The Journal of Bone & Joint Surgery

The Journal of Bone & Joint Surgery, Volume 92, Issue 2

Scientific Articles | February 01, 2010

Physicians’ Ability to Manually Detect Isolated Elevations in Leg Intracompartmental Pressure

Franklin D. Shuler, MD, PhD¹; Matthew J. Dietz, MD¹

¹ Department of Orthopaedics, West Virginia University, P.O. Box 9196, Health Sciences Center, Morgantown, WV 26506-9196. E-mail address for M.J. Dietz: mdietz@hsc.wvu.edu

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Disclosure: In support of their research for or preparation of this work, one or more of the authors received, in any one year, outside funding or grants in excess of $10,000 from the Stryker Corporation, Kalamazoo, Michigan. Neither they nor a member of their immediate families received payments or other benefits or a commitment or agreement to provide such benefits from a commercial entity.

Investigation performed at the Department of Orthopaedics, West Virginia University, Morgantown, West Virginia

J Bone Joint Surg Am, 2010 Feb 01;92(2):361-367. doi: 10.2106/JBJS.I.00411

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Abstract

Background:

Serial physical examination is recommended for patients for whom there is a high index of suspicion for compartment syndrome. This examination is more difficult when performed on an obtunded patient and relies on the sensitivity of manual palpation to detect compartment firmness—a direct manifestation of increased intracompartmental pressure. This study was performed to establish the sensitivity of manual palpation for detecting critical pressure elevations in the leg compartments most frequently involved in clinical compartment syndrome.

Methods:

Reproducible, sustained elevation of intracompartmental pressure was established in fresh cadaver leg specimens. Pressures tested included 20 and 40 mm Hg (negative controls) and 60 and 80 mm Hg (considered to be consistent with a compartment syndrome). Each leg served as an internal control, with three compartments having a noncritical pressure elevation. Orthopaedic residents and faculty were individually invited to manually palpate the leg with a known compartment pressure and to answer the following questions: (1) Is there a compartment syndrome? (2) In which compartment or compartments do you believe the pressure is elevated, if at all? (3) Describe your examination findings as soft, compressible, or firm.

Results:

When a true-positive result was considered to be the correct detection of an elevation of intracompartmental pressures and correct identification of the compartment with the elevated pressure, the sensitivity of manual palpation was 24%, the specificity was 55%, the positive predictive value was 19%, and the negative predictive value was 63%. With increasing intracompartmental pressure, fasciotomy was recommended with a higher frequency (19% when the pressure was 20 mm Hg, 28% when it was 40 mm Hg, 50% when it was 60 mm Hg, and 60% when it was 80 mm Hg). When a true-positive result of manual palpation was considered to be an appropriate recommendation of fasciotomy, regardless of the ability of the examiner to correctly localize the compartment with the critical pressure elevation, the sensitivity was 54%, the specificity was 76%, the positive predictive value was 70%, and the negative predictive value was 63%.

Conclusions:

Manual detection of compartment firmness associated with critical elevations in intracompartmental pressure is poor.

Figures in this Article

Introduction

The diagnosis of compartment syndrome is based on the findings during serial physical examination, with direct measurements of intracompartmental pressure used as an adjunctive tool, particularly in obtunded patients^1-14. The classic physical examination findings associated with established compartment syndrome are pain out of proportion to the injury, increased pressure or firmness of a compartment, paralysis, and paresthesias^12,15-17. A highly sensitive test is preferred for the detection of compartment syndrome because of the substantial consequences of a missed diagnosis, including musculotendinous contractures, neurological deficits, amputation, organ failure resulting from rhabdomyolysis, and even death^11,18-20. Unfortunately, the sensitivity of clinical findings (pain, pain with passive stretch, paresthesia, and paresis) for the diagnosis of compartment syndrome is low (13% to 19%)⁶.

The ability to detect a critical elevation in intracompartmental pressure in an extremity prior to the onset of irreversible tissue ischemia is paramount for the timely diagnosis of compartment syndrome^1,18. The critical pressure threshold varies from patient to patient and depends largely on the degree of limb perfusion, the patient's diastolic blood pressure, and the individual's tolerance of increased tissue pressure^1,19,21,22. In animal models, the threshold at which cellular anoxia produces irreversible tissue damage occurs when intracompartmental pressures are elevated to within 20 mm Hg of the diastolic pressure^7,9,23. In the clinical setting, the pressure threshold for decompressive fasciotomy was determined initially by Whitesides et al.²⁴ and revised by McQueen et al.^1,8 using the relationship between the intracompartmental pressure and the diastolic blood pressure. Their findings established the threshold to be a difference of =30 mm Hg between the diastolic pressure and the anterior leg compartment pressure (delta P [?P]). Intracompartmental pressure has been reported to be variable and is highest at the level of the fracture site and in the anterior and deep posterior compartments of the leg^{1,3,8,10,22,25}.

