recurred despite electrolyte correction.‍ Hemodialysis (HD) was initiated organizing this case report and the final review emergently.‍ No further dysrhythmia occurred after initiation of HD.‍ The and revision of the manuscript; and all authors result of a basic urine drug screen was negative, and a comprehensive approved the final manuscript as submitted and agree to be accountable for all aspects of the work. drug screen (gas chromatography and mass spectroscopy) revealed only a DOI: https:// doi. org/ 10. 1542/ peds. 2018­ 0136 nonsignificant peak for diphenhydramine.‍ Subsequent laboratory evaluation revealed an elevated serum fluoride level.‍ Diagnostic laryngoscopy Accepted for publication May 29, 2018 and upper endoscopy did not reveal evidence of caustic injury.‍ She was Address correspondence to Michael S. Wolf, MD, Division of Pediatric Critical Care Medicine, successfully extubated on hospital day 2 and discharged from the hospital Children’s Hospital of Pittsburgh of University of on day 4 with no neurologic sequelae.‍ With this example, we demonstrate a Pittsburgh Medical Center, 4401 Penn Ave, Faculty potential therapeutic approach to this potentially lethal poisoning.‍ Fluoride Pavilion, Suite 2000, Pittsburgh, PA 15224. E­mail: [email protected] toxicity is typically treated with calcium.‍ However, dysrhythmia may result from calcium-independent direct myocardial toxicity.‍ The kinetics of PEDIATRICS (ISSN Numbers: Print, 0031­4005; Online, 1098­4275). fluoride are amenable to HD, and renal clearance is slow.‍ The potential use Copyright © 2018 by the American Academy of of HD in cases of fluoride poisoning refractory to other therapies warrants Pediatrics further study.‍ FINANCIAL DISCLOSURE: The authors have indicated they have no financial relationships relevant to this article to disclose. Ammonium bifluoride is an inorganic of dysrhythmia is thought to be FUNDING: Dr. Wolf was supported by National 3 Institutes of Health grant T32 HD040686; however, no compound found in glass and metal secondary to hypocalcemia via funding was obtained for this case report. etching products, as well as wheel fluorapatite formation and/or binding 1 POTENTIAL CONFLICT OF INTEREST: The authors cleaners.‍ Fluoride poisoning is of calcium leading to precipitation of 4 have indicated they have no potential conflicts of a common2 cause of preventable insoluble calcium fluoride into tissues.‍ interest to disclose. poisoning.‍ There are scant reports However, a direct cardiotoxic effect of ingestions of ammonium bifluoride of fluoride has also5, 6been implicated To cite: Farkas AN, Wolf MS, Landzberg E, et al. (or other common sources of in animal studies.‍ We report a Treatment of Ventricular Fibrillation Due to Ammo­ fluoride such as hydrofluoric acid) rare case of ingestion of a product nium Bifluoride Poisoning With Hemo dialysis. Pedi- causing ventricular dysrhythmias containing ammonium bifluoride, atrics. 2018;142(3):e20180136 likely because of the rare incidence successfully treated with elimination of such ingestions.‍ The mechanism via hemodialysis (HD) after recurrent Downloaded from www.aappublications.org/news by guest on September 26, 2021 PEDIATRICS Volume 142, number 3, September 2018:e20180136 CASE REPORT CO O ventricular fibrillation occurred bicarbonate (25 mEq), and started 7.‍59, P 2 of 29 mmHg, P 2 of ∼ despite correction of hypocalcemia.‍ on a bicarbonate infusion.‍ Then, 236 mmHg, and a bicarbonate CASE REPORT 90 minutes after arrival, she had a level of 28 mmol/L.‍ The patient brief ventricular fibrillation cardiac was also noted to have marked arrest, which was successfully hypophosphatemia (0.‍9 mg/dL) treated with a 50-J defibrillation.‍ requiring aggressive repletion.‍ A 21-kg 4-year-old girl with no Thereafter, a second bolus of 1.‍6 g A fluoride level obtained 90 minutes pertinent past medical history calcium gluconate was given; 110 into HD was 0.‍37 mg/L (reference presented to an emergency minutes after arrival, there were 2 range <0.‍2 mg/L).