This Article Abstract Full Text (PDF) Free Letters to the Editor: Submit a response Alert me when this article is cited Alert me when Letters to the Editor are posted Alert me if a correction is posted Services E-mail this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My File Cabinet Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by MOHLER, L. R. Articles by GERSHUNI, D. H. Search for Related Content PubMed PubMed Citation Articles by MOHLER, L. R. Articles by GERSHUNI, D. H. Social Bookmarking                   What's this?

Intramuscular Deoxygenation during Exercise in Patients Who Have Chronic Anterior Compartment Syndrome of the Leg*

L. RANDALL MOHLER, M.D., JORMA R. STYF, M.D., PH.D., ROBERT A. PEDOWITZ, M.D., PH.D., ALAN R. HARGENS, PH.D. and DAVID H. GERSHUNI, M.D., SAN DIEGO, CALIFORNIA

Investigation performed at University of California at San Diego, San Diego

	Abstract

Top Abstract Introduction Materials and Methods Results Discussion References

 
Currently, the definitive diagnosis of chronic compartment syndrome is based on invasive measurements of intracompartmental pressure. We measured the intramuscular pressure and the relative oxygenation in the anterior compartment of the leg in eighteen patients who were suspected of having chronic compartment syndrome as well as in ten control subjects before, during, and after exercise. Chronic compartment syndrome was considered to be present if the intramuscular pressure was at least fifteen millimeters of mercury (2.00 kilopascals) before exercise, at least thirty millimeters of mercury (4.00 kilopascals) one minute after exercise, or at least twenty millimeters of mercury (2.67 kilopascals) five minutes after exercise. Changes in relative oxygenation were measured with use of the non-invasive method of near-infrared spectroscopy. In all patients and subjects, there was rapid relative deoxygenation after the initiation of exercise, the level of oxygenation remained relatively stable during continued exercise, and there was reoxygenation to a level that exceeded the pre-exercise resting level after the cessation of exercise. During exercise, maximum relative deoxygenation in the patients who had chronic compartment syndrome (mean relative deoxygenation [and standard error], -290 ± 39 millivolts) was significantly greater than that in the patients who did not have chronic compartment syndrome (-190 ± 10 millivolts) and that in the control subjects (-179 ± 14 millivolts) (p < 0.05 for both comparisons). In addition, the interval between the cessation of exercise and the recovery of the pre-exercise resting level of oxygenation was significantly longer for the patients who had chronic compartment syndrome (184 ± 54 seconds) than for the patients who did not have chronic compartment syndrome (39 ± 19 seconds) and the control subjects (33 ± 10 seconds) (p < 0.05 for both comparisons). CLINICAL RELEVANCE: Patients who had chronic anterior compartment syndrome of the leg had greater relative deoxygenation during exercise as well as delayed reoxygenation after exercise; these findings support an ischemic etiology for chronic compartment syndrome. Near-infrared spectroscopy may be useful as a non-invasive diagnostic tool for the evaluation of patients suspected of having chronic anterior compartment syndrome of the leg.

	Introduction

Top Abstract Introduction Materials and Methods Results Discussion References

 
Patients who have chronic compartment syndrome have recurrent episodes of pain during exercise. The etiology of chronic compartment syndrome is incompletely understood, but there is general agreement that abnormal increases in intramuscular pressure during exercise impair local perfusion, thereby resulting in tissue ischemia and pain⁹. Fasciotomy of the involved compartment has been highly successful both in relieving pain and in allowing a return to full activity, but accurate diagnosis is essential for the appropriate selection of patients for the procedure^{23,24,26,31,33}. A history and a physical examination are inadequate for the purpose of distinguishing chronic compartment syndrome from other causes of exercise-induced pain^21,33; therefore, the definitive diagnosis is made on the basis of measurements of intracompartmental pressure. However, pressures vary with the technique that is used for measurement, the timing of measurement in relation to exercise, the position of adjacent joints, and the depth to which the catheter is inserted^{11,19-21,24,33}. In addition, the measurement of intracompartmental pressure is invasive and is associated with pain and a slight risk of injury.