The clinical diagnosis of compartment syndrome is complicated in an obtunded patient. An examination finding that would not be expected to change on the basis of mental status is the firmness of the compartment to palpation. Direct palpation of the leg is performed as part of the routine clinical examination when there is a high index of suspicion for compartment syndrome. To our knowledge, no study has addressed the sensitivity of direct palpation of the leg for detection of elevated compartment pressure. Our study was designed to establish the sensitivity of manual palpation for detection of critical elevations in isolated intracompartmental pressures in the leg.

Materials and Methods

By adapting animal and cadaver models produced by Moed and Thorderson and Teng et al., we created a cadaver model system capable of generating sustained and reproducible elevations in intracompartmental pressures in the leg^23,26,27. Five fresh, never-frozen cadavers were screened for evidence of previous surgery or injury to the lower extremities. Of these five cadavers, one was excluded from the study because radiographs demonstrated percutaneously placed hardware and a healed fracture in the distal part of the tibia. Four cadavers (eight legs) were used in the final protocol. The average age at the time of death was 74.5 years (range, sixty-five to eighty-seven years). Three of the donors were male, and one was female.

An uninterrupted fluid column was generated for each of the four leg compartments. Four 14-gauge angiocatheters were connected to intravenous tubing with Luer locks. These four tubing assemblies were connected to 1-L bags of normal saline solution and then inserted and secured by suturing into the anterior, lateral, superficial posterior, and deep posterior compartments of one cadaver leg. Different intracompartmental pressures were created by varying the fluid-column height (Fig. 1). An isolated intracompartmental pressure of 20, 40, 60, or 80 mm Hg was established in either the anterior or the deep posterior compartment^8,20, and the three remaining compartments remained at 20 mm Hg to act as internal controls. Twenty millimeters of mercury was chosen as the control pressure on the basis of the intracompartmental pressure measurements in uninjured human legs with the knee extended and the foot in a neutral position^25,27,28. After raising the fluid column to the appropriate height to produce sustained pressure elevations in the control and experimental compartments, we waited twenty minutes to allow for equilibration of the intracompartmental pressures. Direct intracompartmental pressure measurements (preliminary model validation with measurements at the proximal, middle, and distal compartmental levels) confirmed a consistent pressure throughout the entire compartment. In this study, intracompartmental pressures of 20 and 40 mm Hg were considered to not indicate a compartment syndrome, and pressures of 60 and 80 mm Hg were considered to be consistent with a compartment syndrome.

Fig. 1

Generation of sustained elevated compartment pressures. A: Changes in the height of the fluid column (1 L of normal saline solution) produce a steady-state pressure in the isolated compartment. The height (cm) producing the steady-state intracompartmental pressure (mm Hg) is shown. In our model system, a height of 54 cm produced an intracompartmental pressure of 40 mm Hg. All compartments other than the experimental one were maintained at a pressure of 20 mm Hg (a fluid column height of 30 cm)²³. Ant., Lat., SP, and DP = anterior, lateral, superficial posterior, and deep posterior compartments, respectively. B: Photograph of a fresh cadaver leg (the test specimen) with angiocatheters inserted and secured into the four leg compartments. The correct intracompartmental placement of the catheters was confirmed for all specimens by dissection following completion of the study protocol.

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On nonconsecutive days, a new cadaver model was prepared and the pressure of the experimental compartment (anterior or deep posterior) was elevated. Orthopaedic surgery residents and faculty members at a level-I trauma center were invited to palpate the cadaver lower extremity, which was described to them as a "single-limb model of a patient who is obtunded, with a blood pressure of 120/80." The participants were blinded with regard to the height of the fluid column and the other participants’ responses. They were asked three questions: (1) Is there a compartment syndrome? (2) In which compartment or compartments do you believe the pressure is elevated, if at all? (3) Describe your examination findings as soft, compressible, or firm. All compartment pressures were confirmed by direct pressure measurements with a calibrated and zeroed Stryker side-port needle manometer (Stryker, Kalamazoo, Michigan) before and after the participants’ physical examinations. The accuracy and reproducibility of this measurement method has been validated²⁹. After each day's testing, the placement of the angiocatheters into the correct compartment was confirmed by dissection and direct visualization. Of note, intracompartmental pressures of 60 and 80 mm Hg produced muscle bulging following fascial incision, which is consistent with intraoperative findings associated with a fascial release for an acute compartment syndrome in the leg. Additionally, elevated intracompartmental pressures did not alter adjacent compartment pressures; the control compartments remained at 20 mm Hg. Participants were individually escorted into the examination room and exited through a separate door to eliminate discussion of examination findings between participants and a possible bias.

