Venous Ischemic Pancreatitis With Reduced Pancreatic Enzymes Secondary to Extensive Splanchnic Venous Thrombosis: An Unrecognized Vascular Phenotype

Acute pancreatitis is commonly diagnosed on the basis of characteristic abdominal pain, elevation of pancreatic enzymes to greater than three times the upper limit of normal, and supportive imaging findings. However, pancreatic injury may occasionally arise from vascular mechanisms rather than the classical enzyme-mediated inflammatory process. Venous ischemic pancreatitis, secondary to splanchnic venous thrombosis, is an under-recognized clinical entity that may present with normal or even reduced pancreatic enzyme levels, creating a potential diagnostic challenge. We report the case of a 49-year-old woman who presented with severe abdominal pain and radiologic features consistent with pancreatic injury despite both amylase and lipase levels being below the normal reference range. Contrast-enhanced computed tomography (CT) demonstrated a bulky pancreas with areas of hypoenhancement along with extensive thrombosis of the splenic vein, portal vein, and superior mesenteric vein. CT angiography confirmed preserved arterial inflow, supporting venous outflow obstruction as the dominant mechanism of pancreatic ischemia. Comprehensive evaluation excluded common causes of pancreatitis, including gallstone disease, alcohol-related pancreatitis, malignancy, myeloproliferative neoplasms, antiphospholipid syndrome, and major inherited thrombophilias. Therapeutic anticoagulation was initiated promptly, resulting in rapid clinical improvement and preventing progression to bowel ischemia or pancreatic necrosis. This case highlights an under-recognized vascular phenotype of pancreatic injury consistent with venous ischemic pancreatitis and illustrates how careful integration of biochemical findings, vascular imaging, and clinical reasoning can guide timely anticoagulation and dramatically alter clinical outcomes.