Download Diagnostic Techniques in Acute Compartment

CURRENT STATE
OF THE
ART
Diagnostic Techniques in Acute Compartment Syndrome
of the Leg
Babak Shadgan, MD, MSc,*† Matthew Menon, MD, FRCSC, MHSc,‡ Peter J. O’Brien, MD, FRCSC,‡
and W. Darlene Reid, BMR (PT) PhD†§
Objectives: To review the efficacy of the current diagnostic
methods of acute compartment syndrome (ACS) after leg fractures.
Data Sources: A Medline (PubMed) search of the English literature
extending from 1950 to May 2007 was performed using ‘‘compartment syndromes’’ as the main key word. Also a manual search of
orthopaedic texts was performed.
Study Selection and Extraction: The results were limited
to articles involving human subjects. Of 2605 primary titles, 489
abstracts limited to compartment syndromes in the leg and 577
articles related to the diagnosis of compartment syndromes were
identified and their abstracts reviewed. Further articles were identified
by reviewing the references. Sixty-six articles were found to be
relevant to diagnostic techniques for compartment syndrome in the
leg and formed the basis of this review.
Conclusions: Early diagnosis of an ACS is important. Despite its
drawbacks, clinical assessment is still the diagnostic cornerstone of
ACS. Intracompartmental pressure measurement can confirm the
diagnosis in suspected patients and may have a role in the diagnosis
of this condition in unconscious patients or those unable to cooperate.
Whitesides suggests that the perfusion of the compartment depends
on the difference between the diastolic blood pressure and the intracompartmental pressure. They recommend fasciotomy when this
pressure difference, known as the Dp, is less than 30 mm Hg. Access
to a precise, reliable, and noninvasive method for early diagnosis of
ACS would be a landmark achievement in orthopaedic and emergency medicine.
Key Words: compartment syndromes, leg injuries, tibial fractures,
diagnosis, diagnostic methods
(J Orthop Trauma 2008;22:581–587)
Accepted for publication January 12, 2008.
From the *Experimental Medicine, University of British Columbia,
Vancouver, British Columbia, Canada; †Muscle Biophysics Laboratory,
Vancouver Coastal Health Research Institute, Vancouver, British
Columbia, Canada; ‡Trauma Orthopaedic Division, Department of
Orthopedics, University of British Columbia, Vancouver, British
Columbia, Canada; and §Department of Physical Therapy, University
of British Columbia, Vancouver, British Columbia, Canada.
Reprints: Babak Shadgan, MD, MSc, Muscle Biophysics Laboratory, VGH
Research Pavilion, 617-828 W. 10th Avenue, Vancouver, British
Columbia, Canada V5Z 1L8 (e-mail: [email protected]).
The authors did not receive grants or outside funding in support of their
research or preparation of the manuscript.
Copyright Ó 2008 by Lippincott Williams & Wilkins
J Orthop Trauma Volume 22, Number 8, September 2008
INTRODUCTION
Acute compartment syndrome (ACS) is a clinical condition characterized by the increase of pressure within a closed
anatomic space, resulting in a lack of local perfusion to the
tissues within this space.1–3 If untreated, the lack of perfusion
results in irreversible damage to the tissues in the affected
compartment. The results of an unrecognized or untreated
compartment syndrome of the leg include pain, paralysis,
paresthesia, and muscle necrosis with possible rhabdomyolysis. The potential disability associated with a neglected
compartment syndrome is usually irreversible.
Compartment syndrome has been reported in a wide
variety of traumatic and nontraumatic clinical scenarios. The
most common injury resulting in a compartment syndrome is
a fracture of the tibial diaphysis due to the relatively high
incidence of this fracture and the anatomic environment of
closed fascial spaces found in this area.1,3,4–6 This differentially
affects young active individuals.7,8 Permanent disability in this
particular group of patients can place a large burden on the
individual, society, and, often, our medicolegal system.9,10
The reported incidence of compartment syndrome varies
due to differing diagnostic criteria, sampling methods, and
patient populations.1–3,5,11 Reported incidence of compartment
syndrome after tibial fractures ranges from 1.2% to 30.4%.5,12
The incidence is greater in men and in those younger than
35 years. Thirty-six percent of all compartment syndromes
occur after tibial diaphyseal fractures.7 Fractures of the tibial
plateau only develop a compartment syndrome in 3% of cases.4
Treatment of a compartment syndrome consists of
immediate and complete fasciotomy of all fascial compartments involved. In the leg, this involves all 4 anatomic compartments. Wounds are left open for a minimum of 48 hours or
until the compartment syndrome is resolved. Direct closure of
the fasciotomy wounds is attempted; however, plastic surgical
techniques are often required. Delay in the diagnosis or
treatment of the syndrome results in permanent disability.
