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ACG Case Reports Journal logoLink to ACG Case Reports Journal
. 2026 Apr 3;13(4):e02069. doi: 10.14309/crj.0000000000002069

Lingual Asterixis in Hepatic Encephalopathy

Erik Almazan 1,2,, Rintu Saju 1,2, Gala Moreno Lepe 1,2, Nicholas Roberts 1,2, Christopher A Gardner 2,3, Alexander Carbo 1,2
PMCID: PMC13048649  PMID: 41937909

CASE REPORT

A 34-year-old woman with a medical history notable for alcohol use disorder, alcohol-related pancreatitis, and anorexia nervosa presented to our center after a seizure-like episode and required admission to the intensive care unit for metabolic derangements. She had severe hypokalemia (potassium <1.8 mmol/L) and hypoglycemia (37 mg/dL) in the setting of diarrhea and enterocolitis. She also presented with jaundice, transaminase elevations (aspartate aminotransferase 706 U/L, alanine aminotransferase 173 U/L), and hyperbilirubinemia (direct bilirubin 17.3 mg/dL, total bilirubin 22.5 mg/dL). The presentation was consistent with alcohol-associated hepatitis (Maddrey Discriminant Function 119.5) given a history of ongoing alcohol use, the pattern of laboratory abnormalities, and absence of biliary obstruction on imaging. After transfer to the medicine floor, her course was complicated by hepatic encephalopathy. On one examination day, in addition to asterixis of the bilateral upper extremities (Video 1), she exhibited lingual asterixis, a very rare variant of asterixis (Video 2). She was oriented to person, time, and place, but had impaired attention, emotional lability, and asterixis, consistent with grade 2 hepatic encephalopathy according to the West Haven Criteria.

Lingual asterixis, similar to upper extremity asterixis, occurs due to negative myoclonus with intermittent loss of postural tone.1 The finding is elicited by asking the patient to protrude the tongue and may be underrecognized in more severe hepatic encephalopathy, where patients may have difficulty sustaining attention and following examination instructions. In this case, the patient's hepatic encephalopathy resolved after initiation of rifaximin, treatment for presumed Shigella infection, and corticosteroid therapy for alcohol-associated hepatitis.

DISCLOSURES

Author contributions: E. Almazan: conception of work; acquisition of data; interpretation of data; drafted original manuscript; revised manuscript; provided final approval; accountable for all aspects of the work. R. Saju, GM Lepe, N. Roberts, CA Gardner, A. Carbo: acquisition of data; revision of manuscript; provided final approval; are accountable for all aspects of the work. E. Almazan is the article guarantor.

Financial disclosure: None to report.

Informed consent was obtained for this case report.

Contributor Information

Erik Almazan, Email: ealmazan@bwh.harvard.edu.

Rintu Saju, Email: rsaju@bwh.harvard.edu.

Gala Moreno Lepe, Email: gmorenolepe@bwh.harvard.edu.

Nicholas Roberts, Email: nroberts8@mgb.org.

Christopher A. Gardner, Email: cgardner7@mgb.org.

Alexander Carbo, Email: acarbo@bwh.harvard.edu.

REFERENCE

  • 1.Vilstrup H, Amodio P, Bajaj J, et al. Hepatic encephalopathy in chronic liver disease: 2014 Practice Guideline by the American Association for the Study of Liver Diseases and the European Association for the Study of the Liver. Hepatology. 2014;60(2):715–35. [DOI] [PubMed] [Google Scholar]

Articles from ACG Case Reports Journal are provided here courtesy of American College of Gastroenterology

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