Statistical Methods

A response was considered to be true-positive when the participant (1) detected an elevated intracompartmental pressure (60 or 80 mm Hg) and (2) correctly identified the compartment (anterior or deep posterior) with the elevated pressure. The response was defined as false-positive when the participant indicated that the pressure was elevated when in fact it was normal or that the increased pressure was located in a control compartment. A result was considered to be true-negative when the participant indicated "no compartment syndrome" in compartments with a pressure of 20 or 40 mm Hg, and it was considered to be false-negative when the volunteer answered "no compartment syndrome" with regard to compartments with a pressure of 60 or 80 mm Hg. Sensitivity, specificity, and the positive and negative predictive values were determined for the group as a whole and then for each subgroup: junior residents (in their first, second, or third postgraduate year), senior residents (in their fourth or fifth postgraduate year), and attending surgeons (board-certified/fellowship-trained).

Source of Funding

Our group received funding and two Stryker pressure manometers from the Stryker Foundation (Kalamazoo, Michigan). The research grant of $10,443 was used to purchase cadaveric specimens and materials needed to complete this research project.

Results

One hundred and thirty-six separate clinical examinations were performed over the defined range of leg intracompartmental pressures. Using the definition of a true-positive result as the correct detection of an elevated pressure and accurate localization to the experimental compartment, we found manual palpation to have a sensitivity of 24%, a specificity of 55%, a positive predictive value of 19%, and a negative predictive value of 63% (Tables I and II). There were no significant differences based on surgeon experience. Sixty-three examinations were performed by eight junior residents, and the sensitivity of those examinations was 26%, the specificity was 57%, and the positive and negative predictive values were 21% and 64%, respectively. Thirty-nine examinations were performed by six senior residents: the sensitivity was 23%, the specificity was 69%, the positive predictive value was 27%, and the negative predictive value was 64%. Thirty-four examinations were performed by five attending surgeons: the sensitivity was 22%, the specificity was 36%, the positive predictive value was 11%, and the negative predictive value was 56%.

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TABLE I Sensitivity, Specificity, and Positive and Negative Predictive Values for Ability of Palpation to Detect and Localize Isolated Elevated Compartment Pressure

	Sensitivity (%)	Specificity (%)	Positive Predictive Value (%)	Negative Predictive Value (%)
Overall	24	55	19	63
Junior residents	26	57	21	64
Senior residents	23	69	27	64
Attending surgeons	22	36	11	56

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TABLE I Sensitivity, Specificity, and Positive and Negative Predictive Values for Ability of Palpation to Detect and Localize Isolated Elevated Compartment Pressure

	Sensitivity (%)	Specificity (%)	Positive Predictive Value (%)	Negative Predictive Value (%)
Overall	24	55	19	63
Junior residents	26	57	21	64
Senior residents	23	69	27	64
Attending surgeons	22	36	11	56

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TABLE II Breakdown of True-Positive, False-Positive, True-Negative, and False-Negative Responses

	Condition Present
	+	-
Localized by palpation
+	10	43
-	31	52

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TABLE II Breakdown of True-Positive, False-Positive, True-Negative, and False-Negative Responses

	Condition Present
	+	-
Localized by palpation
+	10	43
-	31	52

It was possible for a participant to correctly identify a critical elevation of intracompartmental pressure (the presence of a compartment syndrome) but incorrectly localize this finding to a control compartment. This scenario would result in the recommendation for fascial release and therefore appropriate clinical management. When we changed the definition of a true-positive result by discounting the ability of the examiner to localize the pressure correctly and defined it only as the clinicians’ correct decision to perform a fasciotomy because of an elevated compartment pressure, the overall sensitivity increased to 54%, the specificity increased to 76%, the positive predictive value increased to 70%, and the negative predictive value remained the same.

The frequency of the recommendation for fasciotomy increased with increasing intracompartmental pressures (Fig. 2). The frequency with which an anterior compartment fasciotomy was recommended was 19% of the participants when the pressure was 20 mm Hg, 35% when it was 40 mm Hg, 45% when it was 60 mm Hg, and 56% when it was 80 mm Hg. The frequency with which a fasciotomy in the deep posterior compartment was recommended was 19% when the pressure was 20 mm Hg, 19% when it was 40 mm Hg, 56% when it was 60 mm Hg, and 64% when it was 80 mm Hg. One group (the attending surgeons) recommended fasciotomy in 100% of the cases in which the pressure was 80 mm Hg in the deep posterior compartment.

Fig. 2

Percentage of examinations resulting in a recommendation of fasciotomy, according to the pressure in either the anterior or the deep posterior compartment (A) and according to the seniority of the participant (B). The values in B are an average of the responses based on the examinations of the anterior and deep posterior compartments.

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The participants were also asked to qualify their clinical interpretation of firmness as soft, compressible, or firm (Table III). The participants described the compartment as soft in 59% of the cases in which the pressure was 20 mm Hg in either the anterior or the deep posterior compartment. They described the compartment as firm in only 45% of the cases in which the pressure was 80 mm Hg.

