EpistemisAsterixis
Specialty: Neurology.
Why it occurs
- Hepatic encephalopathy (severe hepatocellular insufficiency or portosystemic shunt)
- Uremic encephalopathy (advanced or acute chronic kidney failure)
- Hypercapnic encephalopathy (CO2 retention in patients with advanced COPD or hypoventilation)
- Drug toxicity (anticonvulsants such as phenytoin, valproate, carbamazepine, or sedatives)
- Generalized metabolic encephalopathy (severe hyponatremia, hypoglycemia, sepsis)
Initial workup
Determination of ammonium in venous or arterial blood, blood urea nitrogen (BUN), serum creatinine, arterial blood gases to quantify pCO2 and acid-base balance; serum levels of anticonvulsant drugs; electroencephalogram (EEG) to observe diffuse slowing and triphasic waves characteristic of metabolic encephalopathies.
red flags
Sudden onset of asterixis accompanied by stupor, progressive obtundation, altered respiratory pattern or signs of acute motor neurological focality, indicating imminent multi-organ failure or severe cerebral edema associated with fulminant acute liver failure.
Standard management
- Lactulose — 15-30 ml orally or enterally every 8-12 hours, adjusting the dose to achieve 2-3 soft stools per day in hepatic encephalopathy
- Rifaximin — 550 mg every 12 hours, to reduce ammonia-producing microbiota
- Immediate suspension of the suspected neurotoxic drug in case of pharmacological cause.
Educational guidance for study. It is NOT a prescription recommendation. The actual choice depends on the cause, the patient, and current guidelines.
- Area
- Neurology
- Listed causes
- 5
- Treatment options
- 3