Introduction etiology or contributing factors. Since the advent of reconstructive surgery, ischemia‐ reperfusion (IR) injury has been a detrimental factor in flap viability and survival. Ischemia is a condition of inadequate blood flow, which is an inevitable part in many clinical situations, such as free tissue transfers, digit/limb replantation, and organ transplantation. Ischemia is the first level of damage and is characterized by oxygen depletion and conversion of cellular metabolism to anaerobic pathways. In case the ischemia period outruns the tolerance of the tissue, inflammation will develop with cell necrosis. Although reperfusion is essential for flap and tissue survival, reperfusion triggers a cascade of pathophysiologic events resulting in tissue injury beyond that caused by the initial ischemia.79 A large volume of experimental data has increased our knowledge of the pathopysiological mechanisms of IR injury and has resulted in strategies to avoid flap loss.80‐83 Increased ischemic time has been shown to correlate with microvascular complications84 and FN85 in the DIEP flap. Although success rates greater than 90% are common in microvascular reconstructive procedures, incidental total flap loss and more commonly PFL still occur. PFL and FN can lead to prolonged hospitalization, additional corrective surgery, and morbidity and also can have an effect on aesthetic outcome. IR injury and nitric oxide Since the discovery of the endothelium‐derived relaxing factor nitric oxide (NO) in 1987, a significant volume of research has been published investigating the role of NO in the vascular endothelium and its role in relation to IR injury.86 Using the PubMed search, ("Reperfusion Injury"Mesh) AND "Nitric Oxide"Mesh lead to 1,646 published studies. NO has been shown to have a protective effect against IR injury and was associated with an increased flap survival in numerous studies.87 IR injury with relation to flap survival is further addressed in this thesis. Objectives This thesis addresses the problem of partial flap loss (PFL) and fat necrosis (FN) in autologous breast reconstruction. PFL and FN are discussed and assessed in relation to the physiological changes after ischemia‐reperfusion (IR) injury and to the role of risk factors. In addition, the use of NO to increase flap blood flow to reduce flap‐related complications is explored. In chapter 1, an overview is given in relation to breast cancer treatment and breast reconstruction techniques. It further focuses on autologous breast reconstruction and PFL and FN. During the first years of autologous breast reconstruction in our institution, a relatively high rate of flap complications was precent despite the fact that reconstructions were performed by an experienced reconstructive surgeon. This initiated the work summarized in this thesis. In chapter 2 a retrospective study is described assessing 19
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