Megavolume Autologous Fat Transfer

Sir: Khouri et al.1 recently published an article about the theory and principle of megavolume autologous fat transfer. They hypothesized that two main principles influence results: graft-to-recipient interface and interstitial fluid pressure limit. They mentioned that free nonvascularized grafts not exceeding 2 mm in radius could survive during the limited time in which plasmatic imbibition nourished the graft until neovascularization was established. This limited time was described as 2 days. They indicated that the decreased interface increased the distance that should diffuse oxygen to reach the grafted adipocytes, causing central necrosis to occur before neovascularization. They reported that the increased interstitial fluid pressure reduced capillary radius, reducing oxygen delivery to grafted adipose tissue. Rubin2 emphasized other variables for fat graft survival not accounted for in the authors’ proposed principles and concluded that if the role of these variables were better elucidated, strategies to optimize all of these factors could be applied in concert. The fat-grafting process, starting from harvest and continuing until long-term survival of the fat, included ischemia-reperfusion injury. Nishikawa et al.3 stated that adipose tissue was the least tolerant to ischemic insult compared with the other cells. Khouri et al.1 explained in an alternate theory that many of the adipocytes died rather soon, but incumbent stem cells survived and transformed their identity to match that of the recipient bed scaffold, in this case, the adipocyte. Eto et al.4 indicated that adipocytes died easily under ischemic conditions, whereas adipose-derived stem/progenitor cells were activated and contributed to adipose tissue repair. We have also revealed that adipose-derived stem cells prevented ischemia-reperfusion injury not only by neovascularization but also by the effect on growth hormones and cytokines of the recipient area.5 The ischemic insult of the fat-grafting process persisted from the traumatic harvest of the fragile adipocytes until neovascularization. In addition, regardless of how much vascularity was in the recipient area, the reperfusion injury continued until the adipocytes survived. The explanation by Khouri et al. of the graft-to-recipient interface mainly focused on the size of the graft, and the dimensions of the cannula still lacked the main mechanism of ischemia-reperfusion injury to the adipocytes during fat grafting. We think that the fat-grafting process can not only be defined as a grafting process but should be accepted as an ischemia-reperfusion injury because of the fragility of the adipocytes. We would like to know the authors’ opinion about the ischemic insult and reperfusion injury during the fat-grafting process. Would the authors suggest any special solution during harvest, or have they been using the standard tumescent technique that would enhance the graft-to-recipient interface? We would be glad if the authors could explain whether there was any special preparation of the fat before injection in their marvelous series of over 1000 fat-grafting procedures. We would like to thank the authors for sharing their experience. DISCLOSURE The authors have no financial interest to declare in relation to the content of this communication. Cagri A. Uysal, M.D., Ph.D. Huseyin Borman, M.D. Department of Plastic and Reconstructive Surgery Baskent University Faculty of Medicine Bahcelievler, Ankara, Turkey