Asterixis is a bilateral, coarse, involuntary movement characterized by brief, sudden lapses in posture due to intermittent loss of muscle tone, often described as a "flapping" tremor. It most commonly affects the wrists and fingers, but may also be seen in the feet, tongue, eyelids, or mouth.

Clinical elicitation

To assess for asterixis:

• Ask the patient to extend both arms, dorsiflex the wrists, and spread the fingers.

• Observe for intermittent, non-rhythmic flapping due to sudden loss of muscle tone.

Alternative assessments:

• In semi-conscious patients: Ask the patient to grip two fingers; rapid alternating release and regrasping indicates asterixis.

• Lower limbs: Dorsiflex the foot and observe for similar tremulous movements at the ankle.

• In the facial region: Look for irregular quivering of the eyelids, tongue, or corners of the mouth during voluntary sustained contraction.

Differential Diagnosis

Asterixis is a clinical sign, not a diagnosis. It commonly indicates underlying metabolic or toxic encephalopathy, including:

1. Hepatic encephalopathy

• Asterixis is a hallmark sign in progressive hepatic encephalopathy.

• May be accompanied by: Lethargy, confusion, personality changes, hyperreflexia, fetor hepaticus, and eventually stupor or coma.

2. Uremic encephalopathy

• Presents with: Lethargy, disorientation, paresthesia, fasciculations, and asterixis.

• Additional features: Polyuria progressing to anuria, metabolic acidosis, hypertension, pericarditis, Kussmaul respirations, and uremic fetor.

3. CO₂ Narcosis (Hypercapnic encephalopathy)

• Occurs in advanced respiratory failure.

• Clinical picture includes: Somnolence, headache, restlessness, confusion, decreased reflexes, and asterixis.

• May progress to respiratory acidosis and coma.

4. Drug-induced asterixis

• Medications such as phenytoin, barbiturates, benzodiazepines, or valproate can precipitate asterixis.

• Dose-related and reversible upon withdrawal.

Clinical significance

Asterixis is often a sign of metabolic encephalopathy and may indicate serious underlying conditions such as:

• Hepatic encephalopathy

• Renal failure (uremic encephalopathy)

• Severe respiratory insufficiency (CO₂ narcosis)

• Drug toxicity (e.g., phenytoin)

Emergency interventions

• Immediate assessment: Neurologic status, vital signs, urine output.

• Monitor for respiratory insufficiency → prepare for intubation/ventilation.

• Be alert for signs of organ failure or metabolic decompensation.

• Establish large-bore IV access, administer oxygen, prepare for fluid/blood resuscitation if indicated.

Organ-specific considerations

Hepatic Disease

• Early: Restlessness, tachypnea, cool/clammy skin.

• Late: Hypotension, oliguria, hematemesis, melena, jaundice.

• Associated with hepatic encephalopathy: Lethargy → Asterixis → Stupor → Coma.

• Other signs: Hyperventilation, fetor hepaticus, positive Babinski, seizures.

Renal Disease

• Assess dialysis history.

• Monitor for hyperkalemia, metabolic acidosis:

  • S/S: Tachycardia, diarrhea, muscle weakness, Kussmaul’s respirations.

  • Treatment: Bicarbonate, insulin, calcium gluconate, dextrose, or sodium polystyrene sulfonate.

Pulmonary Disease

• Signs: Labored breathing, tachypnea, cyanosis, accessory muscle use.

• Risk: Respiratory acidosis → Asterixis → Coma.

• Early HTN → Later hypotension.

• Support: Oxygen or mechanical ventilation.

Other Causes

• Drug-induced: Common culprits include phenytoin, barbiturates, benzodiazepines.

Special considerations

• Comfort care: Elevate HOB, reduce fatigue, relieve itching (oil baths, avoid soaps).

• Nutritional support: Enteral/parenteral nutrition if LOC is impaired.

• Infection prevention: Reposition regularly, strict aseptic technique.

• Skin care: Prevent breakdown in immobile patients.

Patient counseling

• Educate about underlying condition and treatment.

• Teach rest planning and infection prevention strategies.

• Support emotional and physical well-being.

Pediatric Pointers

• Though rare, end-stage hepatic, renal, or pulmonary diseases can cause asterixis in children.

References

1. Crawford, A. & Harris, H. (2013). Cirrhosis: A complex cascade of care. Nursing 2014 Critical Care, 8(4), 26–30.

2. Dijk, J. M., & Tijssen, M. A. (2010). Management of patients with myoclonus. Lancet Neurology, 9, 1028–1036.