S3860 The Hemodynamic Trap: Colonic Perforation Amid Chronic SMA Stenosis and Portal Hypertension in the Quest for Normovolemia

Introduction: The superior mesenteric artery (SMA) supplies the bowel from the duodenum to the splenic flexure; the hepatic flexure is fed by its right and middle colic branches. Chronic mesenteric ischemia has a woman predominance (∼70%). Portal hypertensive colopathy in cirrhosis causes mucosal friability, increasing ischemic colitis risk. Patients with both cirrhosis and ischemic colitis have higher in-hospital mortality. Colonic perforation occurs in ∼15% of ischemic colitis cases. Case Description/Methods: A 65-year-old woman with hepatic cirrhosis secondary to metabolic syndrome presented with hepatic encephalopathy. Labs showed hyperammonemia (137 µmol/L), elevated creatinine (1.14), and lactic acidosis (7.3 mmol/L). By day 6, encephalopathy resolved with lactulose and lactic acidosis improved with intravenous (IV) fluids. On Day 8, she developed right lower chest and abdominal pain, with 1 episode of melena as well as hypoxia. Exam showed mild right upper quadrant tenderness. Point of care ultrasound revealed mild perihepatic ascites and moderate right pleural effusion. Brain natriuretic peptide was 218. Ultrasound confirmed trace ascites not amenable to paracentesis. She was started on IV lasix 40 mg 3 times a day. Subsequent Chest X-rays showed reduction in pleural effusion. On Day 13, she developed severe epigastric pain. Lipase was normal. Computed tomography (CT) abdomen/pelvis revealed a 2.4 cm colonic perforation at the hepatic flexure with adjacent 5 × 2 × 1 cm fluid collection, subtotal occlusion of the celiac and SMA with distal reconstitution, colonic wall thickening (suggesting ischemia), and large gastrohepatic varices. Surgery recommended conservative management with bowel rest and IV fluids. Retrospectively, she was noted to be hypertensive since admission (SBP 130–170s) until diuresis began, after which she became normotensive (SBP 90–110s). On Day 13, lactate rose from 1.4 to 3.3 mmol/L over 4 hours, then stabilized (2.5–3.5). Serial CTs showed decreasing collection and sinus tract formation. Left heart cath confirmed volume overload (wedge pressure 24 mmHg). Discussion: Decompensated cirrhosis is a volume overload state due to low oncotic pressure, splanchnic vasodilation, and high-output failure, leading to cardiac dysfunction and elevated wedge pressure. SMA stenosis reduces renal perfusion, activating RAAS and raising blood pressure to maintain distal flow. On the contrary, in cirrhosis, lower MAP (60–65 mm Hg) is preferred due to lesser adverse events. In our patient, undiagnosed SMA stenosis plus diuresis-induced normotension likely reduced distal flow, contributing to colonic ischemia.