Endotoxemia related to cardiopulmonary bypass is associated with increased risk of infection after cardiac surgery: a prospective observational study

Abstract

IntroductionPrevious studies have documented a high frequency of endotoxemia associated with cardiopulmonary bypass (CPB). Endotoxemia may be responsible for some of the complications associated with cardiac surgery. The purpose of the study was to examine the prevalence of endotoxemia during cardiopulmonary bypass supported aortocoronary bypass grafting surgery (ACB) using a new assay, the Endotoxin Activity Assay (EAA), and explore the association between endotoxemia and post-operative infection.MethodsThe study was a single center prospective observational study measuring EAA during the perioperative period for elective ACB. Blood samples were drawn at induction of anesthesia (T1), immediately prior to release of the aortic cross-clamp (T2), and on the first post-operative morning (T3). The primary outcome was the prevalence of endotoxemia. Secondary outcomes assessed included infection rates, intensive care unit (ICU) and hospital length of stay. An EAA of < 0.40 units was interpreted as "low", 0.41 to 0.59 units as "intermediate", and ≥0.60 units as "high".ResultsA total of 57 patients were enrolled and 54 patients were analyzable. The mean EAA at T1 was 0.38 +/- 0.14, at T2 0.39 +/- 0.18, and at T3 0.33 +/- 0.18. At T2 only 13.5% (7/52) of patients had an EAA in the high range. There was a positive correlation between EAA and duration of surgery (P = 0.02). In patients with EAA ≥0.40 at T2, 26.1% (6/23) of patients developed post-operative infections compared to 3.5% (1/29) of those that had a normal EAA (P = 0.0354). Maximum EAA over the first 24 hours was also strongly correlated with risk of post-operative infection (P = 0.0276).ConclusionsHigh levels of endotoxin occur less frequently during ACB than previously documented. However, endotoxemia is associated with a significantly increased risk of the development of post-operative infection. Measuring endotoxin levels during ACB may provide a mechanism to identify and target a high risk patient population.

Association between Endotoxin Activity and Acute Kidney Injury in Cardiac Patients Undergoing Cardiopulmonary Bypass

“…These findings may be of particular interest since they underline the concept that the variations of EA compared to baseline, more than its value at the beginning of the surgical procedure, could be relevant in describing the role of EA after CPB. In accordance, Klein et al [28] found that the maximum EA over the first 24 h, even though within the normal range, was strongly correlated with an increased risk of postoperative complications. Furthermore, it has been observed that ICU patients with dynamic daily variations in endotoxin levels had a greater degree of total organ dysfunction as measured by the Multi Organ Dysfunction Score [29].…”

Risk factors of sepsis after open congenital cardiac surgery in infants: a pilot study

“…Further, cardiac malfunctioning alone might cause damages in the alimentary tract mucosal barrier resulting in bacterial and endotoxins translocation to systemic circulation and sepsis. In accordance to this hypothesis, Klein et al 30 stated that the duration of cardiopulmonary bypass increased the risk of endotoxemia and postsurgical infection. 30 Further, complex congenital cardiac diseases were substantially related with the risk of necrotizing enterocolitis.…”

“…In accordance to this hypothesis, Klein et al 30 stated that the duration of cardiopulmonary bypass increased the risk of endotoxemia and postsurgical infection. 30 Further, complex congenital cardiac diseases were substantially related with the risk of necrotizing enterocolitis. Even though the enterocolitis was not directly associated with mortality rate, 20% of patients with this inflammatory reaction would die.…”

Acute kidney injury following cardiac surgery

“…[29] The CPB itself provokes a systemic inflammatory response syndrome (SIRS) due to ischemia-reperfusion injury, endotoxemia, operative trauma, non-pulsatile blood flow, and pre-existing left ventricular dysfunction. Inflammatory mediators, such as endotoxin, IL-1b, IL-6, IL-8, and TNF-a, considerably rise during CPB [30] owing to activation of neutrophils and vascular endothelium, elaboration of cytotoxic oxygen-derived free radicals, proteases, cytokines, and chemokines and increased platelet activation, degranulation, and adherence. [31,32] CPB activates factor XII (Hageman factor) to factor XIIa and also results in the activation of intrinsic coagulation system, the kallikrein system, the fibrinolytic system and complement cascade.…”