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TABLE III Description of Firmness of Compartment

Pressure (mm Hg)	Soft (%)	Compressible (%)	Firm (%)
20	59	31	9
40	29	57	13
60	12	47	44
80	20	33	45

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TABLE III Description of Firmness of Compartment

Pressure (mm Hg)	Soft (%)	Compressible (%)	Firm (%)
20	59	31	9
40	29	57	13
60	12	47	44
80	20	33	45

Discussion

Compartment firmness is a direct manifestation of increased intracompartmental pressure and it is the earliest and possibly only objective sign of early compartment syndrome³. Serial evaluation and physical examination is recommended when there is a high index of suspicion for compartment syndrome. During the examination, pain (including pain with passive stretch), pressure, paralysis, paresthesia, and pallor are assessed¹². Ulmer reported that the sensitivity of clinical findings (pain, pain with passive stretch, paresthesia, and paresis) for the diagnosis of compartment syndrome is low, ranging from 13% to 19%⁶. Pain, paralysis, and paresthesias cannot be assessed in obtunded patients. One physical examination finding that would not be expected to change with alterations in mental status and that would be thought to be present prior to the onset of tissue ischemia is compartment firmness. As shown here, palpation of compartment firmness is not a sensitive and reliable method for the noninvasive diagnosis of compartment syndrome.

In the group as a whole, manual palpation had a sensitivity of 54% and a specificity of 76% with regard to its ability to correctly identify critical elevations in intracompartmental pressures in the anterior and deep posterior compartments of the leg. Critical data analysis demonstrated a diminished sensitivity, specificity, and positive predictive value if the participant had to correctly identify the compartment responsible for the increased compartment firmness (sensitivity, 24%; specificity, 55%; and positive predictive value, 19%). As a result of the anatomical location of the deep posterior compartment, we would have expected more difficulty in assessing critical elevations of intracompartmental pressure in that compartment, but the data did not support that conclusion. When the intracompartmental pressure was 80 mm Hg in the deep posterior leg compartment, fasciotomy was recommended 64% of the time, whereas it was recommended 56% of the time when the pressure was 80 mm Hg in the anterior leg compartment.

It is important to note that, as intracompartmental pressures increased, the frequency of the recommendation for fasciotomy also increased. Manual palpation alone produced a high rate of false-positive results, with the participants recommending fascial release in 19% of the cases in which the pressure was 20 mm Hg and in only 60% of the cases in which it was 80 mm Hg. This corresponds well with the 45% frequency with which the compartment was described as firm to palpation when the pressure was 80 mm Hg (Table III). We expected surgeon experience to be an important variable; however, no significant differences in sensitivity and specificity were noted among junior residents, senior residents, and attending surgeons.

One concern about the data presented here is our use of a cadaver model system. This system does not provide a perfusion pressure, which is important for the clinical diagnosis of delta P and of compartment syndrome. Our model system also could not simulate the muscle tone and activation in a living patient. However, this model system would be analogous to the intraoperative assessment of compartment firmness in the setting of pharmacologic skeletal relaxation. An additional limitation of this study were the ages at the time of death (mean, 74.5 years) of the donors of the cadaver specimens from our Human Gift Registry. Our specimens had a corresponding decrease in muscle mass with noted thinning of the soft tissues, which would be expected to result in variability when these data are extrapolated to a younger or more obese population. These age-related changes are beneficial in this model system and represent a positive bias for the detection of fascial firmness. A decrease in the volume of the soft tissue between the fascia and skin should theoretically improve the detection of fascial firmness accompanying changes in intracompartmental pressures. An additional theoretical advantage in the cadaver model system is nontraumatized subcutaneous tissues. Swelling and inflammation of the subcutaneous tissues would be present in compartment syndrome associated with skeletal trauma. This additional barrier to assessment of compartment firmness would be expected to potentially decrease the clinical sensitivity of manual palpation. Our study would therefore be expected to have a positive bias in favor of improving the sensitivity of manual palpation for detecting fascial firmness because of the nontraumatized tissues. Our results clearly showed that, even with these added benefits in the model system, manual palpation still had poor sensitivity for detecting compartment firmness associated with critical elevations in intracompartmental pressure.

Our selection of 20 mm Hg for the control intracompartmental pressure deserves discussion. Gershuni et al. found that pressures in the anterior and deep posterior compartments of the legs of normal volunteers who had the knee extended varied depending on the position of the foot²⁸. They reported that, with full passive ankle dorsiflexion, the average pressures in the anterior and deep posterior compartments were 28 ± 5 mm Hg and 36 ± 4 mm Hg, respectively. Our cadaver specimens had full knee extension and a neutral foot position. A neutral foot position would be expected to decrease the baseline pressures in the anterior and deep posterior compartments compared with the pressures with full passive ankle dorsiflexion²⁸. Direct intracompartmental pressure measurements in uninjured human legs with knee extension and neutral foot flexion have been reported^25,27,28. Prayson et al. measured pressures within the anterior compartment in ten uninjured legs of patients with a contralateral leg fracture who were undergoing surgical repair. The pressures averaged 19.7 mm Hg (subset data analysis with raw data provided by M.J. Prayson)²⁵. Twenty millimeters of mercury was therefore set as the normal baseline pressure for the three control compartments in each leg tested in our study protocol.

