Compartmental Syndromes.
Edited By: Frederick A. Matsen III, M.D., Winston J. Warme, MD
Last updated Friday, October 16, 2009
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Challenging cases
Challenges in diagnosis and treatment
Although the diagnosis and treatment of some compartmental syndromes
may be straightforward, other cases can be quite challenging. In some
instances the physician is pressed to make an early diagnosis of a
compartmental syndrome so that prompt surgical decompression can be
accomplished. In other situations the physician must exclude the
diagnosis of a compartmental syndrome to avoid performing unnecessary
surgery.Seven cases
Having reviewed most of the available information on compartmental
syndromes, the reader may now find it interesting to study some cases
that demonstrate problems in the diagnosis and management of this
condition. Seven such cases are presented below. These cases have been
arranged to challenge the reader to apply his knowledge in selecting
the appropriate laboratory evaluation and treatment without being
biased by what actually occurred. Thus, the history and clinical
evaluation are presented separately from the subsequent course.
In the first three cases, earlier diagnosis and treatment as well as
a better end result might have been possible had the physician
originally treating the patient been more familiar with compartmental
syndromes. The last four cases demonstrate that careful clinical
evaluation and adjunctive diagnostic tests can help resolve some very
challenging diagnostic problems.
Case 1
History and clinical evaluation
A 47-year-old male truck driver was in good health until he noticed
the acute onset of anterior chest pain radiating down both arms while
he performed push-ups. He came to the hospital in acute distress where
a dissecting aneurysm of the ascending aorta was diagnosed. An
emergency surgical repair was performed. This procedure was difficult
and required 5 hours and 12 minutes of cardiopulmonary bypass using the
right femoral artery. Cannulation of this artery in a retrograde manner
produced a relative occlusion of the femoral artery.
After operation the patient was in serious condition in the
intensive care unit. The neuromuscular function of his right leg was
not checked until a consulting physician examined him approximately 14
hours after the conclusion of the original operation. This examination
revealed a tense right leg from the knee to the ankle. The patient was
unable to move his toes and had no sensation in his foot. There was
pain on passive stretch in both the anterior and deep posterior
compartments. His distal pulses were intact.
Laboratory evaluation, treatment, and result
The presence of a tense leg with severe neuromuscular deficits was
deemed sufficient to establish the diagnosis of a compartmental
syndrome and to justify immediate surgical decompression; no additional
time was taken for diagnostic procedures. A four-compartment
parafibular decompression was performed. The contents of all
compartments bulged markedly. The muscle of the anterior compartment
was quite dusky. This patient's subsequent clinical course was
complicated by myoglobinuric renal failure that responded to
hemodialysis. His wound was treated open with daily dressing changes
for 13 days, at which time he was taken to the operating room for
inspection of the wound and skin grafting. The anterior compartment
appeared to be pale, and the extensor digitorum longus muscle was
necrotic and required excision. Minimal debridement of the tibialis
anterior and extensor hallucis longus muscles was performed. The rest
of the leg muscles appeared healthy. A meshed split-thickness graft was
applied. Eighty-five percent of the graft took primarily. The remainder
of the wound was allowed to heal by granulation and epithelialization.
One year after surgery the patient had grade four strength of the
muscles of the lateral, superficial posterior, and deep posterior
compartments. The tibialis anterior muscles, which had apparently been
functionless for over six months, had recovered grade three strength,
and the patient no longer needed a drop foot brace. The patient's
heart, aortic, renal, and cerebral function were all normal.
Comment
This case was made difficult by the patient's critical condition and
by the intensive medical and surgical treatment required to save his
life. In retrospect, prophylactic fasciotomy may have been indicated in
view of the massive postischemic swelling expected after the release of
prolonged occlusion of the femoral artery. The muscle of the anterior
compartment obviously sustained a double ischemic insult, first from
the arterial occlusion and then from the compartmental syndrome. It is
ironic that although the function of his anterior compartment seemed
insignificant while the patient was critically ill, the loss of this
function is now his major disability. It is also instructive to note
the delayed functional return of sufficient anterior compartmental
function to make him brace free.
Case 2
History and clinical evaluation
A l6 year-old boy had surgical correction of a 20-degree valgus
deformity of the right tibia. The osteotomy was performed just distal
to the tibial tubercle along with a proximal fibular osteotomy. On
awaking from anesthesia, the patient was unable to extend his toes or
dorsiflex his foot. Hypesthesia was present in the distribution of the
deep and superficial peroneal nerves. Twenty-four hours after
operation, the patient complained of increasing pain in the leg, which
responded incompletely to removal of the circumferential dressings. A
consulting physician examined the patient two days later and noted
anesthesia in the distribution of the deep peroneal nerve. Strength of
toe flexion was four out of five; strength of toe extension was zero
out of five. The leg was moderately tight on palpation, particularly in
the proximal aspect of the anterior compartment.
Laboratory evaluation, treatment, and result
This patient had at least two causes for the neuromuscular deficits:
a peroneal nerve injury at the time of surgery and an anterior
compartmental syndrome. It was possible that these lesions coexisted.
To help in determining the need for surgical decompression, tissue
pressure was measured at the point of maximum tenseness in the anterior
compartment: a value of 50 mm Hg was obtained.
A four-compartment parafibular decompression was performed; the
contents of the anterior compartment were necrotic, and complete
debridement was subsequently required. The wound was closed eventually
with a meshed split-thickness graft. The patient is currently using a
drop foot brace two months after surgery.