Therefore, the ability to diagnose a compartment syndrome in
a timely manner, before the onset of irreversible ischemic
changes, is crucial to prevent permanent disability.3,5,13
The first sign of a compartment syndrome is excessive
pain disproportionate to the severity of injury in an at-risk
patient. If untreated, paresthesia and paralysis occur. The timing between these symptoms is variable.14 Clinical examination of the patient reveals palpable tightness, an increase in
pain on passive stretch of the compartment involved, progressive paresthesia, and eventually paralysis. The clinical
picture is variable and often only a few signs are present.
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Shadgan et al
Observation of a patient with a developing compartment
syndrome can lead to a delay in diagnosis and treatment. This
delay possibly contributes to permanent disability. Ischemic
contracture complicating tibial fractures has been estimated to
occur in up to 2% of cases.15 Only 13% of patients with
paralysis at the time of their diagnosis recover from this
impairment.2
Health-related quality of life is reported to be decreased
after compartment syndrome of the leg. Giannoudis et al
reported a significant detriment in health-related quality of life,
as measured by the EQ-5D (EuroQol) tool,16 in patients who
had undergone fasciotomy and required a skin graft or those
who had longer closure times.10. Vandervelpen et al showed
that 1 in 4 patients undergoing leg fasciotomies reported late
functional disabilities.17 Fitzgerald et al, who reported on
the sequelae of fasciotomy wounds, found symptoms related to
the skin wounds in up to 77% of patients who had undergone
fasciotomy of the upper or lower limb.18
DIAGNOSIS
Little debate exists as to the necessity of a thorough and
immediate fasciotomy once a compartment syndrome has been
diagnosed. Nor is there disagreement when a clear presentation of clinical signs of compartment syndrome is present
in a high-risk patient. However, diagnosis is often difficult in
patients who cannot give a clear history or participate in
a rigorous clinical examination. This includes children, those
with concomitant neurological injury, the critically ill, and
patients under prolonged general anesthesia. In these patients,
intracompartmental pressure measurements have been used
to screen for the development of compartment syndrome
when clinical examination is either unreliable or equivocal.
Several methods have been investigated as possible diagnostic
adjuncts in the early identification of an ACS. A reliable
screening tool to diagnose a developing compartment syndrome would provide the opportunity to intervene early and
avoid the sequelae of a delayed diagnosis. Although further
investigation is needed, several of these techniques show
promise (Fig. 1).
Pressure Measurements
Whitesides et al19 were the first to apply compartment
pressure measurement to the diagnosis of ACS. Since then,
several techniques have been described, each with limitations
that restrict their reliability or practical use. These include the
needle manometer, the wick catheter, and the slit catheter.19–22
The Stryker intra-compartmental pressure monitor system
(STIC) has become popular as a handheld portable device
that is easily used in a variety of settings without the need for
complex equipment. Continuous pressure monitoring is available by attaching a reliable catheter to an arterial transducer
system.2,5,23 This allows a continuous readout of the pressure
in the compartment and allows us to observe changes over
time. Although there is some technical learning required for
its accurate use, compartment pressure measurements have
been successfully used clinically as an adjunct to clinical
examination.24
Traditionally, the diagnosis of a compartment syndrome
has been on clinical criteria, with objective pressure measurements used as an adjunct for equivocal cases because the
clinical picture is rarely complete. The pressure threshold that
is diagnostic of compartment syndrome has been debated at
length. Experts have advocated fasciotomy for absolute
FIGURE 1. This algorithm shows the
application of ACS diagnostic methods based on ACS pathophysiological stages.
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Diagnostic Techniques in Acute Compartment Syndrome of the Leg
compartment pressures from 30 to 45 mm Hg.1,2,25 This threshold for diagnosis is likely too aggressive and subjects more
patients unnecessarily to fasciotomy and the risks associated
with it. McQueen et al26 have shown that an increase in
compartment pressure after tibial nailing is expected even
without the development of a frank compartment syndrome.
Whitesides et al astutely suggest that the perfusion of the
compartment depends on the difference between the patient’s
blood pressure and the compartment pressure and recommends fasciotomy when the compartment pressure rises to
within 30 mm Hg of the diastolic blood pressure, known as the
Dp (,30 mm Hg).19 White et al27 have shown that an elevated
intramuscular pressure alone is not diagnostic of a compartment syndrome after tibial intramedullary nailing as long as
the Dp remains greater than 30 mm Hg. The use of the Dp has
been consistently shown to be a more reliable indicator of the
conditions necessary to produce a compartment syndrome
than the compartment pressure alone.24,26,27 It also allows
a more reflective measure in patients with abnormal
physiology, such as shock or hypertension.
One difficulty encountered in the development of pressure thresholds for the diagnosis of compartment syndrome is
the lack of gold standard diagnostic criteria for the condition.
A collection of clinical symptoms and signs in experienced
hands serves as the diagnostic criteria in most circumstances.
Attempts to objectify the diagnosis for purposes of validation
of measurement techniques have been made but are not
universally accepted. These include the bulging of muscle
compartments on fasciotomy, and second, clinical follow-up
looking for the sequelae of the syndrome.24,28,29 The first of
these is often dismissed as nonspecific, and the latter does not
allow the identification of successfully treated cases.
