Inhalation Burn from a Fire Extinguisher: A Rare Cause of Acute Phosphate Toxicity

Introduction: Dry chemical fire extinguishers often contain monoammonium phosphate (MAP). Inhalation of MAP can cause upper and lower airway damage leading to acute respiratory distress syndrome. It is also a rare cause of acute phosphate toxicity, leading to a potentially fatal constellation of metabolic derangements including hyperphosphatemia, hypocalcemia, and high anion gap metabolic acidosis in addition to acute kidney injury. Case Description: A 44-year-old male with psychiatric illness and no known kidney disease presented in cardiac arrest after intentionally expelling a fire extinguisher containing MAP into his mouth. He had a prolonged resuscitation and was admitted with acute respiratory failure, non-oliguric AKI, severe, mixed metabolic and respiratory acidosis, hyperkalemia, and marked hyperphosphatemia. Initial chemistry showed: Na 146, K 6.8, Cl 104, C02 9, Ca 11.7, Phos 40, BUN 24, Cr 1.29, anion gap 41, lactic acid 4.8. Arterial blood gas showed: pH 6.77, pCO2 100, pO2 12. The patient was treated initially with inotropes and mechanical ventilation along with bicarbonate infusion. As there was no clinical improvement despite robust urine output, sustained low-efficiency dialysis was started. His metabolic derangements resolved within 24 hours and his creatinine stabilized near 1.3 off dialysis. Unfortunately, the patient died of severe hypoxic brain injury. His family donated his kidneys for transplantation. One of the allografts (for which data are available) functioned well without evidence of acute phosphate nephropathy on subsequent biopsy. Discussion: Organophosphorus poisoning often results from use of pesticides. However, poisoning from inorganic phosphate like MAP is rare. MAP is used as a fertilizer, stabilizing agent to reduce cadmium mobility in soil, and fire retardant or extinguisher. It is recognized to cause respiratory compromise, yet its metabolic consequences are infrequently reported. MAP inhalation and ingestion lead to very high phosphorus levels and a high anion gap metabolic acidosis, due in part to the contribution from the inorganic phosphate anion. It is important to remain aware of this rare poisoning. There is no antidote available. Treatment is supportive and the outcome is often fatal. In this case rapid initiation of dialysis resolved the metabolic abnormalities and prevented long term damage to the kidneys.