Previous studies have demonstrated a relative decrease in the flow of blood to muscle^22,34 as well as impaired oxygenation²⁵ during exercise in patients who have chronic compartment syndrome. Near-infrared spectroscopy is a non-invasive method that can be used to detect changes in the oxygen saturation of hemoglobin³. Hemoglobin absorbs light differently when it is carrying oxygen; consequently, blood changes from deep red to bright red as it becomes saturated with oxygen. Pulse oximeters are used to detect changes in the absorption of visible light, which passes a few millimeters through tissue. Near-infrared light penetrates further, and changes in the infrared part of the spectrum allow for the non-invasive monitoring of oxygen saturation in deeper tissues¹⁵. The purpose of the present study was to determine whether near-infrared spectroscopy can be used as a diagnostic tool for the evaluation of patients suspected of having chronic anterior compartment syndrome of the leg.

	Materials and Methods

Top Abstract Introduction Materials and Methods Results Discussion References

 

Patients and Control Subjects
Eighteen patients were referred to us for the evaluation of possible chronic anterior compartment syndrome of the leg between 1993 and 1995. Although all of the patients had a history of exercise-induced pain in the anterior portion of the leg, the definitive diagnosis of chronic compartment syndrome was based on the measurement of intracompartmental pressures. Chronic compartment syndrome was considered to be present if the intramuscular pressure was at least fifteen millimeters of mercury (2.00 kilopascals) before exercise, at least thirty millimeters of mercury (4.00 kilopascals) one minute after exercise, or at least twenty millimeters of mercury (2.67 kilopascals) five minutes after exercise²¹. Ten patients were diagnosed as having chronic compartment syndrome and eight, as having other sources of pain. Ten healthy volunteers served as controls. The experimental protocol was approved by the Human Subjects Committee of the University of California at San Diego.

Exercise
An isokinetic exercise protocol was used in order to avoid orthostatic changes in pressure during exercise. The patient or subject was seated in a semi-recumbent position, with the hip and knee flexed approximately 45 degrees, on an isokinetic dynamometer (Biodex, Shirley, New York). The control subjects performed dorsiflexion (120 degrees per second) and plantar flexion (450 degrees per second) of the ankle for ten minutes, and the patients exercised until they were unable to continue because of pain in the leg. Intramuscular pressure and relative oxygenation were measured continuously before, during, and for ten minutes after exercise. After a ten-minute recovery period, a tourniquet was applied to the thigh and was inflated to a pressure of 100 millimeters of mercury (13.33 kilopascals) higher than the systolic blood pressure; the patients and subjects then exercised to exhaustion to allow for an estimation of the maximum tissue deoxygenation under ischemic conditions.

Intramuscular Pressure
Intramuscular pressure was measured with the microcapillary infusion technique³² with use of a low-volume catheter with side-holes at the tip (Myopress; Atos Medical, Horby, Sweden) and slow continuous infusion. This technique has a rapid dynamic response and demonstrates a peak pressure with each muscle contraction (muscle-contraction pressure) as well as a trough pressure between contractions (muscle-relaxation pressure). Increased muscle-relaxation pressure corresponds well with increased pressure at rest after exercise. Because muscles have blood flow only during the relaxation phase of exercise, muscle-relaxation pressure has been found to be the most useful parameter for the diagnosis of chronic compartment syndrome during exercise³³.

The skin was anesthetized approximately two centimeters lateral to the tibial tubercle with 1 per cent plain lidocaine; a 16-gauge intravenous catheter then was inserted at a 30-degree angle to the skin and was advanced five centimeters distally, parallel to the tibia. The needle was withdrawn, and a Teflon catheter was inserted through the angiocath and into the muscle. The angiocath then was removed, and the Teflon catheter was secured to the skin. High-pressure tubing was used to create a fluid column to a pressure transducer (model P23 XL; Spectramed, Oxnard, California), which was placed at the level of the tip of the catheter. A flow-limiting device was used to maintain a continuous infusion of three milliliters per hour.

