LETTERs GUIDELINES
Letters to the Editor, discussing material recently published in the Journal, are welcome. They will have the best chance of acceptance if they are received within 8 weeks of an article’s publication. Letters to the Editor may be published with a response from the authors of the article being discussed. Discussions beyond the initial letter and response will not be published. Letters submitted pertaining to published Discussions of articles will not be printed. Letters to the Editor are not usually peer reviewed, but the Journal may invite replies from the authors of the original publication. All Letters are published at the discretion of the Editor. Letters submitted should pose a specific question that clarifies a point that either was not made in the article or was unclear, and therefore a response from the corresponding author of the article is requested. Authors will be listed in the order in which they appear in the submission. Letters should be submitted electronically via PRS’ enkwell, at www.editorialmanager.com/prs/. We reserve the right to edit Letters to meet requirements of space and format. Any financial interests relevant to the content of the correspondence must be disclosed. Submission of a Letter constitutes permission for the American Society of Plastic Surgeons and its licensees and asignees to publish it in the Journal and in any other form or medium. The views, opinions, and conclusions expressed in the Letters to the Editor represent the personal opinions of the individual writers and not those of the publisher, the Editorial Board, or the sponsors of the Journal. Any stated views, opinions, and conclusions do not reflect the policy of any of the sponsoring organizations or of the institutions with which the writer is affiliated, and the publisher, the Editorial Board, and the sponsoring organizations assume no responsibility for the content of such correspondence. The Journal requests that individuals submit no more than five (5) letters to Plastic and Reconstructive Surgery in a calendar year.
Letters Megavolume Autologous Fat Transfer: Part I. Theory and Principles Sir:
K
houri 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 Copyright © 2014 by the American Society of Plastic Surgeons
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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. DOI: 10.1097/PRS.0000000000000539
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 Correspondence to Dr. Uysal Department of Plastic and Reconstructive Surgery Baskent University Faculty of Medicine Fevzi Cakmak Cad. 5. Sok. No. 48 06490 Bahcelievler, Ankara, Turkey [email protected]
www.PRSJournal.com
Volume 134, Number 4 • Letters DISCLOSURE The authors have no financial interest to declare in relation to the content of this communication.
DOI: 10.1097/PRS.0000000000000561
Roger K. Khouri, Jr., B.S. University of Michigan Medical School Ann Arbor, Mich. Miami Breast Center Key Biscayne, Fla.
REFERENCES 1. Khouri RK, Rigotti G, Cardoso E, Khouri RK Jr, Biggs TM. Megavolume autologous fat transfer: Part I. Theory and principles. Plast Reconstr Surg. 2014;133:550–557. 2. Rubin P. Discussion: Megavolume autologous fat transfer: Part I. Theory and principles. Plast Reconstr Surg. 2014;133:558–560. 3. Nishikawa H, Manek S, Barnett SS, Charlett A, Green CJ. Pathology of warm ischaemia and reperfusion injury in adipomusculocutaneous flaps. Int J Exp Pathol. 1993;74: 35–44. 4. Eto H, Kato H, Suga H, et al. The fate of adipocytes after nonvascularized fat grafting: Evidence of early death and replacement of adipocytes. Plast Reconstr Surg. 2012;129:1081–1092. 5. Uysal AC, Mizuno H, Tobita M, Ogawa R, Hyakusoku H. The effect of adipose-derived stem cells on ischemia-reperfusion injury: Immunohistochemical and ultrastructural evaluation. Plast Reconstr Surg. 2009;124:804–815.
Reply: Megavolume Autologous Fat Transfer: Part I. Theory and Principles Sir:
Reperfusion injury is a well-recognized phenomenon in vascularized tissue transfer. Our review, however, studies nonvascularized tissue transfer and the factors essential for revascularization.1 In vascularized tissue transfer, perfusion is restored surgically, leading to a sudden infiltration of blood and inflammatory molecules that induce reperfusion injury. However, in nonvascularized tissue transfer, angiogenesis occurs biologically over the course of days, making reperfusion injury unlikely. For the common two-dimensional skin grafts, angiogenesis requires only adequate contact between the grafted tissue and a functional recipient capillary bed.2 Our review attempts to clarify the surface area–to-volume limitations that occur when the third dimension is added. Extrapolating from the twodimensional grafts, because thick grafts revascularize poorly, we need to avoid graft lobules with a greater than 2-mm radius and carefully disperse them within the three-dimensional recipient scaffold. Furthermore, just as overgrafting is counterproductive in two-dimensional grafts, and we cannot graft more than the size of the recipient wound defect, we need to recognize the limited capacity of a recipient site to accept additional graft volume before the interstitial fluid pressure increases to levels that compromise the capillary circulation. If graft perfusion is not restored before the onset of tissue damage, we need not worry about reperfusion injury.3 It is only after we comply with these requirements for revascularization that we can start discussing reperfusion injury.
