Purpose

Compartment syndrome is a limb threatening condition. Prior research has been limited by an inability to assess functional and histologic changes in muscle over time. This study was designed to assess and quantify functional deficits and histologic changes following acute compartment syndrome of the lower limb in a novel rat model.

Purpose

The anterior inferior tibiofibular ligament (AiTFL) is the primary lateral ligamentous stabilizer of the ankle syndesmosis. Current syndesmosis repair techniques traverse the tibia and fibula, but do not anatomically reconstruct the AiTFL. We compared a novel AiTFL anatomic repair technique (ART) to rigid syndesmosis screw fixation (SCREW).

Purpose: Indomethacin may preserve tissue viability in compartment syndrome. The mechanism of improved tissue viability is unclear, but the anti-inflammatory effects may alter the relative contribution of tissue necrosis versus apoptosis to cellular injury. Existing studies have only considered indomethacin administration prior to induction of compartment syndrome. The purpose of this study was to determine the effect of timing of indomethacin administration on muscle damage in compartment syndrome, and to assess apoptosis as a cause of tissue demise.

Method: Twenty-four Wistar rats were randomized to elevated intracompartmental pressure (EICP) for either 45 or 90 minutes (30mm Hg). In the 45 min group, indomethacin was withheld (group 1), given prior to induction of EICP (group 2) or given 15 min prior to fasciotomy (group 3). In the 90 min group, indomethacin was withheld (group 4) or provided 30 or 60 minutes prior to fasciotomy (groups 5 and 6). Intravital microscopy and histochemical staining assessed capillary perfusion, cell damage and inflammatory activation within EDL muscle. Apoptosis was assessed using ELISA staining for caspase-3. Groups were compared with one-way ANOVA (p< 0.05).

Results: Perfusion improved in indomethacin-treated groups. Nonperfused capillaries decreased from group 1 (50.1±2.5), to groups 2 (38.4±1.8) and 3 (14.13±1.73)(p< 0.0001). Similarly, groups 5 and 6 had 25% fewer non-perfused capillaries compared to group 4 (p< 0.0001). Tissue viability improved in indo-methacin-treated groups. Groups 2 and 3 showed fewer damaged cells (1±0.5% and 8.7±2%) compared to group 1 (20±14%)(p< 0.0001). Groups 5 and 6 showed decreased cell damage (13±1% and 11±1%) compared to group 4 (18±1%) (p< 0.01). Apoptotic activity was present in compartment syndrome. At 30 minutes there were elevated caspase levels in EICP groups (0.47±0.08) compared to controls (0.19±0.02). However, indomethacin treated groups did not differ from controls with regards to caspase levels (p> 0.05).

Conclusion: Indomethacin decreased cell damage and improved perfusion in compartment syndrome. The benefits of indomethacin were partially time dependent; some improvement in tissue viability occurred regardless of timing of administration. Although apoptosis was common in compartment syndrome, the protective effect of indomethacin does not appear to be related to apoptosis.

Purpose: This study was designed to determine whether indomethacin, a potent anti-inflammatory agent, reduces muscle damage secondary to elevated ICP.

Method: 16 adult Wistar rats were randomized to 4 groups. In group 1 (control), no intervention occurred. Group 2 (indo) rats were administered indomethacin (12mg/kg) with no elevation of ICP. Group 3 (CS) rats had elevated ICP (30–40mmHg × 45 minutes) using saline injection. Group 4 rats (CS/indo) had elevated ICP and indomethacin administration. After 45 minutes, hindlimb fasciotomy was performed. The extensor digitorum longus muscle was reflected onto an intravital microscope. Capillary perfusion was measured by comparing the number of continuously perfused capillaries to intermittent and non perfused capillaries. Inflammation was determined using the number of activated (rolling and adherent) white blood cells. Muscle cell damage was measured using differential fluorescent staining. Perfusion, inflammation, and muscle damage were compared in all 4 groups using a one-way ANOVA (p< 0.05).

Results: Perfusion: Indomethacin treatment (CS/indo) increased the proportion of intermittently perfused capillaries (39.1 ± 2.2 vs 30.3 ± 2.7) and decreased nonperfused capillaries (38.4 ± 1.8 vs 50.1 ±2.5) compared to CS (p=0.0002). Control and indo groups demonstrated more continuously perfused capillaries compared to CS or CS/indo groups (p0.05).

