Portal hypertension

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.

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.

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.

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.

Spontaneous bacterial peritonitis is a monomicrobial infection of cirrhotic ascitic fluid without a surgical source, diagnosed by an ascitic fluid neutrophil count of 250 cells/microL or higher on paracentesis. Treatment is prompt IV third-generation cephalosporin plus IV albumin in patients with renal or hepatic dysfunction, followed by indefinite secondary antibiotic prophylaxis because recurrence is common.

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.