No abstract

Seroma formation is a difficult problem to treat and prevent. Its sequelae include wound infection, dehiscence, and skin-flap necrosis. The purpose of this study was to determine the effects of fibrin sealant on seroma formation and wound healing. Seromas were created in a rat model by harvesting the latissimus dorsi muscle. In group I (n = 20), only the latissimus dorsi muscle was harvested. In group II (n = 20), the latissimus dorsi muscle was harvested and fibrin sealant applied. Seromas were routinely aspirated. In group III (n = 20), the latissimus dorsi muscle was harvested, and once a seroma was evident clinically, it was aspirated and injected with fibrin sealant. Fibrin sealant was created by combining virally deactivated fibrinogen and thrombin (American Red Cross, Rockville, Md.). In group I, 90 percent of the animals formed seromas compared with only 20 percent in group II. The average total fluid aspirated in group I was 21 cc versus 6 cc in group II. Sixty percent of the animals in group I and 5 percent in group II required serial drainage for chronic seromas. Skin-flap necrosis occurred in 80 percent of the animals in group I, in 10 percent of group II, and in 40 percent of group III. Histologic evaluation confirmed that group II underwent better wound healing. At necropsy, group I animals with seromas had gross capsular formation; this was not readily apparent in the fibrin sealant groups. We conclude that (1) the harvesting of the rat latissimus dorsi muscle is a reliable model for creating seromas, (2) fibrin sealant effectively prevents seroma formation when applied intraoperatively, (3) wound healing in the seroma rat model is improved with intraoperative fibrin sealant application, (4) closed injection of fibrin sealant for existing seromas cannot be recommended at this time, (5) virally deactivated fibrin sealant retains its hemostatic and adhesive properties, and (6) current clinical trials of virally deactivated fibrin sealant may facilitate its use in the United States.

Keloids are wounding‐induced fibroproliferative human tumor‐like skin scars of complex genetic makeup and poorly defined pathogenesis. To reveal dynamic epigenetic and transcriptome changes of keloid fibroblasts, we performed RNA‐seq and ATAC‐seq analysis on an early passage keloid fibroblast cell strain and its paired normal control fibroblasts. This keloid strain produced keloid‐like scars in a plasma clot‐based skin equivalent humanized keloid animal model. RNA‐seq analysis reveals gene ontology terms including hepatic fibrosis, Wnt‐β‐catenin, TGF‐β, regulation of epithelial‐mesenchymal transition (EMT), STAT3 and adherens junction. ATAC‐seq analysis suggests STAT3 signalling is the most significantly enriched gene ontology term in keloid fibroblasts, followed by Wnt signalling (Wnt5) and regulation of the EMT pathway. Immunohistochemistry confirms that STAT3 (Tyr705 phospho‐STAT3) is activated and β‐catenin is up‐regulated in the dermis of keloid clinical specimens and keloid skin equivalent implants from the humanized mouse model. A non‐linear dose‐response of cucurbitacin I, a selective JAK2/STAT3 inhibitor, in collagen type I expression of keloid‐derived plasma clot‐based skin equivalents implicates a likely role of STAT3 signalling in keloid pathogenesis. This work also demonstrates the utility of the recently established humanized keloid mouse model in exploring the mechanism of keloid formation.

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Ischemically injured reperfused myocardium is characterized by increased 18F-fluorodeoxyglucose uptake as demonstrated by positron emission tomography. To elucidate the metabolic fate of exogenous glucose entering reperfused myocardium, D-[6-14C] glucose and L-[U-13C] lactate were used to determine glucose uptake, glucose oxidation and the contribution of exogenous glucose to lactate production. The pathologic model under investigation consisted of a 3 h balloon occlusion of the left anterior descending coronary artery followed by 24 h of reperfusion in canine myocardium. The extent and severity of myocardial injury after the ischemia and reperfusion were assessed by histochemical evaluation (triphenyltetrazolium chloride and periodic acid-Schiff stains). Thirteen intervention and four control dogs were studied. The glucose uptake in the occluded/reperfused area was significantly enhanced compared with that in control dogs (0.40 +/- 0.14 versus 0.15 +/- 0.10 mumol/ml, respectively). In addition, a significantly greater portion of the glucose extracted immediately entered glycolysis in the intervention group (75%) than in the control dogs (33%). The activity of the nonoxidative glycolytic pathway was markedly increased in the ischemically injured reperfused area, as evidenced by the four times greater lactate release in this area compared with the control value. The dual carbon-labeled isotopes showed that 57% of the exogenous glucose entering glycolysis was being converted to lactate. Exogenous glucose contributed to greater than 90% of the observed lactate production. This finding was confirmed by the histochemical finding of sustained glycogen depletion in the occlusion/reperfusion area. The average area of glycogen depletion (37%) significantly exceeded the average area of necrosis (17%). These data demonstrate enhanced and sustained activity of the nonoxidative glycolytic pathway after a prolonged occlusion with reperfusion in canine myocardium. Because glycogen stores remain depleted, exogenous glucose becomes an important myocardial substrate under these pathologic conditions.

This series demonstrates unique advantages of the LICAP flap for a variety of breast reconstruction problems, including outpatient setting, no muscle sacrifice, flap reliability, and low donor site morbidity. These results confirm previous reports in post bariatric augmentation that the LICAP flap reliably supplies a large skin/adipose flap from the redundant tissue of the lateral chest fold with minimal morbidity even after radiation. The LICAP flap warrants closer consideration in breast reconstruction.

Primary lymphomas of the breast are rare and predominately of B-cell phenotype. Anaplastic large cell lymphoma is a T-cell lymphoma that accounts for only 3% of all non-Hodgkin lymphomas. We present a rare case of primary anaplastic large cell lymphoma of the breast in association with a silicone breast implant capsule in a healthy 40-year-old woman. The patient had bilateral breast implants placed at 21 years of age and presented with painful bilateral breast contractures and associated breast asymmetry. Histology, immunohistochemistry, and T-cell gene rearrangement studies were supportive of a CD 30-positive ALK-1 negative anaplastic large cell lymphoma. This case represents the 14th reported case of primary breast lymphoma in association with breast prosthesis. Of interest is that 11 of these cases were T-cell lymphomas with 8 specifically of the CD30-positive anaplastic large cell lymphoma type. This rare case highlights the importance of histologic examination of breast capsule specimens.

Post-excision RT shows significant reduction in keloid recurrence compared to excision alone. While the recurrence control rates are not statistically different between EBRT and brachytherapy, keloids treated with EBRT recurred significantly later than those treated by HDR brachytherapy by a mean of 2.5 years. Further workup with a randomized control study will help to refine optimal adjuvant RT treatment. LEVEL OF EVIDENCE 3.