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Background: Reduction mammaplasty is one of the most common reconstructive procedures performed in plastic surgery. Multiple comorbidities play a role in postoperative wound healing complications; however, there are insufficient data on the subdermal plexus (SDP) as it relates to these comorbidities. The purpose of this study is to evaluate the relationship between body mass index (BMI) and SDP of the superficial breast tissues and examine the association between SDP and postoperative complications. Methods: After Institutional Review Board approval, screening, and informed consent, patients undergoing reduction mammaplasty were selected. Tissue to be discarded was sent to pathology for analysis of immunohistochemistry directed against endothelial cells to determine the density of the SDP. Patients with BMI <35 and ≥35 kg/m2 were compared. Statistical analysis, including 2-tailed t test and Pearson correlation, was conducted. Results: A significant difference in SDP density (standard deviation) was identified between patients with a BMI ≥35 versus <35 kg/m2 (2.65 capillaries/mm2 ± 1.8 vs 1.56 capillaries/mm2 ± 1.2; P = .033). Patients with no historical use of tobacco versus those who used tobacco showed a significantly increased SDP (2.11 capillaries/mm2 ± 1.6 vs 1.20 capillaries/mm2 ± 0.5; P = .009). A significant relationship between postoperative infection (1.00 capillaries/mm2 ± 1.1; P = .041) and hematoma/seroma (0.788 capillaries/mm2 ± 0.1; P = .003) was identified. No significant relationship was found between SDP and delayed wound healing, nipple-areolar complex complications, fat/flap necrosis, or symptomatic scar occurrence. Conclusions: There is a statistically significant increase in SDP seen with increasing BMI, which does not explain the higher rate of wound healing complications after reduction mammaplasty typically seen in the higher BMI patient population. The association between BMI and complications after reduction mammaplasty remains unclear.

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BACKGROUND: Botulinum toxin-A (BTX) has numerous cosmetic and therapeutic applications. Our previous studies have found that BTX augments pedicled flap survival through both vasodilatory effects and attenuation of the inflammatory response to ischemia in the rat. This study examines the effect of chronic BTX on microcirculatory vascular tone and its response to acute topical vasodilators in muscle flaps. METHODS: The spinotrapezius muscle of Sprague-Dawley rats underwent a single 2-week pretreatment of 0.2 mL saline either with (n = 5) or without (n = 5) 2u BTX. After surgical elevation, an arcade arteriole was observed using a video caliper device. Vessel diameter was measured at 30-second intervals after sequential superfusion of nitroglycerin (100 and 200 µg/mL), multiple concentrations of lidocaine, and a combination of adenosine (10 µM) and nitroprusside (10 µM) to induce maximum dilation. RESULTS: Baseline and dilation diameters were expressed as ratios of pharmacologically induced maximum dilation, whereas percent dilation was defined as the change in diameter over baseline diameter. We found a significant increase in resting diameter with BTX pretreatment (P = 0.0028). Compared with the control group, mean baseline diameter was 15% greater, and percent dilation was 25% less in BTX-pretreated flaps. There was no significant relationship between BTX pretreatment and dilation diameter (P = 0.2895) after adjusting for the effect of acute vasodilators. CONCLUSIONS: Pretreatment with BTX may induce the arteriolar resting diameter to be closer to their maximum potential diameter. Additionally, BTX does not display a synergistic effect with topical vasodilators on vasodilation.

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Ischemia-reperfusion injury is often the final and irreversible factor causing flap failure in microsurgery. The salvage of a microsurgical flap with an ischemia-reperfusion injury contributes to the success of microsurgical flap transfers. Activated protein C (APC), a serine protease with anticoagulant and anti-inflammatory activities, has been shown to improve ischemic flap survival. To date, APC has yet to be applied to models of free flap with ischemia-reperfusion injury. In this study, we aimed to investigate the effect of APC on gracilis flap ischemia-reperfusion injury induced by gracilis vessels clamping and reopening. Sixty male Sprague-Dawley rats were randomly divided into 2 groups. After 4 hours of clamping for ischemia, flaps were reperfused and recombinant human APC (25 µg/kg) or saline was injected in the flaps through pedicles. At 0, 1, 4, 18, and 24 hours after injection (n = 6 for each time point), the tissue samples were harvested. The muscle viability at 24 hours in saline group was 54.8% (15.1%), whereas the APC-treated group was 90.0% (4.3%) (P < 0.05). The induced nitric oxide synthase (iNOS) mRNA expression increased with the time after reperfusion, which were 0.93 (0.25) to 2.09 (0.22) in saline group, and 0.197 (0.15) to 0.711 (0.15) in the APC-treated group. iNOS mRNA expression in the APC-treated group was significantly higher than the saline group at 1, 18, and 24 hours (P < 0.05). Numerous inflammatory cells were observed infiltrating and invading the muscle fibers in the saline group more than the APC-treated group. Increased number of polymorphonuclear cells was also noted in the saline group compared with the APC-treated group (P < 0.05). In conclusion, APC treatment can significantly attenuate ischemia-reperfusion injury and increase the survival of the free flap through down-regulating iNOS mRNA expression and reducing the inflammatory cells. Further research is still needed to be done on various mechanisms in which APC is protective to prevent tissue damage.

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The aging population, in combination with the popularity of breast augmentation with implants, presents surgeons with a growing number of cases involving women undergoing minimally invasive cardiac surgery (MICS) who have breast implants. We present an unusual complication involving the delayed migration of a subpectoral implant into the chest cavity through an iatrogenic defect after a minimally invasive mitral valve repair. This chest wall defect was ultimately repaired with a latissimus dorsi flap. Although MICS has been described in women with breast implants, the documented experience remains limited. Most authors classically recommend explantation of the prosthesis to provide access to the chest wall; however, some have later suggested preserving the implant capsule in situ while performing the cardiac procedure with gentle retraction. From our literature review and experience, we recommend that the posterior capsule should remain intact. If this is not possible, then the chest wall closure should be reinforced with either mesh, soft tissue, or both. Soft tissue options include the conversion from a subpectoral to a subglandular position to use the pectoralis major, or a latissimus dorsi muscle flap. With the increasing number of these cases along with the complexities of minimally invasive procedures, close communication and planning should be undertaken between both cardiothoracic and plastic surgeons when taking care of these patients. Above all, when faced with postoperative complications after MICS, the plastic surgeon must maintain a high index of clinical suspicion and consider the possibility of intrathoracic migration of an implant so that proper workup and planning may be initiated.

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