Ridwan A Lawal, Nestor Malaga, Nida Asif, Fatimah Bello, Juliana Yang
Gastrointestinal perforation in systemic lupus erythematosus (SLE) is uncommon but potentially fatal, and attribution is clinically consequential because perforation may reflect lupus enteritis with mesenteric vasculitis, infection, diverticular or stercoral disease, malignancy, inflammatory bowel disease (IBD), medication-related injury, or a combination of mechanisms. Corticosteroid-associated perforation is therefore best treated as a diagnosis of exclusion rather than as an isolated novel observation. We report a 62-year-old woman with SLE who developed sudden severe right-sided abdominal pain, nausea, vomiting, leukocytosis, lactic acidosis, and radiographic pneumoperitoneum while tapering prednisone from 60 mg/day to 10 mg/day over three months, with 10 mg/day documented at presentation in the available medication history. Computed tomography demonstrated free intraperitoneal air without radiologic diverticulitis or a clear alternative source. Emergent robotic-assisted laparoscopy was converted to open surgery because of extensive purulent contamination. Approximately 1.5 L of pus was evacuated, and a solitary mid-transverse colon perforation was treated with segmental colectomy and primary anastomosis. Gross pathology showed an irregular ulcer with a transmural defect and no mass or diverticulum. Histopathology demonstrated a full-thickness perforated ulcer with acute-on-chronic inflammation and granulation tissue, without vasculitis, thrombosis, ischemic necrosis, granulomas, IBD, or malignancy. The postoperative course was uncomplicated, with the return of bowel function by postoperative day 4 and discharge on day 6. This case is unusual because SLE-associated intestinal perforation is more commonly described in the context of active lupus mesenteric vasculitis or other identifiable etiologies. The report emphasizes a structured exclusion-based diagnostic approach, early source control, and postoperative reassessment of glucocorticoid exposure and steroid-sparing therapy.