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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Overview
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.
Historical Perspective
Trey and Davidson coined the term fulminant hepatic failure in 1970, to describe this reversible condition of severe liver injury. They described a condition that involved the development of encephalopathy within 8 weeks of the appearance of the first symptoms, and an absence of pre-existing liver disease.[1]
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 results from the loss of normal function of hepatic tissue which occurs over a short period of time. It results in the loss of the metabolic, secretory, and regulatory effects of the liver cells. This results in the rapid accumulation of toxic substances, which then manifests in the patient as an altered sensorium, cerebral edema, hemodynamic abnormalities, and even multiorgan 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
There are some diseases or conditions which have a similar presentation to acute liver failure. These include tyrosenemia, fructose intolerance, being affected by the toxin from bacillus cereus, and the HELLP syndrome of pregnancy.
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.
Screening
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.
Natural History
Complications
Prognosis
Diagnosis
Diagnostic Criteria
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