Delayed use of hyperbaric oxygen for treatment of a model anterior compartment syndrome

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Abstract
This study examines the effect of delayed exposure to hyperbaric oxygen on muscle necrosis and edema development following compartment syndromes in the canine hindlimb. Compartment syndromes (100 mm Hg for 8 h) were generated in one anterolateral compartment of six anesthetized dogs. After a 2‐h delay, three 1‐h hyperbaric oxygen treatments (2 atm absolute pure oxygen) were given during the next 12 h. Two days later, technetium‐99m stannous pyrophosphate (99mTc Sn‐PYP) was injected intravenously; 3 h later, samples were obtained from the pressurized and contralateral control muscles, weighed for edema development, counted for 99mTC Sn‐PYP uptake, and evaluated histologically. Hyperbaric oxygen treatments, even when delayed 2 h, reduced muscle necrosis and intramuscular edema to negligible levels (p < 0.05) compared with untreated animals. In addition, muscle morphology remained essentially normal in all hyperbaric oxygen‐treated animals. We conclude that even if hyperbaric oxygen treatments are delayed 2 h, edema and muscle necrosis are reduced significantly in a model compartment syndrome.