Acute exertional
superficial posterior compartment syndrome*
SCOTT J. MUBARAK,† M.D., CHARLES A. OWEN,‡ M.D., STEVE M.D., AND ALAN R. HARGENS,¶ Ph.D., San Diego, California From the Division of Orthopaedic
Acute
GARFIN,§
Surgery, University of California, San Diego
f~cute and chronic exertional tibial
compart-
syndromes involving the four compartments of the leg following strenuous exercise or marching have been more frequently reported since the original description by Vogt in 1943 .17 Exercise-initiated syndromes involving the superficial posterior compartment (gastrocnemius and soleus muscles) are rare. Only Kirby’ and Snook16 describe chronic superficial posterior compartment syndromes in the English literature. We are reporting an acute superficial posterior compartment syndrome initiated by exercise, as well as, reviewing the availment
able literature.
the distance of each day’s run increased. The pain usually subsided 2 to 3 hr after exercise, but in the days prior to admission it lasted the entire day and into the following morning when he began running again. He noted a mild pain at rest on the day of admission, which became unbearable after he ran 3 miles. Prior to his recruitment he had been unaccustomed to vigorous exercise of any sort and had never experienced calf pain. Review of his past medical more severe as
history was unremarkable. Physical
Examination: The
patient
was a
well-
oriented, cooperative, 18-year-old male in moderPertinent physical findings related to his right leg. The leg was very swollen, tense, and tender, especially in the posterior aspect but also the lateral and anterior compartments. The extremity was held in 30° of flexion at the knee and 15°of plantar flexion at the ankle. Extension of the knee or dorsiflexion of the ankle caused excruciating pain in the calf. Passive flexion or extension of the toes caused mild pain in the anterior and posterior leg, respectively. Plantar flexion of the foot caused moderate pain in the anterior compartment. The circumference of the calf 13 cm below the tibial tubercle measured 42 cm on the right compared with 37 cm on the left. Motor examination was intact but limited by extreme pain. Sensory examination showed spotty decrease to light touch and pinprick along the lateral aspect of the right foot, corresponding to the sural nerve distribution. The posterior tibial and dorsalis pedis pulses were palpable. The initial diagnosis was that of a compartment syndrome with primary involvement of the superficial posterior compartment. ate to severe distress.
CASE HISTORY
were
Three weeks prior to his admission on October 1, 1973, an 18-year-old recruit noted pain involving his right calf following episodes of running for more than 1/2 mile. Pain was specifically in his posterior calf and became progressively
History:
* Supported by the Medical Research Service of the Veterans Administration and National Institutes of Health-United States Public Health Service Grant AM18224.
t Assistant Professor of Orthopaedic Surgery, University of California, San Diego, 225 West Dickinson Street, San Diego, California 92103. f Assistant Professor Orthopaedic Surgery, University of California, San Francisco, 4141 Geary Blvd., San Francisco, California
94118.
§ Division of Orthopaedic Surgery, Veterans Administration Hospital, San Diego, California 92161. 1) Orthopaedic Research, Veterans Administration Hospital, 3350 La Jolla Village, San Diego, California 92161.
287
Laboratory Studies: Urinalysis was normal, complete blood count normal, and hematocrit 37. One hr after admission, creatine phosphokinase was 320 IU (normal to 12) and lactate dehydrogenase 260 IU (normal to 200). Twelve hr after admission, creatine
phosphokinase was 270 and lactate dehydrogenase, 145. Thirty-six hr after admission,
for an increase in the hypesin the foot. Four hr after admission the patient was anesthetic in the first web space and hypesthetic on the dorsolateral aspect, and in a spotty distribution on the plantar surface of the foot. Because of the continued progression of signs of an exertional tibial compartment syndrome involving all four compartments, the decision was made to perform decompressive fasciotomy. Intra-
unchanged, except
thetic
area
phosphokinase was 150 and lactate dehydrogenase, 150. Radiographic examination of the leg was normal, except for soft tissue swelling. compartment pressure measurements were not obHospital Course: The extremity was elevated and tained. The patient was taken to the operating room cooled with ice. At 1 hr, examination revealed palpable pulses and normal motor strength, but where four compartment fasciotomies were peractive movements caused more severe pain. Pas- formed using a double skin incision approach (Fig. sive flexion and extension of the toes caused no 1 ). Swelling and hemorrhage were massive in the soleus muscle belly and moderate in the gastrocor at knee extension ankle dorsipain. Attempts flexion caused severe pain in the calf. Sensory nemius muscle belly. The anterior, lateral, and examination now showed decreased sensation to deep posterior compartment muscles were modpinprick and light touch in a spotty distribution erately swollen, but not hemorrhagic. All muscle involving the dorsolateral and plantar foot sur- seemed to be viable. The wounds were left open faces. Two hr after admission the examination was initially and closed 6 days later. Biopsy specimens creatinine
Fig. 1. Bulging soleus and gastrocnemius hemorrhage in that muscle. 288
muscle bellies
after fasciotomy.
