Extremity trauma, including ischemia (e.g., prolonged tourniquet application or crush), is common among battlefield injuries. Injured muscle releases toxins leading to rhabdomyolysis and, potentially, acute kidney injury (AKI). The goal of this study was to characterize sequelae of ischemic extremity injury over 72 h, focusing on time courses of rhabdomyolysis and AKI. Male Sprague Dawley rats were placed into two groups. Ischemic injury was produced in anesthetized rats using bilateral tourniquets (TK; n = 10) for 5 h; control (CON; n = 9) rats were treated identically without TK application. Indicators of rhabdomyolysis and renal function were measured in conscious rats 1 day preinjury (baseline, BL) and then at 1.5, 24, 48, and 72 h post-TK release. Prolonged TK application produced necrosis in both muscle and bone marrow but not in kidney. The wet/dry weights indicated edema in injured limbs at 72 h (4.1 (0.5) (TK) vs. 2.9 (0.1) (CON); p < 0.001). TK rats exhibited a 100-fold increase in creatine kinase activity compared to CON at 1.5 h (20,040 (7265) U/L vs. 195 (86) U/L (mean (SD); p < 0.0001). TK decreased the mean glomerular filtration rate (GFR; p < 0.001) at 1.5 h, but these values recovered by 24 h in concert with elevated urinary flow and alkalinization. Prolonged ischemic extremity injury therefore produced severe rhabdomyolysis without irreversible renal damage.

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.