ABSTRACT

In 1667 Stenson Þrst described ischemic paralysis in the lower limb.1 He observed paralysis of the posterior extremities of an animal following occlusion of the abdominal aorta. A patient with ischemic contracture, presumably from a compartment syndrome, was reported in 1850 by Hamilton according to Hildebrand.2 Research on the pathologic process of ischemic contractures of the extremities started more than 150 years ago. Theories on external compression, inßammation, arterial injury and spasm, venous obstruction, and tissue pressure have been investigated thoroughly for the past 100 years. The effects of strenuous exercise as a cause of acute compartment syndrome were described in the 1940s.3,4

Historical perspectives of the evolution of different theories on etiology, pathogenesis, pathophysiology, and treatment of acute compartment syndrome are discussed in this chapter (Figure 2.1). Reviews of the historical perspectives on the exciting search for clarity regarding ischemic contractures have been presented previously.5,6

In a classic paper from 1881, Von Volkmann presented the hypothesis that Þbrosis and contracture of the muscle in an injured extremity were caused by interrupted arterial blood supply.7 He observed cases where the contracture followed arterial ligature, contusion to extremities, and prolonged external compression (or extrinsic pressure). Since then, prolonged external compression has been accepted as a cause of muscle ischemia.