INTRODUCTION: Use of acellular cadaveric dermis (ACD) in implant-based breast reconstruction provides an alternative to total submuscular placement. We previously reported that biointegrated ACD samples from implant-based breast reconstruction patients had statistically diminished levels of granulation tissue formation, vessel proliferation, chronic inflammatory changes, capsule fibrosis, fibroblast cellularity, and foreign body giant cell inflammatory reaction compared with native breast capsule samples. These findings suggested that certain properties intrinsic to ACD may diminish inflammatory changes that may promote peri-prosthetic capsule formation.1 We sought to further evaluate differences between ACD and native breast capsule specimens through immunohistochemical analysis of key inflammatory markers involved in capsule formation. METHODS: Twenty patients underwent implant-based breast reconstruction using the “dual-plane” ACD (AlloDerm® Regenerative Tissue Matrix, LifeCell Corporation, Branchburg, NJ) technique. During exchange of the tissue expander for the implant, intraoperative biopsies of biointegrated ACD and native subpectoral capsule from the tissue expander envelope were obtained. Immunohistochemical analysis was performed for inflammatory markers: macrophages (CD68), T-cells (CD3), B-cells (CD20), myofibroblasts (αSMA), endothelial cells (CD31), and collagen I and III. Masked biopsy specimens were semi-quantitatively scored by a histopathologist to reflect observed levels of marker staining. Scores were statistically analyzed using the Wilcoxon rank test. RESULTS: ACD samples had statistically diminished levels of all inflammatory markers assessed compared with corresponding native breast capsule samples (P<0.005) (Figure 1). Although all variables were significantly diminished in biointegrated ACD capsules compared with native breast capsules, fibroblast cellularity, granulation tissue, endothelial cells, vessel proliferation, collagen I, and capsule fibrosis had substantially lower P values, suggesting that for those variables, there was an even greater difference between ACD and the native capsule control. Interestingly, although myofibroblasts, collagen III, and B-cell lymphocytes were also decreased in ACD compared with capsular control, these differences were not as significant as the previous variables.Figure 1: Semiquantitative analysis of inflammatory markers with acellular cadaveric dermis (ACD; AlloDerm®) vs. native breast capsule samples (0=none, 3=severe levels of marker staining). *n=21 samples (a bilateral sample was obtained from 1 patient; all other samples were unilateral). P<0.005 for all comparisons.CONCLUSION: This study further supports the theory that ACD has certain intrinsic properties that may limit capsule formation. The decreased inflammatory changes in the ACD samples as evidenced by decreased fibroblast activity, collagen I deposition, and capsular fibrosis, suggest that use of ACD may result in decreased capsule formation. Further investigation is needed to determine the mechanism by which ACD inhibits these inflammatory cells, whether ACD reduces the incidence of breast capsular contracture, and the longevity of this effect.
Through its oversight of residency education in the United States, the Accreditation Council for Graduate Medical Education has mandated new structural changes in resident education with its newly created core competencies and an emphasis on outcomes-based education. These core competencies represent the central areas in which the Accreditation Council for Graduate Medical Education believes a plastic surgery resident should receive adequate and appropriate education and training. In addition, as part of this outcomes-based education, residents are to be evaluated on their level of mastery in these core competencies. Increasingly, the Accreditation Council for Graduate Medical Education will assess the ability of residency programs to integrate the teaching and evaluating of the core competencies in their accreditation process of plastic surgery residency programs. This shift in residency evaluation initiated by the Outcomes Project by the Accreditation Council for Graduate Medical Education will have a significant impact in how plastic surgery residents are taught and, as importantly, evaluated in the coming years. The objectives of this work were as follows: (1) to outline the different methods available to foster a core competency-based plastic surgery training curriculum and (2) to serve as a primer to help both full-time academic and clinical faculty to further develop their curriculum to successfully teach and constructively evaluate their residents in the core competencies in accordance with the Accreditation Council for Graduate Medical Education guidelines. At the conclusion of this review, the reader should have a better understanding of what is necessary to formulate and help foster a plastic surgery core competency curriculum, particularly with an emphasis on the contemporary methods used for outcomes evaluations.
Pregnancy is a relative contraindication for elective surgery. The primary concerns are for the safety of the fetus and the mother. However, there are particular problems involving microvascular surgery due to the pregnancy-associated hypercoagulable state. The authors were presented with a 35-year woman, 20 weeks pregnant, with a degloved foot and ankle associated with an open distal tibia/fibula fracture (Gustilo IIIB). Salvage of her leg required a microvascular tissue transfer. Accordingly, a combined latissimus dorsi-serratus anterior free flap was performed with a saphenous vein graft to the popliteal vessels. The patient was hypercoagulable and there were extensive platelet clots. Her consumption of heparin was enormous. Postoperatively, she was treated with intravenous dextran for 5 days and for 17 days with intravenous heparin. After discharge, she was placed on subcutaneous heparin until she delivered a healthy baby. The flap survived and her leg was salvaged. The hypercoagulable state of pregnancy, as well as thromboprophylaxis, are discussed.
In Brief Learning Objectives: After reviewing this article, the participant should be able to: 1. Describe the epidemiology and etiology of skin cancers. 2. Understand the biology and predisposing conditions. 3. Understand tumor types and their clinical behavior. 4. Discuss the importance of diagnostic biopsy and various treatment options. 5. Understand the basis of surgical management and principles of reconstruction. 6. Review the most recently published literature and understand new concepts in tumor biology. Summary: This article reviews melanoma and nonmelanoma cutaneous malignancies. RELATED VIDEO CONTENT IS AVAILABLE ONLINE.
Human acellular dermal matrix (HADM; previously termed "acellular cadaveric dermis") may limit inflammatory changes believed to play a role in capsular contracture, a common complication of implant-based breast reconstruction. Differences between HADM and native breast capsule specimens were evaluated by immunohistochemical analysis of key inflammatory markers involved in capsule formation. Twenty consecutive patients underwent immediate, 2-stage, implant-based breast reconstruction with dual-plane HADM. During tissue expander–implant exchange, full-thickness biopsies of biointegrated HADM and native breast capsule (internal control) from the tissue-expander envelope were obtained. Immunohistochemical analysis was performed for endothelial cells (CD31), B cells (CD20), T cells (CD3), macrophages (CD68), collagen I and III, and myofibroblasts (α-smooth muscle actin). Observed levels of marker labeling were semiquantitatively scored from 0 (none) to 3 (severe) by a blinded histopathologist and were statistically analyzed with the Wilcoxon rank sum test. A bilateral sample was obtained from 1 patient; all other samples were unilateral. Compared with capsule samples from native breast tissue, HADM samples had significantly lower levels of all inflammatory markers (P < .001). These lower levels of inflammatory markers support previous evidence that HADM may inhibit inflammatory and profibrotic signaling characteristics of breast capsule development and decrease the risk of capsular contracture. Further investigation is needed to determine the mechanism by which HADM inhibits these inflammatory cells, whether HADM reduces the incidence of breast capsular contracture, and if so, the longevity of this effect. Therapeutic
