This investigation seeks to understand how the interfaces between fracture orthoses and the body affect the relative motion between the user and device. Excessive relative motion can inadvertently load the fracture and prevent healing. Identifying interfaces that minimize relative motion will inform the designs of future fracture orthoses. Three types of interfaces are used to off-load the injured limb: a thigh corset, a sling that loaded the ischium, and a sling that loaded the patellar tendon. However, little is known how these interfaces interact or with one another. Eighteen able-bodied participants were fitted with an adjustable interface testing system (ITS) that redirected loads away from the foot and lower leg to more proximal parts of the body using different combinations of the three interfaces. A video motion capture system measured the relative motion between the ITS and the participants while varying the type of interface, load through the ITS, and tightness of the thigh corset. Average relative motion varied from 1.6 to 6.5 cm across all conditions. The thigh corset combined with either the ischial sling or patellar tendon-bearing sling allowed the least relative motion of the interface conditions tested. However, the combinations differ in the sagittal profile they create for the user as well as the breadth of injuries they can treat. All these factors need to be considered in the design of future fracture orthoses.
Background/Objectives: Extremity trauma represents a significant proportion of battlefield injuries and is prevalent in polytraumatized patients from accidents. Delayed antibiotic treatment and surgical intervention can lead to wound infections, contributing to preventable mortality. This preliminary study aimed to develop a conscious swine model of complex extremity trauma that induces systemic inflammatory response syndrome (SIRS). Methods: All surgical procedures were conducted under anesthesia with sufficient analgesia. All swine were instrumented with a telemetry device and catheters at least 3 days prior to any injury. In phase 1 of model development, a complex extremity injury was performed that consisted of skin and muscle loss, bone defect, severe hemorrhage, and 2 h tourniquet application. In phase 2, multi-drug resistant Gram-positive and Gram-negative bacteria were inoculated topically at the injury site to exacerbate pathophysiological changes towards SIRS. Post-injury, conscious animals were assessed a minimum of twice daily, including pain assessment, neurological response, and vital signs. Blood samples were collected for microbiological testing, complete blood cell counts, and biochemical analysis. Results: After establishing SIRS criteria for Sinclair swine, we developed a model of severe extremity trauma leading to SIRS. During phase 1, resuscitative fluids were reduced and discontinued, with animals surviving 24 h and maintaining SIRS for up to 4 h post-recovery. Phase 2 showed that Gram-negative and Gram-positive pathogens can exacerbate and prolong SIRS. After 72 h, localized infection at the injury site was observed in all animals. Conclusions: We established a new swine model of complex extremity trauma with SIRS. Our model is consistent, reproducible, and relevant to prolonged care scenarios, providing a platform for future research into the evaluation of preventative and therapeutic strategies.
Background/Objectives: The diagnosis of acute compartment syndrome (ACS) of the extremities is typically based on subjective clinical signs and symptoms, highlighting the need for user-friendly diagnostic tools to improve accuracy and reliability. This study evaluates the performance of two commercial devices, the MY01® continuous pressure monitoring system and the Moxy Monitor near-infrared spectroscopy-based system, against a reference standard of continuous intracompartmental pressure (ICP) monitoring in a preclinical ACS model. Methods: ACS was induced in the anterior compartment of the distal hind limb in eight Yorkshire pigs using a balloon displacement model. ICP was incrementally elevated and maintained for four hours at >30 mmHg above mean arterial pressure. This was followed by balloon deflation and reperfusion. Final assessments were performed at 24 h post-injury. ICP measurements from the MY01® and muscle oxygen saturation (SmO2) data from the Moxy Monitor were compared to reference ICP measurements. Histologic analysis of muscle tissue was performed to assess the severity of necrosis. Results: The MY01® provided accurate ICP measurements, with a mean bias of 2.21 ± 18.77 mmHg during pre-ischemia, 4.86 ± 10.43 mmHg during reperfusion, and 4.69 ± 3.28 mmHg 24 h post-injury, compared to reference probes. Correlation at 24 h post-injury was (r = 0.86, R2 = 0.73, p < 0.0001). In contrast, the Moxy Monitor failed to detect significant differences in SmO2 between injured and control limbs at 24 h post-injury, despite pronounced ICP differences. Our volumetric displacement ACS model demonstrated its efficacy as a testing platform by allowing for controlled, incremental elevation in ICP and sustaining elevated ICP levels after 24 h. Histologic evaluation confirmed extensive muscle damage, including edema and necrosis. Conclusions: The MY01® provides accurate, continuous ICP monitoring, supporting its clinical utility in ACS diagnosis. However, the use of near-infrared spectroscopy-based systems such as the Moxy Monitor for ACS diagnosis and management should continue to be critically scrutinized.