Some authors have argued that because a rise in
compartment pressure must occur before the development of
a compartment syndrome, an objective pressure measurement
can diagnose a compartment syndrome before the onset of
symptoms and before the development of irreversible sequelae
of the syndrome. Thus, fasciotomy based on continuous pressure measurements for the ‘‘impending’’ compartment syndrome should be the most appropriate treatment so long as the
measurements are adequately sensitive and specific to the
development of a full compartment syndrome. This approach
has been shown to be effective in clinical practice by McQueen
et al24 who reported that no compartment syndromes were
missed in a large prospective series using a Dp of ,30 mm Hg
as the diagnostic criteria for its presence. Despite the apparent
success reported by McQueen et al,30 continuous pressure
monitoring has not become the standard treatment in most
centers. Recently, a prospective randomized trial has attempted
to evaluate the addition of continuous pressure monitoring to
current clinical diagnostic criteria.31The recent development of
a handheld fiber-optic transducer system that uses a unicrystalline piezoelectric semiconductor has eliminated some of the
practical concerns of calibration and blockage that occurred
frequently with catheter-based systems.31
Generalized inflammatory biomarkers such as an elevated
white blood cell count or a positive erythrocyte sedimentation
rate cannot specifically indicate the occurrence of a compartment syndrome.32 Creatine kinase (CK), myoglobin (Mb), and
fatty acid–binding protein (FABP) are low–molecular mass
cytoplasmic proteins present in the myocardial muscles and
skeletal muscles. These proteins have been introduced as
plasma markers for the early detection of myocardial infarction, but at the same time, each of them show similar plasma
release curves after skeletal muscle injury and necrosis. After
skeletal muscle injury, both MB and FABP concentration
significantly increase after 30 minutes, whereas CK concentration reaches a maximum after 2 hours. Both MB and FABP
return to the baseline values at 24 hours after injury, whereas
CK remains elevated for at least 48 hours.33,34 It has been
shown that after intracompartmental ischemia when muscle
necrosis occurs, serum level of CK dramatically increases. It is
recommended that CK values more than 2000 units/L after
surgery can be a warning sign of ACS in ventilated and sedated
patients.35 Compared with the myocardium, the Mb content in
skeletal muscle is higher and the FABP content is lower. The
ratio of MB/FABP in the same blood sample is a useful index
to determine the origin of the proteins. Normal Mb/FABP ratio
in myocardial muscles is about 5 and in skeletal muscle is
more than 20.36 Frequent measurements of these parameters
beginning shortly after tibial fractures could theoretically alert
us to the development of a compartment syndrome; however,
when used clinically, they may not be specific enough to
differentiate between direct skeletal muscle injury due to
trauma, ACS, or myocardial injury.
Anaerobic metabolism of muscle cells within the
ischemic compartment in the early stages of an ACS produces
a high amount of lactic acid. This elevated concentration of
lactate results in a reduced serum pH and may be an indicator
of ACS. However, it is not specific. Measurement and comparison of the local lactate concentrations from the affected
and healthy limbs may increase the specificity rather than
monitoring the plasma lactate level.37
Ischemic modified albumin (IMA) is a relatively new
marker of myocardial ischemia, and IMA concentration can
also be affected by skeletal muscle ischemia.38 An immediate
and transient decrease in plasma concentration of IMA is
reported after skeletal muscle ischemia39 that returns to baseline 1 hour after the initial decrease. Such a transient decrease
in IMA concentration in patients experiencing angina might be
falsely attributed to only myocardial ischemia rather than
potentially arising from a developing ACS. This measure cannot
be a reliable and specific measure for early diagnosis of ACS.
There is no report of a coenzyme or a biomarker specific
to skeletal muscle ischemia to date. Detection of a sensitive
and specific biomarker for skeletal muscle ischemia that is not
influenced by inflammation or tissue injury from trauma would
be a tremendous accomplishment in diagnosis of ACS.
Therefore, more investigation is required.
Biomarkers
Magnetic Resonance Imaging
The traumatic injury associated with tibial fractures and
ACS result in the early onset of inflammatory markers.
Magnetic resonance imaging (MRI) is able to detect soft
tissue edema and swollen compartments on T1-weighted
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spin-echo images.40 However, MRI cannot differentiate the
edema of affected muscles in a compartment syndrome from
the edema of soft tissue injury after trauma.41 MRI can show
the tissue changes in an established compartment syndrome in
a very late stage but fails to identify early changes of an ACS.
MRI is a sensitive and noninvasive diagnostic tool, but the role
of this technology in early diagnosis and monitoring of the
ACS is limited.
