Cirrhosis and Portal Hypertension

Introduction

Cirrhosis is a diffuse injury to the liver characterized by fibrosis and a conversion of the normal hepatic architecture into structurally abnormal nodules.

• The end result is destruction of hepatocytes and their replacement by fibrous tissue. The resulting resistance to blood flow results in portal hypertension and the development of varices and ascites. Hepatocyte loss and intrahepatic shunting of blood result in diminished metabolic and synthetic function, which leads to hepatic encephalopathy (HE) and coagulopathy.

Portal hypertension is characterized by hypervolemia, increased cardiac index, hypotension, and decreased systemic vascular resistance. Ascites is the pathologic accumulation of lymph fluid within the peritoneal cavity. It is one of the earliest and most common presentations of cirrhosis.

CLINICAL PRESENTATION

• The range of presentation of patients with cirrhosis may be from asymptomatic, with abnormal laboratory or radiographic tests, to decompensated with ascites, spontaneous bacterial peritonitis, HE, or variceal bleeding.
• Some presenting characteristics with cirrhosis are anorexia, weight loss, weakness, fatigue, jaundice, pruritis, gastrointestinal (GI) bleeding, coagulopathy, increased abdominal girth with shifting flank dullness, mental status changes, and vascular spiders.

Signs and symptoms :

Asymptomatic Hepatomegaly and splenomegaly Pruritus, jaundice, palmar erythema, spider angiomata, and hyperpigmentation Gynecomastia and reduced libido Ascites, edema, pleural effusion, and respiratory difficulties Malaise, anorexia, and weight loss Encephalopathy.

Laboratory tests :

Hypoalbuminemia, Elevated prothrombin time (PT), Thrombocytopenia Elevated alkaline phosphatase (AST,) Elevated aspartate transaminase, alanine transaminase (ALT), and γ-

TREATMENT

• Goals of Treatment: Treatment goals are clinical improvement or resolution of acute complications, such as variceal bleeding, and resolution of hemodynamic instability for an episode of acute variceal hemorrhage. Other goals are prevention of complications, adequate lowering of portal pressure with medical therapy using β-adrenergic blocker therapy, and support of abstinence from alcohol.

GENERAL APPROACH TO TREATMENT : Approaches to treatment include the following:

✓ Identify and eliminate the causes of cirrhosis (e.g., alcohol abuse).

✓ Assess the risk for variceal bleeding and begin pharmacologic prophylaxis where indicated, reserving endoscopic therapy for high-risk patients or acute bleeding episodes.

✓ The patient should be evaluated for clinical signs of ascites and managed with pharmacologic treatment (e.g., diuretics) and paracentesis. Spontaneous bacterial peritonitis (SBP)should be carefully monitored in patients with ascites who undergo acute deterioration.

✓ HE is a common complication of cirrhosis and requires clinical vigilance and treatment with dietary restriction, elimination of CNS depressants, and therapy to lower ammonia levels.

✓ Frequent monitoring for signs of hepatorenal syndrome, pulmonary insufficiency, and endocrine dysfunction is necessary.

GPrimary Prophylaxis

• All patients with cirrhosis and portal hypertension should be screened for varices on diagnosis.
• The mainstay of primary prophylaxis is the use of a nonselective β-adrenergic blocking agent such as propranolol or nadolol. These agents reduce portal pressure by reducing portal venous inflow via two mechanisms: decrease in cardiac output and decrease in splanchnic blood flow.
• Therapy should be initiated with propranolol, 20 mg twice daily, or nadolol, 20 to 40 mg once daily, and titrated every 2 to 3 days to maximal tolerated dose to heart rate of 55 to 60 beats/min. β-Adrenergic blocker therapy should be continued indefinitely.
• Patients with contraindications to therapy with nonselective β-adrenergic blockers (i.e., those with asthma, insulin-dependent diabetes with episodes of hypoglycemia, and peripheral vascular disease) or intolerance to β-adrenergic blockers should be considered for alternative prophylactic therapy with EVL.