We appreciate Dr. Whitesides’ letter regarding our article. His group’s reporting of their clinical experience and observations created much of our interest in this topic (1). We would also like to acknowledge Dr. Whitesides’ tremendous body of work in this field.

In response to Dr Whitesides’ letter, we would like to point out that the goal of our study was to bring to light a potential clinical complication in the 90o/90o kneeling position by creating a controlled model of the operating room setting through comparisons with other positions, including the supine and 45 o /45 o positions. The definitive explanation of the etiology of the complication of compartment syndrome in the 90o/90o kneeling position was admittedly beyond the scope of our study. Our goal was instead limited to the quantification of factors contributing to this complication.

Overall, we agree with many of Dr. Whitesides’ major points. We acknowledge that leg compartments do not act as uniform hydraulic cylinders, except in acute compartment syndromes caused by an intramuscular arterial bleed. In our study, we did not quantify arteriolar driving pressures and intramuscular pressures locally throughout the leg. In fact, in our discussion, we theorized that local areas of decreased perfusion may create tissue insult and lead to the conditions that can induce compartment syndrome. Additionally, we would like to clarify that we do not question the validity of the theory of differential pressure affecting risk for compartment syndrome. In fact, our group published a paper demonstrating that there are increased differential pressures in the elevated well leg in the hemilithotomy position which can predispose patients to compartment syndrome (2).

In our study, we found that in the 90o/90o kneeling position, leg anterior compartment pressures were significantly elevated to a level of 30.8 ± 5.7 mm Hg. However, in these awake subjects, the ankle blood pressure in the dependent leg was also significantly elevated, thus not meeting the established theoretical criteria for differential pressure, defined as intramuscular pressure relative to either mean arterial pressure or diastolic pressure (2,3,4). Experimentally, we also placed a force sensor under the dependent leg and found there were varying pressures underneath the dependent anterior compartment. These dependent weights and intramuscular pressures in the anterior compartment both significantly correlated with subject weights. This implies, as Dr. Whitesides has observed clinically, that heavier patients with elevated dependent pressures will generate higher intramuscular pressures.

In the clinical setting, after patients are taken out of the 90o/90o kneeling position, our data show that blood pressures at the ankle decrease, with a subsequent increase in differential pressure. This would compound the potential risk for emerging compartment syndrome if the cycle of edema and ischemia, with corresponding increases in intramuscular pressure, would be initiated in the leg compartment during surgical positioning as an inciting event. In addition to differential pressure, time of ischemia is another important factor that contributes to the pathogenesis to acute compartment syndrome.

The referenced works of Heckman et al. and McQueen et al.(3,4), have theorized a critical threshold of differential pressure. The work of Heckman et al. establishes that there are areas of increased tissue pressure localized to limited areas of a compartment. This is consistent with our theory that there are areas in the dependent anterior compartment that create local hypoperfusion and elevated tissue pressure. Additionally, McQueen’s model measures diastolic pressure after a tissue insult, a tibia fracture. As mentioned above, our measurements of ankle blood pressures were taken during the inciting insult of the dependent tissue while in the 90o/90o kneeling position. This snapshot in time does not reflect conditions in an evolving compartment syndrome after the insult occurs and the leg is taken out of this position, thus significantly decreasing ankle blood pressure due to elimination of the leg’s dependent position. This is analogous to measuring differential pressure after this inciting insult of a tibia fracture occurs in the trauma setting.

Anecdotally, we would like to mention that in our heaviest subject (87 kg), in whom we measured the highest intramuscular anterior compartment pressures in the 90o/90o kneeling position of 61 mm Hg, this value never came to a steady state and continued to rise until we terminated the measurements at our maximal IRB approved time of twenty minutes. It should be noted that this was in an unanesthetized subject who was not undergoing clinical scenarios such as those elucidated by Dr. Whitesides which include “prolonged dependent positioning, additional dependent edema, hypotension, or other aspects,” that can further place a patient a risk. This increased risk of elevated tissue pressure in heavy patients again is consistent with Dr. Whitesides stated experience.

