Replication of the compartment syndrome in a canine model: experimental evaluation of treatment

The sequence of acute ischemia, reperfusion, and elevated tissue pressure, with subsequent neuromuscular damage, results in the clinical entity known as the compartment syndrome. We have developed a canine hindlimb model that successfully replicates these clinical features. Surgical devascularization of both hindlimbs at the popliteal level isolates perfusion to a single vascular pedicle. Total ischemia is produced in the left limb for 8 h, while the right limb serves as a surgical control. Ischemia is confirmed by measurement of transfascial oxygen tension (TF-PO2) as well as lactate and blood gases in the venous effluent. Pressure in the anterior compartment of the hindlimb is monitored by the slit catheter technique. After reperfusion, muscle damage is assessed by histology, creatine phosphokinase (CPK), and uptake of technetium-99m pyrophosphate (Tc-PyP), expressed as a ratio of the experimental (L) limb to the control (R) limb (L/R ratio). Muscle necrosis was greatest in untreated controls; the L/R ratio was 8.9 +/- 5.0. Significant diminution of muscle necrosis was achieved by fasciotomy prior to reperfusion (2.6 +/- 0.8), mannitol (1.8 +/- 0.6), albumin-conjugated superoxide dismutase (SOD) 2.8 +/- 0.8), native SOD (2.3 +/- 1.0), fasciotomy combined with SOD (1.9 +/- 0.7), and continuous heparin (1.6 +/- 0.4) (p less than .01 vs controls). When fasciotomy was delayed until 2 h after reperfusion, there was no significant decrease in the L/R ratio (5.4 +/- 1.5; p = .15). Early fasciotomy following prolonged severe limb ischemia remains the treatment of choice, although these results suggest an emerging role for nonsurgical therapies as well. A summary of work done with this model as well as a review of other techniques is presented, along with a discussion of the pathophysiology of the compartment syndrome.