Management of Asterixis
Asterixis itself is not treated directly; management focuses on identifying and treating the underlying cause, most commonly hepatic encephalopathy, which requires ammonia-lowering strategies including lactulose and rifaximin, along with correction of precipitating factors. 1, 2
Diagnostic Workup
The presence of asterixis mandates immediate investigation for the underlying etiology:
Obtain complete metabolic panel to assess for hepatic dysfunction (transaminases, bilirubin, albumin, INR), renal failure (BUN, creatinine), electrolyte disturbances (sodium, potassium, magnesium, phosphate), and hypoglycemia 1, 2
Assess arterial blood gas if hypercapnia from respiratory failure is suspected, as this is a common non-hepatic cause 2, 3
Review medication list for drugs that can induce asterixis: antiepileptics (valproic acid, carbamazepine, phenytoin), levodopa, opiates, anticholinergics, benzodiazepines, lithium, and clozapine 2, 4
Perform neurological examination to distinguish bilateral (81% of cases, suggesting metabolic cause) from unilateral asterixis (19% of cases, suggesting structural brain lesion requiring imaging) 3
Obtain brain imaging (CT or MRI) when unilateral asterixis is present or when structural causes are suspected (stroke, subdural hematoma, epidural abscess, malignancy) 2, 3
Management Based on Etiology
Hepatic Encephalopathy (Most Common Cause)
For overt hepatic encephalopathy with asterixis, the treatment algorithm is:
Identify and treat precipitating factors immediately: gastrointestinal bleeding, infections (particularly spontaneous bacterial peritonitis), electrolyte disturbances, constipation, excessive dietary protein, sedative use, or dehydration 1, 2
Initiate lactulose 15-30 mL orally 2-3 times daily, titrated to achieve 2-3 soft bowel movements per day to reduce ammonia production 2, 5
Add rifaximin 550 mg orally twice daily for patients with recurrent episodes or as adjunct to lactulose, which reduces breakthrough hepatic encephalopathy episodes by 58% and hospitalizations by 50% over 6 months 6
Monitor blood glucose every 2 hours as hypoglycemia mimics hepatic encephalopathy symptoms and is common in acute liver failure 1
Target serum sodium 140-145 mmol/L in patients with hyponatremia, correcting no faster than 10 mmol/L per 24 hours, as hyponatremia correlates with increased intracranial pressure 1
Protect airway in patients with Grade 2 or higher encephalopathy to prevent aspiration pneumonia 1
Important Caveat for Acute Liver Failure
In acute liver failure (ALF), lactulose and rifaximin are NOT recommended as they do not lower ammonia levels effectively in this setting and may delay transfer to transplant centers 1
Non-Hepatic Metabolic Causes
For uremic asterixis: Initiate or optimize renal replacement therapy if meeting criteria for dialysis 2, 3
For hypercapnic asterixis: Provide respiratory support with oxygen therapy, non-invasive ventilation, or mechanical ventilation as indicated 1, 3
For medication-induced asterixis: Discontinue or reduce the offending agent (antiepileptics, benzodiazepines, opiates) and monitor for resolution 2, 4
For electrolyte-related asterixis: Correct hypokalemia, hypomagnesemia, or hypophosphatemia to normal ranges 1, 2
Structural Brain Lesions
- For unilateral asterixis from stroke, subdural hematoma, or focal lesions: Manage the underlying structural pathology according to neurosurgical or stroke protocols 3
Monitoring and Prognosis
Asterixis typically appears at West Haven Grade 1-2 hepatic encephalopathy (early to middle stages with personality changes and sleep disturbances) and disappears as patients progress to stupor and coma (Grade 3-4) 7, 5
Asterixis is usually reversible upon successful treatment of the underlying metabolic or toxic cause 4
The presence of asterixis in cirrhotic patients signals increased mortality risk, with 1-year and 3-year survival rates of 42% and 23% respectively after first overt hepatic encephalopathy episode 1
Critical Pitfalls to Avoid
Do not assume asterixis equals hepatic encephalopathy: It has only 45% specificity and occurs in uremia, hypercapnia, medication toxicity, and structural brain lesions 7, 3
Do not use extracorporeal liver support systems (MARS, Prometheus) as they have not demonstrated survival benefit in randomized controlled trials for acute-on-chronic liver failure 1
Do not restrict protein in chronic hepatic encephalopathy except in severe acute cases, as this worsens nutritional status without clear benefit 1
Do not delay transfer to transplant center for patients with acute-on-chronic liver failure (ACLF) showing asterixis, as early referral is crucial before rapid progression makes transplantation impossible 1