Purpose: Compartment syndrome is a limb-threatening condition. Treatment is urgent decompression by fas-ciotomy. However, orthopedic surgeons are often confronted by a limb at risk for compartment syndrome, in which treatments to preserve tissue might be considered. Hypothermia has shown promise as a technique of maintaining tissue viability in transplant surgery, replant surgery and soft tissue injury. Cooling reduces microvascular dysfunction, inflammation and edema. This study was designed to determine whether tissue cooling might reduce muscle damage in the setting of elevated intracompartmental pressure. Purpose This study investigated the effect of hypothermia on tissue perfusion, viability and the inflammatory response in an animal model of elevated intracompartmental pressure. We hypothesize that hypothermia will preserve muscle tissue viability in an animal model of elevated intracom-partmental pressure. Method: Twenty Wistar rats were randomized. Five animals had elevated intracompartmental pressure for 2 hours (CS). Five had elevated pressure and hindlimb cooling to 25oC (CS-HY). Five had hindlimb cooling to 25oC (HY) and 5 were control animals (C). All animals were anaesthesized for study. Core temperature was maintained over 30oC. Elevated ICP was maintained (30mmHg) using a saline infusion technique (groups CS and CS-HY). After 2 hours, fasciotomies were completed and intravital microscopy was used to measure tissue viability, microvascular perfusion and inflammation. Results: The use of hypothermia reduced tissue damage by approximately 50% in the CS-HY group (8.2% injured cells) compared with the CS group (16.5% injured cells). There was no difference in capillary perfusion comparing the CS and CS-HY groups (p> 0.05). The number of adherent inflammatory cells was fewer comparing the CS-HY with the CS groups, but this did not reach statistical significance with the numbers available for study. Conclusion: Hypothermia preserved tissue viability in an animal model of elevated intracompartmental pressure. Fasciotomy remains the gold standard treatment for established compartment syndrome. However cooling may be useful to preserve tissue viability in extremities that are at risk of developing compartment syndrome. The clinical utility of hypothermia for compartment syndrome requires further study

Purpose: Severe compartment syndrome is associated with renal failure, end organ damage, and systemic inflammatory response syndrome (SIRS). Intravital videomicroscopy (IVVM) is a useful tool to study capillary perfusion and inflammation in end organs such as the liver and lungs. In this study, the systemic effect of hindlimb compartment syndrome was studied using hepatic IVVM. The purpose was to measure the effect of increased hindlimb intracompartmental pressure on hepatocyte viability, inflammation, and blood flow in a rodent model. Method: Ten Wistar rats were randomised into control (C) and Compartment Syndrome (CS) groups. Animals were anaesthetized with 5 % isoflurane. Mean arterial pressure was monitored using a carotid artery catheter. Elevated intracompartmental pressure (EICP) was induced by saline infusion into the anterior compartment of the hind limb and maintained for 2 hours between 30–40mmHg in the CS group. Two hours following fasciotomy, the liver was analyzed using IVVM to quantify capillary perfusion as a measure of microvascular dysfunction. The numbers of adherent and rolling leukocytes in venules and sinusoids were quantified to measure the inflammatory response. Irreversible hepatocyte injury was measured using a fluorescent vital dye which labels the nuclei of severely injured cells. Results: Hepatocellular injury was significantly higher in the CS group (325±103 PI labeled cells/10-1 mm2) compared to controls (30±12 PI labeled cells/10-1 mm2)(p=0.0087). The number of adherent venular white blood cells (WBC) was significantly higher for the CS group (5±2/hpf) than controls (0.2±0.2)(p=0.0099). Volumetric blood flow was not significantly different between CS and controls. Conclusion: After only 2 hours of compartment syndrome in this animal model, the number of activated white blood cells increased 25-fold and liver cellular injury increased 10-fold compared to controls. Marked systemic inflammation and hepatocellular damage was detected in response to isolated limb compartment syndrome. Compartment syndrome is a low-flow ischemia/reperfusion injury with a profound inflammatory response. Further research into the severe end-organ damage associated with compartment syndrome is required

Elevated intracompartmental pressure (ICP) results in tissue damage due to impaired microcirculatory function. The nature of microcirculatory impairment in elevated ICP is not well understood. This study was designed to measure the effects of increased ICP on skeletal muscle microcirculation, inflammation and cell viability using intravital videomicroscopy. Twenty adult male Wistar rats were randomised to four groups: the control group (control) had no intervention; while three experimental groups had elevated ICP maintained for fifteen (15m), 45 (45m), or ninety (90m) minutes. Compartment pressure was continuously monitored and controlled between 30¡V40mmHg in the posterior hindlimb using saline infusion into the anterior hindlimb. Mean arterial pressure was maintained between 80 and 120mmHg. Fasciotomy was then performed and the Extensor Digitorum Longus muscle studied using intravital videomicroscopy. Perfusion was measured by comparing the numbers of continuous, intermittent, and nonperfused capillaries. Inflammation was measured by counting the number of activated (rolling and adherent) leukocytes in post-capillary venules. Muscle cellular Injury was measured using fluorescent vital staining of injured cell nuclei. Perfusion: The number of continuously perfused capillaries decreased from 77 ± 3/mm (control) to 46 ± 10/mm (15m),40±10/mm(45m)and27±8/mm(90m)(p< 0.05). Non-perfused capillaries increased from 13 ± 1 (control) to 16 ± 4 (15m), 30 ± 7 (45m), and 39 ± 5 (90m) (p< 0.05). Inflammation: Activated leukocytes increased from 3.6 ± 0.7/(100ƒÝ)2 (control) to 5.9 ± 1.3 (15m), 8.6 ± 1.8 (45m), and 10.9 ± 3.0/(100ƒÝ)2 (90m) (p< 0.01). Injury: The proportion of injured cells increased from 5 ± 2 % in the control group to 12 ± 3 (15m), 16 ± 7 (45m) and 20 ± 3 % (90m) (p< 0.05). As little as fifteen minutes of 30mmHg ICP caused irreversible muscle damage and microvascular dysfunction. With increased duration, further decreases in capillary perfusion and increases in injury are noted. A severe inflammatory response accompanies elevated ICP. The role of inflammation in compartment syndrome is unknown, but may contribute to cell injury and reduced capillary perfusion