The black
area
in the soleus
represents
of the soleus demonstrated edema and hemorrhage without necrosis, while those of the anterior tibial muscle showed only edema. The patient was treated in a long leg case for 3 weeks and then started on range of motion exercises. He had a complete return of both sensory and motor functions within I week. At 3-month follow-up, he had a full range of motion of both knee and ankle and had normal motor and sensory function of the right leg. DISCUSSION
In 1943 Volt17 first described an acute exertional anterior tibial compartment syndrome induced by marching. In 1957 Blandy and Fuller’ reported two cases of the acute syndrome with lateral compartment involvement. Reneman,15 in his literature review, notes that the anterior compartment has been involved in 46 cases, the lateral alone in 6 cases, and the combination of anterolateral in 6 acute syndromes. Except for the present case, an acute form of the exertional syndrome involving either the superficial posterior to deep posterior compartment has not been described previously. In 1956 Mavor9 presented the first case report of a chronic anterior compartment syndrome brought on by exertion. Since then, more than 60 other documented chronic cases involving either the anterior or a combination of the anterior and lateral compartments have been reported. 15 In 1970 Kirby’ described a case with bilateral chronic superficial posterior compartment syndromes; the symptoms were relieved by fasciotomies. Three additional cases of chronic syndromes in the su-
perficial posterior compartment were reported by Snook. 16 Eleven cases of exertional syndromes involving the deep posterior tibial compartment were reported in 1974 by Puranen.l4 The exact pathogenesis of the exertional tibial compartment syndrome is unknown. Muscle and nerve ischemia caused by elevated compartment pressure appears to be the immediate cause of pain and disability. Studies of this group of patients in 15 our laboratory and by others3, 6. have shown elevated pressures in the involved compartments at rest, and even higher pressures after exertion sufficient to precipitate symptoms. The factors responsible for the prolonged elevation of compartment pressures in certain individuals following exercise remain speculative. Ex-
plained simply, a compartment syndrome is a mechanical problem occurring when a mass of soft tissue (primarily muscle) is too large for the rigid
osseofascial compartment in which it is contained. It is known that once a critical level is reached, a very small increase in volume results in a very large increase in pressure.4 Individual variations in the relationship of muscle bulk to compartment volume may account for the susceptibility of certain individuals to development of the exertional syndromes. It is also of interest that a majority of the cases of exertional syndromes have occurred in well-trained athletes. This suggests that their hypertrophic muscle may decrease the space available for swelling within the relatively fixed volume
compartment.
Wrighe8 stated that muscle increases in bulk by 20%
following exercise. The swelling brought on by acute exercise may be sufficient in these susceptible individuals to raise pressures to critical levels&dquo; and cause muscle and nerve ischemia with
subsequent pain. Cessation of activity before muscle fiber and capillary wall necrosis occur can result in resorption of excess fluid volume, and decrease in compartment pressure with consequent relief of ischemia and pain. Hemorrhage from muscle rupture in either normal or ischemic muscle may also add to the volume and therefore the pressure. Hemorrhage occurred in the soleus in this case and has been reported by others.’, 5,
13
The combination of hemorrhage which is not rapidly absorbed and continuation of the exercise for a prolonged period may produce swelling and elevated pressure above end-arteriolar filling. This results in ischemia of sufficient duration to cause necrosis of capillary walls and muscle. This in turn leads to extravasation of additional edema fluid,&dquo; initiating a self-perpetuating cycle resulting in increasing myonecrosis. Attempts at this stage to decrease the volume of the muscle mass and edema within the compartment by elevation, ice, and other various measures have been uniformly unsuccessful. The only alternative is therefore to increase the size of the compartment by decom-
pressive fasciotomy. This
case
demonstrates both the subacute and
types of the exertional compartment syndrome. For 3 weeks prior to admission, the patient had symptoms in the posterior leg which were acute
