Objectives:Acute compartment syndrome is a devastating condition associated with lasting consequences or even death if not treated in a timely fashion. Current preclinical modeling is inadequate. Ideally a model should mimic human disease. There should be a trauma-induced reperfusion or direct muscle event that causes gradual increased pressure and is amenable to release with fasciotomy. We have attempted to reproduce this mechanism and outcome in a porcine model.Methods:Anterior tibial musculature was injured with vascular occlusion plus exterior tourniquet crush or direct intracompartmental crush through balloon inflation. The injury was maintained for over 5 hours. At that time, the tourniquet or balloon was removed. The injuries were continuously monitored with an intramuscular continuous pressure sensor. Pressure changes were recorded and after 2 hours of postinjury observation, a fasciotomy was performed for the muscle compartment.Results:Pressures were brought to 100 mm Hg during the injury phase. During the two-hour observation period, the balloon catheter technique achieved an average pressure of 25.1 ± SD 8.8 mm Hg with a maximum reading of 38.2 mm Hg and minimum reading of 14.1 mm Hg. During this same period, the ischemia-reperfusion + direct crush technique achieved an average pressure of 33.7 ± SD 7.3 mm Hg, with a maximum reading of 43.5 mm Hg and minimum reading of 23.5 mm Hg. Average pressure postfasciotomy for the balloon catheter technique was 2.4 ± SD 2.5 mm Hg; and for the crush technique, average value postfasciotomy was 4.9 ± SD 3.7 mm Hg—both representing a return to physiologic levels.Conclusion:This is the first preclinical model that shows the same response to injury and treatment as is observed in human physiology. Surgical and nonsurgical therapies for compartment syndrome can now be tested reliably.

Traditional antibiotic treatments for wound infections pose risks associated with microbial resistance, necessitating the exploration of innovative approaches such as nanoparticles as the next generation of antibiotics. In this study, we present a paradigm shift approach for acute and chronic wound care by developing an active wound dressing capable of protecting and eradicating bacteria from the injury site. The focus of this research is on the electroless deposition of large zinc oxide nanoparticles (ZnO NPs) onto spined silk fibroin gauze, targeting a particle size range of approximately 200 nm to minimize cytotoxity. The biocompatibility and antimicrobial efficacy of the ZnO NP-embedded silk wound dressing were evaluated against gram-positive (Staphylococcus aureus) and gram-negative (Pseudomonas aeruginosa) bacteria. The results demonstrate that the ZnO NPs integrated within the silk wound dressing exhibit biocompatibility with 70% cell viability and control microorganism growth against S. aureus and P. aeruginosa, gradually from first 24 hours of exposure. By targeting larger particle size, only the release of a substantial amount of zinc ions were released without generating toxic reactive oxygen species (ROS) that could harm both bacteria and cells. These findings underscore the therapeutic potential of utilizing bioresorbable wound dressings functionalized with large ZnO NPs, thus revolutionizing the landscape of clinical wound care.