Case Report: Non-Catheter-Related arterial hemorrhage as a complication of hemoperfusion in hypertriglyceridemic pancreatitis: mechanistic hypotheses and multidisciplinary strategies.

Hypertriglyceridemia-induced acute pancreatitis (HTG-AP) is a rapidly progressive and increasingly prevalent subtype of acute pancreatitis. Hemoperfusion (HP) is commonly employed as a prompt and effective method to lower serum triglyceride (TG) levels. However, in the context of anticoagulant administration and underlying coagulopathy, this approach may precipitate severe hemorrhagic complications. We report a case involving a female patient with HTG-AP who underwent HP for markedly elevated TG levels. Upon admission, the patient exhibited mildly prolonged thrombin time. Following the second session of HP, she developed hemorrhagic shock. Imaging revealed massive hemoperitoneum initially suspected to result from venous catheterization. Subsequent digital subtraction angiography (DSA) confirmed active arterial bleeding from a branch of the right internal iliac artery, which was successfully managed by embolization. Post-procedural evaluation suggested that the arterial rupture was likely due to increased vascular fragility caused by systemic inflammation from acute pancreatitis, further aggravated by anticoagulant exposure during HP. This case underscores the critical importance of pre-treatment bleeding risk assessment, especially in patients with pre-existing coagulation abnormalities. In cases of acute hemorrhage, clinicians must remain alert to non-iatrogenic bleeding sources associated with the underlying pathology and therapeutic interventions. Individualized anticoagulation strategies and vigilant hemodynamic and coagulation monitoring are essential to mitigate the risk of treatment-associated hemorrhagic events.