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Asterixis

Manuel Mendizabal, M.D., and Marcelo O. Silva, M.D.

N Engl J Med 2010; 363:e14August 26, 2010

Article

Video

Asterixis

Asterixis

A 50-year-old man presented to the emergency room with a 17-day history of jaundice and no other medical history. On physical examination, he had no stigmata of chronic liver disease. Doppler ultrasonography showed patent hepatic vessels and no biliary-duct dilatation. Serum chemical tests were remarkable for elevated liver-function measurements, including a total bilirubin level of 25 mg per deciliter (430 μmol per liter), a direct bilirubin level of 17 mg per deciliter (290 μmol per liter), an aspartate aminotransferase level of 1667 U per liter, an alanine aminotransferase level of 2658 U per liter, an alkaline phosphatase level of 141 U per liter, and an international normalized ratio of 2.7. Further evaluation revealed no evidence of viral or autoimmune hepatitis, Wilson's disease, Epstein–Barr virus, infection with herpes simplex virus, or drug or alcohol use. The patient was admitted, and within days, hepatic encephalopathy and asterixis developed (see video, available at NEJM.org). Asterixis represents the failure to actively maintain a position and is caused by the abnormal function of diencephalic motor centers that regulate the tone of the agonist and antagonist muscles involved in maintaining posture. The patient was placed on a waiting list for urgent liver transplantation. His mental status deteriorated quickly, necessitating intubation. Computed tomography of the brain showed mild cerebral edema, and an epidural catheter was placed to monitor intracranial pressure. The patient underwent emergency liver transplantation with no major complications. Three months after surgery, the patient was well, with no signs of neurologic impairment.

Manuel Mendizabal, M.D.
Marcelo O. Silva, M.D.
Hospital Universitario Austral, Pilar, Argentina