Physical Address
304 North Cardinal St.
Dorchester Center, MA 02124
Variceal Bleeding
Esophageal and gastric variceal bleeding represents a common and potentially life-threatening complication of cirrhosis, and occurs as a consequence of progressive portal hypertension. Patients with cirrhosis are initially categorized as having either compensated or decompensated cirrhosis, the latter defined by the development of overt hepatic decompensation events such as ascites, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatic hydrothorax, or variceal hemorrhage. These complications arise predominantly from the progressive development of portal hypertension ( Fig. 153.1 ) as part of the natural history of cirrhosis, which is defined based on measurement of hepatic venous pressure gradient (HVPG), the difference between the wedged and free hepatic venous pressure. Among patients with compensated cirrhosis, patients may have either normal portal pressure (HVPG < 5 mm Hg), mild portal hypertension (HVPG 6–9 mm Hg), or clinically significant portal hypertension (CSPH) defined as HVPG ≥10 mm Hg. It is this latter group with CSPH who are at risk for developing varices and other decompensation events such as ascites and hepatic encephalopathy.
Clinical Measurement of Portal Hypertension.
Gastroesophageal varices (GEVs) are common and seen in approximately 50% of patients with cirrhosis, including up to 30% and 85% of patients with compensated and decompensated cirrhosis, respectively. Among patients with compensated cirrhosis, varices develop at a rate of 7% to 8% per year, of which variceal hemorrhage occurs at a rate of 10% to 15% per year. Per guidelines of the American Association for the Study of Liver Diseases (AASLD), a screening endoscopy to identify the presence of GEVs is recommended at the time of cirrhosis diagnosis. However, patients who have liver stiffness measurement (LSM) less than 20 kPa on transient elastography and normal platelet count greater than 150,000/mm 3 are deemed to have a low probability (<5%) of having high-risk varices, and therefore endoscopy is not required. Patients who have no varices identified on screening endoscopy do not require further intervention, but should undergo surveillance endoscopy every 2 to 3 years. Patients with compensated cirrhosis who have small varices on screening endoscopy should undergo surveillance endoscopy every 1 to 2 years. Patients with decompensated cirrhosis with any varices, as well as patients with compensated cirrhosis with moderate or large varices, are recommended to undergo primary prophylaxis with a nonselective beta-blocker (NSBB) such as nadolol or propranolol.
Diagnosis: Role of Endoscopy
Endoscopy is useful to identify the presence of varices in patients with cirrhosis and to distinguish high-risk features associated with an increased bleeding risk. Endoscopy is also indicated for patients with acute bleeding to identify the cause of bleeding and for therapeutic intervention. Reports indicate that 10% to 47% of liver disease and upper gastrointestinal bleeding has a nonvariceal source.
The risk for bleeding is related to the severity of liver disease using Child criteria, the presence of red wales, and the size of the varices. The simplest of several grading systems classifies varices from grades 1 to 3. Grade 3 varices are those that occlude the lumen; grade 1 varices disappear completely with insufflation; and grade 2 varices are between grades 1 and 3 in size. Using these scoring systems, patients can be stratified into categories ranging from 6% to 76% risk for bleeding during 1 year of follow-up. One study concluded that varices were most likely to be found during endoscopy in patients with compensated cirrhosis when prothrombin activity was less than 70%, platelet count less than 100 × 10 9 /L, and ultrasonographic portal vein diameter greater than 13 mm.
Primary Prophylaxis
Nonselective beta-adrenergic blocking agents (β-blockers; e.g., propranolol, nadolol) are effective in reducing the risk for a first bleed by 40% to 50% in patients with esophageal varices. Treatment with propranolol begins at 40 mg daily, and doses up to 160 mg daily may be used. Treatment is associated with lower bleed-related mortality and may improve survival.
Endoscopic sclerotherapy has been extensively studied as primary prophylaxis for variceal bleeding, with more than 1500 patients enrolled in trials. With some exceptions, however, sclerotherapy has not been effective, largely because of the high rate of adverse effects, such as pulmonary complications, fever, chest pain, and esophageal ulceration.
Portosystemic shunts are effective in primary prevention but are associated with an unacceptably high incidence of hepatic encephalopathy. A significant proportion of patients fail to tolerate β-blockers or fail to experience a reduction in portal pressure with shunt therapy. Therefore alternative therapies are needed.
Variceal band ligation has been studied as primary prevention ( Fig. 153.2 ) and compared with β-blockers. The largest study showed reduced bleeding, from 43% in the propranolol group to 15% in the ligation group. Risk for bleeding in the propranolol group appeared unusually high, possibly because of underdosage. Band ligation does not appear to reduce overall or bleed-related mortality. Band ligation as primary prophylaxis should be reserved for patients with compensated cirrhosis with large varices or for patients with advanced liver disease with small or large varices who cannot tolerate β-blockers.
Isosorbide mononitrate at 40 mg twice daily can be used if neither ligation nor β-blocker therapy is an option.
You're Reading a Preview
Become a Clinical Tree membership for Full access and enjoy Unlimited articles
If you are a member. Log in here