ABSTRACT
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.
ABSTRACT
Neonatal dilated cardiomyopathy (DCM) is rare with high etiologic heterogeneity. Recently, biallelic, autosomal recessive, pathogenic variants in RPL3L (ribosomal protein L3-like) have been reported in the literature with severe early-onset DCM. In the present brief report, we identified two pathogenic RPL3L variants, each harbored in unaffected heterozygous parents: mother (RPL3L c.1076_1080delCCGTG (p.Ala359Glyfs*4)) and father (RPL3L c.80G > A (p.Gly27Asp)). Pathogenic variants were segregated as autosomal recessive to two offspring born with compound heterozygous RPL3L variants and affected by neonatal DCM. This is the second report in the literature to the best of our knowledge and our findings support the pathogenicity of biallelic RPL3L pathologic variants associated with rapidly progressive neonatal DCM and heart failure with a poor prognosis.