Hepatic failure

Hepatic failure may develop from severe acute and fulminant liver injury with necrosis of liver cells (acute hepaic failure), or from advanced chronic liver disease(chronic hepatic failure)

Acute (fulminant) hepatic failure

Occurs most commonly with acute viral hepatitis. Other causes are hepatotoxic drug reactions, carbon tetrachloride poisoning, acute alcoholic hepatitis and pregnancy induced eclampsia.

Chronic hepatic failure

Most often due to cirrhosis. Other causes include chronic active hepatitis, chronic cholestasis and Wilson’s disease.


The syndrome of acute or chronic hepatic failure produce complex menifestations, majority of which are discussed below.


It usually reflects the severity of liver cells damagesince it occurs due to failure of liver cells to metabolise bilirubin.

Hepatic encephalopathy (Hepatic coma)

The genesis of CNS menifestations in liver disease is considered to be due to toxic products not metabolised by liver reaching the systemic circulation without detoxificationand thus damage the brain.

Hyperkinetic circulation

All forms hepatic failure are associated with a hyperkinetic circulation characterized by peripheral vasodilation, increased splanchnic blood flow and increased cardiac output. There is increased splenic flow but reduced renal flow resulting in impaired cortical perfusion. These changes result in tachycardia, low blood pressure and reduced renal function.

Hepatorenal syndrome

The term hepatorenal syndrome applies to patients of both acute and chronic hepatic failure who develop renal failure as well,in the absence of clinical, laboratory and morphological evidence of other causes of renal dysfunction.

Hepatopulmonary syndrome

The pulmonary changes in chronic hepatic failure such as in cirrhosis consist of pulmonary vasodilation with intra pulmonary arteriovenous shunting. This results in ventilation-perfusion inequality that may lead to impaired pulmonary function, clubbing of fingers and sometimes cyanosis.

Coagulation defects

Impaired synthesis of a number of coagulation factors by the diseased liver may result in coagulation disorders. These include disseminated intravascular coagulation (consumption coagulopathy), thrombocytopenia and presence of fibrin degradation products in the blood.

Ascites and oedema

Chronic liver failure due to cirrhosis may lead to portal hypertension and ascites. Decreased synthesis of albumin by the liver resulting in hypoprotienaemia and consequent fall in plasma oncotic pressure, increased hydrostatic pressure due to portal hypertension and secondary hyperaldosteronism, contribute to the development of ascites and oedema in these patients.

Endocrine changes

These may be found in chronic hepatic failure. The changes are more common in alcoholic cirrhosis in active reproductive life. In the male the changes are towards feminization such as gynaecomastia  and hypogonadism. In the female the changes are less towards musculinisation but atrophy of gonads and breasts occurs.

Skin changes

In alcoholic cirrhosis ‘arterial spiders’ having radiating small vessels from a central arteriole are frequent in the vascular region drained by superior vena cava such as in the neck, face, forearms and dorsum of hands. Less frequently, palmar erthema, especially in the hypothenar and thenar eminences and on the pulp of the fingers, is observed in the chronic liver disease.

Foetor hepaticus

A sweetish and pungent of the breath is found in severe cases of acute and chronic hepatocelllular disease. It appears to be of intestinal origin, possibly due to failure of liver to detoxify sulfur-containing substances absorbed from the gut.

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