Ultrasound
Ultrasonography is a noninvasive diagnostic intervention that can visualize and monitor soft tissue structure and
motion. Several investigators have tried to assess the geometry
and echogenicity of the affected muscles for an early diagnosis
of compartment syndrome by standard sonographic methods
with no consistent success.42 A new ultrasonic intervention
called pulsed phase–locked loop (PPLL) may be useful in the
diagnosis of compartment syndrome.43,44 This technique was
initially developed by Ueno et al45 as a noninvasive method to
monitor intracranial pressure. The PPLL ultrasound is a lowpower ultrasonic device designed to detect submicrometer
displacements between the ultrasound emitter on the skin
surface and any targeted tissue that can reflect the ultrasound
waves.43 The device transmits an ultrasonic wave through the
tissue via a small transducer placed on the skin surface. The
depth of penetration of the ultrasonic waves is set to reach
a specific tissue. The transmitted waves reflect off the targeted
tissue and are received by the same transducer. The PPLL
ultrasound locks on to a characteristic reflection that comes
from a specific tissue. PPLL ultrasound detects the very subtle
movements of fascia that correspond to local arterial pulsation.
These waveforms have a characteristic shape in the normal
compartment. The increased Intracompartmental Pressure
(ICP) during compartment syndrome causes a reduction in
normal fascial displacements in response to arterial pulsation
that decreases the complexity of the fascial displacement
waveform.44 To refine its interpretation, the limitations of this
method such as the effect of possible variations of fascial
movements indicative of normal physiology and anatomy
should be identified. As a noninvasive monitoring device, PPLL
may be a promising method for the early diagnosis of ACS;
however, it requires more investigation.
Scintigraphy
Scintigraphy is a radionuclide imaging intervention.
A 2-dimensional image is obtained after injection of a soluble
radioisotope to evaluate regional perfusion. Scintigraphy
differs from most other imaging methods because it primarily
shows the physiological function of the system being investigated as opposed to its anatomy. It is mostly used to study
myocardial perfusion and peripheral vascular obstructions.
Edwards et al have studied the efficacy of scintigraphy in the
diagnosis of chronic exertional compartment syndrome
(CECS). They reported a sensitivity of 80% and a specificity
of 97% for detection of CECS by using 99-technetium (99Tc)methoxyisobutilisonitrile (MIBI) scintigraphy. They concluded that 99Tc-MIBI can detect compartment syndromes
with good positive and negative predictive values.46 A major
strength of this method is that all 4 compartments of leg can be
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monitored simultaneously. In addition, it is a simple, cheap,
and minimally invasive method. The use of scintigraphy in
ACS is limited by the time required to perform this type of
investigation, the potential lack of specificity in the
traumatized limb, and the inability to perform repeated or
continuous examinations.47
Laser Doppler Flowmetry
Laser Doppler flowmetry (LDF) is a well-developed
technique for the real-time measurement of microvascular
perfusion in tissue. This velocimetry method is based on the
‘‘Doppler effect’’ that describes the shift in the frequency of
a sound or light wave when the wave source and/or the receiver
is moving.48 LDF works by illuminating the tissue with lowpower laser light based on local red blood cell circulation.
Light from 1 optical fiber is scattered by moving red blood
cells. Another optical fiber collects the backscattered light. By
analyzing the differences between the reflected and returned
signals, a functional image is obtained. It is a noninvasive and
highly sensitive method for continuous monitoring of local
blood perfusion. Despite all the advantages, only 1 study has
been performed to assess the capability of this method in
diagnosis of ACS. In that study, Abraham et al49 successfully
used LDF in the diagnosis of CECS. Although there is no
documented experience of using this method for the diagnosis
of ACS, the technique shows potential and requires further
research.
Near-Infrared Spectroscopy
The pathophysiologic mechanism in ACS is an increased
ICP compromising microvascular flow within the affected
compartment that leads to an acute intracompartmental hypoxia
and muscle necrosis. Near-infrared spectroscopy (NIRS) is an
optical technique that can determine the redox state of various
light-absorbing molecules such as hemoglobin. Its function is
based on the relative tissue transparency for light in the nearinfrared spectrum and on the absorption changes of hemoglobin
and Mb when they are in their oxygenated versus deoxygenated
states.50 Based on the different light absorption properties,
NIRS can measure the local changes in concentration of oxygenated and deoxygenated hemoglobin and perfusion in
different tissues including muscle.51 NIRS measures the most
direct pathophysiologic consequence of ACS, intracompartmental tissue oxygen levels, rather than measuring the indirect
mechanism of intracompartmental pressure that may or may
not result in muscle ischemia. In 1977, Jobsis used this
technology for the first time to monitor cerebral and myocardial
oxygenation.52 During the past decade, NIRS has been used to
measure tissue oxygenation especially during investigations of
exercise. The NIRS instrument consists of a probe and an
analyzer chip. The probe contains light-emitting and lightreceiving fibers.
