RESUMO
OBJECTIVES: Acute compartment syndrome is a devastating condition associated with lasting consequences or even death if not treated in a timely fashion. Current preclinical modeling is inadequate. Ideally a model should mimic human disease. There should be a trauma-induced reperfusion or direct muscle event that causes gradual increased pressure and is amenable to release with fasciotomy. We have attempted to reproduce this mechanism and outcome in a porcine model. METHODS: Anterior tibial musculature was injured with vascular occlusion plus exterior tourniquet crush or direct intracompartmental crush through balloon inflation. The injury was maintained for over 5 hours. At that time, the tourniquet or balloon was removed. The injuries were continuously monitored with an intramuscular continuous pressure sensor. Pressure changes were recorded and after 2 hours of postinjury observation, a fasciotomy was performed for the muscle compartment. RESULTS: Pressures were brought to 100 mm Hg during the injury phase. During the two-hour observation period, the balloon catheter technique achieved an average pressure of 25.1 ± SD 8.8 mm Hg with a maximum reading of 38.2 mm Hg and minimum reading of 14.1 mm Hg. During this same period, the ischemia-reperfusion + direct crush technique achieved an average pressure of 33.7 ± SD 7.3 mm Hg, with a maximum reading of 43.5 mm Hg and minimum reading of 23.5 mm Hg. Average pressure postfasciotomy for the balloon catheter technique was 2.4 ± SD 2.5 mm Hg; and for the crush technique, average value postfasciotomy was 4.9 ± SD 3.7 mm Hg-both representing a return to physiologic levels. CONCLUSION: This is the first preclinical model that shows the same response to injury and treatment as is observed in human physiology. Surgical and nonsurgical therapies for compartment syndrome can now be tested reliably.
