Model Of Compartment Syndrome Research Articles

New Noninvasive Ultrasound Technique for Monitoring Perfusion Pressure in a Porcine Model of Acute Compartment Syndrome

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. ACS was generated in right anterior compartments of 7 anesthetized pigs, and contralateral compartments served as normal controls. Intramuscular pressure in all compartments was monitored by slit catheters, whereas intramuscular pressure in experimental compartments was elevated in 10 mm Hg increments by infusing 0.045% albumin in saline. A noninvasive 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 2-way repeated measures analysis of variance and contrast analysis. As PP ranged from 80 to -40 mm Hg, the change in fascial displacement of the infused compartments was significantly greater than that in the control compartments (analysis of variance, P = 0.03). At each PP increment between 40 and -20 mm Hg, fascial displacement in the infused compartments was significantly greater than that in the control compartments (contrast analysis, P < 0.014). 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 noninvasive technique potentially useful for monitoring in ACS.

A Prognostic Model for the Risk of Development of Upper Extremity Compartment Syndrome in the Setting of Brachial Artery Injury

A potentially devastating sequela of brachial artery injury in the setting of upper extremity trauma is the development of compartment syndrome (CS). We performed a retrospective review of 139 trauma patients with brachial artery injury from 1985-2001. Objective characteristics of each case were extracted and analyzed using multivariate logistic regression. Three variables were found to be significant in the final model: estimated intraoperative blood loss as a continuous variable, and presence of a multiple arterial injury and presence of an open fracture as categorical variables. Odds ratio were 1.12, 5.79, and 2.68, respectively. We used these variables to create a summative score for the development of CS with weights assigned proportional to the adjusted odds ratio. Odds of having CS for subjects in group 2 and group 3 are 5.3 and 15.1 times the odds for subjects in group 1, respectively. Applying multivariate regression analysis to the largest series of brachial artery injuries to date, we have developed a predictive scoring model of CS.

Alterations in plasma amine oxidase activities in a compartment syndrome model.

Alterations in plasma amine oxidase activities in a compartment syndrome model.

Can skin surface pressure under a cast reveal intracompartmental pressure?

Although monitoring intracompartmental pressure (IP) under a cast is very important, it is not possible to measure it in every patient undergoing cast treatment. This study aims to answer the question of whether skin surface pressure (SSP) under a cast can reveal IP. A plaster cast was applied to a sculpted inflatable forearm model with dorsal and volar compartments. SSP under the cast was measured at five different localizations from both dorsal and volar sides of the model and compared to the corresponding IP. In the second experiment, a posterior tibial compartment syndrome model was created in both limbs of five rabbits. Correlation analysis was performed between IP and SSP under the cast. All of the SSP measurements taken from the dorsal and volar side of the sculpted forearm model correlated with IP. Mean correlation coefficient of the measurements was 0.995 (P = 0.000) (SD 0.002, range 0.992-0.999). SSP and IP correlation analysis in the posterior tibial compartment syndrome model of 10 limbs in five rabbits revealed a high correlation. The mean correlation coefficient was 0.973 (P = 0.000) (SD 0.024, range 0.916-0.997). Measuring the pressure between the skin and cast can monitor IP. SSP monitoring can help the physician, patient or parents in the follow-up of patients undergoing cast treatment.

Neutrophil mediated microvascular injury in acute, experimental compartment syndrome.

The purpose of this study was to determine the contribution of neutrophils and tissue xanthine oxidase to the skeletal muscle microvascular dysfunction in an ex vivo model of acute compartment syndrome. Adult dogs were rendered neutropenic or depleted of tissue xanthine oxidase before gracilis muscle isolation. Compared with continuously perfused, nonischemic muscles, acute, experimental compartment syndrome resulted in a dramatic increase in microvascular permeability, muscle neutrophil content, and muscle vascular resistance. Neutropenia prevented, whereas xanthine oxidase depletion had no effect on, the microvascular dysfunction and muscle neutrophil infiltration elicited by experimental compartment syndrome. These results suggest that neutrophils contribute to the microvascular dysfunction and blood flow distribution abnormalities elicited by acute, experimental compartment syndrome.