The depth of penetration of NIRS light is about half the
distance between emitter and receiver probes. Specific
wavelengths can be selected for transmission and subsequent
absorption of light for measuring oxygenated and deoxygenated hemoglobin. The difference between emitted and receiver
infrared light signals undergo signal processing by an integrated software program to extract the tissue oxygen saturation
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value. NIRS also has the potential to measure the redox state of
cytochrome c oxidase that can provide more specific information regarding intracellular oxygenation and whether the
oxygen supply is sufficient to meet energy demands at the
cellular level.53 Local ischemia causes an increased extraction
of oxygen by muscular tissue that reduces the level of local
venous oxyhemoglobin.54 NIRS can measure the changes in
tissue hemoglobin saturation and thus has the potential to
provide continuous noninvasive monitoring of intracompartmental ischemia and hypoxia.55
Fewer studies illustrate the utility of NIRS. In a case
report, Tobias and Hoernschemeyer presented the use of
NIRS in monitoring intracompartmental oxygenation of a
1-month-old infant who developed an ACS of the leg after
cardiac surgery.56 Several studies have shown high sensitivity
and specificity of NIRS in the diagnosis of exertional chronic
compartment syndrome,54,57 but no clinical trial is available
regarding the diagnostic value of NIRS in a clinical model of
ACS. In an animal model of limb ACS, Garr et al55 demonstrated a strong correlation between the level of oxyhemoglobin measured by NIRS and perfusion pressure in the
affected muscles. Despite the promising advantages of nearNIRS as a diagnostic tool, it still has some practical limitations, such as low depth of penetration (maximum depth of
30–40 mm) and extraneous variables that could affect the
penetration and reflection of the emitted infrared light signal.
The system needs further technical improvements, and more
clinical investigations are currently under way. NIRS may provide the benefit of a rapid, continuous, noninvasive, sensitive,
and specific tool for early detection of ACS.58
Pulse Oximetry
Pulse oximetry is a noninvasive technique that estimates
the level of arterial oxygen saturation using technology based
on principles somewhat similar to those of the NIRS device.
Diagnostic Techniques in Acute Compartment Syndrome of the Leg
The pulse oximeter emits red and infrared light that is absorbed
by the different levels of oxyhemoglobin and deoxyhemoglobin
during pulsatile flow. The oximeter probe measures the
difference between the emitted and received red and infrared
light during the diastolic and systolic phases of pulsatile flow to
compute the estimated oxygen saturation. It is mainly used in
clinical care units to monitor the level of hypoxemia.59 It cannot
measure intracompartmental tissue oxygen saturation and is
unable to detect intracompartmental hypoperfusion because
pulse oximetry technology requires adequate pulsatile flow to
compute its signal.60 Several reports have demonstrated that
pulse oximetry is not an appropriate aid in the detection or
monitoring of impaired perfusion.61,62
Hardness Measurement Techniques
Several authors have described the use of quantitative
hardness measurement techniques for the diagnosis of compartment syndrome. These techniques are based on the concept that skin surface pressure over a compartment can predict
intracompartmental pressure.63,64 A noninvasive handheld
device formulates a quantitative hardness curve of force
versus depth of indentation by applying a 5-mm-diameter
probe to a limb muscle compartment to estimate the ICP.65
Although the accuracy of this technique is not yet confirmed,66
improvements may enhance the usefulness of this measure as
a noninvasive screening tool for ACS.67
Direct Nerve Stimulation
Two reports22,68 have suggested using direct nerve
stimulation at the site where a nerve enters the compartment in
patients who are unable to voluntarily contract the muscles of
a compartment. This technique can differentiate a motor
dysfunction due to neuropraxia secondary to a high ICP from
a primary nerve injury proximal to the compartment. The lack
of muscular contraction in response to electrical stimulation of
FIGURE 2. Comparison of advantages between diagnostic methods
of ACS.
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the compartment nerve can indicate the ACS, whereas the
presence of a muscle contraction in response to the stimulation
may indicate a proximal nerve injury.59 However, because
paralysis is a late sign of ACS, this method is not useful for
prospective monitoring of high-risk patients.
Vibratory Sensation
Increased ICP alters regional neural function including
the perception of vibratory sensation.59 In a clinical study,
Phillips et al69 demonstrated a direct correlation between
impaired perception of vibration and increasing ICP. They
suggested that diminished response to vibratory stimuli as
measured with a 256 cycle per second tuning fork may be
a useful and very early indication of a developing ACS.70 However, like other subjective measurements, it is not practical in
children, in unconscious patients, or in those unable to cooperate.
Tissue Ultrafiltration
Tissue ultrafiltration is a technique in which small
semipermeable hollow fibers are inserted into tissues for the
removal of local interstitial fluid. It is primarily used as
a laboratory method of assaying the interstitial space. Initially,
Odland et al hypothesized that a tissue ultrafiltration device
can extract local interstitial fluid directly from the involved
muscles.71 Extracted fluid with a higher than expected concentration of metabolic markers of muscle ischemia may
predict ACS. Further refinement of this technique in addition
to identification of a specific biomarker indicative to skeletal
muscle ischemia could be of some benefit to early diagnosis
of ACS.