We believe that our paper has value because it demonstrates that compartment pressures are significantly elevated in the dependent anterior compartment of the 90o/90o kneeling position, a finding not seen in other operative positions. Additionally, we have shown a correlation between subject weight and anterior intramuscular pressures in the 90o/90o kneeling position affecting both absolute and differential pressure, which agrees with Dr. Whitesides point that overweight and muscular subjects are at increased risk for this complication. We agree that further study on local tissue environment would more completely explain this complication if there was clinical interest beyond our work.

References:

1. Whitesides TE Jr, Shuster JK. The kneeling frame and tibial compartment syndrome. Read at The Thirteenth Annual Meeting of the North American Spine Society: 1998 Oct 29; San Francisco, CA.

2. Meyer RS, White KK, Smith JM, Groppo ER, Mubarak SJ, Hargins AR. Intramuscular and blood pressures in legs positioned in the hemilithotomy position: clarification of risk factors for well-leg acute compartment syndrome. J Bone Joint Surg Am. 2002:84:1829-35.

3. Heckman MM, Whitesides TE Jr, Grewe SR, Rooks MD. Compartment pressure in association with closed tibial fractures. The relationship between tissue pressure, compartment, and the distance from the site of fracture. J Bone Joint Surg Am. 1994; 76: 1285-92.

4. McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures. The pressure threshold for decompression. J Bone Joint Surg Br. 1996; 78:99-104.

To the Editor:

In their recent article (1), Leek et al. have brought to our attention a somewhat rare but potentially real problem. The authors studied a group of six asthenic male volunteers, whose leg weight had been calculated, and who knelt in the 90°/ 90° position and two alternative positions for periods of 20 minutes. During that time the tissue pressure (TP) in one area of each of all four compartments was measured, but the axial location of the pressure measurements was not reported. It would appear that they assumed that the compartments acted as true hydraulic cylinders, having uniform tissue pressures throughout. The authors found that the measured pressure in only the anterior compartment in the 90°/ 90° position had a significantly higher mean pressure (30.8 ± 5.7 mmHg) and this value varied significantly with the weight of the leg (p=0.045). However, in neither of the positions nor in any compartment (even the anterior compartment in the 90°/ 90° position) did the measured pressure approach a pressure that would cause a compartment syndrome when compared to the diastolic pressure measured at the ankle. Thus, they did not experimentally explain the etiology of the occurrence of compartment syndrome in this position.

The fact that compartments after injury do not act as a hydraulic unit was shown by three separate studies, each using the Hargins causation model of plasma injection into the center of the compartment (2). Heppenstall et al. (3) in real time metabolic studies, performed P31 MRI measuring pH, pO2, and phosphocreatine stores at the area of pressure measurement. They demonstrated that the pressure differential (ΔP) theory is correct and noted that 10mmHg below diastolic is the point at which ischemic damage occurs, thus corroborating the pressure differential theory first proposed by Whitesides et al. (4,5), Heppenstall et al. (6) also found that at 20mmHg below diastolic, while pO2 and blood flow are diminished, phosphocreatine stores are not diminished and the muscle and neural tissue functionally survive thru 8 hours of such a state. Heckman et al. (7) and Matava, Seiler, et al. (8) both used the Hargins model but measured TP in the central area of injection as well as the proximal and distal locations areas. They also used localized histology, Doppler flow studies, etc, confirming the perfusion pressure differential theories relating to diastolic pressure to challenge the theory that a compartment always acts as a single hydraulic unit.

