Abdominal apoplexy complicating ulcerative colitis: a case report of venous mesenteric hemorrhage.

Introduction: Abdominal apoplexy, or idiopathic spontaneous intraperitoneal hemorrhage, is a rare and potentially fatal vascular emergency defined by spontaneous hemoperitoneum in the absence of trauma, iatrogenic injury, or identifiable intra-abdominal pathology. Fewer than 200 cases have been reported in the literature, and venous-predominant bleeding without an identifiable arterial source represents a particularly uncommon and diagnostically challenging subset. Case presentation: A 52-year-old male with a background of left-sided ulcerative colitis (UC) presented with sudden-onset generalized abdominal pain. Initial computed tomography (CT) of the abdomen and pelvis was unremarkable. Over the next few hours, hemoglobin declined acutely from 160 to 83 g/L. Repeat multiphase CT demonstrated moderate-volume hemoperitoneum and a lobulated hyperdense collection within the transverse mesocolon, with no arterial contrast blush identified. Emergency diagnostic laparoscopy revealed approximately 1.5 L of hemoperitoneum and a large mesocolic hematoma with active bleeding from friable small venous mesenteric branches. The procedure was converted to open laparotomy, with hemostasis achieved via suture ligation and topical hemostatic agents. The patient recovered uneventfully and was well at the 3-month follow-up. Postoperative vasculitis screening excluded systemic arteritis. Discussion: The absence of arterial extravasation, the presence of venous-predominant bleeding, and an initially unremarkable CT followed by catastrophic hemoperitoneum are atypical features that distinguish this case from the arterial-predominant presentations commonly described in the existing literature. The biphasic clinical course is consistent with the double rupture phenomenon, whereby initial hemorrhagic tamponade within the mesocolon precedes free peritoneal rupture. UC-associated mesenteric microvascular fragility is proposed as the underlying predisposing mechanism, supported by the exclusion of systemic vasculitis, aneurysm, trauma, and coagulopathy. Conclusion: This case illustrates two clinically significant features: the double rupture phenomenon, whereby initial hemorrhagic tamponade within the mesocolon precedes catastrophic free hemoperitoneum, and a venous rather than arterial bleeding source, both atypical for abdominal apoplexy. UC-associated mesenteric microvascular fragility is proposed as the underlying predisposing mechanism. A high index of suspicion, serial clinical reassessment, and a low threshold for repeat CT are essential when initial imaging is non-contributory.