Roger K. Khouri, M.D.
180 Crandon Boulevard, Suite 114 Key Biscayne, Fla. 33149 [email protected]
DISCLOSURE The author has no financial interest to declare in relation to the content of this communication. REFERENCES 1. Khouri RK, Rigotti G, Cardoso E, Khouri RK Jr, Biggs TM. Megavolume autologous fat transfer: Part I. Theory and principles. Plast Reconstr Surg. 2014;133:550–557. 2. Greenwood J, Amjadi M, Dearman B, Mackie I. Real-time demonstration of split skin graft inosculation and integra dermal matrix neovascularization using confocal laser scanning microscopy. Eplasty 2009;9:e33. 3. Rezkalla SH, Kloner RA. No-reflow phenomenon. Circulation 2002;105:656–662.
Mandibular Deformity in Hemifacial Microsomia: A Reassessment of the Pruzansky and Kaban Classification Sir:
W
e read with interest the article entitled “Mandibular Deformity in Hemifacial Microsomia: A Reassessment of the Pruzansky and Kaban Classification,” by Wink et al.1 Our group began classifying hemifacial microsomia in a retrospective study of the natural history and progression of the deformity in untreated patients. We concluded that the severity of end-stage facial asymmetry was predicted by the mandibular type2 as designated in Pruzansky’s original classification.3 Subsequently, the criteria for type II deformity were modified for surgical planning4: Wink et al.1 call this the Pruzansky and Kaban classification. The purpose of their study was to use three-dimensional computed tomography to categorize the mandibular deformity in 38 hemifacial microsomia patients. They conclude that three-dimensional imaging highlights inaccuracy and variability of the Pruzansky and Kaban schema and suggest the need to “reexamine the classification of hemifacial microsomia,” presumably referring to the mandibular component. We find flaws in the design and methodology of their research.1 First, their standard was the senior author’s typing of the deformity based on physical examination alone. The Pruzansky and Kaban classification requires both physical examination and imaging. Clinical typing of an infant or toddler is the first step and should be confirmed or revised after obtaining radiographs in childhood. Second, typing by threedimensional imaging only tested the participants’
657e
Letters to the Editor, discussing material recently published in the Journal, are welcome. They will have the best chance of acceptance if they are received within 8 weeks of an article’s publication. Letters to the Editor may be published with a response from the authors of the article being discussed. Discussions beyond the initial letter and response will not be published. Letters submitted pertaining to published Discussions of articles will not be printed. Letters to the Editor are not usually peer reviewed, but the Journal may invite replies from the authors of the original publication. All Letters are published at the discretion of the Editor. Letters submitted should pose a specific question that clarifies a point that either was not made in the article or was unclear, and therefore a response from the corresponding author of the article is requested. Authors will be listed in the order in which they appear in the submission. Letters should be submitted electronically via PRS’ enkwell, at www.editorialmanager.com/prs/. We reserve the right to edit Letters to meet requirements of space and format. Any financial interests relevant to the content of the correspondence must be disclosed. Submission of a Letter constitutes permission for the American Society of Plastic Surgeons and its licensees and asignees to publish it in the Journal and in any other form or medium. The views, opinions, and conclusions expressed in the Letters to the Editor represent the personal opinions of the individual writers and not those of the publisher, the Editorial Board, or the sponsors of the Journal. Any stated views, opinions, and conclusions do not reflect the policy of any of the sponsoring organizations or of the institutions with which the writer is affiliated, and the publisher, the Editorial Board, and the sponsoring organizations assume no responsibility for the content of such correspondence. The Journal requests that individuals submit no more than five (5) letters to Plastic and Reconstructive Surgery in a calendar year.
Letters Megavolume Autologous Fat Transfer: Part I. Theory and Principles Sir:
K
houri 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 Copyright © 2014 by the American Society of Plastic Surgeons
656e
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. DOI: 10.1097/PRS.0000000000000539
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 Correspondence to Dr. Uysal Department of Plastic and Reconstructive Surgery Baskent University Faculty of Medicine Fevzi Cakmak Cad. 5. Sok. No. 48 06490 Bahcelievler, Ankara, Turkey [email protected]
www.PRSJournal.com
Volume 134, Number 4 • Letters DISCLOSURE The authors have no financial interest to declare in relation to the content of this communication.
DOI: 10.1097/PRS.0000000000000561
Roger K. Khouri, Jr., B.S. University of Michigan Medical School Ann Arbor, Mich. Miami Breast Center Key Biscayne, Fla.
