JBJS welcomes reader comments on published articles. Letters to the Editor are reviewed by JBJS editors but are not peer-reviewed. To submit your letter, please follow the "submit a response" link that appears in the content box at the upper right of the full text of the article.

Letters to the Editor to:

Scientific Articles:
Bryan T. Leek, R. Scott Meyer, John M. Wiemann, Adnan Cutuk, Brandon R. Macias, and Alan R. Hargens
The Effect of Kneeling During Spine Surgery on Leg Intramuscular Pressure
J Bone Joint Surg Am 2007; 89: 1941-1947 [Abstract] [Full text] [PDF]
*Letters to the Editor: Submit a response to this article

Electronic letters published:

[Read Letter to the Editor] Dr. Leek and colleagues respond to Dr. Whitesides, Jr.
Bryan Leek, R. Scott Meyer, and Alan R. Hargens   (8 September 2008)
[Read Letter to the Editor] Letter to the Editor
Thomas E. Whitesides, Jr. MD   (8 September 2008)

Dr. Leek and colleagues respond to Dr. Whitesides, Jr. 8 September 2008
Previous Letter to the Editor Top
Bryan Leek ,
R. Scott Meyer, and Alan R. Hargens

Send letter to journal:
Re: Dr. Leek and colleagues respond to Dr. Whitesides, Jr.

bleek{at}ucsd.edu Bryan Leek, et al.

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.
Letter to the Editor 8 September 2008
Next Letter to the Editor Top
Thomas E. Whitesides, Jr. MD,
Professor of Orthopaedics Emeritus
Emory University

Send letter to journal:
Re: Letter to the Editor

twhitesides{at}comcast.net Thomas E. Whitesides, Jr. MD

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