Comment
This case was made difficult by the two possible etiologies of loss
of anterior compartmental function: a compartmental syndrome and a
peroneal nerve palsy. A compartmental syndrome is differentiated from a
nerve palsy by the presence of inappropriate pain and by the
demonstration of increased tissue pressure. Thus, earlier evaluation of
the tenseness of the anterior compartment either by palpation or by
pressure measurement might have prevented the delayed diagnosis of a
compartmental syndrome. Decompression two days after the onset of a
compartmental syndrome cannot be expected to restore normal function.
Prophylactic fasciotomy at the time of the osteotomy may have been
effective in preventing the anterior compartmental syndrome.
Case 4
History and clinical evaluation
An l8-year-old man sustained an anterior dislocation of his left
knee while playing football. After reduction of the knee, examination
revealed a swollen proximal leg, absent active extension of the toes,
hypesthesia in the distributions of the deep and superficial peroneal
nerves, and a diminished dorsalis pedis pulse.
Laboratory evaluation, treatment, and result
An arteriogram revealed a small intimal tear near the origin of the
anterior tibial artery. Stimulation of the peroneal nerve at the
fibular neck produced strong extension of the toes. Anterior
compartment pressure measurements reached a maximum of 15 mm Hg. These
data indicated that the paralysis was not due to compartmental
ischemia, but rather to an injury of the peroneal nerve proximal to the
fibular neck. The arterial lesion was not treated. Peroneal nerve
function gradually returned.
Comment
This case presented a classical differential diagnosis: anterior
compartmental syndrome of the leg versus peroneal nerve palsy versus
occlusion of the anterior tibial artery. The pressure measurements were
helpful in excluding a compartmental syndrome. The results of nerve
stimulation demonstrated that the paralysis of the compartment was not
due to ischemia of the compartmental contents. Thus, peroneal nerve
palsy became the most likely diagnosis.
Case 5
History and clinical evaluation
A 34-year-old woman lay on her left side for 24 hours after a
barbiturate overdosage. After awaking, she noticed an inability to
dorsiflex her foot or extend her toes. The antero-lateral leg was
swollen, but the compartments did not appear clinically tense.
Laboratory evaluation, treatment, and result
Peroneal nerve stimulation distal to the fibular neck elicited
normal foot dorsiflexion and toe extension. Anterior compartment
pressures reached a maximum of 22 mm Hg. Subsequent formal nerve
conduction velocity measurement and electromyography confirmed the
diagnosis of common peroneal nerve palsy from direct pressure. There
was no subsequent evidence of compartmental or crush syndromes.
Myoglobinuria was absent. Neurological function of the leg completely
returned.
Comment
Drug overdosage with prolonged recumbency is a classical etiology of
compartmental syndromes. In this case, however, the lack of pain and
compartmental tenseness as well as the results of the adjunctive
diagnostic tests ruled out the diagnosis of a compartmental syndrome
and helped prevent an unnecessary surgical decompression.
Case 6
History and clinical evaluation
A 60-year-old female pedestrian was hit by an automobile traveling
approximately 70 mph. She sustained multiple trauma, including a
depressed skull fracture, a pelvic fracture, an intertrochanteric
fracture of the right femur, and a spiral fracture of the right tibia
with significant soft tissue injury. This women was obviously at high
risk for a compartmental syndrome in the right leg, but routine
examination was impossible because she was comatose from her head
injury.
Laboratory evaluation, treatment, and result
Intermittent stimulation of the right peroneal nerve provided
assurance that her local neuromuscular status was intact over the first
72 hours, including the time when intracompartmental pressure rose to
its maximum of 45 mm Hg. The patient continued to recover from her
injuries, and, as of two months after her accident, had no neurologic
sequelae in her right lower extremity.
Comment
The Babinski sign and withdrawal reflexes may be of use in
determining the functional status of the leg compartments in a comatose
patient. In this situation further diagnostic assistance may be derived
from tissue pressure monitoring and direct nerve stimulation.
Case 7
History and clinical evaluation
A l3-year-old female cross-country runner experienced pain in the
anterior compartment of the right leg each time she ran. Initially she
could "run through" her symptoms. For the three-month period before
evaluation, however, her symptoms were sufficiently severe to prevent
her from running at all. She had not noticed weakness or sensory
changes in her leg or foot with exercise. Examination at rest was
normal except for slight tenderness in the distal anterior compartment.
Laboratory evaluation, treatment, and result
Repeated dorsiflexion of the foot against resistance reproduced her
symptoms, but was not associated with increased tissue pressure either
by palpation or by pressure measurement. On this basis the diagnosis of
a recurrent compartmental syndrome due to intensive use of muscles was
rejected. The patient subsequently responded to treatment for anterior
tibial tendinitis.
Comment
Recurrent compartmental syndromes are a relatively uncommon cause of
exercise-related pain. The diagnosis should be well established before
surgical treatment is contemplated.
Surgery for Compartmental Syndromes at the University of Washington, Department of Orthopaedics and Sports Medicine, Seattle, Washington
If you are interested in making an appointment to discuss this procedure in Seattle, you can request an appointment using our online referrals website. To request a referral online, please click here. You can also call 206-598-BONE (2663) to make an appointment. Our clinical center is located in Seattle Washington, USA
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