SUMMARY
An ACS is diagnosed by the interpretation of a collection
of clinical signs and symptoms in a high-risk patient. This
requires a detailed examination, a vigilant examiner, and
a cooperative patient. In situations when the examination is
equivocal or unreliable, objective tests that include compartment pressure monitoring can add information for clinical
decision making. The early identification of compartment
syndrome can significantly reduce the physical, financial, and
vocational disability experienced by the injured patient.
Advances in the methods, technology, and application of techniques for the early diagnosis of a compartment syndrome have
renewed interest for their investigation. Serum markers of
muscle damage, the measurement of changes in intracompartmental pressure, and the measurement of compartmental
perfusion and ischemia provide promising opportunities for
clinicians and researchers (Fig. 2). Further efforts in this area
are encouraged.
REFERENCES
1. Amendola A, Twaddel BC. Compartment syndromes. In: Browner BD,
Jupiter JB, Levine AM, et al, eds. Skeletal Trauma; Basic Science,
Management, and Reconstruction. Philadelphia, PA: Saunders; 2003:
268–292.
2. McQueen MM. Acute compartment syndrome. In: Buchholz RW,
Heckman JD, Court-Brown CM, eds. Rockwood and Green’s Fractures
in Adults. Philadelphia, PA: Lippincott Williams & Wilkins; 2006:425–443.
3. Kostler W, Strohm PC, Sudkamp NP. Acute compartment syndrome of the
limb. Injury. 2004;35:1221–1227.
586
4. McQueen MM, Gaston P, Court-Brown CM. Acute compartment syndrome. Who is at risk? J Bone Joint Surg Br. 2000;82:200–203.
5. Mc Queen MM, Christie J, Court-Brown CM. Acute compartment syndrome in tibia diaphyseal fractures. J Bone Joint Surg Br. 1996;78:95–98.
6. Court-Brown CM. Fractures of the tibia and fibula. In: Buchholz RW,
Heckman JD, Court-Brown CM, eds. Rockwood and Green’s Fractures in
Adults. Philadelphia, PA: Lippincott, Williams & Wilkins; 2006:
2079–2146.
7. Court-Brown CM, Koval KJ. The epidemiology of fractures. In: Buchholz
RW, Heckman JD, Court-Brown CM, eds. Rockwood and Green’s
Fractures in Adults. Philadelphia, PA: Lippincott Williams & Wilkins;
2006:96–143.
8. Court-Brown CM, McBirnie J. The epidemiology of tibial fractures.
J Bone Joint Surg Br. 1995;77:417–421.
9. Bhattacharyya T, Vrahas MS. The medical-legal aspects of compartment
syndrome. J Bone Joint Surg Am. 2004;86-A:864–868.
10. Giannoudis PV, Nicolopoulos C, Dinopoulos H, et al. The impact of lower
leg compartment syndrome on health related quality of life. Injury. 2002;
33:117–121.
11. Hope MJ, McQueen MM. Acute compartment syndrome in the absence of
fracture. J Orthop Trauma. 2004;18:220–224.
12. Chang YH, Tu YK, Yeh WL, et al. Tibial plateau fracture with compartment syndrome: a complication of higher incidence in Taiwan. Chang
Gung Med J. 2000;23:149–155.
13. Finkelstein JA, Hunter GA, Hu RW. Lower limb compartment syndrome:
course after delayed fasciotomy. J Trauma. 1996;40:342–344.
14. Olson SA, Glasgow RR. Acute compartment syndrome in lower extremity
musculoskeletal trauma. J Am Acad Orthop Surg. 2005;13:436–444.
15. Ellis H. Disabilities after tibial fractures. J Bone Joint Surg Br. 1958;40-B:
190–197.
16. The Euroqol Group. EuroQol: a new facility for measurement of health
related quality of life. Health Policy. 1990;16:199–208.
17. Vandervelpen G, Goris L, Broos PLO, et al. Functional sequelae in tibial
shaft fractures with compartment syndrome following primary treatment
with urgent fasciotomy. Acta Chir Belg. 1992;92:234–240.
18. Fitzgerald AM, Gaston P, Wilson Y, et al. Long-term sequelae of
fasciotomy wounds. Br J Plast Surg. 2000;53:690–693.
19. Whitesides TEJ, Haney TC, Morimoto K, et al. Tissue pressure measurements as a determinant for the need of fasciotomy. Clin Orthop. 1975;
113:43.
20. Rorabeck CH, Castle GSP, Hardie R, et al. Compartmental pressure
measurements: an experimental investigation using the slit catheter.
J Trauma. 1981;21:446.
21. Mubarak SJ, Hargens AR, Owen CA, et al. The wick catheter technique
for measurement of intramuscular pressure. A new research and clinical
tool. J Bone Joint Surg Am. 1976;58:1016–1020.
22. Matsen F, Winquist R, Krugmire R. Diagnosis and management of
compartmental syndromes. J Bone Joint Surg Am. 1980;162:286–291.
