The pathophysiology of the anterior tibial compartment syndrome: an experimental investigation.
In an experimental study in dogs of the anterior tibial compartment syndrome, three measurements were taken before, during, and following raising pressure in the compartment: blood flow, muscle function, and peroneal nerve conduction. If fasciotomy was performed within 4 hours, peroneal nerve conduction velocity always returned to normal regardless of amount of pressure or length of time pressure was applied; if performed after 12 hours peroneal nerve conduction velocity did not return to normal at any pressure or time condition, suggesting that irreversible damage to the nerve had occurred. Blood flow, as measured by rate of clearance of Xe133, always returned to normal within 2 hours of fasciotomy regardless of the time postinjury or amount of pressure applied. Muscle function (CPK and LDH) did not always return to baseline with fasciotomy and in some instances the absolute values were higher after fasciotomy. Further clinical studies using these measurements are recommended.
D000818:Animals; D000868:Anterior Compartment Syndrome / Q000503:physiopathology* / Q000601:surgery; D001783:Blood Flow Velocity; D003402:Creatine Kinase / Q000097:blood; D004285:Dogs; D000071938:Fasciotomy; D005634:Fructose-Bisphosphate Aldolase / Q000097:blood; D007770:L-Lactate Dehydrogenase / Q000097:blood; D009132:Muscles / Q000503:physiopathology; D009431:Neural Conduction; D010543:Peroneal Nerve / Q000503:physiopathology
D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase; D005634:Fructose-Bisphosphate Aldolase