Abdel Lawendy

What's new in acute compartment syndrome?

Summary: Acute compartment syndrome (ACS) after trauma is often the result of increased size of the damaged tissues after acute crush injury or from reperfusion of ischemic areas. It usually is not solely caused by accumulation of free blood or fluid in the compartment, although that can contribute in some cases. There is no reliable and reproducible test that confirms the diagnosis of ACS. A missed diagnosis or failure to cut the fascia to release pressure within a few hours can result in severe intractable pain, paralysis, and sensory deficits. Reduced blood circulation leads to oxygen and nutrient deprivation, muscle necrosis, and permanent disability. Currently, the diagnosis of ACS is made on the basis of physical examination and repeated needle sticks over a short time frame to measure intracompartmental pressures. Missed compartment syndromes continue to be one of most common causes of malpractice lawsuits. Existing technology for continuous pressure measurements are insensitive, particularly in the deep tissues and compartments, and their use is restricted to highly trained personnel. Newer concepts of the pathophysiology accompanied by new diagnostic and therapeutic modalities have recently been advanced. Among these are the concept of inflammatory mediators as markers and anti-inflammatories as medical adjunct therapy. New diagnostic modalities include near-infrared spectroscopy, ultrafiltration catheters, and radio-frequency identification implants. These all address current shortcomings in the diagnostic armamentarium that trauma surgeons can use. The strengths and weaknesses of these new concepts are discussed to allow the trauma surgeon to follow current evolution of the field.

Indomethacin reduces cell damage: shedding new light on compartment syndrome.

Introduction: 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 before induction of elevated intracompartment pressure. The purpose of this study was to determine the effect of timing of indomethacin administration on muscle damage in elevated intracompartment pressure and to assess apoptosis as a cause of tissue demise. Methods: Twenty-four Wistar rats were randomized to elevated intracompartmental pressure (EICP) for either 45 or 90 minutes (30 mmHg). In the 45-minute cohort, indomethacin was withheld in Group 1 (CS45), given before induction of EICP in Group 2 (CS45Indo0), or given after 30 minutes of EICP/15 minutes before fasciotomy in Group 3 (CS45Indo30). In the 90-minute cohort, indomethacin was withheld in Group 4 (CS90) or given after 30 or 60 minutes of EICP in Groups 5 (CS90Indo30) and 6 (CS90Indo60). Intravital microscopy and fluorescent staining assessed capillary perfusion, cell damage, and inflammatory activation within extensor digitorum longus muscle. Apoptosis was assessed using spectrophotometric assessment of caspase levels. Groups 1 to 3 and 4 to 6 were compared using analysis of variance with P < 0.05 deemed significant. Results: Perfusion and tissue viability improved in indomethacin-treated groups. Nonperfused capillaries decreased from Group 1 (CS45) (50.1 ± 2.5) to Group 2 (CS45Indo0) (38.4 ± 1.8) and Group 3 (CS45Indo30) (14.13 ± 1.73) (P < 0.05). Similarly, Group 5 (CS90Indo30) and Group 6 (CS90Indo60) had 25% fewer nonperfused capillaries compared with Group 4 (CS90) (P < 0.0001). Group 2 (CS45Indo0) and Group 3 (CS45Indo30) showed fewer damaged cells (1% ± 0.5% and 8.7% ± 2%) compared with Group 1 (CS45) (20% ± 14%) (P < 0.0001). Group 5 (CS90Indo30) showed decreased cell damage (13% ± 1%) compared with Group 4 (CS90) (18% ± 1%) (P < 0.01). Group 6 (CS90Indo60) also showed decreased cell damage (11% ± 1%) compared with Group 4 (CS90) (18% ± 1%); however, this difference was not significant (P > 0.05). Apoptotic activity was present with elevated intracompartment pressure. At 30 minutes, there were elevated caspase levels in Group 4 and Group 6 EICP groups (0.47 ± 0.08) compared with control subjects (0.19 ± 0.02) (P < 0.003). However, indomethacin-treated groups did not differ from control subjects with regard to caspase levels (P > 0.05). Conclusion: Indomethacin decreased cell damage and improved perfusion in elevated intracompartment pressure. The benefits of indomethacin were partially time-dependent; some improvement in tissue viability occurred regardless of timing of administration. Although apoptosis was common in elevated intracompartment pressure, the protective effect of indomethacin does not appear to be related to apoptosis. Clinical Relevance: Adjuvant treatment with indomethacin may improve outcome in compartment syndrome.