23. McQueen MM. How to monitor compartment pressures. Tech Orthop.
1996;11:99–101.
24. McQueen MM, Christie J, Court-Brown CM. Compartment pressure
monitoring in tibial fractures. J Bone Joint Surg. 1996;78:99–104.
25. Mubarak SJ, Owen CA, Hargens AR, et al. Acute compartment
syndromes: diagnosis and treatment with the aid of the wick catheter.
J Bone Joint Surg Am. 1978;60:1091–1095.
26. McQueen MM, Christie J, Court-Brown CM. Compartment pressure after
intramedullary nailing of the tibia. J Bone Joint Surg Br. 1990;72:
395–397.
27. White TO, Howell GED, Will EM, et al. Elevated intramuscular
compartment pressures do not influence outcome after tibial fracture.
J Trauma Inj Infec Crit Care. 2003;55:1133–1138.
28. Ulmer T. The clinical diagnosis of compartment syndrome of the lower
leg: are clinical findings predictive of the disorder? J Trauma. 2002;16:
572–577.
29. Janzing HMZ, Broos PLO. Routine monitoring of compartment pressure
in patients with tibial fractures: beware of overtreatment! Injury. 2001;32:
415–421.
30. Williams PR, Russel ID, Mintowt-Czyz WM. Compartment pressure
monitoring—current UK orthopaedic practice. Injury. 1998;29:229–232.
31. Harris IA, Kadir A, Donald G. Continuous compartment pressure
monitoring for tibial fractures: does it influence outcome? J Trauma Inj
Infec Crit Care. 2006;60:1330–1335.
q 2008 Lippincott Williams & Wilkins
J Orthop Trauma Volume 22, Number 8, September 2008
32. Vrouenraets BC, Kroon BB, Klaase JM, et al. Value of laboratory tests in
monitoring acute regional toxicity after isolated limb perfusion. Ann Surg
Oncol. 1997;4:88–94.
33. Sorichter S, Mair J, Koller A, et al. Early assessment of exercise induced
skeletal muscle injury using plasma fatty acid binding protein. Br J Sports
Med. 1998;32:121–124.
34. Van Nieuwenhoven FA, Kleine AH, Keizer HA. Comparison of
myoglobin and fatty acid-binding protein as plasma marker for muscle
damage in man. Eur J Physiol. 1992;421:40.
35. Lampert R, Weih EH, Breucking E, et al. Postoperative bilateral
compartment syndrome resulting from prolonged urological surgery in
lithotomy position. Serum creatine kinase activity CK as a warning signal
in sedated, artificially respirated patients. Anaesthesist. 1995;44:43–47.
36. Van Nieuwenhoven FA, Kleine AH, Wodzig KWH. Discrimination
between myocardial and skeletal muscle injury by assessment of the
plasma ratio of myoglobin over fatty acid-binding protein. Circulation.
1995;92:2848–2854.
37. Qvarfordt P, Christenson JT, Eklof B, et al. Intramuscular pressure, muscle
blood flow, and skeletal muscle metabolism in chronic anterior tibial
compartment syndrome. Clin Orthop Relat Res. 1983;179:284–290.
38. Roy D, Quiles J, Sharma R, et al. Ischemia-modified albumin concentrations in patients with peripheral vascular disease and exercise-induced
skeletal muscle ischemia. Clin Chem. 2004;50:1656–1660.
39. Zapico-Muniz E, Santalo-Bel M, Merce-Muntanola J, et al. Ischemiamodified albumin during skeletal muscle ischemia. Clin Chem. 2004;50:
1063–1065.
40. Rominger MB, Lukosch CJ, Bachmann GF. MR imaging of compartment
syndrome of the lower leg: a case control study. Eur Radiol. 2004;14:
1432–1439.
41. Rominger M, Lukosch C, Bachmann G, et al. Compartment syndrome:
value of MR imaging. Radiology. 1995;197:296.
42. Jerosch J, Geske B, Sons HU, et al. The value of sonography in assessing
intracompartmental pressure in the anterior tibial compartment. Ultraschall Med. 1989;10:206–210.
43. Lynch JE, Heyman JS, Hargens AR. Ultrasonic device for the noninvasive
diagnosis of compartment syndrome. Physiol Meas. 2004;25:N1–N9.
44. Wiemann JM, Ueno T, Leek BT, et al. Noninvasive measurements of
intramuscular pressure using pulsed phase-locked loop ultrasound for
detecting compartment syndromes: a preliminary report. J Orthop
Trauma. 2006;20:458–463.
45. Ueno T, Ballard RE, Macias RB, et al. Non-invasive measurement of
pulsatile intracranial pressure using ultrasound. Acta Neurochir. 1998;71:
66–69.
46. Edwards PD, Miles KA, Owens SJ, et al. A new non-invasive test for the
detection of compartment syndromes. Nucl Med Commun. 1999;20:
215–218.