Oxygenation
Changes in intramuscular oxygenation were measured with use of a continuous dual wavelength-near-infrared spectrometer (RunMan; NIM, Philadelphia, Pennsylvania). This device is used to measure the reflection of light transmitted at wavelengths of 760 and 850 nanometers. Deoxyhemoglobin absorbs more light at 760 nanometers, whereas oxyhemoglobin absorbs more light at 850 nanometers. The difference between the amount of light reflected at these two wavelengths indicates a change in the concentration of oxygenated hemoglobin. Myoglobin has identical absorption characteristics and is not distinguished from hemoglobin with this technique. A probe containing two tungsten-filament lights and photodetectors with filters for wavelengths of 760 and 850 nanometers was positioned on the surface of the leg over the middle third of the anterior compartment, and the difference between the two signals was set to zero with the subject at rest before exercise. The probe measures changes at a mean depth of 2.5 centimeters.

Statistical Analysis
Differences among the three groups were evaluated with analysis of variance. The Fisher protected least-significant-difference test was used for multiple paired comparisons. All results are reported as the mean and the standard error. The level of significance was p < 0.05.

	Results

Top Abstract Introduction Materials and Methods Results Discussion References

 

Exercise
The patients exercised until they were unable to continue because of pain in the leg; those who had chronic compartment syndrome exercised for a mean of 8.2 ± 1.7 minutes and those who did not, for a mean of 9.9 ± 1.6 minutes. All control subjects exercised for ten minutes. There were no substantial differences among the groups with regard to the total work or the rate of work (the total work divided by the duration of exercise), although there were wide individual variations in these parameters. The mean rate of work was 12.3 ± 3.5 newton-meters per minute for the patients who had chronic compartment syndrome, 7.0 ± 2.3 newton-meters per minute for the patients who did not have chronic compartment syndrome, and 9.1 ± 1.3 newton-meters per minute for the control subjects.

Pressure
There were no substantial differences among the three groups with regard to the intramuscular pressure measured at rest before exercise; the mean resting pressure was 11.1 ± 1.4 millimeters of mercury (1.48 ± 0.19 kilopascals) in the patients who had chronic compartment syndrome, 8.9 ± 0.8 millimeters of mercury (1.19 ± 0.11 kilopascals) in the patients who did not have chronic compartment syndrome, and 10.1 ± 1.0 millimeters of mercury (1.35 ± 0.13 kilopascals) in the control subjects. The patients who had chronic compartment syndrome had greater increases in muscle-relaxation pressure during exercise and higher resting pressure throughout the ten-minute recovery period than did the patients who did not have chronic compartment syndrome and the control subjects. A significant difference in muscle-relaxation pressure was first detected between the patients who had chronic compartment syndrome and the control subjects after two minutes of exercise (p < 0.05) (Fig. 1). One minute after the cessation of exercise, the mean resting pressure was 55.4 ± 5.0 millimeters of mercury (7.38 ± 0.67 kilopascals) in the patients who had chronic compartment syndrome, 17.4 ± 4.2 millimeters of mercury (2.32 ± 0.56 kilopascals) in the patients who did not have chronic compartment syndrome, and 16.9 ± 2.9 millimeters of mercury (2.25 ± 0.39 kilopascals) in the control subjects. Five minutes after the cessation of exercise, the values were 41.2 ± 5.8 millimeters of mercury (5.49 ± 0.77 kilopascals), 11.9 ± 2.3 millimeters of mercury (1.59 ± 0.31 kilopascals), and 13.7 ± 1.7 millimeters of mercury (1.83 ± 0.23 kilopascals), respectively.

View larger version (24K): [in this window] [in a new window]   Fig. 1 Graph showing the values for intramuscular pressure measured in the anterior compartment of the leg for the three groups. Data were plotted at equal intervals between two minutes after the initiation of exercise and the completion of exercise to allow for the comparison of changes among groups. The pressure during exercise represents the pressure between contractions (muscle-relaxation pressure). Patients who had chronic compartment syndrome (CCS) had greater increases in pressure during exercise and higher pressure throughout the ten-minute recovery period. (One millimeter of mercury equals 0.1333 kilopascal.)

