Acute liver failure overview

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:

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Historical Perspective

The hepatic and mental disturbance association dates back to Hippocrates. In the sixteenth century, Ballonius was the first to describe hepatic coma. In 1860, Frerichs described the terminal mental changes in patients with cirrhosis and yellow atrophy of the liver. In 1970, Trey and Davidson introduced the term fulminant hepatic failure. Later it was suggested that the term fulminant should be confined to patients who develop jaundice to encephalopathy within 2 weeks. Terms subfulminant hepatic failure and late-onset hepatic failure were coined for onset between 2 weeks to 3 months and for 8 weeks to 24 weeks respectively. The term of acute liver failure was proposed by King's college group.

Classification

Acute liver failure may be classified on the basis of the time interval between the onset of symptoms and the development of encephalopathy as hyperacute, acute, subacute, fulminant, subfulminant and late-onset. The different classification systems used are O’Grady system, Bernuau system, and Japanese system. This classification based on time duration provides helpful clues about etiology, complications, and prognosis such as in hyperacute cases, the cause is usually viral infections or acetaminophen toxicity. The subacute cases can be due to idiosyncratic drug reactions and can also be confused with chronic liver disease. The hyperacute liver failure has a better prognosis than subacute liver failure.

Pathophysiology

Acute liver failure is a sudden and severe loss of liver function with evidence of encephalopathy and coagulopathy with elevated prothrombin time (PT) and (INR) in a person without a preexisting liver disease. The effects of acute liver failure are due to the loss of its metabolic, secretory and regulatory effects. This results in the accumulation of toxic substances and causes deleterious effects. The major pathophysiological mechanisms of morbidity and mortality in patients with acute liver failure are cerebral edema, hypoperfusion to the liver, idiosyncratic drug reactions, depletion of glutathione and viral hepatitis. Cerebral edema in acute liver failure can be due to vasogenic and cytotoxic effects. In cytotoxic type, there is intracellular swelling and blood-brain barrier is intact. In vasogenic type, the blood-brain barrier breaks down and plasma and water accumulate in the extracellular space. The increased ammonia concentration in liver failure in combination with the glutamine produced by the astrocytes causes excess levels of glutamine with the help of enzyme glutamine synthetase. The excess glutamine is cytotoxic and can disturb the osmotic gradient which can result in brain swelling. In acute liver failure, the increased levels of nitric oxide in the circulation can also disrupt the cerebral autoregulation. Acetaminophen is the leading cause of acute liver failure in the United States. Acetaminophen causes dose-related toxicity. Toxicity is rarely seen at normal therapeutic doses (up to 4 g/day) without underlying liver disease. Viral hepatitis is the leading cause of acute liver failure in the developing world. Hepatitis A, B, D (associated with B), and E (in endemic countries) are commonly associated with acute liver failure.

Causes

The causes of acute liver failure can be categorized into viral, drugs and toxins, vascular and metabolic. Common causes of acute liver failure include acetaminophen toxicity, viral hepatitis (most commonly hepatitis A, hepatitis B and hepatitis E), alcoholic hepatitis, autoimmune, sepsis, right heart failure and idiopathic. Acetaminophen toxicity is the most common cause of acute liver failure in the developed world and viral hepatitis (most commonly hepatitis A, hepatitis B and hepatitis E) is most common in the developing world.

Differentiating Acute liver failure from other Diseases

Acute liver failure must be differentiated from other diseases that cause signs and symptoms of jaundice, coagulopathy, and encephalopathy. The differentials include acute hepatitis, cholestatic jaundice, and hemolytic jaundice. The common causes of acute hepatitis causing acute liver failure include acetaminophen toxicity, viral hepatitis, alcoholic hepatitis, autoimmune hepatitis, acute fatty liver of pregnancy, Wilson's disease, ischemic hepatitis and hepatic congestion due to right heart failure and Budd–chiari syndrome.

Risk Factors

Certain conditions can put a person at risk for developing acute liver failure. These include having certain infections, vascular disorders, autoimmune conditions, metabolic diseases, and primary cancers or malignancies.

Natural History, Complications and Prognosis

Acute liver failure is a serious condition which can rapidly progress to death if left untreated. Complications of the illness include cerebral edema, brain herniation, multi-organ failure, systemic inflammatory response syndrome, metabolic derangements, coagulopathy, hemodynamic instability, coma, and death.Several prognostic scoring systems have been devised to predict mortality and to identify who will require early liver transplant. Mortality due to acute liver failure used to be as high as 80%, however this statistic has decreased with the advent of liver transplantation, and better intensive care. There are several prognostic indicator scores used for the prediction of mortality, and to assess the suitability of the patient for transplantation. These include kings college hospital criteria, MELD score, APACHE II and Clichy criteria.

Diagnosis

History and Symptoms

A thorough history should be obtained, with special attention given to a history of ingesting medications or other toxins. Symptoms can include symptoms such as fatigue, nausea, vomiting, abdominal distention, diarrhea, disorientation, and an increased bleeding tendency