ArticleCureus2026
Spontaneous Bacterial Peritonitis as a Rare Complication of a Pancreatic Duct Leak in a Patient Without Cirrhosis: A Case Report.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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5 authors.
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Abstract
Spontaneous bacterial peritonitis (SBP) is classically associated with liver cirrhosis and portal hypertension. Its occurrence in non-cirrhotic patients is rare and poorly characterized. Pancreatic ascites, resulting from disruption of the pancreatic duct (PD) or leakage from a pseudocyst, is an unusual cause of ascites in chronic pancreatitis. The enzyme-rich, exudative nature of this fluid can itself cause chemical peritonitis with neutrophilia, mimicking infection. We report the case of a 50-year-old man with alcohol use disorder and chronic calcific pancreatitis who presented with recurrent massive ascites in the absence of hepatic cirrhosis. Paracentesis revealed a markedly elevated ascitic fluid amylase level (14,619 U/L) and a polymorphonuclear leukocyte (PMN) count exceeding 250 cells/mm³; the ascitic fluid culture was negative. Given the negative culture, we classified the condition as culture-negative neutrocytic ascites (CNNA), with a clinical syndrome highly consistent with SBP, rather than as culture-confirmed SBP. The serum-ascites albumin gradient (SAAG) was 1.5 g/dL, supporting the presence of portal hypertension, which was attributed to nonocclusive portal vein thrombosis (PVT). Imaging identified a PD stricture with upstream dilatation and a leak tracking into the peritoneal cavity. Endoscopic retrograde cholangiopancreatography (ERCP), attempted for therapeutic PD drainage, was unsuccessful because of pancreatic calcifications and distorted ductal anatomy. The admission was further complicated by acute aortoiliac thromboembolism, compartment syndrome, and chylous ascites, all of which were successfully managed with surgical and supportive care. Conservative management with intravenous antibiotics, total parenteral nutrition (TPN), a low-fat diet, and octreotide led to spontaneous resolution of the PD leak, as confirmed by secretin-enhanced magnetic resonance cholangiopancreatography (MRCP). Neutrocytic ascites clinically consistent with SBP may occur in non-cirrhotic patients when a PD leak and localized portal hypertension coexist. However, the anatomical connection between the PD and the gastrointestinal lumen, together with the limited sensitivity of cultures in this setting, means that such cases may be more accurately classified as CNNA. Clinicians should maintain a high index of suspicion for infectious peritoneal complications in patients with pancreatic ascites while using precise terminology that reflects genuine diagnostic uncertainty.
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