Oxygenation
Oxygen saturation decreased rapidly after the initiation of exercise and then remained essentially constant during continued exercise (Fig. 2). The patients who had chronic compartment syndrome had greater relative deoxygenation than did the patients who did not have chronic compartment syndrome and the control subjects. A significant difference in relative oxygenation was first detected between the patients who had chronic compartment syndrome and the control subjects after thirty seconds of exercise. After two minutes of exercise, relative deoxygenation in the patients who had chronic compartment syndrome (relative oxygenation, -228 ± 47 millivolts) was significantly greater than that in the patients who did not have chronic compartment syndrome (-127 ± 17 millivolts) and that in the control subjects (-101 ± 16 millivolts) (p < 0.05 for both comparisons). Similarly, maximum relative deoxygenation was greater in patients who had chronic compartment syndrome (-290 ± 39 millivolts) than in patients who did not have chronic compartment syndrome (-190 ± 10 millivolts) and in control subjects (-179 ± 14 millivolts). No substantial differences in relative oxygenation were detected between the patients who did not have chronic compartment syndrome and the control subjects.

View larger version (23K): [in this window] [in a new window]   Fig. 2 Graph showing the changes in tissue oxygenation in the anterior compartment of the leg as measured with near-infrared spectroscopy in the three groups. Data were plotted at equal intervals between two minutes after the initiation of exercise and the completion of exercise to allow for the comparison of changes among groups. Deoxygenation causes a downward (negative) deflection in the signal. Patients who had chronic compartment syndrome (CCS) had greater relative deoxygenation during exercise and slower reoxygenation after exercise.

The relative deoxygenation during tourniquet ischemia was similar to that during exercise in the group of patients who had chronic compartment syndrome, but this was not the case in the other two groups. There were no substantial differences among the groups with regard to the maximum deoxygenation during tourniquet ischemia (relative oxygenation, -264 ± 46 millivolts in the patients who had chronic compartment syndrome, -203 ± 40 millivolts in the patients who did not have chronic compartment syndrome, and -304 ± 36 millivolts in the control subjects).

	Discussion

Top Abstract Introduction Materials and Methods Results Discussion References

 
Patients who had chronic compartment syndrome had greater relative deoxygenation during exercise compared with patients who had other sources of pain and with healthy control subjects. Impaired tissue perfusion secondary to increased intramuscular pressure was anticipated on the basis of the findings of previous studies^8,18,29,30. In the present study, however, patients who had chronic compartment syndrome had greater deoxygenation after only thirty seconds of exercise, which was before intracompartmental pressure had increased substantially. Early differences in oxygen saturation, which appear to precede impaired delivery of oxygen, may result from increased extraction of oxygen from the intracompartmental circulation. The oxidative capacity of skeletal muscle increases in response to reduced blood flow¹⁰; as a result, the metabolic capacity of skeletal muscle is increased in patients who have arterial insufficiency^4,14. Similar changes may occur in patients who have chronic compartment syndrome because of insufficient blood flow to muscles during exercise. Varelas et al.³⁵ reported increased endurance capacity in patients who had chronic compartment syndrome compared with control subjects. Therefore, the early increase in deoxygenation observed in patients who had chronic compartment syndrome may reflect an increased ability to extract oxygen.

During exercise, the level of oxygenation in patients who had chronic compartment syndrome was consistently lower than the levels in patients who did not have chronic compartment syndrome and in control subjects who were exercising at similar rates. After exercise, reoxygenation was delayed in the former group compared with the two latter groups. The interval between the cessation of exercise and the recovery of the resting level of oxygenation is affected by both the intensity of the exercise and the delivery of oxygen. Chance et al.⁶ found that the recovery time increased with the intensity of work performed by competitive rowers, and several other authors have reported increased times for recovery for patients who had impaired delivery of oxygen because of arterial insufficiency^7,16,17. Delayed reoxygenation in patients who have chronic compartment syndrome probably reflects a combination of greater deoxygenation during exercise and impaired delivery of oxygen due to increased intramuscular pressure.