The segmental nature of the clinical picture of compartment syndrome in extremity injury was thoroughly settled, in my view, by Heckman et al. (9) in a prospective tibial fracture study that rebutted the theories presented by Hargens and Mubarak et al. (2 & 10). Heckman et al.(9). found that 75% of patients with acute closed tibial fractures who did not require fasciotomy had developed TP of 30mm.Hg or more in a compartment over a significant period of time, even up to 4 days, and developed no sequelae. This has been further corroborated by McQueen et al. (11). Also, more recent direct microscopic observation of capillary perfusion in controlled external pressure by Hartsock et al. (12) shows cessation of capillary flow at 25mmHg below mean arterial pressure (thus about 10mm.Hg below diastolic).

Despite the above evidence, Leek et al. (1) have assumed in this study that compartments act hydraulically, thus assuming that the weight of the leg acted equally against all areas of the table pad. They cite absolute pressure studies (2 & 10) to explain their inability in this study to demonstrate the mechanism of difficulty with this position. It is more likely that the explanation lies in overweight patients, prolonged dependent positioning, prominence of the anterior compartment muscles, additional dependent edema, hypotension, or other aspects that could lower the ΔP. As all reported clinical instances of this complication occurred in obese patients who underwent prolonged procedures in the 90/90 position (13, & 14), it would appear that the authors would have gotten more useful data if they had studied overweight and muscular subjects -- thus, with their modern force transducer matrix used in the 90°/ 90° position, they could measure TP only in areas of obvious high contact pressure

I agree with the authors that, with our current knowledge of this problem, it would be inappropriate to risk this position with a patient susceptible to this complication. Consideration of the established principles of circulatory physiology should be used in the positioning of surgical patients.

The author did not receive any outside funding or grants in support of his research for or preparation of this work. Neither he nor a member of his immediate family received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity. No commercial entity paid or directed, or agreed to pay or direct, any benefits to any research fund, foundation, division, center, clinical practice, or other charitable or nonprofit organization with which the author, or a member of his immediate family, is affiliated or associated.

References

1. Leek BT, Meyer RS, Wiemann JM, Cutak A. Macias BR, Hargens AR. The Effect of Kneeling During Spine Surgery on Leg Intramuscular Pressure. J Bone Joint Surg Am. 2007; 89:1941-1947.

2. Hargens AR, Schmidt DA, Evans KL, Gonsalves MR, Cologne JB, Garfin SR, Mubarak SJ, Hagan PL, Akeson WH. Quantitation of skeletal-muscle necrosis in a model compartment syndrome. J Bone Joint Surg Am. 1981; 63:631-6.

3. Heppenstall RB, Sapega AA, Scott R, Shenton D, Park YS, Maris J, Chance B. The compartment syndrome. An experimental and clinical study of muscular energy metabolism using phosphorus nuclear magnetic resonance spectroscopy. Clin Orthop Relat Res. 1988; 226:138-55.

4. Whitesides TE Jr, Harada H, Morimoto K. The response of skeletal muscle to temporary ischemia: an experimental study. J Bone Joint Surg Am. 1971:53:1027-8.

5. Whitesides TE Jr, Harada H, Morimoto K. Compartment syndromes and the role of fasciotomy, its parameters and techniques. AAOS Instructional Course Lectures 1977: 26; 179-196.

6. Heppenstall RB, Sapega AA, Izant T, Fallon R, Shenton D, Park YS, Chance B. Compartment syndrome; a quantitative study of high-energy phosphorus compounds using 31P-magnetic resonance spectroscopy. J Trauma. 1989; 19:1113-9.

7. Heckman MM, Whitesides TE Jr., Grewe SR, Judd RL, Miller M, Lawrence JH 3rd. Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model. J Orthop Trauma. 1993; 7: 199-210.

8. Matava MJ, Whitesides TE Jr., Seiler JG 3rd, Hewan-Lowe K, Hutton WC. Determination of the compartment pressure threshold of muscle ischemia in a canine model. J Trauma. 1994; 37:50-8

9. Heckman MM, Whitesides TE Jr, Grewe SR, Rooks MD. Compartment pressure in association with closed tibial fractures. The relationship between tissue pressure, compartment, and the distance from the site of fracture. J Bone Joint Surg Am. 1994; 76: 1285-92.

