A major pathway of closed soft-tissue injury is failure of microvascular perfusion combined with a persistently enhanced inflammatory response. We therefore tested the hypothesis that hypertonic hydroxyethyl starch (HS/HES) effectively restores microcirculation and reduces leukocyte adherence after closed soft-tissue injury. We induced closed soft-tissue injury in the hindlimbs of 14 male isoflurane-anaesthetised rats. Seven traumatised animals received 7.5% sodium chloride-6% HS/HES and seven isovolaemic 0.9% saline (NS). Six non-injured animals did not receive any additional fluid and acted as a control group. The microcirculation of the extensor digitorum longus muscle (EDL) was quantitatively analysed two hours after trauma using intravital microscopy and laser Doppler flowmetry, i.e. erythrocyte flux. Oedema was assessed by the wet-to-dry-weight ratio of the EDL. In NS-treated animals closed soft-tissue injury resulted in massive reduction of functional capillary density (FCD) and a marked increase in microvascular permeability and leukocyte-endothelial cell interaction as compared with the control group. By contrast, HS/HES was effective in restoring the FCD to 94% of values found in the control group. In addition, leukocyte rolling decreased almost to control levels and leukocyte adherence was found to be reduced by ~50%. Erythrocyte flux in NS-treated animals decreased to 90 ± 8% (mean . sem. ), whereas values in the HS/HES group significantly increased to 137 ± 3% compared with the baseline flux. Oedema in the HS/HES group (1.06 ± 0.02) was significantly decreased compared with the NS-group (1.12 ± 0.01). HS/HES effectively restores nutritive perfusion, decreases leukocyte adherence, improves endothelial integrity and attenuates oedema, thereby restricting tissue damage evolving secondary to closed soft-tissue injury. It appears to be an effective intervention, supporting nutritional blood flow by reducing trauma-induced microvascular dysfunction

Compartment syndrome, a devastating consequence of limb trauma, is characterised by severe tissue injury and microvascular perfusion deficits. We hypothesised that leucopenia might provide significant protection against microvascular dysfunction and preserve tissue viability. Using our clinically relevant rat model of compartment syndrome, microvascular perfusion and tissue injury were directly visualised by intravital video microscopy in leucopenic animals. We found that while the tissue perfusion was similar in both groups (38.8% (standard error of the mean (. sem). 7.1). , 36.4. % (. sem. 5.7), 32.0% (. sem. 1.7), and 30.5% (. sem. 5.35) continuously-perfused capillaries at 45, 90, 120 and 180 minutes compartment syndrome, respectively versus 39.2% (. sem. 8.6), 43.5% (. sem. 8.5). , . 36.6% (. sem. 1.4) and 50.8% (. sem. 4.8) at 45, 90, 120 and 180 minutes compartment syndrome, respectively in leucopenia), compartment syndrome-associated muscle injury was significantly decreased in leucopenic animals (7.0% (. sem. 2.0), 7.0%, (. sem. 1.0), 9.0% (. sem. 1.0) and 5.0% (. sem. 2.0) at 45, 90, 120 and 180 minutes of compartment syndrome, respectively in leucopenia group versus 18.0% (. sem. 4.0), 23.0% (. sem. 4.0), 32.0% (. sem. 7.0), and 20.0% (. sem. 5.0) at 45, 90, 120 and 180 minutes of compartment syndrome in control, p = 0.0005). This study demonstrates that the inflammatory process should be considered central to the understanding of the pathogenesis of cellular injury in compartment syndrome. Cite this article: Bone Joint J 2015;97-B:539–43

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

We report the outcomes of 20 patients (12 men, 8 women, 21 feet) with Charcot neuro-arthropathy who underwent correction of deformities of the ankle and hindfoot using retrograde intramedullary nail arthrodesis. The mean age of the patients was 62.6 years (46 to 83); their mean BMI was 32.7 (15 to 47) and their median American Society of Anaesthetists score was 3 (2 to 4). All presented with severe deformities and 15 had chronic ulceration. All were treated with reconstructive surgery and seven underwent simultaneous midfoot fusion using a bolt, locking plate or a combination of both. At a mean follow-up of 26 months (8 to 54), limb salvage was achieved in all patients and 12 patients (80%) with ulceration achieved healing and all but one patient regained independent mobilisation. There was failure of fixation with a broken nail requiring revision surgery in one patient. Migration of distal locking screws occurred only when standard screws had been used but not with hydroxyapatite-coated screws. The mean American Academy of Orthopaedic Surgeons Foot and Ankle (AAOS-FAO) score improved from 50.7 (17 to 88) to 65.2 (22 to 88), (p = 0.015). The mean Short Form (SF)-36 Health Survey Physical Component Score improved from 25.2 (16.4 to 42.8) to 29.8 (17.7 to 44.2), (p = 0.003) and the mean Euroqol EQ‑5D‑5L score improved from 0.63 (0.51 to 0.78) to 0.67 (0.57 to 0.84), (p = 0.012).

Single-stage correction of deformity using an intramedullary hindfoot arthrodesis nail is a good form of treatment for patients with severe Charcot hindfoot deformity, ulceration and instability provided a multidisciplinary care plan is delivered.

Cite this article: Bone Joint J 2015;97-B:76–82.