The most important determinant of poor outcome from acute compartment syndrome is a delay in diagnosis. Compartment firmness is a fundamental finding in all cases of compartment syndrome in alert and obtunded patients. Firmness, a direct manifestation of increased intracompartmental pressure, is the earliest, and may be the only, objective finding of early compartment syndrome³. Previous studies have highlighted the low sensitivity of noninvasive physical examination for establishing this diagnosis^6,15,30-32. This study confirms that the sensitivity of manual palpation of compartmental firmness is poor for the detection of elevated intracompartmental pressures in the leg and should not be used in isolation. The most accurate readily available technique should be used to establish the diagnosis of compartment syndrome²⁹. We have challenged the assertion that the diagnosis of acute compartment syndrome is primarily clinical, especially in obtunded patients. We conclude that one should consider a more reliable means of assessing intracompartmental pressure in patients for whom there is a high index of suspicion for compartment syndrome and in obtunded patients with limited physical examination findings.

Acknowledgements

Note: The authors thank Nina Clovis, Vincent Kish, Suzanne Smith, Dr. Brian J. Cross, and Dr. Michael J. Prayson for their contributions to this project. They also thank all of the residents and faculty of the West Virginia University Department of Orthopaedics who participated in this research project.

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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.[PubMed]

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

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.[PubMed]

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 the fracture. J Bone Joint Surg Am. 1994;76:1285-92.[PubMed]

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Topics

compartment syndrome ; cadaver ; internship and residency ; palpation ; leg ; pressure-physical agent ; stupor ; fasciotomy ; medical residencies

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Franklin D. Shuler, MD, PhD

Posted on March 25, 2010

Drs. Shuler and Dietz respond to Drs. Steinberg, Gross, and colleagues

West Virginia University, Morgantown, West Virginia

We appreciate the comments from Drs. Steinberg, Gross, Mooney and Frick. Many of the items generated in these letters were addressed in the review process for manuscript publication. We are happy to provide the following additional information.

First, in response to Dr. Steinberg, the model system was a â€œfresh, never frozenâ€ model system as highlighted in the Materials and Methods. This fact addresses many of the concerns generated in your comments. Second, normal saline was used to establish the elevations in intra-compartmental pressures by adapting the animal and cadaveric model systems described by Moed and Thorderson and Teng et al. (1,2). Saline was chosen for our model system due to the relatively rapid examination protocol which was completed within 20 minutes following intracompartmental pressure equilibration. This short period of elevated pressure did not cause the production of subcutaneous edema due to the release of fluid into the subcutaneous tissues. Dissection was performed each day at the end of the testing protocol to ensure accurate intracompartmental placement of the angiocatheters. As stated in the article, "intracompartmental pressures of 60 and 80 mmHg produced muscle bulging following fascial incision...â€ We appreciate your comments and should have also stated that this dissection did not encounter subcutaneous fluid or tissue edema and therefore would not produce an impediment toward detecting fascial firmness. Finally, we strongly disagree with the third comment on cadaver age producing an â€œoverwhelmingly negative impact on the model.â€ Thin, elderly cadavers were selected to promote a â€œpositive biasâ€ for the detection of fascial firmness (other factors included non-traumatized tissues and potentially high prevalence of elevated compartment pressures). Our results clearly showed that, even with these added benefits, manual palpation has a poor sensitivity and poor positive predictive value for the detection of compartmental firmness associated with critical elevations in intracompartmental pressures.

In response to Drs. Gross, Mooney and Frick, sound scientific methodology was used in the experimental protocol. First, we agree that a cadaver model system for this clinical problem does have both strengths and weaknesses as addressed in the manuscript and in comments above. Second, the term â€œstiffsâ€ in your title would attract attention but over-dramatizes the true state of the fresh, never frozen cadaver specimens used in this experimental protocol. Fascial displacement and firmness was not tested in rigor mortis and would not be expected to be altered by livor mortis. Livor mortis is noted in the great toe in Figure 1B and refers to gravitational pooling of blood postmortem causing a red-purple discoloration of skin. This discoloration can blanch with pressure initially but, over time, the discoloration becomes fixed and unable to blanch with finger pressure. The statement made by Dr. Gross et al. that skin in these areas â€œcould not be depressed by finger pressureâ€ is false. Skin in areas of livor mortis are compressible and this does not present an impediment to detecting fascial firmness associated with elevations in intracompartmental pressures.

The comments and insight are appreciated. Following the discussion provided above, we feel that the fresh cadaver model system provided an adequate representation of a clinical process without inflicting pain or harm on volunteers. As for the medicolegal implications, this article in no way demonstrates a failure in our abilities to diagnose compartment syndrome; it simply highlights the limitations of manual palpation.

References

1. Moed BR, Thorderson PK. Measurement of intracompartmental pressure: a comparison of the slit catheter, side-ported needle, and simple needle. J Bone Joint Surg Am. 1993;75:231-5.