10. Zweifach SS, Hargens AR, Evans KL, Smith RK, Mubarak SJ, Akeson WH. Skeletal muscle necrosis in pressurized compartments associated with hemorrhagic hypotension. J Trauma 1980; 20:941-7.

11. McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures. The pressure threshold for decompression. J Bone Joint Surg Br. 1996; 78:99-104.

12. Hartsock LA, O’Farrell D. Seaber D, Urbaniak JR. The effect of increased compartment pressure on the microcirculation of skeletal muscle. Microsurgery. 1998; 18: 67-71.

13. Geisler FH, Laich DT, Goldflies M, Shepard A. Anterior tibial compartment syndrome as a positioning complication of the prone-sitting position for lumbar surgery. Neurosurgery. 1993:33:117.

14. Whitesides TE Jr, Shuster JK. The kneeling frame and tibial compartment syndrome. Read at The Thirteenth Annual Meeting of the North American Spine Society: 1998 Oct 29; San Francisco, CA

EDITOR'S NOTE: The authors were invited to respond to this letter, but to date, have not done so.

To the Editor:

In their recent article(1), Leek et al. have brought to our attention a somewhat rare but potentially real problem. The authors studied a group of six asthenic male volunteers, whose leg weight had been calculated, and who knelt in the 90°/ 90° position and two alternative positions for periods of 20 minutes. During that time the tissue pressure (TP) in one area of each of all four compartments was measured, but the axial location of the pressure measurements was not reported. It would appear that they assumed that the compartments acted as true hydraulic cylinders, having uniform tissue pressure throughout. The authors found that the measured pressure in only the anterior compartment in the 90°/ 90° position had a significantly higher mean pressure (30.8 ± 5.7 mmHg) and this value varied significantly with the weight of the leg (p=0.045). However, in neither of the positions nor in any compartment (even the anterior compartment in the 90°/ 90° position) did the measured pressure approach a pressure that would cause a compartment syndrome when compared to the diastolic pressure measured at the ankle. Thus, they did not experimentally explain the etiology of the occurrence of compartment syndrome in this position.

The authors do recognize that this study had limitations relative to the clinical situation that I described in a previous presentation to NASS(2). I personally operated on an overweight male patient (BMI=38.2) with very prominent leg musculature, performing in the 90°/ 90° position a difficult third repair of a lumbo-sacral problem that entailed a 5+ hour procedure. He developed significant left anterior compartment swelling overnight and 14 hours post-op had pain but no neural or motor deficit. Tissue pressures were measured every 5 cm. with the highest pressure peaking at 42mm.Hg in one area with BP of 126/72 (ÄP = 30 mm.Hg). The patient was observed and 2 hours later, still being neurologically intact with full motion, the same area of peak previous pressure had developed a pressure of 85mm.Hg with surrounding areas measuring from 42 to 48mm.Hg (Figs, 1 & 2). Fasciotomy was performed with a normal neurological and functional result(Fig. 3).

Two additional very large patients upon whom I performed relatively long procedures had bilateral anterior compartment swelling without pain immediately post-op with TP in both legs of 24-28mm.Hg in the peak areas. Both resolved within 2 hours to TP < 15mm.Hg with no symptoms or sequelae.

I was subsequently consulted for medico-legal defense in an instance of florid compartment syndrome involving use of the 90°/ 90° position. Suspecting a pattern, I obtained permission from the governance of NASS to carry out a survey of the then 1500 members requesting basic information with anonymity of the patients and confidentiality of the surgeon as there were already litigations against physicians, hospitals, and the manufacturer of the Andrews Frame and Table(OSI). Nineteen surgeons reported 20 patients with compartment syndrome diagnosed clinically; all were treated by fasciotomy. Three were bilateral. Fourteen patients had poor results (residual paralysis) and 6 had good results (no "foot drop"). There were 17 males with prominent anterior compartment musculature and an average weight of 123kg. (95-176kg.). The 3 females had an average weight of 93kg. Average operating time was 5.7 hours(3.5-8).