relieved by rest, indicating that the phenomenon reversible. The run on the day of admission precipitated edema and hemorrhage sufficient to produce the self-perpetuating edema-ischemia cycle. The physical fmdings of tenseness over the involved muscles and the marked pain on passive was
289
stretch of the gastrosoleus are consistent with the muscle ischemia and necrosis. Sensory deficit was present in the sural nerve that traverses the involved compartment. This case presented in 1973 prior to initiating clinical use of the wick catheter (July 1, 1974).l0 Since then we have used the wick to diagnose and treat acute and chronic compartment syndromes. Normal intracompartment pressure is 4 t 4 mm Hg. A pressure of 30 mm Hg or greater seems to be the critical level for immediate fasciotomy, based on our evaluation of more than 50 patients with suspected acute compartment syndromes.&dquo; Our preliminary data on chronic syndromes indicate that their resting and postexercise compartment pressures are significantly elevated compared with normals. The details of this data will be the subject of a future publication. SUMMARY
This
case
report of
an
acute
exertional compart-
syndrome involving predominantly the superficial posterior compartment emphasizes several important facts: ( 1 ) The subacute recurring syndromes, if left untreated, may develop into an acute syndrome. (2) The diagnostic findings separating the acute syndrome from the chronic forms are marked pain with passive stretch of the involved muscles, paresis, and sensory deficit. 8, 12, 15 (3) In the acute form, immediate fasciotomy is mandatory and often results in full recovery. (4) All four major compartments of the leg are susceptible to chronic or acute compartment syndromes initiated by exertion. These compartments can be decompressed as necessary through a limited skin incision as recently reported.&dquo; (5) The need for an easily obtainable and reproducible method for measuring intracompartment pressures (e.g., the wick catheter technique) is indicated. ment
REFERENCES 1.
Blandy JP, Fuller R: March gangrene. J Bone Joint Surg 39B: 679-693, 1957
290
2. Carter AB, Richards RB, Zachary B: The anterior tibial syndrome. Lancet 2: 928-934, 1949 3. French EB, Price WH: Anterior tibial pain. Br Med J 2: 1290-1296, 1962 4. Hargens AB, Akeson WH, Mubarak SJ, et al: Fluid balance within canine anterolateral compartment and its relationship to compartment syndromes. J Bone Joint Surg 60A: 499-505, 1978 5. Horn CE: Acute ischaemia of the anterior tibial muscle and the long extensor muscles of the toes. J Bone Joint Surg 27: 615-622, 1945 6. Kennelly BM, Blumberg L: Bilateral anterior tibial claudication. JAMA 203: 487-491, 1968 7. Kirby NG: Exericse ischaemia in the fascial compartment of soleus. J Bone Joint Surg 52B: 738-740, 1970 8. Leach RE, Hammond G, Stryker WS: Anterior tibial compartment syndrome. Acute and chronic. J Bone Joint Surg 49A: 45462, 1967 9. Mavor GE: The anterior tibial syndrome. J Bone Joint Surg 38B: 513-517, 1956 10. 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 58A: 1016-1020, 1976 11. Mubarak SJ, Owen CA: Double incision fasciotomy of the leg for decompression in compartment syndromes. J Bone Joint Surg 59A: 184-187, 1977 12. Mubarak SJ, Owen CA, Hargens AR, et al: Acute compartment syndromes: diagnosis and treatment with the aid of wick catheter. J Bone Joint Surg (in
press) 13. Pearson C, Adams RD, Denny-Brown D: Traumatic necrosis of pretibial muscles. N Engl J Med 231:
213-217, 1948 14. Puranen J: The medial tibial syndrome. J Bone Joint Surg 56B: 712-714, 1974 15. Reneman RS: The Anterior and the Lateral Compartment Syndrome of the Leg. Hague, Mouton and Co, 1968 16. Snook GA: Intermittent claudication in athletes. J Sports Med 3: 71-75, 1975 17. Vogt PR: Ischemic muscular necrosis following marching. Unpublished paper, Oregon State Medical Society Meeting, September 4, 1943. Cited by CE Horn (1945) 18. Wright S: Applied Physiology. Tenth edition. London, Oxford University Press, 1961
superficial posterior compartment syndrome*
SCOTT J. MUBARAK,† M.D., CHARLES A. OWEN,‡ M.D., STEVE M.D., AND ALAN R. HARGENS,¶ Ph.D., San Diego, California From the Division of Orthopaedic
Acute
GARFIN,§
Surgery, University of California, San Diego
f~cute and chronic exertional tibial
compart-
syndromes involving the four compartments of the leg following strenuous exercise or marching have been more frequently reported since the original description by Vogt in 1943 .17 Exercise-initiated syndromes involving the superficial posterior compartment (gastrocnemius and soleus muscles) are rare. Only Kirby’ and Snook16 describe chronic superficial posterior compartment syndromes in the English literature. We are reporting an acute superficial posterior compartment syndrome initiated by exercise, as well as, reviewing the availment
able literature.
