S3524 Anchored in Albumin: Non-Cirrhotic Portal Hypertension from Extrinsic Portal Venous Compression Following Necrotizing Pancreatitis

Introduction: Non-cirrhotic portal hypertension (NCPH) is a heterogeneous and underrecognized cause of ascites, with variable etiologies ranging from prehepatic (e.g., portal vein thrombosis or compression), intrahepatic (e.g., nodular regenerative hyperplasia, schistosomiasis), and posthepatic causes. Clinically, patients have a similar presentation to cirrhotic patients which can include variceal formation, splenomegaly, and ascites. However, NCPH patients will differ as their synthetic liver function is usually preserved. In patients without known liver disease or significant alcohol use, identifying the underlying mechanism for ascites can be challenging. Case Description/Methods: We present a case of recurrent ascites that eventually diagnosed with NCPH secondary to extrinsic compression of the portal venous confluence. A 72-year-old man with medication-induced necrotizing pancreatitis developed recurrent ascites and peripheral edema. Initially, the primary team thought that the patient’s hypervolemia was attributed to hypoalbuminemia from severe malnutrition. Despite nutritional improvement and a rising serum albumin, fluid accumulation progressed. Further evaluation included cross-sectional abdominal imaging that revealed a persistent 4.5 cm peripancreatic walled-off necrosis near the pancreatic head and moderate ascites. His diagnostic paracentesis had low amylase, ruling out pancreatic ascites, and findings consistent with portal hypertensive ascites. Venous-phase contrast computed tomography demonstrated marked narrowing at the confluence of the main portal vein, splenic vein, and superior mesenteric vein, indicating vascular compression. Discussion: This case highlights the diagnostic complexity of ascites in non-cirrhotic patients with prior pancreatic pathology. While hypoalbuminemia is a contributor to third-spacing, patients that still have persistent ascites despite initial management warrants further evaluation. For this patient, his well-documented history is a risk factor for vascular pathology. In patients with abdominal inflammation, malignancy, or prior surgical intervention prehepatic thrombosis and vascular compression should be considered. Computed tomography imaging was key in identifying the anatomical cause and allows for the patient to receive appropriate intervention above further hepatic testing. NCPH is more commonly associated with intrahepatic causes, but this case underscores the importance of considering vascular etiologies in the appropriate clinical context.