Introduction: Extracorporeal liver assist device has been described in the literature as a promising strategy for acute liver failureIntroduction: Extracorporeal liver assist device has been described in the literature as a promising strategy for acute liver failure in the setting of acetaminophen toxicity as a bridge to liver transplant. In the largest study of paracetamol overdose treated with MARS™ therapy, patients with Grade 2 encephalopathy (n=14) had a mean MELD score 23 ± 13[1]. There was a higher rate of native liver recovery and 6 month survival with Molecular Adsorbent Recirculating System (MARS™) than the control group. However, there is a lack of uniform protocols to guide clinical management. Therefore, the use has not been widely disseminated in the USA, despite acetaminophen toxicity as the leading cause of acute liver failure and a leading cause of drug fatalities. We present a case where extracorporeal liver assist device, MARS, was used in fulminant liver failure secondary to acetaminophen toxicity with recovery of hepatic and neurologic function without organ transplantation. Case Description: A 39 year-old woman with past medical history of chronic pancreatitis status post pancreatectomy and splenectomy, roux-en-y bypass with malnutrition requiring tube feeds, pulmonary emboli on anticoagulation, and bipolar disorder, presented with acute on chronic left abdominal pain for which she takes oxycodone. She also reported dark bloody fluid from her PEG, epistaxis, nausea and vomiting for one day. She was noted to have an elevated INR of 6.3, WBC 15.9 x109/L, hemoglobin 8 g/dL, glucose of 20's mg/dL, and lactate of 8.8 mmol/L. She was given dextrose and antibiotics then transferred for ICU admission. She continued to have abdominal pain out of proportion to her exam and became hypotensive with BP 80's/40's. Recheck of INR was >10 and AST was 700 U/L. Abdominal CT and ultrasound were negative. Despite adequate fluid resuscitation and timely antibiotics, her lactate remained elevated. Acetaminophen level was found to be 42 mcg/mL. Over the phone, her mother noted 75 missing Percocet pills of her own prescription. After 12 hours, she had increasing somnolence with rising ammonia 268 mcg N/dL, a MELD score 24, and rising transaminases (AST 8150 U/L, ALT 3450 U/L). Within hours after intubation, she exhibited decorticate posturing and ICP monitor was emergently placed. Opening pressure was 45 mmHg then decreased within seconds to 6 to 7 mmHg, and later increased episodically >25 mmHg which responded to mannitol bolus. Through multidisciplinary discussion, she was not considered for liver transplant due to complex psychosocial and medical issues. MARS™ was initiated on day 1 with a second session on day 2. Ammonia dropped to 165 mcg N/dL after the first session then to 40 mcg N/dL after the second. She slowly improved and ICP monitor was removed on day 5 and extubated on day 7. She remained on hemodialysis but never required vasopressors. After 3 weeks, she recovered synthetic and metabolic liver function (Albumin 2.7, INR 1.9, AST 70 u/L, ALT 42u/L, glucose 103, Alkaline phosphatase 141 u/L, total bilirubin 25.2 mg/dL from a peak of 42 on day 9, MELD score of 39, platelets 239 x109/L), was neurologically intact, and discharged to a psychiatric unit. Discussion: With limited organ donation, other modalities could be considered for patients with fulminant liver failure, namely extracorporeal liver assist device (ELAD). It is generally well tolerated except for thrombocytopenia, which our patient exhibited but normalized in a week. With two sessions, neurologic and hepatic function recovery was remarkable considering her initial neurological symptoms. The change of ammonia was more dramatic than previously described. One can hypothesize that early initiation of ELAD in fulminant liver failure could be a bridge to transplantation as well as aiding native hepatic recovery in non-organ transplant candidates.