Conclusion: Treatment of elevated ICP with indomethacin improved microvascular perfusion and reduced cell damage. The protective mechanism of indomethacin is unknown, but may be related to an anti-oxidative and vasodilatory effect. Treatment of elevated intracompartmental pressure with indomethacin dramatically reduces muscle damage and may have important future clinical benefit. Further research is required to determine the mechanism of action.

Elevated intracompartmental pressure (ICP) results in muscle damage. Previous studies identified severe inflammation associated with elevated ICP. This study was designed to determine whether indomethacin, a potent anti-inflammatory agent, reduces muscle damage secondary to elevated ICP. We hypothesised that administration of indomethacin reduces muscle damage from elevated ICP.

Sixteen adult Wistar rats were randomised to four groups. In group One (control), no intervention occurred. Group Two (indo) rats were administered indomethacin (12mg/kg) with no elevation of ICP. Group Three (CS) rats had elevated ICP (30–40mmHg X 45 minutes) using saline injection. Group Four rats (CS/indo) had elevated ICP and indomethacin administration. After forty-five minutes, hindlimb fasciotomy was performed. The extensor digitorum longus muscle was reflected onto an intravital microscope. Capillary perfusion was measured by comparing the number of continuously perfused capillaries to intermittent and non perfused capillaries. Inflammation was determined using the number of activated (rolling and adherent) white blood cells. Muscle cell damage was measured using differential fluorescent staining. Perfusion, inflammation, and muscle damage were compared in all four groups using a one-way ANOVA (p< 0.05).

Perfusion: Indomethacin treatment (CS/indo) increased the proportion of intermittently perfused capillaries (39.1 ± 2.2 vs 30.3 ± 2.7) and decreased nonperfused capillaries (38.4 ± 1.8 vs 50.1 ±2.5) compared to CS (p=0.0002). Control and indo groups demonstrated more continuously perfused capillaries compared to CS or CS/indo groups (p< 0.0001). Muscle damage: Indomethacin treatment of elevated ICP reduced the proportion of damaged cells from 0.20 ± 0.14 (CS) to 0.01 ± 0.0.005 (CS/indo, p< 0.0001). There were no differences between CS/indo, control, or indo groups. Inflammation: CS and CS/indo groups demonstrated greater inflammatory activation compared to control and indo groups (p< 0.001). There were no differences in inflammatory activation between CS and CS/indo (p> 0.05).

Treatment of elevated ICP with indomethacin improved microvascular perfusion and reduced cell damage. The protective mechanism of indomethacin is unknown, but may be related to an anti-oxidative and vasodilatory effect. Treatment of elevated intracompartmental pressure with indomethacin dramatically reduces muscle damage and may have important future clinical benefit.

Screw fixation of the injured syndesmosis restores stability, but may reduce ankle motion. We wished to determine whether functional and radiographic results are improved by removal of syndesmosis screws. In addition, we studied whether large fragment screws have an advantage compared to small fragment screws. We hypothesised that retained intact syndesmosis screws are detrimental to ankle function.

One hundred and seven adults with ankle fractures requiring syndesmosis screw fixation between 2001 and 2005 were retrospectively studied. Indications for syndesmosis fixation were a positive intraoperative external rotation stress test or inadequate lateral column buttress. Weight bearing was encouraged six weeks postoperatively. Syndesmosis screws were only removed for tenderness, prominence or ankle dorsiflexion < 0.05.

The LEM score for patients with intact screws was 70 ± 26 compared with 85 ± 20 for broken, loosened or removed screws (p=0.05). The OM score for patients with intact screws was 48 ± 36 compared with 63 ± 27 for broken, loosened or removed screws (p=0.12). There was no difference in outcome comparing broken, loosened, and removed screws. The tibiofibular clear space for intact screws was 3.3 ± 1.3 compared with 4.1 ± 1.7 for removed, broken or loosened screws (p=0.02). There was no difference in outcome comparing large and small fragment screws.

Patients with broken, loosened or removed syndesmosis screws have better functional outcome compared to intact screws. The syndesmosis allows fibular rotation, shortening and translation during gait; the presence of an intact syndesmosis screw may restrict this motion. There was no disadvantage to leaving broken or loosened screws in-situ.