
Abstract
Intractable bleeding during cardiac surgery is a rare but life-threatening complication. We describe a novel management approach in which the patient was supported with venoarterial extracorporeal membrane oxygenation until hemostasis could be achieved. This approach serves as an unloading technique for the heart while allowing compression of bleeding sites and safe transfusion without hemodynamic instability or myocardial dysfunction.
Extracorporeal membrane oxygenation (ECMO) has become a crucial life-supporting intervention since the 1970s, with a continued rise in its use.1 The growing body of literature reflects ECMO’s evolving role as a vital rescue therapy for critically ill patients in cardiorespiratory failure, transplant bridging, and severe trauma and as a salvage strategy for postcardiotomy cardiogenic shock across various cardiac surgeries.2 Intraoperatively, ECMO has been shown to play a role in lung transplantation or in patients who cannot be weaned off cardiopulmonary bypass at the end of the procedure.3,4 To date, there are limited reports, to our knowledge, of ECMO use primarily intended for hemostatic rather than for circulatory support, particularly in the cardiac surgery setting. In this report, we describe the deliberate initiation of venoarterial (VA) ECMO primarily to facilitate hemostasis in the setting of diffuse, unlocalized intraoperative bleeding in a patient who had not yet had frank hemodynamic collapse.
The patient is a 56-year-old woman with a history of hypertension, dyslipidemia, and kidney transplantation 18 years earlier. She presented with heart failure symptoms including fatigability and dyspnea on exertion worsening during a period of 2 weeks. She was hemodynamically stable with a significant finding of a holosystolic murmur and mild troponin (1246 ng/L) and significant B-type natriuretic peptide elevation (2340 pg/mL). Echocardiography showed an ejection fraction of 25%, regional wall motion abnormalities, severe mitral regurgitation, and moderate aortic stenosis. Angiography showed multivessel coronary artery disease with a 70% right coronary artery stenosis and 90% mid–left anterior descending artery stenosis. Notably, her creatinine concentration, at baseline between 2.0 and 2.2 mg/dL, peaked at 4.0 mg/dL.
The cardiothoracic surgery team evaluated her and recommended high-risk cardiac surgery that entails 2-vessel bypass and aortic and mitral valve replacement. As no exact risk calculator existed for this operation, we used coronary artery bypass grafting and aortic valve replacement as an approximation and indicated a predicted mortality of 26.3%, mostly driven by her renal disease and previous transplant and steroid use.
During surgery, there was a moderate amount of pericardial adhesion from prior uremic pericarditis. It was immediately noted that her tissues were remarkably friable. Extra care was taken at every step to execute this operation that included mitral valve replacement with a 25-mm bioprosthetic valve, aortic valve replacement with a 19-mm bioprosthetic valve, and 2 vessel bypasses with a left internal mammary artery graft to left anterior descending artery and a saphenous vein graft to the posterior descending artery. Given the friability of the aortic tissues and concern for excessive bleeding, aortic root enlargement was not pursued to minimize operative complexity and bleeding risk. The cardiopulmonary bypass time and cross-clamp time were particularly long, attributed to the difficulty in handling the friable tissue.
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