Introduction
Chronic exertional compartment syndrome (CECS) is defined as a condition in which
exercise or heavy exertion creates elevated pressures within the closed space of an
extremity muscular compartment which subsequently causes consistently recurring symptoms
and/or disability by progressive impairment of the neuromuscular function of the involved
compartment [[1 ],[2 ],[3 ],[4 ],[5 ],[6 ]]. The diagnosis of CECS is primarily made on careful history that demonstrates consistent
appearance of symptoms in the same compartments in the lower extremities with exertion.
Symptoms may consist of an aching pain, squeezing sensation, sharp pains, or possible
paresthesias in the feet. It is not uncommon for bilateral mirror image compartments
to be involved. Confirmation of the diagnosis is generally made with direct invasive
intra-compartmental pressure measurements [[1 ],[4 ],[7 ],[8 ]]. We present a case where non-invasive, non-painful neurosensory testing successfully
diagnosed the problem of exertional compartment syndrome and was used to help guide
and document successful management of the disorder in a patient with suspected deep
distal posterior compartment syndrome.
Case report
A 25 year old male was originally seen in our office after the diagnosis of chronic
exertional compartment syndrome (CECS) of the anterior and lateral compartments had
been made by invasive pressure measurements of those compartments. He was originally
referred to our office for the treatment of chronic leg pain due to a neuroma of a
superficial peroneal nerve, injured during an anterior and lateral compartment fasciotomy
to treat his CECS. This painful neuroma was treated successfully by neuroma resection
and implantation of the proximal end of the superficial peroneal nerve into the extensor
digitorum communis muscle [[9 ]]. His anterior and lateral compartment pain had resolved with the original fasciotomies.
He was then discharged from our care.
He returned to our office one year later with complaints of bilateral exercise induced
pain in the backs of his legs from the lower calf to the ankle that he stated felt
“just like the front of my legs did, though slightly less intense.” After five minutes
of running he began to complain of tightness and a dull aching pain that progressed
to severe pain eventually causing him to stop exercising. His pain was also associated
with paresthesias and numbness in the soles of his feet. The pain and numbness persisted
for five to ten minutes after stopping his exercise, but the tightness lasted longer.
On exam, the patient was an athletic appearing male with normal pulses in dorsalis
pedis and posterior tibial vessels. He was tender to pressure applied immediately
posterior to the tibia overlying the distal deep posterior compartment. He had no
tenderness to percussion of the tibia itself or to palpation of the tibial edge. He
was not tender in the midline of the posterior calf over the proximal tibial nerve
[[10 ]]. His gastrocnemius muscle was slightly tender. He did have a Tinel sign over both
tarsal tunnels with radiation to the sole of his feet.
Due to his symptoms of exercise induced numbness and paraesthesias, non-invasive,
non-painful neurosensory testing was performed with the Pressure Specified Sensory
Device™ (Sensory Management Services, LLC, Baltimore, Maryland, USA) at rest to measure
base line cutaneous pressure thresholds for one and two point static touch and to
measure two point discrimination in the skin innervated by medial plantar and medial
calcaneal branches of the tibial nerve ([Figures 1 ]. and [2 ]). The anterior lateral dorsum of the foot and the dorsal web-space between the first
and second toe – the usual distribution of the superficial peroneal and deep peroneal
nerve branches respectively – were also measured. The study was repeated immediately
after 10 minutes of running on a treadmill – the time interval to reproduce his symptoms.
Following the running, there was widening of two point discrimination in the distribution
of the calcaneal nerve and the medial plantar nerve indicating loss of large fiber
tibial nerve function suggesting the diagnosis of exertional compartment syndrome
of the deep posterior compartment causing compression of the tibial nerve ([Table 1 ]).
Table 1
Neurosensory Measurements Before & After Stress Testing
Cutaneous Pressure Thresholds for Static Two-Point Discrimination*
Prior to 1st Posterior Distal Compartment Release (A)
After 1st Posterior Distal Compartment Release (B)
After 2nd Posterior Distal Compartment Release (C)
RIGHT LEG
Tibial Nerve
Before Exercise
After Exercise
Before Exercise
After Exercise
Before Exercise
After Exercise
Hallux Pulp
mm
10
15
8
12
5
5
gm/mm
2
43
60
46
52
63
66
Medial Heel
mm
11
15
8
12
8
5
gm/mm
2
40
58
82
79
96
68
Peroneal Nerve
1st web space
mm
5
5
8
10
5
5
gm/mm
2
60
88
60
68
53
56
Dorsolateral**
NA
NA
NA
NA
NA
NA
LEFT LEG
Tibial Nerve
Hallux Pulp
mm
4
8
10
10
5
5
gm/mm
2
38
97
40
52
79
75
Medial Heel
mm
5
15
8
8
5
5
gm/mm
2
45
82
92
69
52
64
Peroneal Nerve
1st web space
mm
5
5
8
8
5
5
gm/mm
2
35
77
95
80
73
52
Dorsolateral
mm
7
7
7
7
7
7
gm/mm
2
37
78
90
79
53
71
*Two-point static-touch; normative values in the foot for someone less than 45 years
of age have a pressure of about 15 gm/mm2 to discriminate one from two static points at 6 mm distance apart. ** The right superficial
peroneal nerve was resected previously and the anterior and lateral compartments released
previously.
