Does the Use of Incisional Negative-Pressure Wound Therapy Prevent Mastectomy Flap Necrosis in Immediate Expander-Based Breast Reconstruction?

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I note with interest the excellent article by Kim et al., demonstrating that incisional negative-pressure wound therapy effectively prevented mastectomy flap necrosis in immediate expander-based breast reconstruction with acellular dermal matrices.1 The study had an elegant retrospective cohort study design, and was powered to show reduced overall complications, infections, dehiscence, and major flap necrosis requiring surgical correction. I believe this to be a very valuable contribution to the literature regarding perioperative wound care, and specifically in the prevention of wound complications.
In the Discussion section, the authors correctly refer to the effective splinting of the incision line with negative-pressure wound therapy, which in my view is the dominant beneficial mechanism. In a study using PICO (Smith & Nephew, London, United Kingdom) versus conventional dressings in the context of bilateral breast reductions, the most obvious early beneficial effect appeared to be improvements in the experience of pain on the side with the incisional negative-pressure wound therapy.2 This appears to support the rationale of reduced movement across the incision line, and likely reduces the incidence of dehiscence.
Unfortunately, the authors cited work using laser Doppler flow to show the augmentation of soft-tissue perfusion.3 In this regard, the authors have failed to recognize the contribution that Kairinos et al. have made in both in vivo and in vitro studies, much of which has been published in this Journal, toward our understanding of the biomechanism of negative-pressure wound therapy.4–9 Irrespective of the wound dimensions, the filler, or the interface, negative-pressure wound therapy actually exerts a small positive pressure on the wound bed on application of negative pressure to the filler material.4–9 The perfusion initially reduces while the pressure is applied, and this is important in our concept of why granulation forms so well under negative-pressure wound therapy in the context of an open wound, as a result of the release of growth factors such as vascular endothelial growth factor, and specifically why more granulation occurs when using intermittent or variable settings.4–9 Unfortunately, our understanding of perfusion was perverted by the use of laser Doppler in many of the negative-pressure wound therapy studies, a measure dependent on a constant diameter of vessels in the examined wound. Under positive pressure, laser Doppler will interpret perfusion as greater when it may actually be reduced, because the velocity of flow is greater in smaller vessels.

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