Association Between Intraoperative Hyperoxia and Acute Kidney Injury After Cardiac Surgery: A Retrospective Observational Study

Objective Optimal oxygen management during cardiac surgery has not been established, and studies on the effects of perioperative hyperoxia on postoperative acute kidney injury (AKI) are scarce. The association between intraoperative hyperoxia and AKI after cardiac surgery involving cardiopulmonary bypass was evaluated for the present study. Design Retrospective observational study. Setting A tertiary teaching hospital. Participants Adult patients who underwent cardiac surgery with cardiopulmonary bypass from November 2006–December 2018. Interventions None. Measurements and Main Results The area above arterial oxygen partial pressure (PaO2) threshold of 300 mmHg (AOT300, mmHg × h) was used as a metric of intraoperative hyperoxia and was associated with postoperative AKI, using the logistic regression analysis. Data also were fitted using the restricted cubic spline model. Sensitivity analyses were conducted using different PaO2 thresholds (150, 200, 250, and 350 mmHg). A total of 2,926 patients were analyzed. Intraoperative AOT300 independently was associated with the risk of AKI (odds ratio 1.0009; 95% confidence interval 1.0002-1.0015). A PaO2 increment of 100 mmHg above PaO2 300 mmHg for an hour was associated with an increased risk of AKI by 9.4% (1.0009100 ≈ 1.094). In the spline model, the log-odds of AKI increased as AOT300 increased. In the sensitivity analyses, AOT250 and AOT350 also significantly were associated with the risk of AKI, whereas AOT150 and AOT200 were not. As the PaO2 threshold increased from 150 to 350 mmHg, the odds ratio gradually increased. Conclusions Intraoperative hyperoxia significantly was associated with the risk of AKI after cardiac surgery involving cardiopulmonary bypass. Optimal oxygen management during cardiac surgery has not been established, and studies on the effects of perioperative hyperoxia on postoperative acute kidney injury (AKI) are scarce. The association between intraoperative hyperoxia and AKI after cardiac surgery involving cardiopulmonary bypass was evaluated for the present study. Retrospective observational study. A tertiary teaching hospital. Adult patients who underwent cardiac surgery with cardiopulmonary bypass from November 2006–December 2018. None. The area above arterial oxygen partial pressure (PaO2) threshold of 300 mmHg (AOT300, mmHg × h) was used as a metric of intraoperative hyperoxia and was associated with postoperative AKI, using the logistic regression analysis. Data also were fitted using the restricted cubic spline model. Sensitivity analyses were conducted using different PaO2 thresholds (150, 200, 250, and 350 mmHg). A total of 2,926 patients were analyzed. Intraoperative AOT300 independently was associated with the risk of AKI (odds ratio 1.0009; 95% confidence interval 1.0002-1.0015). A PaO2 increment of 100 mmHg above PaO2 300 mmHg for an hour was associated with an increased risk of AKI by 9.4% (1.0009100 ≈ 1.094). In the spline model, the log-odds of AKI increased as AOT300 increased. In the sensitivity analyses, AOT250 and AOT350 also significantly were associated with the risk of AKI, whereas AOT150 and AOT200 were not. As the PaO2 threshold increased from 150 to 350 mmHg, the odds ratio gradually increased. Intraoperative hyperoxia significantly was associated with the risk of AKI after cardiac surgery involving cardiopulmonary bypass.