‍ The result of department with vomiting and coma “ ” additional episodes of ventricular a basic urine drug screening was shortly after ingestion of reportedly ’ fibrillation treated with 50- and negative, and a comprehensive urine just a sip of a chemical being stored “ ’ 85-J defibrillation, respectively.‍ drug screen (gas chromatography/ in her family s garage.‍ This chemical ’ A continuous infusion of calcium mass spectroscopy) revealed was later identified as Meguiar s ” gluconate at 400 mg per hour was only a nonsignificant peak of Professional s Choice Detailer, ∼ then started, and she was treated diphenhydramine.‍ Electrocardiogram Wheel Brightener, with the safety with a total of 4 g of magnesium that was obtained 6 hours after data sheet indicating the presence – sulfate.‍ A repeated ionized calcium initial presentation revealed sinus of 5% to 10% ammonium bifluoride – level was 1.‍33 mmol/L.‍ tachycardia at a rate of 123, QRS as well as water (70% 90%), – duration of 82 ms, and QT and sodium xylene sulfonate (1% 5%), The patient was then transported QTc intervals of 304 and 435, ethoxylated alcohols (0.‍5% 1.‍5%), via air ambulance with a pediatric respectively, without ST segment and ammonium fluoride (<0.‍5%).‍ On ’ ° critical care transport team to a or T wave abnormalities; ionized arrival, the patient had vital signs of tertiary children s hospital and calcium was 1.‍39 mmol/L at temperature (35.‍9 C), blood pressure required 2 additional defibrillations that time.‍ (75 over 39 mmHg), pulse (87 for ventricular fibrillation en route beats per minute), respiratory rate There were no further episodes despite the ongoing infusion of (6 breaths per minute), and pulse of dysrhythmia after initiation calcium gluconate (although no oximetry (98% on a nonrebreather of HD, and the patient remained additional bolus dosing was given).‍ face mask).‍ The physical examination hemodynamically stable (Fig 1).‍ Immediately on arrival to our PICU, was notable for obtundation, the The patient underwent diagnostic a point-of-care ionized calcium was presence of vomitus, and recent fecal ’ laryngoscopy and upper endoscopy found to be 1.‍23 mmol/L.‍ Five hours incontinence.‍ The patient was given revealing no evidence of caustic after the patient s initial emergency intravenous normal saline boluses injury.‍ She was successfully department arrival, the patient was for hypotension, with the lowest extubated on hospital day 2 and placed on HD; hemodynamics were measured pressure being 45 over discharged from the hospital on day 4 deemed sufficient for intermittent 31 mmHg.‍ She was intubated for with no neurologic sequelae.‍ HD (heart rate was 130 beats per respiratory depression and airway minute, and blood pressure was 95 DISCUSSION protection.‍ Blood work obtained over 33 mmHg).‍ The treatment was shortly after arrival revealed an provided with a Fresenius Optiplex arterial blood gas with a pH of CO O 16NR dialyzer via a 9 French, 12-cm Ammonium bifluoride ingestions 7.‍156, P 2 of 44.‍3 mmHg, P 2 of catheter placed in the left femoral have been previously reported 115.‍7 mmHg, and bicarbonate level vein.‍ The treatment was performed to cause central nervous system of 15.‍7 mmol/L.‍ This metabolic with blood flow at 200 to 250 mL per depression, hypocalcemia, and acidosis occurred despite a normal 1 minute, dialysate flow at 800 mL per ventricular dysrhythmia.‍ Although lactate (1.‍1 mmol/L).‍ A point-of-care minute, and no ultrafiltration for 4 there were other ingredients present ionized calcium was 0.‍88 mmol/L.‍ hours with dialysate concentrations within the wheel cleaner ingested in Serum chemistries were notable for of sodium 139 mmol/L, potassium this case, they were minimally toxic a potassium level of 3.‍4 mmol/L, ’ 4 mmol/L, bicarbonate 35 mmol/L, and unlikely to have contributed magnesium level of 2.‍2 mg/dL, – and calcium 3.‍5 mmol/L.‍ Additional to the patient s presentation.‍ This calcium level of 6.‍0 mmol/L (range: μ testing obtained on arrival included case of ammonium
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