A) Interpretation: the distance required to discriminate one from two point static-touchincreased
for the tibial nerve on both the right and left sides after exercise, consistent with
bilateral (right worse than left) posterior compartment syndrome. Note that the peroneal
nerve measurements on the left and right did not change, and that the anterior and
lateral compartments had been released previously.
B) Interpretation: There is still an increase in the right tibial nerve measurements
for discrimination of one from two point static-touch, indicating that despite fasciotomy
of the deep compartment on the right, there is still compression of the tibial nerve
in the distal deep compartment. Neurosensory testing demonstrates that another fasciotomy
is still required. The lack of change in left tibial nerve may be a timing phenomenon
as the right leg was tested first after the patient stopped running.
C) Interpretation: After complete decompression of the deep distal posterior compartment
bilaterally, there is now no increase in the distance required to discriminate one
from two static-touch points, consistent with complete release of the deep distal
posterior compartments and return of normal tibial nerve function.
Figure 1 . This obtains a true measurement of the distance that a patient can feel two distinct
points and the pressure which is required to feel those two points.
Figure 2 . This obtains a true measurement of the distance that a patient can feel two distinct
points and the pressure which is required to feel those two points.
To confirm the diagnosis, traditional invasive, immediate, post-exercise compartment
pressures of the superficial and deep posterior compartments were obtained using a
device with a side port needle measurement system (Stryker Instruments, Kalamazoo,
Mich.). The superficial posterior compartment (SPC) measured 40 mmHg on the right
and 24 mmHg on the left. The deep posterior compartment (DPC) measured 62 mmHg on
the right and 28 mmHg on the left. To rule out other causes of posterior leg pain
an MRI was performed and demonstrated no vascular anomalies, no evidence of stress
fractures, medial tibial periostitis, tumors, or other abnormalities.
Bilateral superficial posterior and deep distal posterior fasciotomies were performed
through a proximal and distal two incision medial approach. Postoperatively, the patient
recovered without incident. However, at three months he still complained of similar
symptoms, but they were more isolated to the posterior distal half of the lower extremity
over the distal deep compartment muscles. The patient’s exam still demonstrated pain
with compression just posterior to the tibia in the lower half of his legs. Due to
his complaints of persistent pain and numbness, his non-invasive neurosensory testing
was repeated before and after running 10 minutes on a treadmill ([Table 1 ]). Again he demonstrated loss of two point discrimination in the calcaneal and medial
plantar nerve that suggested continued tibial nerve dysfunction brought on by exertion.
Therefore he was taken back to the operating room for a repeat fasciotomy of the distal
deep compartments. It was discovered that the patient had an unusual anatomic variant
of his deep distal compartment as described by Detmer [[11 ]], and therefore the compartment had not been fully released during the first operation.
The soleus muscle wrapped around medial side of the tibia unusually far, and it completely
obscured the deep distal compartment. The fascia that had originally been released
turned out to be the fascia overlying the unusually large and medially placed soleus.
Only after peeling the soleus completely off the medial edge of the tibia in the distal
lower leg was a second deeper layer of thickened fascia found beneath it. This too
was released longitudinally to open the true deep distal compartment that encased
the posterior tibial neurovascular bundle, the flexor digitorum longus, posterior
tibialis, and flexor hallucis muscles.
The patient recovered well from his second operation and was allowed to progress in
his exercise regimen starting three weeks after surgery. After his first attempted
posterior distal compartment release, he was able to run only a half of a mile before
he would need to rest and allow his legs to recover. Three months after his second
posterior distal compartment release, he was able to run over three miles with out
resting. At 15 months after the second posterior distal compartment fasciotomy, the
patient states that he had a 90% improvement in the numbness and posterior leg pain
since surgery.
We tested him a third time with the non-invasive neurosensory testing before and after
running on a treadmill for 12 minutes and this demonstrated minimal change in two
point discrimination indicating minimal change in tibial nerve function, thus demonstrating
resolution of nerve compressions caused by his deep distal posterior exertional compartment
syndrome.
Discussion
To our knowledge this is the first case where non-invasive neurosensory testing with
the Pressure-Specified Sensory Device™ was used during a provocative test to assist
in making the diagnosis and then to help guide surgical management of CECS in an athlete.
