Acute Liver Failure Clinical Presentation

Updated: Jun 13, 2017
  • Author: Gagan K Sood, MD; Chief Editor: BS Anand, MD  more...
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Presentation

History

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)

Next:

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

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