2462 Rapid Development of Bleeding Esophageal Varices After Placement of Continuous Flow Left Ventricular Assist Device

Abstract

INTRODUCTION: Upper gastrointestinal bleeding – typically due to arterio-venous malformations - is common in patients with continuous-flow LVAD, and is due to acquired von Willebrand disease and systemic anticoagulation. We present a patient with compensated cirrhosis in whom large esophageal varices developed within a few weeks of LVAD placement, resulting in hemorrhage and eventual fatal outcome. CASE DESCRIPTION/METHODS: A 62-year old male with a history of non-ischemic cardiomyopathy presented with recurrent pulmonary edema requiring intra-aortic balloon pump (IABP) to maintain stability. Workup for placement of a LVAD was initiated. An abdominal CT scan unexpectedly revealed cirrhotic liver changes. The patient had no physical exam stigmata of advanced liver disease. The INR was 1.1, platelets 170,000, albumin 3.7, transaminases and bilirubins were normal. EGD revealed no varices. A liver biopsy revealed a portal-systemic gradient of 20 mmHg and histology confirmed cirrhosis but revealed no specific etiology. The patient's MELD score of 11 and Child-Pugh class A were consistent with well-compensated cirrhosis, and the patient underwent uneventful placement of a LVAD. Seventeen days after placement, the patient sustained an acute upper GI bleeding episode. Emergent EGD revealed large, actively bleeding esophageal varices, which were successfully ligated. Over the following days, the patient developed ascites, hepatic encephalopathy and renal failure. Twelve days later, the patient developed recurrent bleeding. EGD revealed active bleeding in the esophagus and a large clot. No specific bleeding source could be identified and endoscopic attempts at hemostasis were unsuccessful. Placement of a transjugular intrahepatic portosystemic shunt was considered, but the patient's MELD score of 40 was prohibitively high. The patient continued to bleed and expired on the following morning. DISCUSSION: We hypothesize that the fluid shifts and increased hepatic arterial inflow following LVAD placement caused rapid increases in esophageal variceal pressures and bleeding. The patient's low cardiac output prior to LVAD placement likely masked the extent of his portal hypertension. In hindsight, the markedly elevated pre-LVAD portal-systemic gradient was the clearest predictor of post-LVAD variceal complications in our patient. Our experience suggests that even well-compensated cirrhotic patients with significant portal hypertension are at risk for variceal bleeding after LVAD placement.