The gold standard for diagnosis of CECS is invasive intra-compartmental pressure measurements
before, during, and/or after exercise with a wick catheter, slit catheter, or sideport
needle [[1 ],[4 ],[12 ]]. In addition to elevated pressures seen before, during, and after exercise, there
is a delayed return of the intracompartamental pressure to base line when compared
to controls [[13 ]]. This invasive technique caries with it some discomfort and a small risk of injury
to neurovascular structures, furthermore, it may be difficult to tell exactly where
the tip of the needle is measuring [[1 ],[6 ],[12 ]]. Non-invasive techniques including magnetic resonance imaging, near-infrared spectroscopy,
and laser doppler flowmetry, have been described to diagnose CECS in the lower extremities
[[6 ],[12 ],[14 ],[15 ]]. Several studies have successfully used non-invasive vibration thresholds to diagnose
acute compartment syndrome [[16 ],[17 ]]. Progressive loss of motor strength was used to demonstrate CESC non-invasively
in the upper extremity [[18 ]].
Pathophysiologic mechanisms underlying the cause of this syndrome are not fully understood,
but generally it is believed that exercise causes an abnormally high intra-compartmental
pressure, thus impairing local tissue perfusion and, therefore, causing ischemic pain
[[5 ],[12 ],[15 ],[19 ]]. However, there is some evidence that ischemia may not be the underlying mechanism
of pain [[7 ],[14 ]]. Matsen and colleagues studied the effect of compartment pressure on motor nerve
conduction velocity, compound muscle-action potential amplitude, sensation to light
touch and pin prick [[20 ]]. They found a “consistent sequence in the appearance of abnormalities in neuromuscular
function during compression.” Subjective numbness appeared first followed by hypesthesia
to light touch and pinprick, and then motor weakness [[20 ]]. This work supports the use of sensibility testing as a means to detect early changes
in compartment syndromes.
The function of large myelinated nerve fibers measured by the detection of vibratory
sensation has been shown to be a sensitive indicator of acute compartment syndrome
as well as chronic nerve compression and nerve regeneration [[8 ],[16 ],[17 ],[21 ],[22 ]]. Although vibratory stimulation with a tuning fork or vibrometer is clinically
useful, the major drawback is that this form of stimulation sets up a waveform stimulus
and will potentially stimulate nerve fibers outside the field of interest and lead
to potential misinterpretation [[23 ]].
The Pressure-Specified Sensory Device™ offers the clinician, reliable, valid quantitative
measurements of pressure threshold and nerve fiber density data by asking the patient
to indicate at what distance he can feel two distinct pressure points to the skin.
This distance between the points is an indication of the functional nerve fiber density,
while the pressure required to feel those two different points is a measure of sensory
fiber threshold [[23 ],[24 ],[25 ],[26 ]]. Neurosensory testing with the Pressure-Specified Sensory Device™ has been proven
to be more sensitive and specific than either vibration or Semmes-Weinstein monofilaments
in identifying large fiber peripheral nerve dysfunction in patients with chronic nerve
compression and peripheral neuropathy [[23 ],[24 ],[25 ]].
The limitations of this technique are that neurosensory testing is a subjective test
rather than a purely objective one. It requires a cooperative and truthful patient
and a trained technician to perform it. At this time we do not have clinical normative
values that describe what amount of sensory change is considered to be pathologic,
and further testing needs to be performed.
Neurosensory testing also needs to be performed quickly after the patient stops the
exercise in order to pick up the changes in reversible sensory change. It is currently
unknown how long these sensory changes can be detected with this device, and clinical
study needs to be performed to better determine this. With regards to this particular
patient, testing was performed on both feet within 4–5 minutes of stopping his exercise.
Clearly it must be emphasized that this represents only a single case report and further
studies to determine population norms, control values, and to determine clinically
significant sensory changes must to be performed to prove that this is a useful technique
to use for routine purposes to diagnose and follow patients with complaints consistent
with CECS.
Conclusion
With an accurate, valid, non-invasive measurement system, it may be more important
to determine treatment based end organ function of the most sensitive organ – the
nerve – rather than on pressures in the compartments involved with CECS. If one could
accurately determine the real-time function of the peripheral nerve the compartment
then one could begin to refine the clinical treatment of patients with suspected CECS.
While compartment pressure measurements are a reliable method of evaluation of patients
with suspected CECS, in this report, neurosensory testing demonstrated that a non-painful,
non-invasive method was also helpful in directing care in a patient with CECS.
Abbreviations
CECS:
Chronic exertional compartment syndrome
Competing interests
One author, ALD has a proprietary interest in the Pressure- Specified Sensory Device
™, and the company Sensory Management Services, LLC that markets it.
Authors’ contributions
EHW: writing, design, interpretation of data, direct patient care, DED: design, patient
care, intellectual content, GPG: design, direct patient care, acquisition of data,
intellectual content, ALD: writing, interpretation of data, intellectual content
Consent
Written informed consent was obtained from the patient for publication of this Case
report and accompanying images.
