Description
Acute liver failure is a rare but serious medical condition characterized by the rapid loss of liver function within a short period, typically days to weeks. It can be caused by various factors such as viral infections (like hepatitis), drug toxicity (such as acetaminophen overdose), autoimmune disorders, and metabolic diseases. Symptoms may include jaundice (yellowing of the skin and eyes), confusion, bleeding, and abdominal swelling. Immediate medical attention is crucial, often requiring hospitalization and intensive care. Treatment involves addressing the underlying cause, managing complications, and, in severe cases, evaluating the need for a liver transplant. Early intervention and close medical monitoring are vital for improving outcomes in acute liver failure.
Summary Listen
- Acute liver failure (ALF) is a rare but deadly condition characterized by rapid liver dysfunction in the absence of pre-existing chronic liver disease. Key diagnostic criteria include jaundice, coagulopathy (INR > 1.5), and encephalopathy, appearing within 26 weeks. Viral hepatitis and anti-tuberculosis drugs are common causes in India, while acetaminophen overdose predominates in the West.
- Etiology is crucial for management and prognosis. The O'Grady system defines hyperacute (encephalopathy within 7 days of jaundice), acute (within 4 weeks), and subacute (4-26 weeks) liver failure. The Indian definition mirrors this but tailors it to the local scenario, emphasizing that the development of encephalopathy and coagulopathy within 28 days of jaundice constitutes acute liver failure.
- Clinical features are initially nonspecific, including fatigue, anorexia, and jaundice. Encephalopathy is graded from mild confusion to coma, and the presence and severity of encephalopathy guides management and transplantation decisions. Cerebral edema arises from ammonia buildup, astrocyte swelling, and inflammation breaching the blood-brain barrier.
- Evaluation involves identifying the cause (viral serologies, autoimmune markers, toxicology screens), assessing prognosis (prothrombin time, serum chemistry, arterial blood gas, ammonia levels), and excluding alternative diagnoses. CT scans or MRIs of the brain are utilized to rule out intracranial bleeding or cerebral edema.
- Management prioritizes maintaining cerebral perfusion pressure (CPP) above 50 mm Hg and intracranial pressure (ICP) below 20 mm Hg. Volume resuscitation with crystalloids and albumin is crucial, maintaining mean arterial pressure above 65 mm Hg. Norepinephrine is the preferred vasopressor, with vasopressin as a second-line option. Hypocapnia is no longer routinely recommended.
- Renal replacement therapy (RRT), particularly continuous RRT, addresses hyperammonemia, fluid overload, and electrolyte imbalances. Anticoagulation during RRT should use citrate to minimize bleeding risk. Prophylactic transfusions of blood products are discouraged unless active bleeding occurs.
- Infections are a leading cause of death. While prophylactic antibiotics are debated, a high index of suspicion is necessary with worsening encephalopathy or persistent fever. Antifungal therapy is indicated in prolonged antibiotic use and multi-organ failure.
- Liver transplantation (LT) is the definitive treatment. King’s College criteria guide referral for transplantation. Specific therapies address underlying causes, such as antivirals for hepatitis B or N-acetylcysteine for acetaminophen toxicity. While liver assist devices hold promise, they are not yet standard treatment.
- Long-term outcomes depend on the need for LT. Patients surviving ALF without LT typically regain normal liver function due to liver regeneration. Transplant recipients require lifelong immunosuppression and face associated complications.
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