Thus, the pattern emerged of a uniformly obese and usually male patient with prominent musculature on whom a long procedure was performed in a kneeling 90°/ 90° position. To test this theory, three Emory staff male volunteers of differing body habitus(Fig. 4) knelt in the 90°/ 90° position onto ultra-sensitive engineering pressure test paper(Figs. 5, 6, & 7). One was tall and very thin with a BMI of 18.3, one was heavy with muscular but well rounded and padded legs and a BMI of 33.2, and another was short with abdominal adiposity and prominent leg musculature without adipose padding and a BMI of 29.8. Only the later(Fig. 8) had a localized high pressure area noted in either leg. This was over the prominent musculature in the mid-portion of the left anterior compartment. A "slit" catheter was inserted and, on 90°/ 90° repositioning, a TP of 72mmHg. was measured(Fig. 9 & 10). His systemic BP now, as then, is 124/74 and his ankle BP now in the 90°/ 90° position is 190/99. With a ÄP of 27mm.Hg to diastolic, this person might be at risk for muscle injury if a prolonged procedure, hypotension, dependant edema, etc occurred.

Our feeling was that the most efficient method of rapid surgeon and care-taker personnel education was that all owners of the Andrews table should be informed and be given brochures with the appropriate information to distribute to all involved personnel. The manufacturer strenuously objected and professed profound disbelief of the data. Due to the confidentiality involved and the multiple litigations in progress at that time (even by patients without resultant disability), this material was not published. It was, however, presented to the 1998 NASS Annual Meeting in San Francisco in more detail than appeared in the brief program abstract(2). Thus, there is objective data concerning the occurrence of this problem that would support the use of an alternative to the 90°/ 90° kneeling position in appropriate clinical situations. In fact, the use of the position has substantially decreased. At our institutions, it is rarely used, if at all.

While the group from UCSD has admitted the validity of the differential perfusion pressure theories in this and another recent paper(3), this was for decades not the case. Clinicians and researchers at Emory University established the differential perfusion pressure theory on extensive laboratory research in the late 1960's. Seasoned by significant clinical experience, this was disseminated extensively in the 1970's with presentation initially at AAOS in 1971(4) followed by ACS and other local and national podia along with publications(5,6,7) and convention exhibits. Annual AAOS Instructional Course presentations were first organized and given at the Las Vegas Meeting in 1973, and published in the AAOS Instructional Course Lecture Series, 1977(8). Fasciotomy was suggested as pressure approached 20mm. Hg below diastolic pressure as this was the obvious result of our research and had been validated by extensive clinical experience by myself and others. A definite time line of tolerated muscle ischemia was determined in the initial research and has been validated clinically in current cardiac practice and by those that perform peripheral vascular injury repair. This effort received an AAOS/ORS Kappa Delta Award in 1980. As noted in this paper(1), the UCSD group performed research in the 1970's suggesting that necrosis began at an absolute pressure level of 30mm.Hg and advised fasciotomy at this point(9). An absolute pressure of 20mm.Hg was suggested in the presence of hypotension(10). In these experiments, as in this current one, they apparently assumed that muscle compartments act as true hydraulic cylinders thus producing equal pressure throughout. Their experimental model was to inject plasma in a canine leg anterior compartment in the center of the compartment and measure TP at the proximal and distal ends -- at a distance from where the injection was occurring to cause elevation of the compartment pressure. As later shown, this led to erroneous results both in their technetium monitoring results and histologic studies.

Since Sir Herbert Seddon documented it in the forearm in 1956(11) and later in the leg(12), it also has been known from clinical experience in reconstructive surgery of post-compartment syndrome contractures that the infarct requiring resection is located in the area of the greatest injury to the muscle and often with adjacent remnant functional muscle.