Near-infrared spectroscopy for monitoring of tissue oxygenation of exercising skeletal muscle in a chronic compartment syndrome model.

Variations in the levels of muscle hemoglobin and of myoglobin oxygen saturation can be detected non-invasively with near-infrared spectroscopy. This technique could be applied to the diagnosis of chronic compartment syndrome, in which invasive testing has shown increased intramuscular pressure associated with ischemia and pain during exercise. We simulated chronic compartment syndrome in ten healthy subjects (seven men and three women) by applying external compression, through a wide inflatable cuff, to increase the intramuscular pressure in the anterior compartment of the leg. The tissue oxygenation of the tibialis anterior muscle was measured with near-infrared spectroscopy during gradual inflation of the cuff to a pressure of forty millimeters of mercury (5.33 kilopascals) during fourteen minutes of cyclic isokinetic dorsiflexion and plantar flexion of the ankle. The subjects exercised with and without external compression. The data on tissue oxygenation for each subject then were normalized to a scale of 100 per cent (the baseline value, or the value at rest) to 0 per cent (the physiological minimum, or the level of oxygenation achieved by exercise to exhaustion during arterial occlusion of the lower extremity). With external compression, tissue oxygenation declined at a rate of 1.4 +/- 0.3 per cent per minute (mean and standard error) during exercise. After an initial decrease at the onset, tissue oxygenation did not decline during exercise without compression. The recovery of tissue oxygenation after exercise was twice as slow with compression (2.5 +/- 0.6 minutes) than it was without the use of compression (1.3 +/- 0.2 minutes).

Effects of adenosine on pressure-flow relationships in an in vitro model of compartment syndrome.

Blood flow through skeletal muscle is best modeled with a vascular waterfall at the arteriolar level. Under these conditions, flow is determined by the difference between perfusion pressure (Pper) and the waterfall pressure (Pcrit), divided by the arterial resistance (Ra). By pump perfusing an isolated canine gastrocnemius muscle (n = 6) after it was placed within an airtight box, with and without adenosine infusion, we observed an interaction between the pressure surrounding a muscle (as occurs in compartment syndrome) and baseline vascular tone. We titrated adenosine concentration to double baseline flow. We measured Pcrit and Ra at box pressures (Pbox), which resulted in 100 (Pbox = 0), 90, 75, and 50% flow without adenosine; and 200, 180, 150, 100, and 50% flow with adenosine. Without adenosine, each 10% decline in flow was associated with a 5.7 mmHg increase in Pcrit (P < 0.01). With adenosine, the same decrease in flow was associated with a 2.6-mmHg increase in Pcrit (P < 0.01). Values of Pcrit at 50% of flow were almost identical. Each 10% decrease in flow was also associated with 2.2% increase in Ra with or without adenosine (P < 0.001). Ra decreased with adenosine infusion (P < 0.05), and there was no interaction between adenosine and flow (P > 0.9). We conclude that increases in pressure surrounding a muscle limit flow primarily through changes in Pcrit with and without adenosine-induced vasodilation. The interaction between Pbox and adenosine with respect to Pcrit but not Ra suggests that Pbox affects the tone of the vessels responsible for Pcrit but not Ra.

The effect of antecedent ischemia on the tolerance of skeletal muscle to increased interstitial pressure.