Previous studies have shown decreased blood flow and oxygenation in patients who have chronic compartment syndrome. One of us (J. R. S.) and colleagues³⁴ found that muscle blood flow was decreased when patients who had chronic compartment syndrome had development of increased intramuscular pressure and pain during exercise. Royle et al.²⁵ reported that the partial pressure of oxygen in intracompartmental muscle decreased significantly during exercise in patients who had chronic compartment syndrome. However, some authors have reported that ischemia may not be the source of pain in these patients^1,2. Amendola et al.¹ used radioisotope uptake to estimate local blood flow during exercise and found no consistent ischemic changes in five patients who had chronic compartment syndrome, as compared with control subjects. Balduini et al.² used nuclear magnetic resonance spectroscopy to detect changes in the concentration of phosphocreatine and found no differences between twelve patients in whom the intracompartmental pressure met their criterion for chronic compartment syndrome and fourteen patients in whom it did not. In the patients who had chronic compartment syndrome in the present study, deoxygenation during exercise reached a level similar to that during tourniquet ischemia; this extreme deoxygenation suggests that ischemia plays a substantial role in the pathophysiology of chronic compartment syndrome.

Although near-infrared spectroscopy is painless and non-invasive, it has limitations compared with current techniques of pressure measurement. The signal indicates changes in the absorption of light in all tissues through which the light has passed. Although skin and subcutaneous fat contribute very little to the total signal¹³, superficial muscles absorb infrared rays; as a result, deeper muscles (such as those in the deep posterior compartment of the leg) cannot be isolated for study. Moreover, as the path length of the light in the tissue must be known in order to calculate the absolute concentration of chromophores²⁷, this technique can be used only to detect changes and trends in relative oxygenation. As a result, the technique is not useful in the setting of an acute compartment syndrome, in which changes in oxygenation may develop before monitoring.

At the present time, it is not possible to develop diagnostic criteria on the basis of the magnitude of deoxygenation because the continuous dual wavelength- near-infrared spectrometer does not provide absolute values of oxygenation. However, the time-course of events is independent of absolute oxygenation. In the present study, the interval between the cessation of exercise and the return to the resting level of oxygenation was significantly longer for the patients who had chronic compartment syndrome. With use of the value for the control group as the standard, the mean recovery time plus two standard deviations was 103 seconds. Five of the ten patients who had chronic compartment syndrome and only one of the eight who did not had abnormally prolonged reoxygenation, making this criterion only mildly sensitive but rather specific for the diagnosis of chronic compartment syndrome. Recently, the techniques of time and frequency resolution have been applied to near-infrared spectroscopy for continuous measurement of path length^{5,12,27,28,36}. Newer instruments soon may be capable of providing quantitative data regarding tissue oxygenation and allow for the development of more useful diagnostic criteria.

In the present study, patients who had chronic anterior compartment syndrome of the leg had greater relative deoxygenation during exercise as well as delayed reoxygenation after exercise. The finding that deoxygenation during exercise reached levels similar to those during tourniquet ischemia in such patients suggests that ischemia plays a major role in the pathophysiology of chronic compartment syndrome. The results of the present study suggest that near-infrared spectroscopy may be useful as a non-invasive diagnostic tool for the evaluation of patients suspected of having chronic anterior compartment syndrome of the leg.

NOTE: The authors thank Sandra Van Leuven, Ph.D., and Michael A. Lopez, B.S., for their expert technical assistance.

	Footnotes

 
*No benefits in any form have been received or will be received from a commercial party related directly or indirectly to the subject of this article. Funds were received in total or partial support of the research or clinical study presented in this article. The funding sources were National Aeronautics and Space Administration Grant 199-26-12-34 and the Veterans Administration Medical Center, San Diego, California.

Department of Orthopaedic Surgery, University of California at San Diego, 200 West Arbor Drive 8894, San Diego, California 92103-8894.

Department of Orthopaedics, University of Göteborg, S-416 85 Göteborg, Sweden.

Life Science Division (239-11), National Aeronautics and Space Administration Ames Research Center, Moffett Field, California 94035-1000.

