To Mesh or Not to Mesh: What Is the Ideal Meshing Ratio for Split Thickness Skin Grafting of the Lower Extremity?

Split-thickness skin grafts can provide effective autologous wound closure in patients with dysvascular comorbidities. Meshing the graft allows for reduced donor site morbidity and expanded coverage. This study directly compares outcomes across varying meshing ratios used to treat chronic lower extremity wounds. Patients who received split-thickness skin grafts to their lower extremity for chronic ulcers from December 2014 to December 2019 at a single center were retrospectively reviewed. Patients were stratified by meshing ratios: nonmeshed (including pie crusting), 1.5:1, and 3:1. The primary outcome was clinical "healing" as determined by surgeon discretion at 30 days, 60 days, and the latest follow-up. Secondary outcomes included postoperative complications, graft loss, ulcer recurrence, progression to amputation, and mortality. A total of 321 patients were identified. Wound sizes and location differed significantly, with 3:1 meshing applied to the largest wounds (187.8 ± 157.6 cm2; 1.5:1 meshed, 110.4 ± 103.9 cm2; nonmeshed 38.7 ± 55.5 cm2; p < .0001) mostly of the lower leg (n = 18, 75%; 1.5:1 meshed, n = 23, 43.4%; nonmeshed n = 62, 25.7%; p < .0001). Meshed grafts displayed a significantly higher proportion of healing at 30 and 60 days, but no differences persisted by the final follow-up (16.5 ± 20.5 months). Longitudinally, nonmeshed STSG was associated with most graft loss (46, 19.1%; p = .011) and ulcer recurrence (44, 18.3%; p = .011). Of the 3 meshing ratios, 3:1 exhibited the lowest rates of complications. Our results suggest that 3:1 meshing is a safe option for coverage of large lower extremity wounds to minimize donor site morbidity.

Intraoperative Invasive Blood Pressure Monitoring in Flap-Based Breast Reconstruction: Does It Change Outcomes?

Despite the lack of guidelines regarding the use of intra-arterial lines in postmastectomy breast reconstruction (PMBR), they continue to be used in this setting. In this study of patients undergoing PMBR, we aimed to (1) identify factors associated with intra-arterial line placement, (2) analyze the correlation between intra-arterial monitoring and noninvasive blood pressure (NIBP) monitoring, and (3) investigate whether hemodynamic management differs significantly between patients undergoing intra-arterial blood pressure monitoring versus NIBP. METHODS: All patients undergoing flap-based PMBR between 2017 and 2019 were retrospectively reviewed. Patients were pair-matched based on flap donor site, BMI, and age to identify factors associated with intra-arterial line placement. Methods described by Bland and Altman1 were utilized to determine agreement between intra-arterial line measurements and NIBP. RESULTS: Thirty-two patients were included with 16 patients in the intra-arterial line group and 16 in the NIBP group. None of the factors studied were significantly related to the likelihood of intra-arterial line placement. Agreement analysis demonstrated that mean arterial pressures calculated from intra-arterial line readings were as much as 23 points lower or 12 points higher than those from NIBP. Bias calculations with this extent of difference suggest poor correlation between intra-arterial line readings and NIBP. There was no difference between groups in rate of administration of blood-pressure altering medications (hypertensive: n = 3, 18.8%, P = 1.000; hypotensive: n = 7, 3.8%, P = 1.000). CONCLUSION: Our findings highlight the need for more definitive guidance regarding the use of intra-arterial monitoring in patients undergoing PMBR.

Mesenchyme-specific deletion of Tgf-ß1 in the embryonic lung disrupts branching morphogenesis and induces lung hypoplasia.

Proper lung development depends on the precise temporal and spatial expression of several morphogenic factors, including Fgf10, Fgf9, Shh, Bmp4, and Tgf-ß. Over- or under-expression of these molecules often leads to aberrant embryonic or postnatal lung development. Herein, we deleted the Tgf-ß1 gene specifically within the lung embryonic mesenchymal compartment at specific gestational stages to determine the contribution of this cytokine to lung development. Mutant embryos developed severe lung hypoplasia and died at birth due to the inability to breathe. Despite the markedly reduced lung size, proliferation and differentiation of the lung epithelium was not affected by the lack of mesenchymal expression of the Tgf-ß1 gene, while apoptosis was significantly increased in the mutant lung parenchyma. Lack of mesenchymal expression of the Tgf-ß1 gene was also associated with reduced lung branching morphogenesis, with accompanying inhibition of the local FGF10 signaling pathway as well as abnormal development of the vascular system. To shed light on the mechanism of lung hypoplasia, we quantified the phosphorylation of 226 proteins in the mutant E12.5 lung compared with control. We identified five proteins, Hrs, Vav2, c-Kit, the regulatory subunit of Pi3k (P85), and Fgfr1, that were over- or under-phosphorylated in the mutant lung, suggesting that they could be indispensable effectors of the TGF-ß signaling program during embryonic lung development. In conclusion, we have uncovered novel roles of the mesenchyme-specific Tgf-ß1 ligand in embryonic mouse lung development and generated a mouse model that may prove helpful to identify some of the key pathogenic mechanisms underlying lung hypoplasia in humans.