• Kelsie A Kiser, Akiko Tanaka, Harleen K Sandhu, Charles C Miller, Samuel D Leonard, Hazim J Safi, and Anthony L Estrera.
• Memorial Hermann Hospital, Houston, Tex.
• J. Thorac. Cardiovasc. Surg. 2022 Mar 1; 163 (3): 914-921.e1.

ObjectiveCell salvage (CS) reduces intraoperative blood transfusion. However, it may cause deformity of the red blood cells and loss of coagulation factors, which may lead to unwanted sequelae. Thus, we hypothesized that extensive CS would lead to adverse outcomes after descending/thoracoabdominal aortic aneurysm (D/TAAA) repair.MethodsBetween 1991 and 2017, 2012 patients undergoing D/TAAA repair were retrospectively reviewed. After we excluded patients without reported intraoperative CS amount, patients were enrolled in the study (N = 1474) and divided into 2 groups: low CS (salvaged units <40, N = 983) and high CS (salvaged units ≥40, N = 491). Analyses were performed to verify the extensive CS as the risk factor for adverse outcomes.ResultsPreoperative demographics showed that the high-CS group had a significantly greater incidence of male patients (72% vs 58%), heritable aortic disease (24% vs 17%), redo (27% vs 20%), greater glomerular filtration rate (mL/min/1.73 m2, 75 vs 66) and more extensive aneurysms (TAAA extent II-IV). The high-CS group had significantly more postoperative complications compared with the low-CS group, including respiratory failure, renal failure, cardiac complications, neurologic deficits, bleeding, and 30-day mortality. Multivariable analysis confirmed high CS was an independent risk factor for renal failure along with long bypass time, older age, and extent of repairs. There was an incremental risk of renal failure and 30-day mortality proportional to salvaged cell unit (P < .001 in both).ConclusionsIncreased salvaged cell units were associated with adverse postoperative outcomes after D/TAAA repairs. Risk of renal failure and mortality increased proportionally to the salvaged cell units.Copyright © 2020 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.

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