	References

Top Abstract Introduction Materials and Methods Results Discussion References

 

1. Amendola, A.; Rorabeck, C. H.; Vellett, D.; Vezina, W.; Rutt, B.; and Nott, L.: The use of magnetic resonance imaging in exertional compartment syndromes. Am. J. Sports Med., 18: 29-34, 1990.[Abstract/Free Full Text]
2. Balduini, F. C.; Shenton, D. W.; O'Connor, K. H.; and Heppenstall, R. B.: Chronic exertional compartment syndrome: correlation of compartment pressure and muscle ischemia utilizing ³¹P-NMR spectroscopy. Clin. Sports Med., 12: 151-165, 1993.[Medline]
3. Benaron, D. A.; Benitz, W. E.; Ariagno, R. L.; and Stevenson, D. K.: Noninvasive methods for estimating in vivo oxygenation. Clin. Pediat., 31: 258-273, 1992.
4. Bylund, A. C.; Hammarsten, J.; Holm, J.; and Scherstén, T.: Enzyme activities in skeletal muscles from patients with peripheral arterial insufficiency. European J. Clin. Invest., 6: 425-429, 1976.[Medline]
5. Chance, B.; Maris, M.; Sorge, J.; and Zhang, M. Z.: A phase modulation system for dual wavelength difference spectroscopy of haemoglobin deoxygenation in tissues. Proc. SPIE, 1204: 481-491, 1990.
6. Chance, B.; Dait, M. T.; Zhang, C.; Hamaoka, T.; and Hagerman, F.: Recovery from exercise-induced desaturation in the quadriceps muscles of elite competitive rowers. Am. J. Physiol., 262: 766-C775, 1992.
7. Cheatle, T. R.; Potter, L. A.; Cope, M.; Delpy, D. T.; Coleridge Smith, P. D.; and Scurr, J. H.: Near-infrared spectroscopy in peripheral vascular disease. British J. Surg., 78: 405-408, 1991.[Medline]
8. Clayton, J. M.; Hayes, A. C.; and Barnes, R. W.: Tissue pressure and perfusion in the compartment syndrome. J. Surg. Res., 22: 333-339, 1977.[Medline]
9. Eisele, S. A., and Sammarco, G. J.: Chronic exertional compartment syndrome. In Instructional Course Lectures, The American Academy of Orthopaedic Surgeons. Vol. 42, pp. 213-217. Rosemont, Illinois, The American Academy of Orthopaedic Surgeons, 1993.
10. Elander, A.; Idström, J. P.; Scherstén, T.; and Bylund-Fellenius, A. C.: Metabolic adaptation to reduced muscle blood flow. I. Enzyme and metabolite alterations. Am. J. Physiol., 249: 63-E69, 1985.
11. Gershuni, D. H.; Yaru, N. C.; Hargens, A. R.; Lieber, R. L.; O'Hara, R. C.; and Akeson, W. H.: Ankle and knee position as a factor modifying intracompartmental pressure in the human leg. J. Bone and Joint Surg., 66-A: 1415-1420, Dec. 1984.[Abstract/Free Full Text]
12. Haida, M.; Miwa, M.; Shiino, A.; and Chance, B.: A method to estimate the ratio of absorption coefficients of two wavelengths using phase-modulated near infrared light spectroscopy. Analyt. Biochem., 208: 348-351, 1993.
13. Hampson, N. B., and Piantadosi, C. A.: Near infrared monitoring of human skeletal muscle oxygenation during forearm ischemia. J. Appl. Physiol., 64: 2449-2457, 1988.[Abstract/Free Full Text]
14. Holm, J.; Björntorp, P.; and Scherstén, T.: Metabolic activity in human skeletal muscle. Effect of peripheral arterial insufficiency. European J. Clin. Invest., 2: 321-325, 1972.[Medline]
15. Jöbsis, F. F.: Noninvasive, infrared monitoring of cerebral and myocardial oxygen sufficiency and circulatory parameters. Science, 198: 1264-1267, 1977.[Abstract/Free Full Text]
16. Komiyama, T.; Shigematsu, H.; Yasuhara, H.; and Muto, T.: An objective assessment of intermittent claudication by near-infrared spectroscopy. European J. Vasc. Surg., 8: 294-296, 1994.
17. McCully, K. K.; Halber, C.; and Posner, J. D.: Exercise-induced changes in oxygen saturation in the calf muscles of elderly subjects with peripheral vascular disease. J. Gerontol., 49: 128-B134, 1994.
