Acute Infectious Hepatitis with Fulminant Hepatic Failure – A Study of 289 Cases

Deshpande, R.S., M.B., B.S., D.P.H. Medical Superintendent In-charge, Kasturba Hospital for Infectious Diseases, Sane Guruji Marg, Bombay, India

Acute infectious hepatitis is by far the most common form of hepatitis. It occurs sporadically and in epidemics. The virus appears in the blood, intestinal contents and liver at various stages of the disease. It is usually transmitted by the faecaloral route. Unsanitary conditions foster its spread especially when human excreta contaminate food or water or where there is more intimate personal contact.

It may have very mild, moderate or severe manifestations. It could be anicteric, but usually, in the majority of cases, jaundice appears. Anorexia, nausea and occasional vomiting which occur especially at the sight of food, are early symptoms. The urine becomes dark brown and a day or two later, frank jaundice appears. Darkening of the urine and a lightening of faeces heralds the development of jaundice starting on the sclera and spreading in varying depths to all over the body. Patients become febrile and feel miserable (Sherlock 1973) 38.

Viral hepatitis, as observed in India, is frequently of prolonged duration with a predisposition to complications like subacute hepatic necrosis or acute fulminant necrosis or acute hepatic failure. Such cases are commonly those in whom a superimposed direct nutritional deficiency increases the susceptibility of the liver cells to necrosis – in Asia and Africa diets usually lack in first class proteins (Davidson 1968)11. The development of drowsiness in a patient with acute infectious hepatitis should be regarded as a danger sign. Treatment to prevent complications that are so often the cause of death must be instituted.

Hepatic precoma and coma occur frequently in patients with severe forms of acute viral hepatitis and in severe liver disease. There are several days of confusion followed by stupor, which is a precoma condition and is followed by coma. Hepatic coma is in fact a common accompaniment of most forms of severe liver disease, and hepatocellular failure may follow a severe attack of acute viral hepatitis.

Etiopathological Features

Fulminant hepatic failure is defined as a clinical syndrome associated with massive necrosis of liver cells or with sudden severe impairment of hepatic function. It is characterised by acute onset of progressive and severe mental changes starting with confusion and rapidly advancing to stupor or coma. In nearly all cases there is widespread inflammation in the portal tracts and in the lobules. The cause is presumed to be the virus in most cases (Brit. med. Bull. 1972)6

The liver undergoes necrosis (Autolysis) and releases breakdown products into the circulation. A great increase of serum amino-acid concentrate is usual when the liver undergoes necrosis. Perhaps these aminoacids are harmful to the brain function when their serum concentration is high. The liver is the chief site for disposal of aminoacids by deamination. Decrease of this function contributes considerably to the hyperaminoacidaemia associated with massive liver necrosis. Coma has been attributed to abnormalities in ammonia metabolism. This, by far, is the most likely hypothesis. The molecular basis of ammonia interaction is not settled though most likely (Sheldon Jacobson 1973)19. The cerebral disturbances manifested by patients with liver disease may be the result of many other toxins besides ammonia.

Normally, a great many substances are detoxified and metabolised or excreted by the liver. Some are substances, which depress the cerebral oxygen consumption and brain function, and eventually result in coma.

There is a concept of portal systemic encephalopathy for patients going into coma. The concept considers cerebral intoxication by intestinal contents, which have not been metabolised by the liver, the toxins produced by intestinal bacteria, ammonia toxicity and other nitrogenous substances and L-tryptophane, which is particularly toxic and other metabolic abnormality. These metabolic changes are acid base electrolyte changes, hypoxia, transfer of ionised ammonia across the cell membrane, changes in carbohydrate metabolism, fatty acid metabolism, and undue sensitiveness of the brain to insults. There is difficulty in mobilising and storing carbohydrates and in manufacturing proteins. This syndrome is most frequently associated with viral hepatitis in the fulminant form.

The rapid onset of coma is presumed to be of metabolic origin rather than due to structural changes (Williams 1970)48. Disordered cerebral function may be due to a lack of an essential substance produced by the normal liver. Failure of the damaged liver to detoxicate these substances is thought to be the main factor but other metabolic changes as well as alterations in acid base balance and possibly in cerebral blood flow may be additive. Disordered brain function (Encepholopathy) results from substances reaching the brain which are made by bacterial action on protein in the colon due to by-passing the liver cells where they are normally metabolised. The accumulation of toxins especially protein-bound non-dialysable toxins and the lack of essential metabolates may play a part in the pathogenesis of hepatic coma. This, by far, is the most likely hypothesis. The primary site of the action is thought to be on the alerting mechanisms situated in the reticular formation. Recently a lot of interest has been created in the effects of neutrotransmitter amines in hepatic coma. (Parkes et al, 1970)30

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