acute liver failure(redirected from Acute hepatic failure)
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acute liver failureA 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 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).
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.