Background: The “Wide Awake Local Anesthesia No Tourniquet” (WALANT) technique is gaining popularity in hand surgery owing to its benefits of reduced cost, shorter hospital stay, improved safety, and the ability to perform active intraoperative examinations. The aim of this study is to analyze the cost savings and efficiency of performing A1 pulley release for treatment of trigger finger using the WALANT technique in a major city hospital procedure room (PR) as compared with the standard tourniquet, operating room (OR) approach. Methods: Patients who underwent trigger finger release between 2012 and 2017 were identified. Demographic and procedural information were obtained. Patients were followed for an average of 82 and 242 days in the PR and OR groups, respectively. Results: Thirty-nine PR and 37 OR patients were identified. Case length and turnover time were shorter in the PR group [21.4 ± 7 versus 23.5 ± 14.3 min (P = 0.942) and 31.1 ± 11.1 and 65.3 ± 17.7 min (P < 0.001), respectively). The cost of the instrument tray utilized was calculated as $3,304.25 in the main OR and $993.79 in the PR. Cost per minute for all personal services in the OR was calculated to be $44/min, a cost that was virtually absent in the PR. Complication rates did not differ between both groups. Conclusion: Performing A1 pulley release for treatment of trigger finger using the WALANT technique is both cost effective and time efficient compared to performing the same procedure in the main OR of a major city public hospital.

Chronic hyperglycemia impairs intracellular redox homeostasis and contributes to impaired diabetic tissue regeneration. The Keap1/Nrf2 pathway is a critical regulator of the endogenous antioxidant response system, and its dysfunction has been implicated in numerous pathologies. Here we characterize the effect of chronic hyperglycemia on Nrf2 signaling within a diabetic cutaneous regeneration model. We characterized the effects of chronic hyperglycemia on the Keap1/Nrf2 pathway within models of diabetic cutaneous wound regeneration. We assessed reactive oxygen species (ROS) production and antioxidant gene expression following alterations in the Nrf2 suppressor Keap1 and the subsequent changes in Nrf2 signaling. We also developed a topical small interfering RNA (siRNA)–based therapy to restore redox homeostasis within diabetic wounds. Western blotting demonstrated that chronic hyperglycemia–associated oxidative stress inhibits nuclear translocation of Nrf2 and impairs activation of antioxidant genes, thus contributing to ROS accumulation. Keap1 inhibition increased Nrf2 nuclear translocation, increased antioxidant gene expression, and reduced ROS production to normoglycemic levels, both in vitro and in vivo. Topical siKeap1 therapy resulted in improved regenerative capacity of diabetic wounds and accelerated closure. We report that chronic hyperglycemia weakens the endogenous antioxidant response, and the consequences of this defect are manifested by intracellular redox dysregulation, which can be restored by Keap1 inhibition. Targeted siRNA-based therapy represents a novel, efficacious strategy to reestablish redox homeostasis and accelerate diabetic cutaneous tissue regeneration.

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Therapeutic, III.

Early debridement and coverage of exposed hardware are crucial to successfully treating these LVAD infections.