Reconstruction of the chest wall.

Chest wall reconstructions can be a complex and challenging procedure and may require a multidisciplinary approach. The most common indications for chest wall reconstruction are repair of defects due to tumor resection, infection, radiation necrosis, congenital deformities or trauma. The repair of complex chest wall defects presents a challenging problem for the reconstructive surgeon. Although the majority of such defects can be repaired with the use of local and regional musculocutaneous flaps, more complicated cases require increasingly sophisticated reconstructive techniques. As defects increase in size, microsurgical techniques are necessary to augment blood flow to pedicled flaps or to provide free flap coverage from distant sites. A better understanding of the respiratory mechanics and local anatomy is crucial in managing these complex defects.

Recombinant leptin administration improves early angiogenesis in full-thickness skin flaps: an experimental study.

BACKGROUND: Leptin is a potent direct angiogenic factor that stimulates endothelial cell migration and activation in vitro, and angiogenesis in vivo. In addition, leptin seems to play an important role in angiogenesis as it promotes the formation of new blood vessels. OBJECTIVE: To determine the effect of local application of exogenous leptin on the survival of full thickness skin flaps in an experimental animal model. MATERIALS AND METHODS: Ninety Sprague-Dawley rats were used in this study. A full thickness dorsal flap (10 cm x 2 cm) with the pedicle located at the level of the iliac crest was designed. Animals were divided into ten groups of nine animals each. In the distal two thirds of the flap and by means of subdermal injection at 8 different locations, rats were injected with 100 ng/ml leptin, 250 ng/ml leptin, 500 ng/ml leptin, 1000 ng/ml leptin (groups A, B, C and D), 1 microg/ml VEGF (group E), or 1 ml saline (control group), respectively. For each of the four leptin doses used, another animal group was injected with a combination of leptin/antileptin: 100 ng/ml leptin with 150 ng/ml antileptin, 250 ng/ml leptin with 375 ng/ml antileptin, 500 ng/ml leptin with 750 ng/ml antileptin or 1000 ng/ml leptin with 1500 ng/ml antileptin (groups A1, B1, C1 and D1, respectively), in order to study the inhibition of the leptin factor. Nine rats served as controls and were injected with 1 ml saline solution. Rats were sacrificed 3, 7 and 9 days postoperatively. After sacrifice of the animals, the skin was grossly arranged on its appearance, colour and texture. Full thickness skin flaps were dissected for histological examination. A qualitative analysis of angiogenesis in the flap was conducted following a standard hematoxylin and eosin stain. The wound tissue samples from each experimental group underwent immunohistochemical evaluation of microvessel density by endothelial cell staining with mouse anti-rat CD 34 monoclonal antibody. RESULTS: Immunohistochemical staining revealed that more granulation tissue and improved angiogenesis were observed in group D (1000 ng/ml leptin) flaps compared to those in the VEGF, leptin/antileptin and saline groups. In addition, skin flap survival rate in group D (1000 ng/ml leptin) and group E (1 microg/ml VEGF) were significantly better than those of the other groups. The most impressive formation of new blood vessels was noted in the groups with the higher leptin doses. Surgical wounds in the control, as well as in the leptin/antileptin groups, did not demonstrate any new vessels. CONCLUSION: Exogenous administration of recombinant leptin increases early skin flap angiogenesis in an experimental animal model. Local application of leptin could efficiently improve survival of ischemic skin flaps.

Exogenously-administered leptin increases early incisional wound angiogenesis in an experimental animal model.

