Acute Liver Failure (ALF)

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ALF manifests as jaundice with increased INR and decreased consciousness.

ALF is present when there is an increase in the INR (> 1.5) and when hepatic encephalopathy appears in a patient previously not known to have serious underlying liver disease.

The interval between the first increase in bilirubin and the onset of hepatic encephalopathy also determines the prognosis. Hyperacute liver failure is present if this interval is less than 1 week. This may be accompanied by cerebral edema and cerebral compression. If the interval is longer than 6 to 8 weeks, subacute liver failure is present. The clinical picture then corresponds to the end stage of a patient with cirrhosis, without cirrhosis being present. Mortality in this type is caused by bacterial infections.

Hepatitis A and acetaminophen cause hyperacute liver failure. Hepatitis B usually leads to acute liver failure. Liver failure provoked by DILI leads to subacute liver failure. This type is now considered the most important cause of ALF.

If the patient meets the criteria for urgent liver transplantation, he has a mortality of more than 90% within 2 weeks if he does not receive a transplant. However, if the patient recovers, a complete spontaneous recovery follows.

Scores that help to assess the need for liver transplantation include the King's College Criteria. They are based on age, etiology, the interval between the rise in bilirubin and the finding of hepatic encephalopathy, the INR and bilirubin level. The subacute forms have the worst prognosis.

Therefore, a patient without previous liver disease who develops an INR > 1.5 should be referred immediately to a centre where urgent liver transplantation is possible. In that case, supportive therapy with N-acetylcysteine ​​can be given. This results in an improvement of peripheral tissue oxygenation.

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