Chapter 7 Table 7.2 Partial flap loss in zones I–IV in study groups. Zone I Zone II Zone III Zone IV Sham (n7) 0 0 1 4 IR injury* I (n7) 2 3 6 7 IR injury* II (n7) 3 3 6 7 *IR injury = ischemia‐reperfusion injury. Discussion Since the first successful transplant of a free flap by Goldwyn in 196315, there has been a continued improvement in free flap transfer techniques and flap design. An excellent example of this process is breast reconstruction, in which the pedicled TRAM flap has evolved to the DIEP flap with improved results and minimal donor site morbidity and postoperative complications.16 However, reconstructive surgery is a constant battle against flap ischemia. Despite the improvements made, PFL and/or FN continues to be a relative common complication, occurring up to 62% in all cases, depending on the technique used.2 Further refinements have failed to completely eliminate these complications. The aim of this study was to investigate the cause and possible therapeutic targets for minimizing PFL and/or FN. In this study, PFL occurred mostly, in descending order, in zone IV, zone III, zone II, and zone I. This pattern of PFL is also observed in TRAM/DIEP flaps clinically. Although the results in this study are not completely new and the outcome is as expected, the main focus of this experimental study is to further enlighten the pathophysiological process that causes PFL. It is the first study that addresses the fact that PFL of the TRAM/DIEP flap is not solely attributable to flap design or intrinsic vascular anatomy. This study has revealed that IR injury may also be an important factor in the pathophysiological process of PFL and necrosis. The clinical consequence of these findings is that future endeavors aimed at reducing/eliminating PFL and/or FN must also focus on IR injury and not solely on the anatomical distribution of vessels. There is broad experimental evidence focusing on different pathophysiologic steps of IR injury, which successfully reduce the rate of (partial) flap loss.12‐14,17 In this study, we used a mouse abdominal flap model based on the deep inferior epigastric artery. The choice for the mouse was the availability of knockout mice for future studies. It is generally accepted that the design of the flap can be a cause of PFL. Venous congestion is often caused by variable venous anatomy across the midline or insufficient venous perforator caliber.2,7,8,18,19 Decision making is thus an important step in perforator selection with regard to PFL and/or FN, venous congestion, and flap survival. Therefore, multiple techniques have been developed to augment the venous drainage of the flap.9,20‐24 However, venous congestion and any flap complication were 106
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