Pathogenesis of inner environment changes in acute muscular compartment syndrome

Acute compartment syndrome results from a pressure increase within an anatomically defined space delineated by a non-elastic surrounding. Every muscle group, encased by fascia/bone, presents a compartment with a potential to develop increased pressure under certain conditions. Increase in pressure within the compartment causes a decrease in perfusion pressure, leading to ischemia and pathological utilisation of energy substrates on the cellular level. Initially, the malfunction of cellular metabolism is functional and reversible. Later progress of these changes leads into irreversible myonecrosis. Restitution of blood supply reverses the local ischemia, however, the following reperfusion syndrome associated with oxidative stress, leads to further pathological sequelae. Re-established blood circulation carries the end-products of myonecrosis and activated immunocompetent cells from the site of lesion into the whole body. Furthermore, locally activated endothelium becomes a significant source of systemic inflammatory mediators. Pro-inflammatory conditions induce the response of anti-inflammatory regulatory mechanisms and their mutual interaction determines both local and systemic outcome of the disease.