Non-occlusive mesenteric ischemia complicated by ischemic hepatitis presenting as severe lactic acidosis: a case report.

Background: Non-occlusive mesenteric ischemia (NOMI) and ischemic hepatitis (IH) are severe target-organ injuries caused by splanchnic hypoperfusion and are associated with substantial mortality, particularly in elderly patients with panvascular disease. When intestinal and hepatic hypoperfusion occur concurrently, intestinal anaerobic metabolism may increase lactate production, whereas ischemic hepatocellular injury may impair lactate clearance. Together, these mechanisms can lead to severe or even refractory lactic acidosis. Case presentation: An 84-year-old man was admitted for progressive black discoloration of the skin on his left foot lasting more than 1 month. His medical history included hypertension, type 2 diabetes mellitus, cerebral infarction, lower-extremity arteriosclerosis obliterans, prior lower-limb endovascular intervention, and left femoral artery stent implantation. He had been receiving long-term dual antiplatelet therapy (DAPT). On postoperative day 10 after debridement and skin grafting of the left foot, he suddenly developed coffee-ground emesis, followed by tachypnea and lethargy. Although blood pressure remained relatively stable during this episode, he developed tachycardia, mottled skin, severe anemia, metabolic acidosis, and marked hyperlactatemia, with lactate levels exceeding 20 mmol/L. After transfer to the intensive care unit (ICU), fasting, fluid resuscitation, blood transfusion, acid-base correction, and continuous renal replacement therapy (CRRT) were initiated, with gradual improvement in acid-base balance and metabolic status. Contrast-enhanced abdominal computed tomography (CT) revealed extensive atherosclerosis of the abdominal aorta and its branches, mural thrombi, penetrating atherosclerotic ulcers, and ischemic changes in the bowel and right hepatic lobe. After multidisciplinary evaluation, the patient was diagnosed with NOMI complicated by IH. Following comprehensive intensive treatment, his condition stabilized, and he was discharged successfully. Conclusion: NOMI should be considered in elderly patients with panvascular disease and perioperative volume fluctuations who present with unexplained hyperlactatemia and metabolic acidosis. Clinicians should recognize that splanchnic hypoperfusion may affect multiple target organs simultaneously. Early recognition and timely multidisciplinary management may help improve outcomes in this high-risk population.