Liver transplantation

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.

Cirrhotic ascites is fluid accumulation in the peritoneal cavity driven by portal hypertension and splanchnic vasodilation, confirmed by a serum-ascites albumin gradient of 1.1 g/dL or more on diagnostic paracentesis. Management proceeds from sodium restriction and combination diuretics to large-volume paracentesis with albumin and TIPS for refractory disease, with every new or worsening episode screened for spontaneous bacterial peritonitis.

Gastroesophageal varices are dilated portosystemic collateral veins that form as portal pressure rises in cirrhosis, and their rupture causes acute variceal hemorrhage, a GI emergency treated with vasoactive therapy, prophylactic antibiotics, and urgent endoscopic band ligation. Screening endoscopy in cirrhotics guides primary prophylaxis with a nonselective beta-blocker or ligation, and survivors of a bleed require combined beta-blocker and serial ligation for secondary prophylaxis.

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.

Hepatorenal syndrome is functional renal failure in a patient with cirrhosis and ascites, driven by splanchnic vasodilation and compensatory renal vasoconstriction, and it is diagnosed only after excluding shock, nephrotoxins, and structural kidney disease and after creatinine fails to improve with diuretic withdrawal and an albumin challenge. Treatment is a splanchnic vasoconstrictor (terlipressin first-line) with intravenous albumin as a bridge to liver transplantation, the only curative therapy.

Hepatopulmonary syndrome is intrapulmonary vascular dilatation and right-to-left shunting that develops in patients with portal hypertension, producing hypoxemia with the hallmark signs of platypnea and orthodeoxia. Contrast-enhanced echocardiography confirms the shunt, and liver transplantation is the only effective treatment.

Hepatocellular carcinoma is a primary liver cancer that arises almost exclusively in cirrhosis and can be diagnosed non-invasively when multiphase CT or MRI shows arterial-phase hyperenhancement with portal-venous washout in a lesion at least 1 cm. Treatment is stratified by tumor burden, liver function, and vascular or extrahepatic spread, ranging from resection or ablation through transplantation and transarterial chemoembolization to systemic atezolizumab-bevacizumab for advanced disease.

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.

Hepatitis C virus is a bloodborne RNA virus, transmitted mainly by injection drug use, that produces mostly asymptomatic acute infection and chronic infection in 60% to 80% of cases. Diagnosis is by HCV antibody followed by HCV RNA, and direct-acting antiviral regimens cure more than 90% of patients, reducing but not eliminating the risk of cirrhosis and hepatocellular carcinoma.

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.

Primary biliary cholangitis is an autoimmune, T cell-mediated destruction of small and medium intrahepatic bile ducts that presents with fatigue and pruritus in middle-aged women and a cholestatic liver chemistry pattern. Diagnosis requires two of three criteria (elevated alkaline phosphatase, positive antimitochondrial antibody, compatible biopsy), and lifelong ursodeoxycholic acid is first-line treatment, with obeticholic acid or fibrates added for inadequate biochemical response.

Alcohol-associated hepatitis is an acute steatohepatitic syndrome, fever, tender hepatomegaly, jaundice, and leukocytosis, arising on a background of heavy chronic alcohol use. Severity is graded by the Maddrey discriminant function and the Model for End-Stage Liver Disease score, and severe disease is treated with prednisolone after infection and bleeding are excluded, guided by the day-7 Lille score.

Acute liver failure is the abrupt onset of hepatic synthetic dysfunction, defined by coagulopathy with an INR of 1.5 or higher plus any grade of hepatic encephalopathy, occurring within 26 weeks of illness onset in a patient without preexisting liver disease. Acetaminophen overdose is the leading cause in the United States, and management centers on N-acetylcysteine when acetaminophen is implicated, intensive supportive care, and early referral to a liver transplant center.

Drug-induced liver injury (DILI) is liver damage from a prescription, over-the-counter, or herbal agent, ranging from asymptomatic transaminase elevation to acute liver failure. Diagnosis rests on excluding other causes and a temporal drug link; management is prompt discontinuation of the offending agent, with N-acetylcysteine for acetaminophen toxicity.

Abnormal liver chemistries are evaluated by first classifying the pattern as hepatocellular (AST/ALT predominant), cholestatic (ALP/bilirubin predominant), or isolated hyperbilirubinemia, then pursuing an ordered, pattern-specific workup for viral, autoimmune, metabolic, toxic, infiltrative, and obstructive causes.

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.