Case presentation

A 43-year-old woman, gravida 2 para 1, underwent cesarean delivery at the referring hospital. She had no relevant medical history, no known connective tissue disorder, and no family history of vascular disease. Although the procedure was reported to have been uncomplicated, detailed operative information regarding intra-abdominal adhesions, peritoneal or mesenteric findings, surgical manipulation, and abdominal closure techniques was not available. On postoperative day 4, she developed sudden upper abdominal pain. She had not experienced similar abdominal symptoms before delivery.

On presentation, her blood pressure was 168/71 mmHg. Physical examination revealed mild abdominal distension and epigastric tenderness without rebound tenderness, guarding, or other peritoneal signs. Laboratory testing showed leukocytosis with a white blood cell count of 12,300/µL, anemia with a hemoglobin level of 7.8 g/dL, a mildly elevated C-reactive protein level of 1.78 mg/dL, and fibrinogen of 403 mg/dL. The anemia and pelvic hemoperitoneum initially raised concern for postoperative bleeding. In contrast, the leukocytosis and mildly elevated C-reactive protein level were considered nonspecific findings in the early postoperative and postpartum setting and were not, by themselves, considered evidence of bowel ischemia or severe intra-abdominal infection.

CT revealed pelvic hemoperitoneum. Contrast-enhanced CT demonstrated an intimal flap in the superior mesenteric artery (Figure 1), consistent with ISMAD. No contrast extravasation was observed. The distal branches of the superior mesenteric artery were patent, and there were no radiologic findings suggestive of intestinal ischemia, including bowel wall thickening, reduced bowel wall enhancement, pneumatosis intestinalis, or portal venous gas. The principal diagnostic clues were the sudden onset and upper abdominal location of the pain, which were not fully explained by the pelvic hemoperitoneum, and the identification of an intimal flap in the superior mesenteric artery on contrast-enhanced CT. The patency of the distal branches and absence of radiologic signs of bowel ischemia were also important in guiding conservative management.

Figure 1: Contrast-enhanced computed tomography showing isolated superior mesenteric artery dissection after cesarean delivery.An intimal flap is visible within the superior mesenteric artery (arrowhead), consistent with arterial dissection. The distal branches remain patent, and there is no contrast extravasation or radiologic evidence of bowel ischemia.

Because active arterial bleeding was absent, the pelvic hemoperitoneum was considered more likely to have originated from the cesarean section site than from the arterial dissection. The absence of arterial rupture, distal branch occlusion, and bowel ischemia supported nonoperative management. Conservative treatment with strict blood pressure control, close observation, repeated clinical assessment, and blood transfusion was selected. Her abdominal pain gradually improved, and no signs of intestinal ischemia or hemodynamic instability developed during hospitalization.

She was discharged without complications. Follow-up contrast-enhanced CT performed 12 months later showed that the dissection had become less conspicuous. The patient remained recurrence-free and had no subsequent abdominal symptoms.