Acute Liver Failure Clinical Presentation

Updated: Jun 13, 2017
  • Author: Gagan K Sood, MD; Chief Editor: BS Anand, MD  more...
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The patient's history is valuable for suggesting the likely causes of acute liver failure and guiding appropriate interventions. If the patient is incapacitated, closely question family members, caretakers, and friends.

In taking the history, collect details on the following:

  • Date of onset of jaundice and encephalopathy
  • Alcohol use
  • Medication use (prescription and illicit or recreational)
  • Herbal or traditional medicine use
  • Family history of liver disease (Wilson disease)
  • Exposure to risk factors for viral hepatitis (travel, transfusions, sexual contacts, occupation, body piercing)
  • Exposure to hepatic toxins (mushrooms, organic solvents, phosphorus contained in fireworks).
  • Evidence of complications (eg, renal failure, seizures, bleeding, infection)

Physical Examination

Physical examination includes careful assessment and documentation of the patient's mental status and search for stigmata of chronic liver disease. Jaundice is often but not always present. Right upper quadrant tenderness is variably present. The liver span may be small, indicative of significant loss of volume due to hepatic necrosis. An enlarged liver may be seen with heart failure, viral hepatitis, or Budd-Chiari syndrome.

The development of cerebral edema may ultimately give rise to manifestations of increased intracranial pressure (ICP), including papilledema, hypertension, and bradycardia.

The rapid development of ascites, especially if observed in a patient with fulminant hepatic failure accompanied by abdominal pain, suggests the possibility of hepatic vein thrombosis (Budd-Chiari syndrome).

Hematemesis or melena as a result of upper gastrointestinal bleeding may complicate fulminant hepatic failure.

Typically, patients are hypotensive and tachycardic as a result of the reduced systemic vascular resistance that accompanies fulminant hepatic failure, a pattern that is indistinguishable from septic shock. Although this presentation may be intrinsic to hepatic failure, it is important to consider the possibility of a superimposed infection (especially spontaneous bacterial peritonitis).

Assess the patient for signs of encephalopathy. See the table below.

Table. Grading of Hepatic Encephalopathy (Open Table in a new window)

Grade Level of Consciousness Personality and Intellect Neurologic Signs Electroencephalogram (EEG) Abnormalities
0 Normal Normal None None
Subclinical Normal Normal Abnormalities only on psychometric testing None
1 Day/night sleep reversal, restlessness Forgetfulness, mild confusion, agitation, irritability Tremor, apraxia, incoordination, impaired handwriting Triphasic waves (5 Hz)
2 Lethargy, slowed responses Disorientation to time, loss of inhibition, inappropriate behavior Asterixis, dysarthria, ataxia, hypoactive reflexes Triphasic waves (5 Hz)
3 Somnolence, confusion Disorientation to place, aggressive behavior Asterixis, muscular rigidity, Babinski signs, hyperactive reflexes Triphasic waves (5 Hz)
4 Coma None Decerebration Delta/slow wave activity