Minimizing Systemic Inflammation During Cardiopulmonary Bypass in the Pediatric Population

Abstract

Cardiopulmonary bypass (CPB) is known to cause a systemic inflammatory response. Inflammation includes several cascade activations: complement, cytokine, and coagulation. The early phase is triggered by blood contact with the synthetic bypass circuit and the late phase by ischemia-reperfusion and endotoxemia. Systemic inflammatory response syndrome (SIRS) is constant following cardiac surgery; however, a compensatory anti-inflammatory response is also constant and the clinical manifestations (varying from uncomplicated SIRS to shock and multiple organ dysfunction) depend on the balance between the two responses. When overexpressed, the inflammatory response may significantly increase a patient's risk. Minimization of systemic inflammation is a major concern and several strategies aiming to inhibit the inflammatory response are described. None of them is satisfactory, but the "control" of the inflammatory response extent is likely to require a multimodal approach. This review aims to describe the strategies proposed to reduce CPB-related systemic inflammation.

Systemic inflammatory response syndrome after pediatric congenital heart surgery: Incidence, risk factors, and clinical outcome

“…Left panel presents the amount of fulfilled SIRS criteria at time of first diagnosis. SIRS was defined as presence of at least two out of four criteria (abnormal heart rate, respiratory rate, temperature and leukocyte count) . At least either abnormal temperature or leukocyte count was considered as one obligate criterion.…”

“…SIRS is frequently observed in children after open‐heart surgery and has been associated with both cardiopulmonary bypass and surgical trauma . Following cardiac surgery the pathophysiological mechanisms of SIRS involve a cytokine‐mediated general capillary leakage followed by intravascular volume depletion, generalized edema, circulatory compromise, and altered microcirculation . The inflammatory process may further impair the function of the lung, myocardium, kidney, liver, intestine, and brain …”

Promotion of anoxia‑reoxygenation‑induced inflammation and permeability enhancement by nicotinamide phosphoribosyltransferase‑activated MAPK signaling in human umbilical vein endothelial cells

“…During CPB, oxygen is supplied to the lung only through the bronchus, thus, ischemia and hypoxia may occur in the lung. Therefore, the lung is often reperfused, resulting in anoxia-reoxygenation (A-R)-induced acute injury (3). A-R has been reported to induce inflammation and enhance the cellular permeability of pulmonary vascular endothelial cells, which then led to pneumonedema, inducing hyoxemia, acute respiratory distress syndrome and even mortality (4).…”

Key Points for Curbing Cardiopulmonary Bypass Inflammation

“…According to Durandy (2014), one of the greatest challenges is how to modulate the systemic inflammatory response so that excessive inflammation in controlled while preserving a level of inflammation needed for host defense and wound healing 8 . Further research is required to substantiate this.…”

“…In fact, while inflammation is frequent following pediatric CPB, serious consequences only affect a small number of patients 8,9 . Also, many studies were performed in small groups of patients and were, therefore, likely to beunderpowered 8,10 .…”