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Chapter: Medicine and surgery: Hepatic, biliary and pancreatic systems

Acute hepatitis - Patterns of liver disease

Acute inflammation of the liver parenchyma. - Definition, Incidence, Aetiology, Pathophysiology, Clinical features, Complications, Investigations, Management, Prognosis.

Patterns of liver disease


Acute hepatitis




Acute inflammation of the liver parenchyma.



The causes of acute hepatitis:


·        Acute viral hepatitis may be caused by the hepatotrophic viruses (A, B and E) or other viruses such as Epstein–Barr virus, cytomegalovirus and yellow fever virus.


·        Alcohol-induced hepatitis.


·        Nonalcoholic steatohepatitis.


·        Drug-induced hepatocellular damage which may be histologically indistinguishable from viral hepatitis, e.g. paracetamol.


·        Wilson’s disease.




Cellular damage results in impairment of normal liver function: bilirubin is not excreted properly resulting in jaundice and conjugated bilirubin in the urine, which appears dark. Less bile reaches the gut, so that the stool contains less stercobilinogen and appears pale. There is reduced protein synthesis, e.g. albumin and clotting factors.


Dying hepatocytes release enzymes, mainly transaminases.


Swelling of the liver results in stretching of the liver capsule which may result in pain.

Clinical features


The features of acute liver damage are malaise, jaundice, anorexia, nausea, right upper quadrant pain and in severe cases, evidence of liver failure. In cases of acute viral hepatitis, there is often a history of a ‘flulike’ illness preceding the onset of jaundice. On examination there may be an enlarged, tender liver, pale stools and dark urine. Stigmata of chronic liver disease should be looked for to exclude acute on chronic liver disease.




Acute viral hepatitis has a histological appearance which can be mimicked by drug reactions. Hepatocytes undergo ballooning degeneration appearing swollen and vacuolated. There is a lymphocytic infiltration. Cell death is by apoptosis and results in the formation of Councilman bodies. As regeneration occurs the normal architecture is disrupted. In severe cases, necrosis spreads from one portal tract to the central vein or from central vein to central vein, so that confluent areas of necrosis form termed bridging necrosis.




Fulminant liver failure, chronic hepatitis, and cirrhosis.




Serum bilirubin and transaminases (aspartate transaminase (AST) and alanine aminotransferase (ALT)) are raised in acute liver injury.


Prothrombin time and albumin should be measured. Ultrasound may be needed to exclude obstructive


jaundice, if applicable.


Serological testing will identify viral infections.


Specific tests depend on suspected causes, e.g. paracetamol levels. A liver biopsy may be required if the cause is not identified.




In most cases supportive management is the only available treatment. This includes careful fluid balance, adequate nutrition and anti-emetics. Where possible removal of the causative agent, e.g. alcohol or specific therapies should be given (see Wilson’s Disease page 211 and Paracetamol poisoning page 527). Patients require serial liver function tests (including clotting) to follow the course of the hepatitis.

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