18. Matsen, F. A., III; King, R. V.; Krugmire, R. B., Jr.; Mowery, C. A.; and Roche, T.: Physiological effects of increased tissue pressure. Internat. Orthop., 3: 237-244, 1979.[Medline]
19. Nakhostine, M.; Styf, J. R.; van Leuven, S.; Hargens, A. R.; and Gershuni, D. H.: Intramuscular pressure varies with depth. The tibialis anterior muscle studied in 12 volunteers. Acta Orthop. Scandinavica, 64: 377-381, 1993.[Medline]
20. Pedowitz, R. A., and Gershuni, D. H.: Diagnosis and treatment of chronic compartment syndrome. Crit. Rev. Phys. and Rehab. Med., 5: 301-313, 1993.
21. Pedowitz, R. A.; Hargens, A. R.; Mubarak, S. J.; and Gershuni, D. H.: Modified criteria for the objective diagnosis of chronic compartment syndrome of the leg. Am. J. Sports Med., 18: 35-40, 1990.[Abstract/Free Full Text]
22. Qvarfordt, P.; Christenson, J. T.; Eklöf, B.; Ohlin, P.; and Saltin, B.: Intramuscular pressure, muscle blood flow, and skeletal muscle metabolism in chronic anterior tibial compartment syndrome. Clin. Orthop., 179: 284-290, 1983.
23. Rorabeck, C. H.; Fowler, P. J.; and Nott, L.: The results of fasciotomy in the management of chronic exertional compartment syndrome. Am. J. Sports Med., 16: 224-227, 1988.[Abstract/Free Full Text]
24. Rorabeck, C. H.; Bourne, R. B.; Fowler, P. J.; Finlay, J. B.; and Nott, L.: The role of tissue pressure measurement in diagnosing chronic anterior compartment syndrome . Am. J. Sports Med., 16: 143-146, 1988.[Abstract/Free Full Text]
25. Royle, S. G.; Ross, E. R. S.; and Rithalia, S. V. S.: Intracompartmental pressure and intramuscular pO² in chronic compartment syndrome. J. Bone and Joint Surg., 75-B (Supplement II): 142, 1993.
26. Schepsis, A. A.; Martini, D.; and Corbett, M.: Surgical management of exertional compartment syndrome of the lower leg. Long-term followup. Am. J. Sports Med., 21: 811-817, 1993.[Abstract/Free Full Text]
27. Sevick, E. M.; Weng, J.; Maris, M.; and Chance, B.: Analysis of absorption, scattering, and hemoglobin saturation using phase modulation spectroscopy. Proc. SPIE, 1431: 264-275, 1991.
28. Sevick, E. M.; Chance, B.; Leigh, J.; Nioka, S.; and Maris, M.: Quantitation of time- and frequency-resolved optical spectra for the determination of tissue oxygenation. Analyt. Biochem., 195: 330-351, 1991.
29. Sheridan, G. W., and Matsen, F. A., III: An animal model of the compartmental syndrome. Clin. Orthop., 113: 36-42, 1975.
30. Sheridan, G. W.; Matsen, F. A., III; and Krugmire, R. B., Jr.: Further investigations on the pathophysiology of the compartmental syndrome. Clin. Orthop., 123: 266-270, 1977.
31. Styf, J. R., and Körner, L. M.: Chronic anterior-compartment syndrome of the leg. Results of treatment by fasciotomy. J. Bone and Joint Surg., 68-A: 1338-1347, Dec. 1986.[Abstract/Free Full Text]
32. Styf, J. R., and Körner, L. M.: Microcapillary infusion technique for measurement of intramuscular pressure during exercise. Clin. Orthop., 207: 253-262, 1986.
33. Styf, J. R., and Körner, L. M.: Diagnosis of chronic anterior compartment syndrome in the lower leg. Acta Orthop. Scandinavica, 58: 139-144, 1987.[Medline]
34. Styf, J.; Körner, L.; and Suurkula, M.: Intramuscular pressure and muscle blood flow during exercise in chronic compartment syndrome. J. Bone and Joint Surg., 69-B(2): 301-305, 1987.
35. Varelas, F. L.; Wessel, J.; Clement, D. B.; Doyle, D. L.; and Wiley, J. P.: Muscle function in chronic compartment syndrome of the leg. J. Orthop. and Sports Phys. Ther., 18: 586-589, 1993.[Medline]
36. Wilson, B. C.; Sevick, E. M.; Patterson, M. S.; and Chance, B.: Time-dependent optical spectroscopy and imaging for biomedical applications. Proc. IEEE, 80: 918-930, 1992.