47. Elliott KG, Johnstone AJ. Diagnosing acute compartment syndrome.
J Bone Joint Surg Br. 2003;85:625–632.
48. Briers JD. Laser Doppler, speckle and related techniques for blood
perfusion mapping and imaging. Physiol Meas. 2001;22:R35–R66.
49. Abraham P, Leftheriotis G, Saumet JL. Laser Doppler flowmetry in the
diagnosis of chronic compartment syndrome. J Bone Joint Surg Br. 1998;
80:365–369.
50. Van Beekvelt MC, Colier WN, Wevers RA, et al. Performance of nearinfrared spectroscopy in measuring local O2 consumption and blood flow
in skeletal muscle. J Appl Physiol. 2001;90:511–519.
q 2008 Lippincott Williams & Wilkins
Diagnostic Techniques in Acute Compartment Syndrome of the Leg
51. Mancini DM, Bolinger L, Li H, et al. Validation of near-infrared spectroscopy in humans. J Appl Physiol. 1994;77:2740–2747.
52. Jobsis FF. Noninvasive, infrared monitoring of cerebral and myocardial
oxygen sufficiency and circulatory parameters. Science. 1977;198:1264–
1267.
53. Arbabi S, Brundage SI, Gentilello LM. Near-infrared spectroscopy:
a potential method for continuous, transcutaneous monitoring for
compartmental syndrome in critically injured patients. J Trauma Inj
Infec Crit Care. 1999;47:829–833.
54. van den Brand JG, Nelson T, Verleisdonk EJ, et al. The diagnostic value of
intracompartmental pressure measurement, magnetic resonance imaging,
and near-infrared spectroscopy in chronic exertional compartment syndrome: a prospective study in 50 patients. J Sports Med. 2005;33:699–704.
55. Garr JL, Gentilello LM, Cole PA, et al. Monitoring for compartmental
syndrome using near-infrared spectroscopy: a noninvasive continuous
transcutaneous monitoring technique. J Trauma. 1999;46:613–618.
56. Tobias JD, Hoernschemeyer DG. Near-infrared spectroscopy identifies
compartment syndrome in an infant. J Pediatr Orthop. 2007;27:311–313.
57. Van den Brand JG, Verleisdonk EJ, Van der Werken C. Near infrared
spectroscopy in the diagnosis of chronic exertional compartment
syndrome. Am J Sports Med. 2004;32:452–456.
58. Giannotti G, Cohn SM, Brown M, et al. Utility of near-infrared
spectroscopy in the diagnosis of lower extremity compartment syndrome.
J Trauma Inj Infec Crit Care. 2000;48:396–401.
59. Styf J. Compartment Syndromes Diagnosis, Treatment and Complications. Boca Raton, FL: CRC Press LLC; 2004.
60. David HG. Pulse oximetry in closed limb fractures. Ann R Coll Surg Engl.
1991;73:283–284.
61. Mars M, Maseko S, Thomson S, et al. Can pulse oximetry detect raised
intracompartmental pressure? S Afr J Surg. 1994;32:48–50.
62. Mars M, Hadley GP. Failure of pulse oximetry in the assessment of raised
limb intracompartmental pressure. Injury. 1994;25:379–381.
63. Uslu MM, Apan A. Can skin surface pressure under a cast reveal intracompartmental pressure? Arch Orthop Trauma Surg. 2000;120:319–322.
64. Arokoski JP, Surakka J, Ojala T, et al. Feasibility of the use of a novel soft
tissue stiffness meter. Physiol Meas. 2005;26:215–228.
65. Steinberg BD. Evaluation of limb compartments with increased interstitial
pressure. An improved noninvasive method for determining quantitative
hardness. J Biomechanics. 2005;38:1629–1635.
66. Dickson KF, Sullivan MJ, Steinberg B, et al. Noninvasive measurement of
compartment syndrome. Orthopedics. 2003;26:1215–1218.
67. Joseph B, Varghese RA, Mulpuri K, et al. Measurement of tissue
hardness: can this be a method of diagnosing compartment syndrome
noninvasively in children? J Pediatr Orthop. 2006;15 (part B):443–448.
68. Sheridan GW, Matsen FA III, Krugmire RB Jr. Further investigations on
the pathophysiology of the compartmental syndrome. Clin Orthop Relat
Res. 1977;123:266–270.
69. Phillips JH, Mackinnon SE, Beatty SE, et al. Vibratory sensory testing in
acute compartment syndromes: a clinical and experimental study. Plast
Reconstr Surg. 1987;79:796–801.
70. Dellon AL, Schneider RJ, Burke R. Effect of acute compartmental
pressure change on response to vibratory stimuli in primates. Plast
Reconstr Surg. 1983;72:208–216.
71. Odland R, Schmidt AH, Hunter B, et al. Use of tissue ultrafiltration for
treatment of compartment syndrome: a pilot study using porcine
hindlimbs. J Orthop Trauma. 2005;19:267–275.
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