BACKGROUND: Leptin is a potent direct angiogenic factor that stimulates endothelial cell migration and activation in vitro, as well as angiogenesis in vivo. In addition, leptin seems to play an important role in clinical angiogenesis by promoting the development of new blood vessels. OBJECTIVE: To determine the effect of exogenously administered leptin on incisional wound healing in an experimental animal model. MATERIALS AND METHODS: Sixty-three Sprague-Dawley male mice were used for the study. Full thickness incisional wound was considered as the wound model. The mice were divided into seven groups of nine animals each. Surgical wounds were injected with murine recombinant leptin. Three different leptin doses of 100 pg/ml, 200 pg/ml and 500 pg/ml were used in different animal groups (A, B and C). For each of the three leptin doses used, another animal group was evaluated with a combined injection of leptin and antileptin: 100 pg/ml leptin with 50 pg antileptin, 200 pg/ml leptin with 100 pg antileptin, 500 pg/ml leptin with 250 pg antileptin (A1, B1, and C1), in order to study the inhibitory effect on the leptin factor. Nine mice served as controls. These were injected with 0.3 ml water for injection solution. Mice were sacrificed 3, 7 and 9 days postoperatively. After sacrifice of the animals, the skin was grossly assessed for appearance, colour and texture. Full thickness incisional wounds were dissected for histological examination. A qualitative analysis of angiogenesis in the surgical wound was conducted following a standard hematoxylin and eosin stain. The wound tissue samples from each experimental group underwent immunohistochemical evaluation of microvessel density by endothelial cell staining with mouse anti-rat CD34 monoclonal antibody. RESULTS: The most impressive growth of new blood vessels appeared seven and nine days after treatment with the highest leptin doses. There were no significant differences in microvessel density at seven or nine postoperative days among different groups treated with leptin. None of the wounds from the control group, or those from animal groups treated with the combined injection of leptin and antileptin developed any new vessels. CONCLUSION: Exogenous administration of leptin may increase early tissue angiogenesis in the incisional wound of an experimental animal model.

Melanoma of the head and neck: a review.

Melanoma of the head and neck and its treatment are complex issues. The behavior of head and neck melanoma is aggressive, and it has an overall poorer prognosis than that of other skin sites. Current understanding of the behavior of head and neck melanoma is reviewed and treatment strategies are presented. Controversies in treatment include the role of lymphoscintigraphy with sentinel node biopsy, nodal dissection, margin size, role of radiation therapy, and reconstruction. The therapeutic goal is to treat melanoma aggressively while minimizing the effects of treatment on patient's quality of life. Due to its biological behavior, head and neck melanoma should be treated in an aggressive manner when morbidity is not significantly increased. Patient's specific treatment is imperative.

Dermatofibrosarcoma protuberans: clinicopathological aspects of an unusual cutaneous tumor.

Dermatofibrosarcoma protuberans is a rare cutaneous tumor with particular characteristics and a high frequency of recurrence after inadequate primary treatment. Its histopathological diagnosis might be difficult. Dermatofibrosarcoma protuberans can be safely distinguished from other similar neoplasms of mesenchymal origin based on the immunohistochemical expression of CD34 antigen and the genetic presence of specific chromosomal translocations. Although rarely metastatic, it is followed by a significantly high rate of locoregional failure due to an indolent subcuticular tissue spread. Aggressive surgical management is the therapeutic approach of choice. A wide resection with microscopically disease-free margins is always recommended. Mohs' micrographic surgery together with advanced reconstructive techniques provides satisfactory results even for tumors involving the face or distal extremities.

Merkel cell carcinoma: clinicopathological aspects of an unusual neoplasm.

Merkel cell carcinoma (MCC) is a rare, aggressive cutaneous cancer that predominately affects elderly Caucasians with fair skin and has a propensity for local recurrence and regional lymph node metastases. It can occur on the face, the trunk, the genitalia, and the perianal region. The median age of the patients is 69 years, but it may occur earlier and more frequently in immunosuppressed patients. MCC usually arises in the dermis and extends into the subcutis. It may be difficult to accurately diagnose MCC by light microscopy alone and ancillary techniques, including electron microscopy and immunohistochemistry, may be necessary for a definitive diagnosis. The management of MCC is dependent on the stage of the disease and is hampered by its rarity and lack of randomized trials. Nonetheless, for localized disease most guidelines include wide local excision of the primary tumor either alone or followed by radiation therapy. Sentinel lymph node biopsy can be helpful in staging and prognosis, but its benefit in survival remains to be seen. Systemic chemotherapy may be considered as an adjuvant following surgery or to treat locoregional or distant disease. The prognosis of MCC is variable. In patients with localized disease the course is indolent and is well-controlled with local excision alone. On the other hand, many tumors are aggressive and have a tendency for locoregional recurrence and distant metastases. Such patients have a grim prognosis, with a median survival of 9 months. Successful outcome most often is seen in patients with early diagnosis and complete excision.

Malignant hidradenoma: a report of two cases and review of the literature.