CiteULike

Connotea

Del.icio.us

Facebook

Technorati

Twitter

This article has been cited by other articles:

				M. S. Shuler, W. M. Reisman, T. E. Whitesides Jr., T. L. Kinsey, E. M. Hammerberg, M. G. Davila, and T. J. Moore Near-Infrared Spectroscopy in Lower Extremity Trauma J. Bone Joint Surg. Am., June 1, 2009; 91(6): 1360 - 1368. [Abstract] [Full Text] [PDF]

				J. G. H. van den Brand, T. Nelson, E. J. M. M. Verleisdonk, and C. van der Werken The Diagnostic Value of Intracompartmental Pressure Measurement, Magnetic Resonance Imaging, and Near-Infrared Spectroscopy in Chronic Exertional Compartment Syndrome: A Prospective Study in 50 Patients Am. J. Sports Med., May 1, 2005; 33(5): 699 - 704. [Abstract] [Full Text] [PDF]

				T D A Barbour, C A Briggs, S N Bell, C J Bradshaw, D J Venter, and P D Brukner Histology of the fascial-periosteal interface in lower limb chronic deep posterior compartment syndrome Br. J. Sports Med., December 1, 2004; 38(6): 709 - 717. [Abstract] [Full Text] [PDF]

				R. F. Pell IV, H. S. Khanuja, and G. R. Cooley Leg Pain in the Running Athlete J. Am. Acad. Ortho. Surg., November 1, 2004; 12(6): 396 - 404. [Abstract] [Full Text] [PDF]

				J. G. H. van den Brand, E. J. M. M. Verleisdonk, and C. van der Werken Near Infrared Spectroscopy in the Diagnosis of Chronic Exertional Compartment Syndrome Am. J. Sports Med., March 1, 2004; 32(2): 452 - 456. [Abstract] [Full Text] [PDF]

				M. J. Fraipont and G. J. Adamson Chronic Exertional Compartment Syndrome J. Am. Acad. Ortho. Surg., July 1, 2003; 11(4): 268 - 276. [Abstract] [Full Text] [PDF]

				F. J. Leversedge, P. J. Casey, J. G. Seiler III, and J. W. Xerogeanes Endoscopically Assisted Fasciotomy : Description of Technique and In Vitro Assessment of Lower-Leg Compartment Decompression Am. J. Sports Med., March 1, 2002; 30(2): 272 - 278. [Abstract] [Full Text] [PDF]

				A. A. Schepsis, S. S. Gill, and T. A. Foster Fasciotomy for Exertional Anterior Compartment Syndrome: Is Lateral Compartment Release Necessary? Am. J. Sports Med., July 1, 1999; 27(4): 430 - 435. [Abstract] [Full Text] [PDF]

This Article Abstract Full Text (PDF) Free Letters to the Editor: Submit a response Alert me when this article is cited Alert me when Letters to the Editor are posted Alert me if a correction is posted Services E-mail this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to My File Cabinet Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by MOHLER, L. R. Articles by GERSHUNI, D. H. Search for Related Content PubMed PubMed Citation Articles by MOHLER, L. R. Articles by GERSHUNI, D. H. Social Bookmarking                   What's this?

Stanford University Libraries' HighWire Press (TM) assists in the publication of JBJS Online.
Copyright © 1997 by The Journal of Bone and Joint Surgery, Inc. Online ISSN: 1535-1386.
The Journal of Bone and Joint Surgery®, JBJS®, JB&JS®, and eJBJS® are registered in the U.S. Patent and Trademark Office.