This study used an experimental model (canine hind limb) of compartment syndrome, monitored with phosphorus 31 nuclear magnetic resonance spectroscopy, to determine the pressure threshold for metabolic deterioration in skeletal muscle previously subjected to ischemia. Our results show that muscle subjected to 6 h of antecedent ischemia has a lower tolerance to increased tissue pressure than otherwise normal muscle. The threshold was found to occur at a delta P (difference between mean blood pressure and limb compartment pressure) of 40 mm Hg, compared with a delta P of 30 mm Hg in muscle that was not subjected to antecedent ischemia. In addition, once the critical pressure threshold of postischemic muscle was crossed, there was a more rapid rate of high-energy phosphate depletion than that seen in normal muscle pressurized to the same degree beyond its delta P threshold. For compartment syndromes that appear after relatively atraumatic ischemia (i.e., drug overdose-induced limb compression, proximal arterial trauma causing distal limb ischemia, etc.), of < or = 6 h, fasciotomy should be performed at a delta P < or = 40 mm Hg. Compartment pressure elevation after local blunt muscle trauma and ischemia may well require earlier or even prophylactic fasciotomy. Fasciotomy in ongoing postischemic compartment syndromes should be considered particularly urgent owing to the rapid rate of metabolic deterioration that is observed once the critical delta P threshold is crossed. The type of compartment syndrome should always be considered when interpreting tissue pressure measurements as indications for fasciotomy.

Pressure-flow relationships in in vitro model of compartment syndrome.

Compartment syndrome is a condition in which an increase in intramuscular pressure decreases blood flow to skeletal muscle. According to the Starling resistor (i.e., vascular waterfall) model of blood flow, the decrease in flow could occur through an increase in arterial resistance (Rart) or an increase in the critical closing pressure (Pcrit). To determine which explains the decrease in flow, we pump perfused a canine gastrocnemius muscle placed within an airtight box, controlled box pressures (Pbox) so that flow ranged from 100 to 50%, and measured Pcrit, Rart, arterial compliance, small venular pressure (measured by the double-occlusion technique), and venous pressure. An increase in Pbox limited flow mainly through an increase in Pcrit (75-85%), with only small changes in Rart (15-25%) and no change in arterial compliance. Increases in Pbox also produced a vascular waterfall in the venous circulation, but small venular transmural pressure always remained less than control levels. We conclude that increases in Pbox mostly limit blood flow through increases in Pcrit and that Rart plays a minor role. Transmural pressure across the small venules decreases with increases in intramuscular pressure, which contradicts the currently held belief that compartment syndrome is due to a cycle of swelling-ischemia-swelling.

Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model: Heckman MM, Whitesides TE, Grewe JR, Judd RL, Miller M, Lawrence JM. Orthop Trauma. 1993;7:199–210

Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model: Heckman MM, Whitesides TE, Grewe JR, Judd RL, Miller M, Lawrence JM. Orthop Trauma. 1993;7:199–210

Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model.

Our objective was to define the critical tissue pressure at which irreversible muscle damage occurs and to compare our results to those thresholds advocated in the orthopaedic literature. A standard plasma infusion compartment syndrome model was created in a canine model. Four dogs were in each of four experimental groups with compartment pressure maintained as follows: (a) 30 mm Hg with support of diastolic blood pressure to a level > 50 mm Hg; (b) 20 mm Hg less than diastolic pressure; (c) 10 mm Hg less than diastolic blood pressure; (d) a level equal to the animal's diastolic blood pressure. All animals were sacrificed 14 days after the procedure. Histology revealed the following: (a) tissues pressurized to 30 mm Hg in a normotensive dog demonstrated no significant abnormalities; (b) tissues pressurized to 20 mm Hg less than diastolic revealed occasional cells undergoing regeneration but no evidence of infarction or fibrosis; (c) tissues pressurized to 10 mm Hg less than diastolic showed scattered small areas of infarction and fibrosis; and (d) tissues pressurized to diastolic blood pressure demonstrated more widespread infarction and scarring. The ischemic threshold of muscle, beyond which irreversible tissue damage occurs, is directly related to the difference in compartment and perfusion pressure. Our findings document this pressure to be 10 mm Hg less than diastolic blood pressure or within 30 mm Hg of mean arterial pressure. This data refutes the use of absolute tissue pressure values as a guide to the necessity of fasciotomy. To abort an impending compartment syndrome and avoid irreversible tissue injury and their sequelae, fasciotomy should be done if tissue pressure reaches within 10-20 mm Hg of diastolic pressure.