The fact that segmental pressure gradients occur in this experimental model and, thus, that the compartment does not act as a hydraulic unit was shown by three separate studies, each using the Hargins causation model of plasma injection into the center of the compartment. Heppenstall et al, in real time metabolic studies, performed P31 MRI measuring pH, pO2, and phosphocreatine stores at the area of pressure measurement. They demonstrated that the pressure differential (ÄP) theory is correct and note that 10mmHg below diastolic is the point at which ischemic damage occurs (13). Also at 20mmHg below diastolic, while pO2 and blood flow are diminished, phosphocreatine stores are not diminished and the muscle and neural tissue functionally survive thru 8 hours of such a state(14). This effort received an AAOS/ORS Kappa Delta Award in 1986. Heckman et al.(15) and Matava, Seiler, et al.(16) both used the Hargins model but measured TP in the central area of injection as well as the proximal and distal locations areas. They also used localized histology, Doppler flow studies, etc, confirming the perfusion pressure differential theories relating to diastolic pressure and disproved the theory that a compartment acts as a single hydraulic unit.

The segmental nature of the clinical picture in extremity injury was thoroughly settled by Heckman et al.(17) in a prospective tibial fracture study that also disproved the absolute theories presented by Hargens and Mubarak et al.(9). They also found that 75% of those with acute closed tibial fractures who did not require fasciotomy had developed TP of 30mm.Hg or more in a compartment over a significant period of time and developed no sequelae. This has been further corroborated by McQueen et al.(18). Also, recent direct microscopic observation of capillary perfusion in controlled external pressure by Hartsock et al. shows cessation of capillary flow at 25mmHg below mean arterial pressure (thus about 10mm.Hg below diastolic)(19).

Despite the above evidence, Leek et al.(1) make the same assumption (that compartments acts hydraulically) in this study, thus assuming that the weight of the leg acted equally against all areas of the table pad. They also use the faulty 1970's absolute pressure studies(9,10) as a possible way to explain their inability in this study to demonstrate the mechanism of difficulty with this position. This is not acceptable with the current knowledge of circulatory dynamics. It is more likely that the explanation lies in overweight patients, prolonged dependent positioning, prominence of the anterior compartment muscles, additional dependent edema, hypotension, or other aspects that could lower the ÄP.

I agree with the authors that, with our current knowledge of this problem, it would be inappropriate to risk this position with a patient susceptible to this complication using current monitoring methods to definitively prove our theories. Consideration of the established principals of circulatory physiology should be used in the positioning of surgical patients.

Fig. 1. Left leg at time of localized anterior compartment high pressure measurement.

Fig. 2. Monitor showing measurement of 85mmHg.

Fig. 3. Standing 3 months post-op. A 12mm. area of muscle slough with delayed healing occurred at the area of highest pressure measurement.

Fig. 4. Three volunteers of differing body habitus.

Fig. 5. The large volunteer with BMI of 33.2 with well rounded and adipose padded leg in the 90°/90° kneeling position on pressure sensitive paper.

Fig. 6. Pressure sensitive paper of this subject showing no area of pressure concentration.

Fig. 7. Pressure sensitive paper of tall and lean subject with BMI of 18.3 showing only knee and tibial crest pressure.

Fig. 8. Pressure sensitive paper superimposed on area of increased pressure contact in subject with prominent musculature and BMI of 29.8.

Fig. 9. "Slit" catheter in place for monitoring.

Fig. 10. Subject in 90°/90° position with monitor reading 72mmHg.

References:

1. Leek BT, Meyer RS, Wiemann JM, Cutuk A, Macias BR, Hargens AR. The effect of kneeling during spine surgery on leg intramuscular pressure. J Bone Joint Surg Am. 2007;89:1941-1947.

2. Whitesides TE Jr, Shuster JK. The kneeling frame and tibial compartment syndrome. Read at The Thirteenth Annual Meeting of the North American Spine Society: 1998 Oct 29; San Francisco, CA.

