Abstract
(1) Alkaline phosphatase (AP) is consumed during cardiopulmonary bypass (CPB). A high AP depletion leads to an impaired outcome after cardiac surgery. However, data is scarce on the postoperative course of AP under venoarterial ECMO (VA-ECMO) support. (2) A total of 239 patients with VA-ECMO support between 2000 and 2019 at the Department of Cardiac Surgery (Vienna General Hospital, Austria) were included in this retrospective analysis. Blood samples were collected at several timepoints (baseline, postoperative day (POD) 1–7, POD 14 and 30). Patients were categorized according to the relative AP drop (<60% vs. ≥60%) and ECMO duration (<5 days vs. ≥5 days). (3) Overall, 44.4% reached the baseline AP values within 5 days—this was only the case for 28.6% with a higher AP drop (compared to 62.7% with a lower drop; p = 0.000). A greater AP drop was associated with a significantly higher need for renal replacement therapy (40.9% vs. 61.9%; p = 0.002) and an impaired 1-year survival (51.4% vs. 66.0%; p = 0.031). (4) CPB exceeds the negative impact of VA-ECMO; still, ECMO seems to delay alkaline phosphatase recovery. A greater initial AP drop bears the risk of higher morbidity and mortality.
Highlights
The deleterious effects of cardiopulmonary bypass (CPB) are profound and involve various cellular levels—inter alia: endothelial hyperpermeability, ischemia–reperfusion injury, and direct endothelial cell injury [1,2]
Two hundred and thirty-nine patients were included in the retrospective data analysis after reviewing their eligibility
The study cohort was divided according to the venoarterial extracorporeal membrane oxygenation (ECMO) (VA-ECMO) support duration and the initial drop of alkaline phosphatase
Summary
The deleterious effects of cardiopulmonary bypass (CPB) are profound and involve various cellular levels—inter alia: endothelial hyperpermeability, ischemia–reperfusion injury, and direct endothelial cell injury [1,2]. Systemic inflammatory response syndrome (SIRS) virtually occurs in a third of patients after CPB and carries the potential for endorgan damage and increased morbidity [3]. This complex biochemical mechanism is not entirely understood. Systemic inflammation is triggered by a release of endogenous molecules. Adenosine triphosphate (ATP) is released from inflammatory or apoptotic cells [4] or from cells under duress—such as in the case of ischemic stress, where cell membranes experience temporal damage [5]. Alterations in flow patterns induce ischemic conditions within the gastrointestinal tract (GIT), resulting in an increased endothelial permeability with an impaired intestinal barrier function [6,7]
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