Varices

Hepatobiliary disease occurs due to bile duct obstruction from abnormal bile composition and flow. Hepatomegaly, splenomegaly, and cholecystitis may be present. Hepatic steatosis may also be present due to effects of malnutrition. The progression from cholestasis (impaired bile flow) to portal fibrosis and to focal and multilobar cirrhosis, esophageal varices, and portal hypertension takes several years. Many patients are compensated and asymptomatic but maybe susceptible to acute decompensation in the event of extrinsic hepatic insult from viruses, medications, or other factors.7... 

O Portal hypertension is the precipitating factor for the complications of cirrhotic liver disease—ascites, spontaneous bacterial peritonitis (SBP), variceal bleeding, and hepatic encephalopathy. Lowering portal pressure can reduce the complications of cirrhosis and decrease morbidity and mortality. 

Non-selective P-blockers are first-line treatment for preventing variceal bleeding they vasoconstrict the splanchnic bed through multiple mechanisms. 

Cirrhosis is the progressive replacement of normal hepatic cells by fibrous scar tissue. This scarring is accompanied by the loss of viable hepatocytes, which are the functional cells of the liver. Progressive cirrhosis is irreversible and leads to portal hypertension that is in turn responsible for many of the complications of advanced liver disease. These consequences include (but are not limited to) spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, and variceal bleeding.1... 

The splanchnic system drains venous blood from the GI tract to the liver. In portal hypertension there is increased resistance to drainage from the originating organ so collateral vessels (varices) develop in the esophagus, stomach, and rectum to compensate for the increased blood volume. Varices divert blood meant for hepatic circulation back to the systemic circulation this has the unintended deleterious effect of decreasing clearance of medications and potential toxins through loss of first-pass metabolism. Varices are weak superficial vessels, and any additional increase in pressure can cause these vessels to rupture and bleed.15... 

Patients with previously stable cirrhosis who develop acute encephalopathy often have an identifiable precipitating event that can account for the increased production and/or decreased elimination of these toxins. Infections, variceal hemorrhage, renal insufficiency, electrolyte abnormalities, and increased dietary protein have all been associated with acute development of HE. 

Hemorrhage associated with variceal bleeding may be associated with nausea, vomiting, and hematemesis. Patients may also present with pallor, fatigue, and weakness from blood loss. 

In patients with bleeding varices, digestion of swallowed blood represents a high protein load this causes nausea and can precipitate symptoms of HE. 

Anemia (decreased hemoglobin and hematocrit) occurs as a result of variceal bleeding, decreased erythrocyte production, and hypersplenism. 

In some cases, cirrhosis is diagnosed incidentally before the patient develops symptoms or acute complications. Other patients may have decompensated cirrhosis at initial presentation they may present with variceal bleeding, ascites, SBP, or HE. Patients may also have some of the laboratory abnormalities and/or signs and symptoms listed above that are associated with cirrhosis.28... 

Patients with ascites or known varices must be assumed to have portal hypertension and are treated as such, even if direct measurements of portal pressure have not been made.29... 

Balloon tamponade involves the application of direct pressure to the area of bleeding with an inflatable balloon attached to a nasogastric tube. It is an option for patients in whom drug therapy and band ligation fail to stop variceal bleeding. Balloon tamponade is used only when other methods have failed. Once the direct pressure of the balloon is removed, rebleeding often occurs, so balloon tamponade is only a temporary measure prior to more definitive treatment such as shunting.11... 

Drug therapy for portal hypertension and cirrhosis can alleviate symptoms and prevent complications but it cannot reverse cirrhosis. Drug therapy is available to treat the complications of ascites, varices, spontaneous bacterial peritonitis, hepatic encephalopathy, and coagulation abnormalities. 

Non-selective fi-blockers such as propranolol and nadolol are first-line treatments to reduce portal hypertension. This effect reduces bleeding and decreases mortality in patients with known varices. Use of (1-blockers to prevent variceal formation is controversial. 

Only non-selective p-blockers reduce bleeding complications in patients with known varices. Blockade of P, receptors reduces cardiac output and splanchnic blood flow. 02-Adrenergic blockade prevents p2-receptor-mediated splanchnic vasodilation while allowing unopposed a-adrenergic effects this enhances vasoconstriction of both the systemic and splanchnic vascular beds. The combination of P, and P2 effects makes the non-selective p-blockers preferable to car-dioselective agents in treating portal hypertension.1,36,41... 

Initiation of prophylactic antibiotics is recommended during acute variceal bleeding this is typically done with an oral fluoroquinolone (e.g., ciprofloxacin 500 mg twice daily x 7 days) or an IV third-generation cephalosporin. Prophylactic antibiotic therapy reduces in-hospital infections and mortality in patients hospitalized for variceal bleeding.44... 

Patients who have previously experienced spontaneous bacterial peritonitis and have low-protein ascites (ascitic fluid albumin less than 1 g/dL [less than 10 g/L]) are candidates for long-term prophylactic therapy. Recommended regimens include either a single trimethoprim-sulfamethoxazole doublestrength tablet 5 days per week (Monday through Friday) or ciprofloxacin 750 mg once weekly.19,46 Any patient who has experienced an episode of variceal bleeding should also receive prophylactic antibiotics. 

What is the prognosis for this patient who has developed ascites, variceal bleeding, and hepatic encephalopathy within 3 months ... 

Consider antibiotic prophylaxis for SBP in patients with a history of variceal bleeding or prior SBP. 

Sharara AI, Rockey DC. Gastroesophageal variceal hemorrhage. N Engl J Med 2001 345 669-681. 

Chronic hepatitis (disease lasting longer than 6 months) is usually associated with hepatitis B, C, and D. Chronic viral hepatitis may lead to the development of cirrhosis, which may induce end-stage liver disease (ESLD). Complications of ESLD include ascites, edema, jaundice, hepatic encephalopathy, infections, and bleeding esophageal varices. Therefore, prevention and treatment of viral hepatitis may prevent ESLD. 

Esophageal varices Dilated blood vessels in the esophagus. 

Variceal bleeding Gastric or esophageal bleeding from collateral vessels (varices). 

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