OBJECTIVE: The aim of this study was to investigate the utility of direct measurement of tissue oxygenation during compartment syndrome (CS) and tourniquet-induced ischemia in a large animal model. We hypothesize that as compartment pressure (CP) rises, circulation within the compartment will decrease resulting in a decreased level of oxygen in the muscle. METHODS: This study used a dog model of both CS- and tourniquet-based ischemia. In 15 animals, CS was induced in 1 hind limb with varying degrees of severity using an infusion model. Tourniquet ischemia was induced in the contralateral hind limb for varying durations. The partial pressure of oxygen (PmO2) was continuously monitored using a polarographic oxygen probe in the muscle of both hind limbs. CP was monitored in the CS limb. PmO2 and CP were analyzed after fasciotomy, performed after approximately 7 hours of warm ischemia, or release of tourniquet. RESULTS: With the application of tourniquet ischemia, PmO2 fell from 38.40 to 1.30 mm Hg (P < 0.001) and subsequently rose after release of the tourniquet to 39.81 mm Hg (P < 0.001). Elevated CP induced by infusion was relieved by fasciotomy (52.04-11.37 mm Hg postfasciotomy, P < 0.001). PmO2 readings in the infusion model were significantly higher in pre-CS than during CS (31.77 mm Hg vs. 3.88 mm Hg, P < 0.001) and rebounded after fasciotomy (50.24 mm Hg, P < 0.001), consistent with hyperemic response. CONCLUSIONS: Increased CP caused an observable decrease in PmO2 that was reversed by fasciotomy. PmO2 can be directly measured in real time with a polarographic tissue pO2 probe. This study is the first step of evaluating an alternative method for diagnosing acute CS.
OBJECTIVE: The aim of this study was to investigate the utility of direct measurement of tissue oxygenation during compartment syndrome (CS) and tourniquet-induced ischemia in a large animal model. We hypothesize that as compartment pressure (CP) rises, circulation within the compartment will decrease resulting in a decreased level of oxygen in the muscle. METHODS: This study used a dog model of both CS- and tourniquet-based ischemia. In 15 animals, CS was induced in 1 hind limb with varying degrees of severity using an infusion model. Tourniquet ischemia was induced in the contralateral hind limb for varying durations. The partial pressure of oxygen (PmO2) was continuously monitored using a polarographic oxygen probe in the muscle of both hind limbs. CP was monitored in the CS limb. PmO2 and CP were analyzed after fasciotomy, performed after approximately 7 hours of warm ischemia, or release of tourniquet. RESULTS: With the application of tourniquet ischemia, PmO2 fell from 38.40 to 1.30 mm Hg (P < 0.001) and subsequently rose after release of the tourniquet to 39.81 mm Hg (P < 0.001). Elevated CP induced by infusion was relieved by fasciotomy (52.04-11.37 mm Hg postfasciotomy, P < 0.001). PmO2 readings in the infusion model were significantly higher in pre-CS than during CS (31.77 mm Hg vs. 3.88 mm Hg, P < 0.001) and rebounded after fasciotomy (50.24 mm Hg, P < 0.001), consistent with hyperemic response. CONCLUSIONS: Increased CP caused an observable decrease in PmO2 that was reversed by fasciotomy. PmO2 can be directly measured in real time with a polarographic tissue pO2 probe. This study is the first step of evaluating an alternative method for diagnosing acute CS.
Authors: Natalie A Wisniewski; Scott P Nichols; Soya J Gamsey; Steve Pullins; Kit Y Au-Yeung; Bruce Klitzman; Kristen L Helton Journal: Adv Exp Med Biol Date: 2017 Impact factor: 2.622