Perioperative Inflammation and Microcirculation in Surgery: Clinical Strategies for Improved Surgical Outcomes

Abstract

Impaired microcirculation secondary to underlying vascular endothelial dysfunction is increasingly recognized to play a central role in the pathophysiology associated with numerous postoperative complications. Noxious stimuli, including direct injury from surgical trauma and hypoxia (e.g., ischemia-reperfusion injury), trigger adrenergicinflammatory-thrombotic-immune cascades to impair the microcirculation, with consequent perfusion-related postoperative complications. The endothelium, characterized by exquisite sensitivity to inflammation and low proliferative potential, has limited self-repair capacity that is dependent on circulating bone marrow-derived endothelial progenitor cells for regeneration. As such, the extent to which the endothelial physical and functional integrity is preserved mirrors not only underlying cardiovascular health but is also an important factor in susceptibility to postoperative morbidity. This review explores the effect of perioperative inflammation on the microcirculation and some of the current protective strategies available to clinicians. "Prehabilitation," with preoperative exercise to improve the underlying endothelial function and bone marrow responsiveness for endogenous endothelial repair mechanisms, and anti-inflammatory strategies to limit activation of the endothelial-thrombotic-inflammatory cascades may provide clinical strategies to preserve the microcirculation to engender optimal surgical outcomes.

Association of preoperative plasma suPAR levels with intraoperative sublingual microvascular perfusion in patients undergoing major non-cardiac surgery

“…The impairment of microcirculatory perfusion may be independent of systemic hemodynamics. 43,52,53 This was also evident in this study, which revealed only a weak correlation between MAP and De Backer score during the intraoperative period. De Backer et al reported that the microcirculatory perfusion might only deteriorate when MAP is lower than 60-65 mmHg.…”

“…In patients with chronic inflammation, the endothelium has been activated much earlier than the time of surgery and is associated with elevated suPAR levels. 12,43 In these individuals, graded changes in venular shear rate even for brief periods elicit progressive recruitment of both rolling and firmly adherent leukocytes. 44,45 The activated leukocytes cause oxidative and enzymatic degradation of the glycocalyx and further impair microvascular perfusion.…”

Оптимізація Хірургічного Лікування Та Профілактика Розвитку Гострої Спайкової Тонкокишкової Непрохідності

“…Як відомо із літературних джерел, саме інтраопераційний період є визначальним етапом формування ускладнень та основним етапом формування спайкового процесу [3]. В цей період важливим моментом є не лише вплив маніпуляцій у черевній порожнині, негативний вплив препаратів для наркозу, а й такий фактор, як стан мікроциркуляції, ступінь ендогенної інтоксикації та температурний гомеостаз [4][5][6].…”