Measurement of intracompartmental pressure

An experimental model of acute compartment syndrome involving the anterolateral compartment of the hindlimb in dogs was used to compare three methods of measurement of intracompartmental pressure: the simple-needle technique, use of the slit catheter, and use of the side-ported needle. No statistical difference was found between the values obtained with the slit catheter and those obtained with the side-ported needle; the mean difference was 1.4 millimeters of mercury throughout the range of compartment pressures that were measured. The side-ported needle appeared to be as accurate as the slit catheter for the measurement of compartment pressures (p = 0.355, 1-beta = 0.9). The values obtained with use of the simple needle were consistently higher than those obtained with the other two methods (p < 0.001): an average of 18.3 millimeters of mercury higher than the values measured with the slit catheter and 19.3 millimeters of mercury higher than those measured with the side-ported needle. Clinically, the side-ported needle or the slit catheter can be used to obtain accurate measurements of compartment pressure. Use of the simple 18-gauge needle is not recommended for this purpose.

Are free radical scavengers beneficial in the treatment of compartment syndrome after acute arterial ischemia?

Because it is postulated that compartment syndrome developing secondary to an acute arterial occlusion may be due to reperfusion injury, oxygen-derived free radicals have been implicated in its genesis. To assess the possible beneficial effect of free radical scavengers in this setting, we used a previously established in vivo canine model of compartment syndrome to compare four groups: group I, no treatment; group II, prophylactic fasciotomy; group III, intravenous albumin conjugated superoxide dismutase (SOD); group IV, intravenous mannitol (hydroxyl radical scavenger). Both hind limbs were completely devascularized at the popliteal level except for an isolated pedicle to the anterior compartment. The right limb served as the nonischemic control, whereas the left underwent 8 hours of ischemia followed by reperfusion. Continuous monitoring of transfascial oxygen tension (tfPO2) demonstrated severe ischemia during occlusion (tfPO2 5.7 ± 5.1 mm Hg) and restoration of blood flow with reperfusion (mean tfPO2 50 to 60 mm Hg). Measurements of compartment pressure were significantly higher after reperfusion in groups I, III, and IV when compared with those of group II (p < 0.001, groups I and II; p < 0.01, group IV). Extent of muscle necrosis assessed by technetium pyrophosphate scanning and expressed as a ratio of left to right legs was as follows: group I, 8.9 ± 5.0; group II, 2.6 ± 0.5; group III, 2.8 ± 0.8; group IV, 1.8 ± 0.6. Muscle contraction studies 16 hours after reperfusion indicated abnormal findings in all but group II. In conclusion, administration of free radical scavengers did not preserve normal neuromuscular function despite a significant reduction in muscle damage. The effects of ischemia-reperfusion and increased compartment pressure appear additive. Fasciotomy at the time of reperfusion after prolonged ischemia remains the treatment of choice to avoid functional impairment.

Long-term Myoneural Function After an Induced Compartment Syndrome in the Canine Hindlimb

For evaluation of long-term myoneural function in a compartment syndrome model of the canine hindlimb, five conditioned dogs had injections of autologous plasma into the hindlimb anterolateral muscle compartment, maintaining the pressure at 40 mmHg for eight hours. A newly described technique for measuring muscle function was used before pressurization and at weekly intervals following pressurization for a period of one month. Two days after pressurization, isometric twitch torque and tetanic torque showed a significant decrease (p less than .05) when compared with baseline values. Time to peak tension, one-half relaxation time, and endurance tests showed no significant change throughout the four-week testing. At four weeks following pressurization, no muscle dysfunction was noted, and muscle examined histologically was normal. Therefore, the initial muscle dysfunction present was reversed by skeletal muscle recovery or regeneration. Although no long-term muscle dysfunction occurred in this study of dogs, there may exist a lower tolerance to elevated intramuscular pressure in humans. Since dogs have only fatigue-resistant muscle fibers with higher oxidative capacity than human fibers, dog muscle may have a greater regenerative capacity than human muscle. Therefore, exact extrapolation of these dog studies to clinical compartment syndromes is difficult. Although muscle function was recovered in these animal experiments, human muscle may have less capacity to recover. It is advisable to decompress muscle compartments at a pressure of 30 mmHg as soon as clinical symptoms of a compartment syndrome appear.