OBJECTIVES-Acute compartment syndrome (ACS) is the result of decreased perfusion pressure (PP) and the diagnosis frequently requires invasive monitoring. Our objective was to test a new noninvasive ultrasound device for correlating PP with measurements of fascial displacement in a controlled porcine model of ACS. We hypothesized that fascial displacement in experimental compartments with impaired PP would be significantly greater than that in control compartments with normal baseline PP.METHODS-ACS was generated in right anterior compartments of seven anesthetized pigs while contralateral compartments served as normal controls. Intramuscular pressure (IMP) in all compartments was monitored by slit catheters while IMP in experimental compartments was elevated in 10 mmHg increments by infusing 0.045% albumin in saline. A non-invasive ultrasound device continuously recorded fascial displacement corresponding to arterial pressure pulses in all compartments. Mean fascial displacement amplitude was grouped by PP and analyzed using twoway repeated measures ANOVA and contrast analysis.RESULTS-As PP ranged from 80 to -40 mmHg, the change in fascial displacement of the infused compartments was significantly greater than that in the control compartments (ANOVA, p = 0.03). At each PP increment between 40 and -20 mmHg, fascial displacement in the infused compartments was significantly greater than that in the control compartments (contrast analysis, p < 0.014).CONCLUSIONS-Fascial displacement is significantly greater in muscle compartments with decreased PP. Furthermore, changes in PP are associated with changes in fascial displacement over a clinically relevant range of PP, making this non-invasive technique potentially useful for monitoring in ACS.
Negative pressure wound therapy has become ubiquitous in orthopedic surgery and it is therefore important to understand the physiologic conditions of this therapy. The purpose of this study was to determine the magnitude and depth of negative pressure transmission into underlying muscle tissue in a wound model. We hypothesized that the negative pressure is not transmitted beyond 2 mm into underlying muscle tissue. Using both an isolated muscle and a live animal wound model, we applied open cell foam dressing to the tissue. Using a series of vacuum-assisted closure negative pressure settings (0, -75, -125, -200 mmHg) interstitial fluid pressure was measured in the underlying tissue with a solid-state pressure transducer catheter at 1/10 mm depth intervals. In the ex vivo isolated-muscle model, the effect of negative pressure wound therapy on interstitial fluid pressure was extinguished and not significantly different than controls at a depth <2 mm. In the live animal wound model, the magnitude of interstitial fluid pressures corresponded directly with negative pressure settings (p<0.01) and inversely with depth into muscle (p<0.01). Interstitial fluid pressures were significantly (p<0.05) less than control interstitial fluid pressures (0 mmHg setting) at depths of 0.5, 0.4, and 0.9 mm below the foam/muscle interface when the applied pressures were -75, -125, and -200 mmHg, respectively. Negative pressure wound therapy penetrates no more than 1 mm into rabbit wound tissue at the highest negative pressure setting (-200 mmHg) when using open-cell foam dressing.
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