Acute liver failure

Hepatic encephalopathy is a reversible spectrum of brain dysfunction from insufficient hepatic clearance and portosystemic shunting of gut-derived toxins, graded by the West Haven criteria and almost always triggered by an identifiable precipitant such as infection, gastrointestinal bleeding, constipation, or an electrolyte disturbance. Diagnosis is clinical, and management proceeds by treating the precipitant first, then titrating lactulose and adding rifaximin for recurrence prevention.

Hepatitis A virus is a fecal-oral RNA virus that causes acute, host-immune-mediated hepatitis with a prodrome followed by jaundice, aminotransferases often exceeding 1,000 U/L, and full recovery in at least 90% of patients within 3 to 6 months. Diagnosis rests on HAV IgM, treatment is supportive, and prevention centers on a 2-dose inactivated vaccine plus prompt postexposure prophylaxis.

Hepatitis B virus is a bloodborne and sexually transmitted DNA virus that causes acute hepatitis and, when infection becomes chronic, progresses through immune-tolerant, immune-active, immune-control, and reactivation phases toward cirrhosis and hepatocellular carcinoma. Diagnosis rests on hepatitis B serology, chronic infection is treated with entecavir or tenofovir, and reactivation during immunosuppression is prevented with prophylactic antiviral therapy.

Autoimmune hepatitis is a chronic inflammatory hepatitis, four times more common in women, marked by elevated aminotransferases, autoantibodies, and hypergammaglobulinemia, confirmed by liver biopsy after excluding other causes. Treatment is immunosuppression with prednisone, usually combined with azathioprine, continued for at least 2 to 3 years before withdrawal is considered.

Wilson disease is an autosomal recessive disorder of the ATP7B copper-transporting ATPase causing toxic copper accumulation in the liver, brain, and cornea, presenting with hepatic and/or neuropsychiatric disease usually before age 40; diagnosis rests on ceruloplasmin, urinary copper, and Kayser-Fleischer rings, and lifelong treatment is chelation with penicillamine or trientine, or zinc, unless liver transplant is required.

Acute fatty liver of pregnancy is a rare, life-threatening third-trimester disorder of microvesicular hepatic steatosis driven by a fetal-maternal fatty-acid oxidation mismatch (classically LCHAD deficiency); it is treated by immediate delivery, the only intervention that reverses the maternal disease.

Cirrhosis is end-stage hepatic fibrosis with regenerative nodules, staged as compensated or decompensated by the onset of ascites, variceal hemorrhage, encephalopathy, or jaundice. Severity is graded by Child-Pugh class and MELD, and management centers on treating the underlying cause, surveillance for varices and hepatocellular carcinoma, and timely transplant referral once decompensation appears.

Sepsis is life-threatening organ dysfunction caused by a dysregulated host response to infection, identified by an acute rise in SOFA score of 2 points or more in a patient with known or suspected infection. Survival depends on recognizing the pattern early and completing the hour-1 bundle: lactate, blood cultures before antibiotics, broad-spectrum antibiotics such as cefepime 2 g IV every 8 hours, and 30 mL/kg crystalloid for hypotension or a lactate of 4 mmol/L or higher.

HELLP syndrome is a thrombotic microangiopathy of pregnancy, a severe-feature variant of preeclampsia defined by hemolysis, transaminases at least twice the upper limit of normal, and a platelet count under 100,000/uL. Delivery is the only curative treatment; management pairs blood pressure control and magnesium sulfate seizure prophylaxis with prompt, gestational-age-guided delivery.