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A6922 - A Case of Massive Acetaminophen Toxicity Needing Emergent Hemodialysis
Author Block: I. Melgarejo1, G. Devendra2; 1Internal Medicine, University of Hawaii Internal Medicine Residency Program, Honolulu, HI, United States, 2Critical Care, Queens Medical Center, Honolulu, HI, United States.
Acetaminophen toxicity is one of the most common toxic ingestions in the US. Massive doses of acetaminophen induce irreversible hepatocyte damage. We now present a case of a 31year-old female with bipolar disorder who was found unconscious with an empty bottle of acetaminophen. Time of ingestion is unknown with initial acetaminophen (APAP) level of 909. On presentation, she was obtunded with vital signs: BP 129/100 mmHg, HR 133 bpm, RR 20 cpm T 36.7C. Initial laboratory data includes WBC 14,670/dL Hgb 13.mg/dL 264, glucose 310 mg/dL, Na 136 K 3.3 meq/dL, HCO3 14meq/L with pH 7.23 and anion gap 27. Liver and renal function test was normal. Salicylates and urine drug screen was unremarkable. Activated charcoal, bicarbonate drip, N-acetylcysteine (NAC) bolus plus infusion was administered. APAP level was checked four hours after starting the NAC drip, and it decreased to 606 however but blood pH was 7.13.She underwent hemodialysis for five hours. APAP levels decreased to 185 and pH improved after treatment. Her liver function tests remained normal until acetaminophen levels were undetectable. The next day she became more awake and was liberated from the ventilator. She was later transferred to psychiatric unit and discharged. The main cause of toxicity in massive acetaminophen overdose is the rapid accumulation of NAPQI which induces hepatocyte damage. Another effect of APAP toxicity is pyroglutamic acidosis5. The exact mechanism is unknown, other studies suggests it is related to glutathione depletion3. The accumulation of pyroglutamic acid results to high anion gap acidosis4 and metabolic encephalopathy which resulted from damage to the lipid layer7. Extracorporeal treatments (ECT) is effective in cases of methanol and polyethylene glycol toxicity but its role acetaminophen toxicity is not well studied. Extracorporeal Treatments in Poisoning (EXTRIP) Workgroup recognizes NAC as an efficient antidote. EXTRIP recommends urgent hemodialysis if the patient presents with signs of mitochondrial dysfunction as evidenced by coma, lactic acidosis and severe acidosis. The rate of infusion of N-acetylcysteine must also be doubled during dialysis as NAC is a dialyzable substance2. In summary, our case highlights the utility of hemodialysis in APAP toxicity. While NAC is recognized as an efficient antidote, dialysis must be highly considered if the patient presents with signs of mitochondrial toxicity1.