Fasciotomy for Compartmental Hypertension and Acute Compartment Syndrome

Pathophysiology

Two separate biophysical phenomena can result in compartmental hypertension and the development of compartment syndrome ( Box 1 ). First, and relatively uncommonly, muscle compartment size may be limited or restricted. Examples include the occasionally deleterious effects of casts, splints, or other circumferential dressings; surgical closure of muscle fascial defects; or circumferential scars resulting from thermal injury.

Much more common are the various forms of injury that increase the volume of tissues within an inexpansile compartment. This may be a result of edema, hematoma or blood or, occasionally, iatrogenic causes such as unintended extravasation of intravenous fluids or misdirected irrigation volumes. The vast majority of patients with clinically evident compartment syndrome develop this problem either in the calf muscles or the forearm muscles because these two sets of muscle compartments (four in the leg, three in the upper extremity) are bound by fascia that is much more inelastic than that surrounding muscles elsewhere in the body.

Patients with severe acute arterial insufficiency of the extremities that is successfully reversed are at risk for developing compartment syndrome. The ischemia–reperfusion pathophysiology that underlies this particular form of compartmental hypertension has been extensively studied by Hobson, Walker, and Blaisdell, among others. The underlying mechanism in post–ischemia–reperfusion compartmental hypertension appears to arise from the generation of toxic oxygen radicals, the effect of which, among others, is to render capillary beds leaky. When blood flow is restored (reperfusion), intravascular fluid—plasma—extravasates into the extracellular space. In most sites in the body, the affected tissues simply swell. However, in the forearm and the calf, the inelastic fascia surrounding the muscle compartments prevents such tissue expansion, resulting instead in an inexorable rise in tissue pressure, increasing encroachment on venous outflow and later on arteriolar inflow, producing a reduction in capillary perfusion pressure and a resulting loss of tissue nutrition. Unrelieved compartmental hypertension inevitably results in tissue necrosis diffusely throughout the affected compartment.

Skeletal muscle undergoes infarction initially at its depths, dying from the inside out. Muscle that is initially healthy and viable appearing at the time of initial decompression may be found to have proceeded to complete infarction at subsequent assessment. Ischemia itself does not result in compartmental hypertension. Rather, the ischemic tissue bed, once it is successfully revascularized, should be considered at risk for developing compartmental hypertension if the inevitable post-reperfusion tissue swelling could potentially occur within an inelastic fascial envelope.