Case Report: Ischemic bowel necrosis following intra-aortic balloon pump support in a patient with cardiogenic shock.

Background: The intra-aortic balloon pump (IABP) is a widely used mechanical circulatory support device for patients with acute myocardial infarction complicated by cardiogenic shock. Although generally safe, IABP use may impair visceral organ perfusion and lead to rare but severe complications, including ischemic bowel necrosis. Case presentation: A 59-year-old man was admitted after experiencing a cardiac arrest caused by an extensive acute anterior myocardial infarction. Following successful cardiopulmonary resuscitation, emergency coronary angiography revealed total occlusion of the mid-segment of the left anterior descending artery. Primary percutaneous coronary intervention was performed with implantation of a drug-eluting stent and IABP support, achieving a thrombolysis in myocardial infarction grade 3 flow. On the fourth postoperative day, the patient developed progressive abdominal distension, absent bowel sounds, and refractory septic shock. Contrast-enhanced computed tomography revealed small bowel dilation with air-fluid levels, hepatic portal venous gas, and pneumatosis intestinalis, findings suggestive of ischemic bowel necrosis. Further evaluation indicated that the distal end of the intra-aortic balloon was positioned below the origin of the superior mesenteric artery, suggesting that a mismatch between the aortic anatomy and balloon length contributed to mesenteric hypoperfusion in the setting of cardiogenic shock and high-dose vasopressor therapy. The IABP counterpulsation ratio was adjusted to 1:2, and broad-spectrum antibiotics were administered. Despite these interventions, the patient's condition continued to deteriorate, with persistent high fever and circulatory collapse. The family ultimately decided to discontinue treatment due to unsustainable vital signs and a poor prognosis. Conclusion: This case highlights a rare and catastrophic complication following coronary stent implantation and IABP therapy in a patient with cardiogenic shock. Bowel ischemia in this setting is rarely attributable to a single mechanism: systemic hypoperfusion after cardiac arrest, IABP-related reduction in mesenteric blood flow due to balloon-aortic length mismatch, vasopressor-induced splanchnic vasoconstriction, and ischemia-reperfusion injury likely acted in concert. Clinicians should remain highly vigilant for early signs of ischemic bowel necrosis in patients receiving IABP support, particularly those requiring high doses of vasoactive agents, and should be aware that serum lactate trends may not reliably reflect splanchnic perfusion. Early recognition through serial abdominal examination and timely imaging is essential.