INTRODUCTION: Malignant tumors of the sweat glands are very rare. Clear cell hidradenoma is a lesion with histopathological features resembling those of eccrine poroma and eccrine spiradenoma. The biological behavior of the tumor is aggressive, with local recurrences reported in more than 50% of the surgically-treated cases. MATERIALS AND METHODS: Two patients are presented, the first with tumor in the right axillary region, the second with a recurrent tumor of the abdominal wall. The first patient underwent wide excision with clear margins and axillary lymph node dissection and the second patient underwent wide excision of the primary lesion and bilateral inguinal node dissection due to palpable nodes. RESULTS: The patients had uneventful postoperative courses. No additional treatment was administered. However, sixteen months after surgery, patient 2 developed extensive and massive recurrence involving almost the whole abdominal wall. Although he had received several chemotherapeutic agents, the disease had a relentless course and the patient succumbed two and a half years following surgery. CONCLUSION: Malignant tumors of the sweat glands are very rare neoplasms with no discrete clinical characteristics. It is necessary to suspect any lesion which shows evidence of enlargement and to verify its status by histological evaluation. Additional resection is generally required, with at least 2-cm clear margins, since surgery is the only effective treatment.

Penetration of clarithromycin in experimental pleural empyema model fluid.

BACKGROUND: The degree of penetration of clarithromycin into the pleural fluid has not been studied. OBJECTIVE: To determine the degree to which clarithromycin penetrates into empyemic pleural fluid using a new rabbit model of empyema. METHODS: An empyema was created via the intrapleural injection of 1 ml turpentine followed 24 h later by instillation of 5 ml (10(10)) Escherichia coli bacteria (ATCC 35218) into the pleural space of New Zealand white rabbits. After an empyema was verified by thoracentesis and pleural fluid analysis, clarithromycin 30 mg/kg was administered intravenously. Antibiotic levels were determined on samples of pleural fluid and blood samples collected serially over 12 h. Antibiotic levels were estimated using HPLC. RESULTS: The antibiotic penetrated well into the empyemic pleural fluid (AUC(PF)/AUC(serum) ratio of 1.57). The time to equilibration between the pleural fluid and blood antibiotic levels was 8 h. The peak pleural fluid level (Cmax(PF) of 2.88 microg/ml) occurred 1 h (Tmax(PF) of 1 h) after infusion and decreased thereafter. The Cmax(serum) was 3.53 microg/ml at 1 h after administration. CONCLUSION: The levels of clarithromycin in the pleural fluid after intravenous administration are inhibitory for most of the usual pathogens causing empyema. The degree of penetration of clarithromycin should be considered when macrolides are selected for the treatment of patients with empyema.

Penetration of newer quinolones in the empyema fluid.

The degree of penetration of newer quinolones into the pleural fluid has not been studied. The objective of the present study was to determine the degree to which moxifloxacin and levofloxacin penetrate into empyemic pleural fluid using a new rabbit model of empyema. An empyema was created via the intrapleural injection of turpentine (1 mL), followed 24 h later by instillation of 2 mL (1 x 10(10)) Escherichia coli bacteria (ATCC 35218) into the pleural space of New Zealand white rabbits. After an empyema was verified by thoracentesis and pleural fluid analysis, moxifloxacin and levofloxacin (25 mg.kg(-1) for both, i.v.) were administered. Antibiotic levels were determined in samples of pleural fluid and in blood collected serially over 12 h. Antibiotic levels were measured using HPLC. Each of the antibiotics penetrated well into the empyemic pleural fluid. Antibiotic penetration was the greatest for moxifloxacin (area under the curve (AUC) for pleural fluid/blood (AUCPF/AUCblood) ratio=1.37) followed by levofloxacin (ratio=1.13). The time to equilibration between the pleural fluid and blood antibiotic levels was more rapid for moxifloxacin (3.9 h) than for levofloxacin (4.4 h). With moxifloxacin, the peak pleural fluid concentration (Cmax,PF) was 2.77 microg.mL(-1) and occurred at a time to maximum pleural fluid concentration (Tmax,PF) of 6 h after infusion and decreased thereafter. The peak blood concentration (Cmax,blood) was 4.81 microg.mL(-1) at 1 h after administration. With levofloxacin, the peak pleural fluid level (Cmax,PF=1.39 microg.mL(-1)) occurred at 6 h (Tmax,PF=6 h) after infusion. The Cmax,blood was 1.88 microg.mL(-1) at 1 h after administration. In conclusion, differences were found in the degree of penetration of the two quinolones into infected pleural fluid in rabbits. The clinical significance of these differences is unknown. More studies are needed to evaluate the pharmacokinetic parameters in the pleural space in humans.