3. Meyer RS, White KK, Smith JM, Groppo ER, Mubarak SJ, Hargins AR. Intramuscular and blood pressures in legs positioned in the hemilithotomy position: clarification of risk factors for well-leg acute compartment syndrome. J Bone Joint Surg Am. 2002:84:1829-35.

4. Whitesides TE Jr, Harada H, Morimoto K. The response of skeletal muscle to temporary ischemia: an experimental study. J Bone Joint Surg Am. 1971:53:1027-8.

5. Whitesides TE Jr, Haney TC, Morimoto K, Harada H. Tissue pressure measurements as a determinant for the need of fasciotomy, Clin Orthop Relat Res. 1975:113;43-51.

6. Whitesides TE Jr, Haney TC, Harada H, Holmes HE, Morimoto K. A simple method for tissue pressure determination. Arch Surg. 1975:110; 1311-3.

7. Whitesides TE Jr, Perdue GD, Smith RB. A simple direct method of measuring tissue pressure and its applications in ascertaining the necessity for fasciotomy. J Cardiovasc Surg. 1976:17; 83-4.

8. Whitesides TE Jr, Harada H, Morimoto K. Compartment syndromes and the role of fasciotomy, its parameters and techniques. AAOS Instructional Course Lectures 1977: 26; 179-196.

9. Hargens AR, Schmidt DA, Evans KL, Gonsalves MR, Cologne JB, Garfin SR, Mubarak SJ, Hagan PL, Akeson WH. Quantitation of skeletal-muscle necrosis in a model compartment syndrome. J Bone Joint Surg Am. 1981; 63:631-6.

10. Zweifach SS, Hargens AR, Evans KL, Smith RK, Mubarak SJ, Akeson WH. Skeletal muscle necrosis in pressurized compartments associated with hemorrhagic hypotension. J Trauma 1980; 20:941-7.

11. Seddon HJ. Volkmann's contracture; treatment by excision of the infarct. J Bone Joint Surg Br. 1956; 38: 152-74.

12. Seddon HJ, Volkmann's ischaemia in the lower limb. J Bone Joint Surg Br. 1966; 48: 627-636.

13. Heppenstall RB, Sapega AA, Scott R, Shenton D, Park YS, Maris J, Chance B. The compartment syndrome. An experimental and clinical study of muscular energy metabolism using phosphorus nuclear magnetic resonance spectroscopy. Clin Orthop Relat Res. 1988; 226:138-55.

14. Heppenstall RB, Sapega AA, Izant T, Fallon R, Shenton D, Park YS, Chance B. Compartment syndrome; a quantitative study of high-energy phosphorus compounds using 31P-magnetic resonance spectroscopy. J Trauma. 1989; 19:1113-9.

15. Heckman MM, Whitesides TE Jr., Grewe SR, Judd RL, Miller M, Lawrence JH 3rd. Histologic determination of the ischemic threshold of muscle in the canine compartment syndrome model. J Orthop Trauma. 1993; 7: 199-210.

16. Matava MJ, Whitesides TE Jr., Seiler JG 3rd, Hewan-Lowe K, Hutton WC. Determination of the compartment pressure threshold of muscle ischemia in a canine model. J Trauma. 1994; 37:50-8.

17. Heckman MM, Whitesides TE Jr, Grewe SR, Rooks MD. Compartment pressure in association with closed tibial fractures. The relationship between tissue pressure, compartment, and the distance from the site of fracture. J Bone Joint Surg Am. 1994; 76: 1285-92.

18. McQueen MM, Court-Brown CM. Compartment monitoring in tibial fractures. The pressure threshold for decompression. J Bone Joint Surg Br. 1996; 78:99-104.

19. Hartsock LA, O'Farrell D. Seaber D, Urbaniak JR. The effect of increased compartment pressure on the microcirculation of skeletal muscle. Microsurgery. 1998; 18: 67-71.