MANAGEMENT OF UPPER GASTROINTESTINAL BLEEDING IN THE PATIENT WITH CHRONIC LIVER DISEASE

The basic management is similar for all patients with upper gastrointestinal (UGI) bleeding regardless of the cause or whether chronic liver disease is present or absent. All patients with massive UGI hemorrhage should be admitted to an intensive care unit (ICU) for resuscitation and close monitoring to minimize endoscopic complications or bleeding-related complications such as aspiration, shock, cardiac arrhythmia, and death. 114 Prompt and adequate intravascular volume replacement must be instituted immediately for all patients with severe UGI bleeding. Two large-bore (18-gauge or larger) peripheral intravenous catheters should be placed for venous access to minimize the risk of shock. Inadequate resuscitation before endoscopy is an important cause of endoscopy-related morbidity and mortality in the setting of ongoing or recurrent massive UGI bleeding. Packed red blood cell transfusions are indicated for patients with active bleeding and diminished intravascular volume to maintain the hematocrit value 30% or greater. Many patients with chronic liver disease have some degree of coagulopathy (e.g., prolonged prothrombin time or partial thromboplastin time) and thrombocytopenia caused by poor hepatic synthetic function and hypersplenism. Attempts should be made to correct or improve the underlying coagulopathy with fresh frozen plasma and subcutaneous vitamin K injection, although the latter measure does not have any immediate effect. Platelet transfusions are indicated if the platelet count is below 50,000/mm 3 and there is evidence of active bleeding or if therapeutic endoscopy is anticipated. Bleeding may diminish or stop completely following these measures. These steps may have only a minimal effect on these bleeding parameters because of primary fibrinolysis, low-grade disseminated intravascular coagulation, and hypersplenism. Other temporizing measures that may slow or stop variceal bleeding include mechanical balloon tamponade and pharmacologic agents such as vasopressin, somatostatin, or octreotide (see treatment of variceal bleeding, later). These therapies are adjunctive and should not be instituted before endoscopic confirmation of variceal bleeding. The patient with chronic liver disease who presents with massive UGI bleeding is often unable to give a history because of hepatic encephalopathy. Therefore, this information must be obtained from family members or friends. Important historical information to elicit should include the onset and severity of the bleeding episode, a prior history of UGI bleeding (e.g., prior variceal or nonvariceal bleeding), medications (e.g., aspirin, nonsteroidal anti-inflammatory drugs [NSAIDs], warfarin), the cause and severity of liver disease (Child-Pugh classification [see article by Jaffe and colleagues]), previous nonbleeding complications of end-stage liver disease (e.g., encephalopathy, ascites, spontaneous bacterial peritonitis), and recent interventions (e.g., liver biopsy, percutaneous transhepatic cholangiography, sclerotherapy). This information directs the diagnostic evaluation and helps guide further management. Patients with gastric or duodenal varices may develop massive variceal hemorrhage in the absence of esophageal varices. Because up to 50% of patients with documented esophageal varices have a nonvariceal source of bleeding, diagnostic endoscopy must be performed to determine the cause of acute UGI bleeding. Thus, variceal bleeding cannot be differentiated from a nonvariceal hemorrhage based solely on clinical information.