2. Teng AL, Huang JI, Wilber RG, Wilber JH. Treatment of compartment syndrome: transverse fasciotomy as an adjunct to longitudinal dermatofasciotomy: an in vitro study. J Orthop Trauma. 2005;19:442-7.

Matthew J. Dietz, MD

Posted on March 11, 2010

Drs. Dietz and Shuler respond to Dr. Schmidt

Department of Orthopaedics, West Virginia University, Morgantown, West Virginia

We appreciate Dr. Schmidtâ€™s comments on prevalence and its effect on predictive values. His statements support the conclusion that the physiciansâ€™ ability to manually detect critical elevations in intracompartmental pressure is poor using a cadaver model system and â€œeven worse in clinical useâ€.

In our article, the positive predictive value (PPV) describes the proportion of cadavers with critical elevations in intracompartmental pressures that were correctly detected by manual palpation. The formula used for this calculation is PPV = number true positives Ã· (number of true positives + number of false positives). This formula assumes that the ratio of the number of cadavers in the elevated compartment pressure group and the number of cadavers in the control group is equivalent to the reported prevalence of compartment syndrome. The prevalence of compartment syndrome varies significantly in the literature ranging from 2.7% to 35% (1-3). It was this prevalence variability that allowed us to report PPV and negative predictive value (NPV) in our paper because the tested prevalence of 30% (41 of 136 had elevated intracompartmental pressure) is not significantly different than the prevalence reported in the literature. However, we agree that if the prevalence of compartment syndrome is significantly lower than 30%, positive and negative likelihood ratios would have been reported.

We want to be clear that PPV is affected by the prevalence. However, the prevalence of compartment syndrome is affected by the decompression threshold used to establish the diagnosis. If a pressure threshold of 30mmHg is used to recommend fasciotomy, then the prevalence of compartment syndrome would be greater than using a pressure of 40mmHg or delta P (3,4). If the prevalence of clinical compartment syndrome is lower than in our model system, the following equations would be used:

PPV = (sensitivity)(prevalence)/ [(sensitivity)prevalence) + (1-specificity)(1-prevalence)]

NPV = (specificity)(1-prevalence)/ [(specificity)(1-prevalence) + (1-sensitivity)(prevalence)]

Using the prevalence data quoted by Dr. Schmidt, the reported positive predictive value would decrease from 19% to 6% and the negative predictive value would increase from 63% to 87%. This difference becomes even greater if the prevalence of compartment syndrome is lower than 10%. The model system used in our report had its strengths and weaknesses addressed in the manuscript. However, the model was designed to promote a â€œpositive biasâ€ for the detection of fascial firmness: non-traumatized tissues, thin elderly cadavers, and potentially high prevalence of elevated compartment pressures. Our results clearly showed that even with these added benefits, manual palpation has a poor sensitivity for the detection of compartmental firmness associated with critical elevations in intracompartmental pressures with the PPV and NPV affected by the selected definition of critical elevation requiring fascial release.

References

1. Moehring HD, Voigtlander JP. Compartment pressure monitoring during intramedullary fixation of tibial fractures. Orthopedics. 1995;18:631-5.

2. Mullett H, Al-Abed K, Prasad CV, Oâ€™Sullivan M. Outcome of compartment syndrome following intramedullary nailing of tibial diaphyseal fractures. Injury. 2001;32:411-3.

3. Ovre S, Hvaal K, Holm I, StrÃ¸msÃ¸e K, Nordsletten L, Skjeldal S. Compartment pressure in nailed tibial fractures. A threshold of 30mmHg for decompression gives 29% fasciotomies. Arch Orthop Trauma Surg. 1998;118:29-31.

4. Prayson MJ, Chen JL, Hampers D, Vogt M, Fenwick J, Meredick R. Baseline compartment pressure measurements in isolated lower extremity fractures without clinical compartment syndrome. J Trauma. 2006;60:1037-40.

Richard H. Gross, MD

Posted on February 23, 2010

Studying Compartmental Pressure in "Stiffs"

Medical University of South Carolina, Charleston, South Carolina

To the Editor:

The paper â€œPhysiciansâ€™ Ability to Manually Detect Isolated Elevations in Leg Intracompartmental Pressureâ€ may potentially have a substantial medicolegal impact. Therefore, one would expect sound scientific methodology supporting the authorsâ€™ conclusion that â€œManual detection of compartment firmness associated with critical elevations in intracompartmental pressure is poorâ€ (1).

The authors list two papers as references for describing their technique. Moed and Thorderson performed a study of the slit catheter using anesthetized dogs (2). Teng et al. used cadaveric human legs to study the merits of a transverse fascial incision compared with a longitudinal fascial incision, but noted, â€œa cadaveric model does not represent true living physiologic tissue and complex interplay that occurs during soft-tissue trauma and swelling that lead to compartment syndromeâ€ (3).

