What's new in acute compartment syndrome?

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Abstract

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. Copyright © 2012 by Lippincott Williams & Wilkins.

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APA

Harvey, E. J., Sanders, D. W., Shuler, M. S., Lawendy, A. R., Cole, A. L., Alqahtani, S. M., & Schmidt, A. H. (2012, December). What’s new in acute compartment syndrome? Journal of Orthopaedic Trauma. https://doi.org/10.1097/BOT.0b013e31826df980

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