3182 Spontaneous Bacterial Peritonitis in Cardiac Ascites: A Rare but Deadly Occurrence

Abstract

INTRODUCTION: Spontaneous bacterial peritonitis (SBP) is frequently described in cirrhotic patients who develop infected ascitic fluid. The phenomenon of SBP in cardiac ascites is rare. Here we present a unique case of a patient who was admitted for advanced cardiorenal syndrome in the setting of a gastroenteritis that likely promoted a bacterial translocation resulting in SBP. CASE DESCRIPTION/METHODS: An 85M presented from a nursing facility with lethargy, confusion and non-bloody diarrhea. Medical history was significant for congestive heart failure (CHF) and chronic kidney disease. No history of alcohol use. Upon arrival to the hospital, he was noted to be confused with a mildly distended abdomen, asterixis and two plus lower extremity pitting edema. The patient was admitted for a CHF exacerbation and metabolic encephalopathy. Initial labs revealed a BNP 3915, WBC 11,500, BUN 89, creatinine 3.5, total bilirubin 2, AST 22, ALT 9, and INR 1.27. An abdominal CT scan showed a moderate amount of intraperitoneal fluid. A diagnostic paracentesis was performed. The aspirated fluid was dark yellow and opaque with a serum ascites albumin gradient of 1.9 g/dL, total fluid protein 3.3 g/dL, 1,115 PMNs cells/mm3, 49% polymorphonuclear leukocytes. To much surprise, these findings demonstrated cardiac ascites resulting in SBP. There was no evidence of cirrhosis. Antibiotic treatment was initiated. Unfortunately, the patient exhibited a rapid decline renal function, and expired shortly afterwards. DISCUSSION: Due to the liver's extensive vascular supply it is prone to hemodynamic disturbances which can result in passive hepatic congestion from right sided heart failure. Recent studies have supported the diagnostic utility of serum BNP levels to distinguish ascites from cirrhosis or heart failure. It has been generally well accepted that the low occurrence of SBP in cardiac ascites may be related to the protein rich ascitic fluid that has both opsonic and bactericidal activity. Interestingly, the “gut hypothesis” suggests that intestinal hypoperfusion and congestion can lead to altered gut morphology, permeability, and the growth of microbiota that may ultimately stimulate bacterial translocation and endotoxin release. This case tends to shed light on a few quintessential points for clinicians to be aware of, including the potential intersection between the microbiota and metabolic effects of CHF and the necessity to lower the diagnostic threshold for SBP cardiac ascites in patient's presenting for a CHF exacerbation.