Perfusion classification in a IR injury DIEP flap model Introduction The deep inferior epigastric perforator (DIEP) flap is a reliable choice of autologous breast reconstruction. It allows reconstruction of a natural breast with the advent of minimal donor site morbidity and low complication rate. However, fat necrosis (FN) and partial flap loss (PFL) to a lesser extent are quite common with reported rates of 6% to 35% in the literature.1‐3 FN as a sequela of necrosis leads to palpable lump formation, which is occasionally accompanied by pain in some patients. This can be an emotional burden in breast cancer patients and may lead to secondary corrective surgery. Arterial and venous anatomy of both free and pedicled flap follows the principles of angiosomes and venosomes as first described by Taylor et al.4,5 As a result of this, the human body can be theoretically divided by various angiosomes and venosomes. These angiosomes and venosomes are connected by anastomosis, choke vessels, arteriovenous shunts, valves in the venous system, and a bidirectional venous system of the postcapillary venulles.4,5 In modern reconstructive surgery, flaps are designed to preferably incorporate one angiosome in order to increase viability and reduce complications such as PFL. However, in breast reconstructive surgery, where more volume is needed, the flap design incorporates several angiosomes. As a result, despite significant advances in flap design and preoperative planning, PFL is still a relatively common complication leading to FN or PFL. In addition, the dominant artery supplying the angiosomes and dominant vein draining the venosomes of a flap are not always in the same pedicle. This is particularly true for the DIEP flap, where venous congestion continues to be a common complication, especially in the distal part (zone IV) of the flap, resulting in PFL or FN.1,2,6 This clinical observation was confirmed in anatomical and clinical studies.7,8 Therefore, the removal of flap parenchyma more distal from the vascular pedicle or the addition of venous anastomosis appears to reduce the severity venous congestion. These measures however, do not appear to reduce the incidence of PFL and FN.9,10 Moreover, in simultaneous bilateral breast reconstruction with a DIEP flap using only zones 1 and 2, there is still a rate of up to 12.5% FN in the literature.11 In addition, the overall incidence of FN is much higher than previously reported in the literature despite the complete removal of zone IV.3 This raises the question that other pathophysiological mechanisms may be contributing to PFL. Large volumes of experimental data have emerged, defining the complex pathophysiological events following IR. IR injury is a significant mechanism negated by most clinical studies. IR injury cannot be prevented because it is a part of the procedure, and it affects the entire flap. As the distance from the vascular pedicle increases, the number and size of collateral microcirculation decreases, which makes the distal parts of a free flap theoretically more vulnerable for IR injury. Intervention studies with experimental IR models targeting various specific steps and thus potential clinical therapies have been promising.12‐14 101
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