Advanced Biventricular Heart Failure Leading to the Formation of a Gastric Bezoar: The Implications of Heart Failure on the Gastrointestinal Tract

Abstract

While dyspnea or increasing peripheral edema come to mind when thinking of worsening heart failure (HF), seemingly unrelated symptoms such as nausea or bloating can indicate exacerbation. We highlight the significant gastrointestinal (GI) symptoms that result from HF, with emphasis on impaired gastric and intestinal motility. A 43 year-old man with cardiomyopathy (CM) presented with worsening abdominal pain, distention and nausea for 4 months. Physical exam showed jugular venous distention, peripheral edema, diminished breath sounds and a murmur. The abdomen was soft, mildly distended and tender. Labs showed B-type natriuretic peptide of 1374pg/ml. Blood gas showed a lactic acid of 3.2mmol/L. Platelet count was 66K/UL and international normalized ratio was 2.3. Total bilirubin was 4.0mg/dl with direct of 1.9mg/dl; aspartate aminotransferase of 98IU/L, alanine aminotransferase of 121IU/L and an alkaline phosphatase of 87IU/L. Computerized tomography showed wall thickening of the stomach, ascites, diffuse anasarca and thickening in the sigmoid colon. Echocardiogram showed an ejection fraction of 21-25% and global CM. Upper endoscopy revealed a gastric bezoar. The patient was given a can of Pepsi Cola and kept nil per os for repeat endoscopy, which showed resolution of the bezoar. Cardiac catheterization showed normal coronaries and reduced cardiac output (CO). Gastric emptying study confirmed gastroparesis. We look at the pathophysiology of HF and its effect on the structure and function of the GI tract. The small and large intestine display bowel wall edema with increased wall thickness leading to impaired nutrition of the enterocytes resulting in decreased absorptive function of the bowel. In the sigmoid colon, increased thickness correlates with increased concentrations of C-reactive protein and leukocytes. The intestine is one of the most perfused organs at rest, receiving 25% of the CO. At maximal exercise, gut perfusion drops to 4% of the CO. Increased sympathetic stimulation causes vessel constriction and decreased bowel perfusion. Small changes in CO lead to significant ischemia causing decreased motility and absorption and increased bowel wall permeability. Hepatic congestion from blood backup into the liver results in delayed gastric emptying, slowed gut motility, increased bowel permeability and bacterial translocation. Presented case demonstrates pathophysiology of frequently seen but often underappreciated GI manifestations of heart failure.2631_A Figure 1. CT scan of the abdomen showing wall thickening of the cardia of the stomach2631_B Figure 2. Gastric Bezoar2631_C Figure 3. Body or the stomach, on second EGD, 24 hours after can of Pepsi Cola