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’

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