The authors make no mention of rigor mortis and livor mortis, well-known features of cadavers that dramatically alter the tactile properties of muscle and skin change after death. There are good reasons cadavers are called â€œstiffsâ€ (4). Classically, â€œrigor commences about 2 hours after death and it persists for some 30 hours or so before the muscles soften and the stiffness passes offâ€ (5).

Most important in regard to the current study is the question of â€œtextureâ€, which Bendall describes as â€œsoft and sticky before rigor and later becomes hard and dryâ€ (6). The only study we could find specifically addressing this issue was by a reference (in German) by Bendall to Mangold, in 1927, with a scientific method of compressing the muscle with a weighted steel ball. Not surprisingly, the texture is low for several hours, then becomes rapidly harder, followed by a slower decrease.

Livor mortis is secondary to postmortem pooling of blood, which appears to be present in the great toe and the anterior leg of Fig 1B (in the current paper). Sannohe studied this phenomenon in 19 cadavers, noting that the skin could not be depressed by finger pressure, but was compressible with a tweezers. He concluded that progressive immobility of intravascular red cell clumps was responsible (7).

We feel the authors must further justify the scientific methodology of this paper and question whether testing the ability to manually detect raised intracompartmental pressure should be performed on cadaver specimens.

The authors did not receive any outside funding or grants in support of their research for or preparation of this work. One or more of the authors, or a member of his or her immediate family, received, in any one year, payments or other benefits of less than $10,000 or a commitment or agreement to provide such benefits from a commercial entity (Synthes Spine). 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 authors, or a member of their immediate families, are affiliated or associated.

References

1. Shuler FD, Dietz MJ. Physicians' ability to manually detect isolated elevations in leg intracompartmental pressure. J Bone Joint Surg Am. 2010;92:361-7.

2. Moed BR, Thorderson PK. Measurement of intracompartmental pressure: a comparison of the slit catheter, side-ported needle, and simple needle. J Bone Joint Surg Am. 1993;75:231-5.

3. Teng AL, Huang JI, Wilber RG, Wilber JH. Treatment of compartment syndrome: transverse fasciotomy as an adjunct to longitudinal dermatofasciotomy: an in vitro study. J Orthop Trauma. 2005;19:442-7.

4. Goldblatt D. Stiffs. Semin Neurol. 1991;11:295-300.

5. Evans WED. The chemistry of death. Springfield, Il: Charles C. Thomas; 1963.

6. Bendall JR. Postmortem changes in muscle. In: Bourne GH, editor. The structure and function of muscle. 2nd ed. New York: Academic Press; 1973. p 243-309.

7. Sannohe S. Change in the postmortem formation of hypostasis in skin preparations 100 micrometers thick. Am J Forensic Med Pathol. 2002;23:349-54.

Bruce Steinberg, MD

Posted on February 22, 2010

Detection of Compartment Syndrome by Palpation Cannot be Accurately Tested with a Cadaver Model

Jacksonville Orthopaedic Institute, Jacksonville, Florida

To the Editor:

I have recently read the article, â€œPhysiciansâ€™ Ability to Manually Detect Isolated Elevations in Leg Intracompartmental Pressure,â€ (1). The study â€œwas performed to establish a sensitivity of manual palpation for detecting critical pressure elevations in the leg compartments most frequently involved in clinical compartment syndrome.â€ Unfortunately, for multiple reasons, a fresh frozen cadaver model cannot be used to accurately determine if this clinical examination is effective. The authors should consider several human volunteer in-vivo models that have been utilized to simulate compartment syndrome (2-5).

In a living individual when muscle hardness is quantitatively tested, a curve is formulated of pressure applied to indentation distance (2). This curve has been described previously with a spring model (6). When the examiner palpates a limb muscle compartment, the digit is pressed into the compartment, the examiner senses the difference between normal muscle and the same muscle becoming harder as it is compacted. In living individuals, when the intracompartmental pressure is increased, the quantitative hardness curves change with the mid-portion of the curve becoming similar to the muscle compaction characteristic. In addition, the slope of the curve becomes greater, indicating the need for more force for indentation (2). With the cadaver model, this differential of hardness does not take place. When a quantitative hardness curve is obtained in a fresh frozen cadaver limb, the curve is close to linear after the compression of subcutaneous tissue. In the living model, the curves are curvilinear, becoming more linear as the intramuscular pressure increases. This could be the reason why close to 40% of the attendingsâ€™ examinations (most experienced examiners) in the study at 20 mmHg resulted in the recommendation of fasciotomy.

Another criticism of the model is that, when normal saline is used as the injectable into a compartment, it diffuses through the fascial membrane quickly leading to edema of the subcutaneous tissue especially at the higher pressures which distorts the examination. Another choice for injectable is outdated blood bank plasma. This seems to work better because of the higher osmolarity of the fluid (7).

Another weakness of the cadaver model is that the average age was 74.5 years. Individuals who develop compartment syndrome are usually males between the ages of 18 and 40 years (8-12). The decreased elasticity of fascia and skin along with decreased muscle bulk with the significantly higher age combined with a nonliving specimen, certainly has an overwhelming negative impact on this model.

