Postoperative Acute Refractory Hypoxemia After Acute Type A Aortic Dissection Surgery: Supporting the Two-Hit Mechanism of Transfusion-Related Acute Lung Injury. A Retrospective Cohort Study

Acute type A aortic dissection (ATAAD) surgery is often complicated by postoperative acute refractory hypoxemia (ARH). Multiple risk factors contribute to ARH, and perioperative blood transfusion is a potential risk factor. This study investigates the association between perioperative blood product transfusion and ARH in ATAAD surgical patients. This retrospective cohort study included 282 patients who underwent surgical repair of ATAAD between 2015 and 2020. Perioperative blood product transfusion volumes, postoperative oxygenation indices, laboratory and radiological findings were analyzed. The primary outcome, ARH, was defined as moderate-to-severe hypoxemia (P/F ≤ 200 mmHg) within 72 hours postoperatively. Multivariate logistic regression was used to identify risk factors for ARH, confounders were adjusted for, and platelet transfusion association was further evaluated. Acute refractory hypoxemia occurred in 35.8% of the total patient cohort. At baseline, ARH patients had significantly higher BMI and a high prevalence of hypertension and coronary artery disease. Marfan syndrome was significantly more prevalent in the non-ARH group. Platelet transfusion was administered in 81.2% of patients, and a significantly higher frequency of ARH patients received platelet transfusion [p=0.013; Adjusted OR 95% CI; 3.43 (1.54-7.63)]. A synergistic effect was observed between high preoperative C-reactive protein (CRP) and platelet transfusion in the resulting ARH [p < 0.001; adjusted OR 95% CI: 16.06 (3.02-85.50)]. After multivariate logistic regression analysis, platelet transfusion, high CRP, brachiocephalic trunk involvement, and prolonged hypothermic circulatory arrest time were independent risk factors for postoperative ARH after ATAAD surgery. ARH patients required a significantly longer duration of mechanical ventilation. Platelet transfusion was independently associated with risk of postoperative ARH, supporting a potential TRALI-like mechanism. Findings suggest that in high-risk ATAAD surgery, the synergistic effect of preoperative systemic inflammation and platelet transfusion may contribute to lung injury compatible with the "two-hit" model. This potential pathway requires further investigation.