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This case examines the rapid progression of multi-organ failure due to rhabdomyolysis in a patient with alcoholic cirrhosis.

May 20, 2026

A51-41 Fulminant Multi-Organ Failure in Alcoholic Cirrhosis: A Catastrophic Cascade of Rhabdomyolysis, Hepatic Failure, and Cerebral Edema

Key Points

This case examines the rapid progression of multi-organ failure due to rhabdomyolysis in a patient with alcoholic cirrhosis.
Described clinical presentation of a 33-year-old woman with alcoholic cirrhosis.
Utilized laboratory findings to assess levels of electrolytes, liver enzymes, and metabolic indicators.
Reported treatment interventions including vasopressors, bicarbonate therapy, and transfer to specialized care.
Patient developed severe metabolic acidosis (pH 6.99), hyperkalemia (K 9.6 mmol/L), and multi-organ failure within 24 hours.
Neurologic status deteriorated due to cerebral edema from hyperammonemia despite intensive medical interventions.
Early transfer to a liver-transplant-capable ICU was deemed vital as standard therapies were ineffective.

Abstract

Abstract Introduction Acute-on-chronic liver failure (ACLF) can rapidly evolve into catastrophic multi-organ failure when combined with shock and metabolic injury. We describe a young woman with alcoholic cirrhosis who developed fulminant hepatic failure, rhabdomyolysis-associated hyperkalemia, and cerebral edema leading to impending herniation. Case Presentation A 33-year-old woman with alcoholic cirrhosis presented with three days of weakness, vomiting, and poor intake. On arrival, she was encephalopathic and hypotensive (SBP 60 mm Hg). Laboratory findings included Na 123 mmol/L, K 6.6 mmol/L, bicarbonate 12 mEq/L, lactate 8.9 mmol/L, creatinine 2.4 mg/dL, total bilirubin 7.0 mg/dL, INR 2.1, AST 5,000 U/L, ALT 619 U/L, and ammonia 186 µmol/L. She was intubated for airway protection and transferred to the ICU on norepinephrine, vasopressin, and phenylephrine infusions. Within 24 hours, she developed mixed distributive shock, rhabdomyolysis (CK 39,000 U/L; myoglobin 20,000 ng/mL), and severe metabolic acidosis (pH 6.99, HCO3 8 mEq/L, lactate 16.4 mmol/L). Hyperkalemia rebounded to 9.6 mmol/L despite repeated calcium, insulin/dextrose, and bicarbonate therapy. Lipase 1,206 U/L suggested alcohol-related pancreatitis. Urine output was 100 mL/24 h. Nephrology attributed AKI to hepatorenal syndrome and ATN; gastroenterology identified transaminases far exceeding levels expected for alcoholic hepatitis, consistent with ACLF; neurology noted cerebral edema with probable herniation secondary to hyperammonemia. Despite quadruple vasopressors, continuous bicarbonate infusion, lactulose, rifaximin, N-acetylcysteine, mannitol, and broad antimicrobials, the patient’s acidosis and neurologic status worsened. She was transferred to a tertiary liver-transplant-capable ICU. Discussion This case highlights the lethal intersection of rhabdomyolysis, ACLF, and hyperammonemic cerebral edema. Profound metabolic acidosis, shock liver, and refractory hyperkalemia accelerated neurologic injury. Early recognition and transfer to transplant-capable centers are vital when conventional therapy fails. Conclusion Cirrhotic patients can deteriorate precipitously into fulminant hepatic failure with multi-organ collapse. Hyperammonemia-induced cerebral edema must be anticipated, and neuroprotective interventions initiated promptly. This abstract is funded by: N/A

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A51-41 Fulminant Multi-Organ Failure in Alcoholic Cirrhosis: A Catastrophic Cascade of Rhabdomyolysis, Hepatic Failure, and Cerebral Edema

Key Points

Abstract

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