acute liver failure

(redirected from Acute hepatic failure)

acute liver failure

A condition characterised by an abrupt onset of the signs (e.g., jaundice) and symptoms (e.g., ascites) due to hypoalbuminaemia of a liver incapable of maintaining its normal activity and metabolic functions, which indicates severe damage to 80–90% of native tissue.

Acute hepatitis (autoimmune, drugs, toxin, viral), decompensated chronic liver disease (haemochromatosis, Wilson’s disease), acute exacerbation of chronic liver disease (e.g., autoimmune hepatitis), hepatic infiltration by cancer (most commonly lymphoma).

Acute liver failure, hepatitic vs toxic
Pattern of necrosis
Coagulative vs Lytic

Uniform vs Patchy

± ++ to +++

acute liver failure

The development of severe liver damage with encephalopathy and jaundice within eight weeks of the onset of liver disease. Coagulopathy, electrolyte imbalance, and cerebral edema are common. Death is likely without liver transplantation. Synonym: fulminant hepatic failure; fulminant hepatitis


The most common causes of acute liver failure are viral hepatitis, acetaminophen overdose (and other drug reactions), trauma, ischemia, acute fatty liver of pregnancy, and autoimmune disorders.


Early symptoms are often nonspecific and mFay include nausea, vomiting, dizziness, lightheadedness, or drowsiness. As liver injury becomes more obvious, bile permeates the skin, producing jaundice. Alterations in mental status (lethargy or coma) and bleeding caused by coagulopathy may develop.


The diagnosis is suggested by jaundice and altered mental status in addition to elevations in liver function tests and prolongation of the protime and international normalized ratio (INR).

Patient care

Affected patients should be hospitalized, usually in intensive care under very close monitoring. General patient care concerns apply. Airway support and mechanical ventilation are often needed. Fluids and/or pressors, such as dopamine, may be needed to maintain blood pressure and cardiac output. Nutritional support with a low salt, protein-restricted diet, and most calories supplied by carbohydrates, blood product infusions (fresh frozen plasma and platelets), and lactulose are usually administered. Potassium supplements help to reverse the affects of high aldosterone levels; potassium-sparing diuretics increase urine volume. Ascitic fluid is removed by paracentesis or shunt placement to relieve abdominal discomfort and aid respiratory effort. Portal hypertension requires shunt placement to divert blood flow, and variceal bleeding is treated with vasoconstrictor drugs, balloon tamponade, vitamin K administration, and perhaps surgery (to ligate bleeding portal vein collateral vessels).

Medications that are normally metabolized by the liver and medications that may injure the liver further should be avoided. Patients who have overdosed on acetaminophen may benefit from the administration of acetylcysteine if it can be administered within 12 hr of a single ingestion.

Liver transplantation is the definitive treatment for acute liver failure. Early transplant evaluation should be carried out for every patient for whom there is a donated organ available. Without transplantation, the mortality from acute liver injury may reach 80%.

The patient’s level of consciousness should be assessed frequently, with ongoing orientation to time and place. Girth should be measured daily. Signs of anemia, infection, alkalosis, and GI bleeding should be documented and reported immediately. A quiet atmosphere is provided. Physical restraints are applied as minimally as possible, with chemical restraint prohibited. If the patient is comatose, the eyes are protected from corneal injury using artificial tears and/or eye patches.

The prognosis for the illness should be discussed in a sensitive but forthright fashion and emotional support provided to family members. Agency social workers, the hospital chaplain, and other support personnel should be involved in the patient’s care as appropriate to individual needs.

See also: failure
References in periodicals archive ?
In conclusion, we report four cases of acute hepatic failure, which developed in patients who had received immunosuppressive agents for their rheumatologic conditions.
Subgroup 2 included patients who were thought to have died directly from deterioration of acute hepatic failure.
A low FVIII level in acute hepatic failure indicates presence of DIC.
Acute hepatic failure associated with low-dose sustained release niacin.
Acute hepatic failure characterized by hepatic encephalopathy, severe coagulopathy, jaundice, and hydroperitoneum is associated with high patient mortality, for which there is still no available therapy except liver transplantation limited by the chronic shortage of donor livers (Lee, 1994; Van Thiel et al.
Acute hepatic failure in India: A perspective from the East.
Acute hepatic failure and severe liver injury, in some cases fatal, have been reported in patients treated with KETEK.
During January-June 2004, the Kenya Ministry of Health (MOH) and partners identified 317 cases of acute hepatic failure in eastern Kenya; 125 cases occurred in persons who subsequently died during the illness.
Acute hepatic failure, ARDS, renal failure, DIC, coagulopathy, and decerebrate convulsions are among the fatal complications.
HBV infection occurs primarily in hepatocytes and long-term infection causes hepatic inflammation that leads to acute and chronic hepatic dysfunction including acute hepatic failure, cirrhosis, and hepatocellular carcinoma.
We report the case of a female presenting with diffuse gastrointestinal symptoms progressing to acute hepatic failure and multiple organ dysfunction, diagnosed as resulting from colchicine overdose after being listed for liver transplant for four days.
Ham JM, Fitzpatrick P: Acute pancreatitis in patients with acute hepatic failure.

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