Concurrent acute pancreatitis and splanchnic vein thrombosis in a heavy smoker: a dynamic D-dimer-based diagnostic algorithm and mechanistic insights—a case report

Splanchnic vein thrombosis (SVT) concurrent with acute pancreatitis (AP) at initial diagnosis is rare and its pathophysiology remains unclear. We describe a heavy smoker who presented with AP with occult non-occlusive SVT, which paradoxically progressed to complete thrombotic occlusion. A 52-year-old male heavy smoker (40–60 cigarettes/day for 30 years) presented with epigastric pain and was diagnosed with AP after excluding common etiologies. On admission, D-dimer was markedly elevated at 9.15 mg/L (18 times the upper limit of normal). By day 12, despite radiological resolution of pancreatic inflammation and a significant c-reactive protein (CRP) reduction (139.16 to 45.35 mg/L), he developed mesenteric ischemia. Laboratory findings revealed a paradoxical “dynamic decoupling”: D-dimer further escalated to 9.52 mg/L, fibrinogen (FIB) was consumed to 2.72 g/L, and antithrombin III (AT-III) was critically depleted to 45%. Contrast-enhanced CT confirmed complete thrombotic occlusion of the superior mesenteric, splenic, and portal veins; retrospective review verified non-occlusive SVT at onset. Standard systemic anticoagulation failed to halt thrombotic progression, reaching a “pharmacological ceiling” due to profound AT-III depletion. Transjugular endovascular intervention (thrombus aspiration and catheter-directed thrombolysis) successfully reversed the intestinal ischemia. In heavy smokers with AP, an initial D-dimer exceeding 18 times the upper limit of normal should prompt early contrast-enhanced CT to exclude occult SVT. When standard systemic anticoagulation fails due to a “pharmacological ceiling” of depleted antithrombin, timely endovascular escalation is a key salvage strategy.