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The use of pedicled and free flaps for tissue transfer and coverage has become a common practice in modern plastic surgery. An area that presents considerable challenge for tissue coverage is the groin. Defects in this area are complicated by issues such as prior surgery; scar contracture; extension of the defect beyond the borders of the groin; radiation damage; high probability of infection; and involvement of vital underlying structures, the genitalia, and perineal and perianal area. Therefore, the choice of donor site and flap usage is often difficult. Multiple methods of tissue transfer closure have been reported in the literature for repair of such defects and are reviewed in the following text. Here the authors present the case of a 30-year-old Caucasian woman born with a congenital giant hairy nevus of her left lower back, buttock, posterior thigh, and flank, who underwent wide local excision and skin grafting as a newborn. After several operations, the closure broke down and was left to heal by secondary intention. She has since developed excessive scar tissue leading to pain with ambulation secondary to scar contracture involving her labia majora. In this report, the wound was repaired with a free DIEP flap with excellent result and resolution of all symptoms.

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ABSTARCT: BACKGROUND: Secondary lymphedema following breast cancer therapy remains a major problem. Vascularized lymph node transfer (VLNT) is a surgical treatment for lymphedema that has shown promising results, but limited studies in the United States have investigated outcomes for single-stage VLNT to the axilla. The goal of this prospective, ongoing study was to investigate the clinical, psychosocial, and functional outcomes of patients who underwent VLNT for the treatment of upper extremity lymphedema after breast cancer therapy. STUDY DESIGN: VLNT to the axilla were performed on patients with upper extremity lymphedema after breast cancer therapy. Patients were evaluated preoperatively and postoperatively at 1-, 3-, 6-, 9-, and 12-month intervals by circumferential measurements, pain/heaviness scales, and the LYMQOL questionnaire. RESULTS: Fifty patients met the study criteria. Preliminary results showed a decrease in arm volumes by 34.57 % at 1 month, 52.03 % at 3 months, 42.34 % at 6 months, 65.23 % at 9 months, and 58.68 % at 12 months. Pain and heaviness consistently decreased over time to 0.38 and 1.67 respectively at 12 months. Overall quality of life scores steadily improved from 5.72 preoperatively to 7.79 at 12 months. There was a significant decrease in the number of infections of the affected arm postoperatively and a decreased need for physiotherapy. Complications occurred in 17 patients and consisted mainly of minor wound complications. CONCLUSIONS: VLNT continues to demonstrate its value as a safe and effective treatment option for lymphedema after breast cancer therapy. Significant reductions in volume are accompanied by a decrease in symptoms and improvement in quality of life.

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The advantages of endoscopic carpal tunnel release, compared with traditional open techniques, include smaller incisions, less scar tenderness, and faster recoveries. However, endoscopic carpal tunnel release has also been associated with higher complication rates. The goal of this study was to evaluate the safety and functional outcomes of minimal-incision open carpal tunnel release. In this prospective study involving a 2-year period, 104 patients (149 hands) underwent open carpal tunnel release with a 1-cm incision. Prospective data on complications among 104 patients were recorded, and functional outcomes among 20 patients were assessed by using the Michigan Hand Outcomes Questionnaire, the Jebsen-Taylor Hand Function Test, and pinch/grip strength testing. Data were collected before the operation and 3 weeks and 6 months after the operation. Complications included three wound infections and one carpal tunnel syndrome recurrence, 18 months after the initial release procedure. Michigan Hand Outcomes Questionnaire scores improved significantly between the preoperative and postoperative periods. There were no significant changes in Jebsen-Taylor Hand Function Test results or pinch/grip strength. Minimal-incision open carpal tunnel release can be performed safely and is associated with good functional outcomes.

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Lipopolysaccharide (LPS)-binding protein (LBP) greatly facilitates LPS activation of monocytic cells through the CD14 receptor, triggering activation of innate immune responses. An acute phase protein, LBP is produced predominantly by the liver; however, we and others have shown that LBP is produced extrahepatically in multiple locations, including the lung. The importance of LBP in the lung has remained unclear. LBP may make the host more acutely sensitive to LPS and development of septic complications; alternatively, it may be protective, aiding in detection, opsonization, and killing of bacteria. Our objective was to determine the role LBP plays in local pulmonary immune defenses to bacterial challenge. LBP knockout mice and age-matched C57BL/6 wild-type controls were challenged with direct intratracheal inoculation of Klebsiella pneumoniae. We observed a significant increase in mortality, earlier onset of bacteremia, and greater pulmonary bacterial loads in LBP knockout mice compared with controls. Total lung myeloperoxidase (MPO) activity, neutrophil recruitment to the alveolar space, and levels of KC--a chemokine involved in neutrophil recruitment--in bronchoalveolar lavage (BAL) fluid and lung homogenates were found to be significantly diminished in knockout mice compared with controls. Together, our findings suggest that LBP is essential in local pulmonary innate immune responses against bacteria.

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Upregulation of CD14 in Kupffer cells has been implicated in the pathogenesis of several forms of liver injury, including alcoholic liver disease. However, it remains unclear whether CD14 mediates lipopolysaccharide (LPS) signaling in this specialized liver macrophage population. In this series of experiments, we determined the role of CD14 in LPS activation of Kupffer cells by using several complementary approaches. First, we isolated Kupffer cells from human livers and studied the effects of anti-CD14 antibodies on LPS activation of these cells. Kupffer cells were incubated with increasing concentrations of LPS in the presence and absence of recombinant human LPS binding protein (LBP). With increasing concentrations of LPS, human Kupffer cell tumor necrosis factor-alpha (TNF-alpha) production (a marker for Kupffer cell activation) increased in a dose-dependent manner in the presence and absence of LBP. In the presence of anti-human CD14 antibodies, the production of TNF-alpha was significantly diminished. Second, we compared LPS activation of Kupffer cells isolated from wild-type and CD14 knockout mice. Kupffer cells from CD14 knockout mice produced significantly less TNF-alpha in response to the same amount of LPS. Together, these data strongly support a critical role for CD14 in Kupffer cell responses to LPS.

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BACKGROUND: Skin is equipped with an array of immune mediators aimed at fighting invading microbes. CD14 has been shown to play a key role in modulating the activation of cells by LPS. Since LPS levels within burn wounds are often found to be elevated, we sought to examine the expression of CD14 within human skin following thermal injury. METHODS: Patients who sustained partial thickness burns, were recruited into the study (n=57). Total RNA was isolated from both burn and normal (control) skin. Northern blot analysis and TaqMan RT-PCR were used to determine skin CD14 mRNA levels. Immunohistochemistry was used to localize CD14 expression in burned and normal skin. RESULTS: Quantitative PCR showed significantly increased CD14 expression levels in the immediate post-burn period (P<0.05 burn versus non-burn). Immunohistochemistry revealed more pronounced CD14 staining 24 h after the injury, reaching normal levels approximately 5-7 days post-burn. CONCLUSION: CD14 expression peaks within the first week post-burn before declining, reaching normal levels after 14 days. This loss of supranormal CD14 expression locally within the wound may contribute to a weakened host defense response 5-6 days after injury, when patients become especially vulnerable to infection.

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