Negative Pressure Wound Therapy in Facilitating Wound Healing After Surgical Decompression for Metastatic Spine Disease.

BACKGROUND: The risk of wound-related complications, including surgical site infections (SSIs), in patients undergoing surgery for metastatic spine disease (MSD) is high. Consequently, patients requiring wound revision surgery face delay in resuming oncological care and incur additional hospitalization. Recent reports suggest that negative pressure wound therapy (NPWT) applied on a closed wound at the time of surgery significantly reduces postoperative wound complications in degenerative spine disease and trauma setting. Here, we report a single institution experience with incisional NPWT in patients undergoing surgery for MSD. METHODS: We compared rates of wound complications requiring surgical revision in a surgical cohort of patients with or without NPWT from 2015 to 2020. Adult patients with radiographic evidence of MSD with mechanical instability and/or accelerated neurological decline were included in the study. NPWT was applied on a closed wound in the operating room and continued for 5 days or until discharge, whichever occurred first. RESULTS: A total of 42 patients were included: 28 with NPWT and 14 without. Patient demographics including underlying comorbidities were largely similar. NPWT patients had higher rates of prior radiation to the surgical site (36% vs. 0%, P = 0.017) and longer fusion constructs (6.7 vs. 3.9 levels, P < 0.001). Three patients (21%) from the control group and none from the NPWT group contracted SSI requiring wound washout (P = 0.032). CONCLUSIONS: Our data suggest that SSI and wound dehiscence are significantly reduced with the addition of incisional NPWT in this vulnerable population.

CRISPR Cas9-mediated deletion of biliverdin reductase A (BVRA) in mouse liver cells induces oxidative stress and lipid accumulation.

Obesity is the predominant cause of non-alcoholic fatty liver disease (NAFLD), which is associated with insulin resistance and diabetes. NAFLD includes a spectrum of pathologies that starts with simple steatosis, which can progress to non-alcoholic steatohepatitis (NASH) with the commission of other factors such as the enhancement of reactive oxygen species (ROS). Biliverdin reductase A (BVRA) reduces biliverdin to the antioxidant bilirubin, which may serve to prevent NAFLD, and possibly the progression to NASH. To further understand the role of BVRA in hepatic function, we used CRISPR-Cas9 technology to target the Blvra gene in the murine hepa1c1c7 hepatocyte cell line (BVRA KO). BVRA activity and protein levels were significantly lower in BVRA KO vs. wild-type (WT) hepatocytes. Lipid accumulation under basal and serum-starved conditions was significantly (p < 0.05) higher in BVRA KO vs. WT cells. The loss of BVRA resulted in the reduction of mitochondria number, decreased expression of markers of mitochondrial biogenesis, uncoupling, oxidation, and fusion, which paralleled reduced mitochondrial oxygen consumption. BVRA KO cells exhibited increased levels of ROS generation and decreased levels of superoxide dismutase mRNA expression. In conclusion, our data demonstrate a critical role for BVRA in protecting against lipid accumulation and oxidative stress in hepatocytes, which may serve as a future therapeutic target for NAFLD and its progression to NASH.