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. Shuler FD, Dietz MJ. Physicians' ability to manually detect isolated elevations in leg intracompartmental pressure. J Bone Joint Surg Am. 2010;92:361-7.

2. Steinberg BD. Evaluation of limb compartments with increased interstitial pressure. An improved noninvasive method for determining quantitative hardness. J Biomech. 2005;38:1629-35.

3. Clayton JM, Hayes AC, Barnes RW. Tissue pressure and perfusion in the compartment syndrome. J Surg Res. 1977;22:333-9.

4. Willy C, Gerngross H, Sterk J. Measurement of intracompartmental pressure with use of a new electronic transducer-tipped catheter system. J Bone Joint Surg Am. 1999;81:158-68.

5. Wiemann JM, Ueno T, Leek BT, Yost WT, Schwartz AK, Hargens AR. Noninvasive measurements of intramuscular pressure using pulsed phase-locked loop ultrasound for detecting compartment syndromes: a preliminary report. J Orthop Trauma. 2006;20:458-63.

6. Horikawa M, Ebihara S, Sakai F, Akiyama M. Non-invasive measurement method for hardness in muscular tissues. Med Biol Eng Comput. 1993;31:623-7.

7. Steinberg BD, Gelberman RH. Evaluation of limb compartment with suspected increased interstitial pressure. A noninvasive method for determining quantitative hardness. Clin Orthop Relat Res. 1994;300:248-53.

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

9. Shadgan B, Menon M, Oâ€™Brien, PJ, Reid WD. Diagnostic techniques in acute compartment syndrome of the leg. J Orthop Trauma. 2008;22:581-7.

10. Sheridan GW, Matsen FA 3rd. Fasciotomy in the treatment of the acute compartment syndrome. J Bone Joint Surg Am. 1976;58:112-5.

11. Simpson NS, Jupiter JB. Delayed onset of forearm compartment syndrome: a complication of distal radius fracture in young adults. J Orthop Trauma. 1995;9:411-8.

12. Matsen FA 3rd, Winquist RA, Krugmire RB Jr. Diagnosis and management of compartment syndromes. J Bone Joint Surg Am. 1980;62:286-91.

Andrew H. Schmidt, MD

Posted on February 17, 2010

Clinical Predictive Value of Manual Detection of Elevated Intracompartmental Pressure

Hennepin County Medical Center, Minneapolis, Minnesota

To the Editor:

I read with interest the article by Shuler and Dietz regarding the ability of physicians to detect elevated intracompartmental pressure by manual palpation (1). The authors of this paper report the sensitivity, specificity, and positive and negative predictive values of manual palpation in recognizing cadaver legs with intracompartmental pressures of either 60 or 80 mm Hg (considered to represent the presence of compartment syndrome) compared to legs with lower pressures of 20 or 40 mm Hg (considered to represent absent compartment syndrome). Although I agree with their conclusion that manual detection of significantly elevated intracompartmental pressure is poor, I think that the positive predictive value of this diagnostic test is likely to be even worse in clinical use than what they found in their model.

In their discussion, the authors did not mention that the prevalence of â€œcompartment syndromeâ€ among their cadaver legs was 30% (41 of 136), which is higher than in most actual clinical situations. Since prevalence affects the calculation of predictive values, the predictive values reported by the authors are different than what would be the case in a clinical situation. In a patient with a tibia fracture, a realistic number to use for the prevalence of acute compartment syndrome might be 5% or 10%. Thus, assuming the same sensitivity and specificity of the exam, in real-life the positive predictive value will be lower and the negative predictive value higher than what the authors report. For example, if one uses a prevalence of acute compartment syndrome in a patient with a tibial shaft fracture of 10% instead of 30%, the positive predictive value becomes 6% (instead of the 19% reported) and the negative predictive value becomes 87% (instead of 63% reported). The difference becomes even greater if the prevalence of compartment syndrome is less than 10%. These estimates of the positive and negative predictive value of manual detection of elevated compartment pressure in a more realistic clinical situation further support the authors' conclusion that manual detection of critical elevation in compartment pressure of the leg is poor, although determining which legs do not have elevated compartment pressure is fairly easy.

The author did not receive any outside funding or grants in support of his research for or preparation of this work. The author, or a member of his immediate family, received, in any one year, payments or other benefits in excess of $10,000 or a commitment or agreement to provide such benefits from a commercial entity (Twin Star Medical, Medtronic, DGIMed, Smith & Nephew, Thieme Inc.). 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.

Reference

1. Shuler FD, Dietz MJ. Physicians' ability to manually detect isolated elevations in leg intracompartmental pressure. J Bone Joint Surg Am. 2010;92:361-7.

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Franklin D. Shuler, Matthew J. Dietz; Physicians’ Ability to Manually Detect Isolated Elevations in Leg Intracompartmental Pressure. The Journal of Bone & Joint Surgery. 2010 Feb;92(2):361-367.

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