REFERENCES 1. Khouri RK, Rigotti G, Cardoso E, Khouri RK Jr, Biggs TM. Megavolume autologous fat transfer: Part I. Theory and principles. Plast Reconstr Surg. 2014;133:550–557. 2. Rubin P. Discussion: Megavolume autologous fat transfer: Part I. Theory and principles. Plast Reconstr Surg. 2014;133:558–560. 3. Nishikawa H, Manek S, Barnett SS, Charlett A, Green CJ. Pathology of warm ischaemia and reperfusion injury in adipomusculocutaneous flaps. Int J Exp Pathol. 1993;74: 35–44. 4. Eto H, Kato H, Suga H, et al. The fate of adipocytes after nonvascularized fat grafting: Evidence of early death and replacement of adipocytes. Plast Reconstr Surg. 2012;129:1081–1092. 5. Uysal AC, Mizuno H, Tobita M, Ogawa R, Hyakusoku H. The effect of adipose-derived stem cells on ischemia-reperfusion injury: Immunohistochemical and ultrastructural evaluation. Plast Reconstr Surg. 2009;124:804–815.
Reply: Megavolume Autologous Fat Transfer: Part I. Theory and Principles Sir:
Reperfusion injury is a well-recognized phenomenon in vascularized tissue transfer. Our review, however, studies nonvascularized tissue transfer and the factors essential for revascularization.1 In vascularized tissue transfer, perfusion is restored surgically, leading to a sudden infiltration of blood and inflammatory molecules that induce reperfusion injury. However, in nonvascularized tissue transfer, angiogenesis occurs biologically over the course of days, making reperfusion injury unlikely. For the common two-dimensional skin grafts, angiogenesis requires only adequate contact between the grafted tissue and a functional recipient capillary bed.2 Our review attempts to clarify the surface area–to-volume limitations that occur when the third dimension is added. Extrapolating from the twodimensional grafts, because thick grafts revascularize poorly, we need to avoid graft lobules with a greater than 2-mm radius and carefully disperse them within the three-dimensional recipient scaffold. Furthermore, just as overgrafting is counterproductive in two-dimensional grafts, and we cannot graft more than the size of the recipient wound defect, we need to recognize the limited capacity of a recipient site to accept additional graft volume before the interstitial fluid pressure increases to levels that compromise the capillary circulation. If graft perfusion is not restored before the onset of tissue damage, we need not worry about reperfusion injury.3 It is only after we comply with these requirements for revascularization that we can start discussing reperfusion injury.
Roger K. Khouri, M.D.
180 Crandon Boulevard, Suite 114 Key Biscayne, Fla. 33149 [email protected]
DISCLOSURE The author has no financial interest to declare in relation to the content of this communication. REFERENCES 1. Khouri RK, Rigotti G, Cardoso E, Khouri RK Jr, Biggs TM. Megavolume autologous fat transfer: Part I. Theory and principles. Plast Reconstr Surg. 2014;133:550–557. 2. Greenwood J, Amjadi M, Dearman B, Mackie I. Real-time demonstration of split skin graft inosculation and integra dermal matrix neovascularization using confocal laser scanning microscopy. Eplasty 2009;9:e33. 3. Rezkalla SH, Kloner RA. No-reflow phenomenon. Circulation 2002;105:656–662.
Mandibular Deformity in Hemifacial Microsomia: A Reassessment of the Pruzansky and Kaban Classification Sir:
W
e read with interest the article entitled “Mandibular Deformity in Hemifacial Microsomia: A Reassessment of the Pruzansky and Kaban Classification,” by Wink et al.1 Our group began classifying hemifacial microsomia in a retrospective study of the natural history and progression of the deformity in untreated patients. We concluded that the severity of end-stage facial asymmetry was predicted by the mandibular type2 as designated in Pruzansky’s original classification.3 Subsequently, the criteria for type II deformity were modified for surgical planning4: Wink et al.1 call this the Pruzansky and Kaban classification. The purpose of their study was to use three-dimensional computed tomography to categorize the mandibular deformity in 38 hemifacial microsomia patients. They conclude that three-dimensional imaging highlights inaccuracy and variability of the Pruzansky and Kaban schema and suggest the need to “reexamine the classification of hemifacial microsomia,” presumably referring to the mandibular component. We find flaws in the design and methodology of their research.1 First, their standard was the senior author’s typing of the deformity based on physical examination alone. The Pruzansky and Kaban classification requires both physical examination and imaging. Clinical typing of an infant or toddler is the first step and should be confirmed or revised after obtaining radiographs in childhood. Second, typing by threedimensional imaging only tested the participants’
657e