the distance of each day’s run increased. The pain usually subsided 2 to 3 hr after exercise, but in the days prior to admission it lasted the entire day and into the following morning when he began running again. He noted a mild pain at rest on the day of admission, which became unbearable after he ran 3 miles. Prior to his recruitment he had been unaccustomed to vigorous exercise of any sort and had never experienced calf pain. Review of his past medical more severe as
history was unremarkable. Physical
Examination: The
patient
was a
well-
oriented, cooperative, 18-year-old male in moderPertinent physical findings related to his right leg. The leg was very swollen, tense, and tender, especially in the posterior aspect but also the lateral and anterior compartments. The extremity was held in 30° of flexion at the knee and 15°of plantar flexion at the ankle. Extension of the knee or dorsiflexion of the ankle caused excruciating pain in the calf. Passive flexion or extension of the toes caused mild pain in the anterior and posterior leg, respectively. Plantar flexion of the foot caused moderate pain in the anterior compartment. The circumference of the calf 13 cm below the tibial tubercle measured 42 cm on the right compared with 37 cm on the left. Motor examination was intact but limited by extreme pain. Sensory examination showed spotty decrease to light touch and pinprick along the lateral aspect of the right foot, corresponding to the sural nerve distribution. The posterior tibial and dorsalis pedis pulses were palpable. The initial diagnosis was that of a compartment syndrome with primary involvement of the superficial posterior compartment. ate to severe distress.
CASE HISTORY
were
Three weeks prior to his admission on October 1, 1973, an 18-year-old recruit noted pain involving his right calf following episodes of running for more than 1/2 mile. Pain was specifically in his posterior calf and became progressively
History:
* Supported by the Medical Research Service of the Veterans Administration and National Institutes of Health-United States Public Health Service Grant AM18224.
t Assistant Professor of Orthopaedic Surgery, University of California, San Diego, 225 West Dickinson Street, San Diego, California 92103. f Assistant Professor Orthopaedic Surgery, University of California, San Francisco, 4141 Geary Blvd., San Francisco, California
94118.
§ Division of Orthopaedic Surgery, Veterans Administration Hospital, San Diego, California 92161. 1) Orthopaedic Research, Veterans Administration Hospital, 3350 La Jolla Village, San Diego, California 92161.
287
Laboratory Studies: Urinalysis was normal, complete blood count normal, and hematocrit 37. One hr after admission, creatine phosphokinase was 320 IU (normal to 12) and lactate dehydrogenase 260 IU (normal to 200). Twelve hr after admission, creatine
phosphokinase was 270 and lactate dehydrogenase, 145. Thirty-six hr after admission,
for an increase in the hypesin the foot. Four hr after admission the patient was anesthetic in the first web space and hypesthetic on the dorsolateral aspect, and in a spotty distribution on the plantar surface of the foot. Because of the continued progression of signs of an exertional tibial compartment syndrome involving all four compartments, the decision was made to perform decompressive fasciotomy. Intra-
unchanged, except
thetic
area
phosphokinase was 150 and lactate dehydrogenase, 150. Radiographic examination of the leg was normal, except for soft tissue swelling. compartment pressure measurements were not obHospital Course: The extremity was elevated and tained. The patient was taken to the operating room cooled with ice. At 1 hr, examination revealed palpable pulses and normal motor strength, but where four compartment fasciotomies were peractive movements caused more severe pain. Pas- formed using a double skin incision approach (Fig. sive flexion and extension of the toes caused no 1 ). Swelling and hemorrhage were massive in the soleus muscle belly and moderate in the gastrocor at knee extension ankle dorsipain. Attempts flexion caused severe pain in the calf. Sensory nemius muscle belly. The anterior, lateral, and examination now showed decreased sensation to deep posterior compartment muscles were modpinprick and light touch in a spotty distribution erately swollen, but not hemorrhagic. All muscle involving the dorsolateral and plantar foot sur- seemed to be viable. The wounds were left open faces. Two hr after admission the examination was initially and closed 6 days later. Biopsy specimens creatinine
Fig. 1. Bulging soleus and gastrocnemius hemorrhage in that muscle. 288
muscle bellies
after fasciotomy.
The black
area
in the soleus
represents
of the soleus demonstrated edema and hemorrhage without necrosis, while those of the anterior tibial muscle showed only edema. The patient was treated in a long leg case for 3 weeks and then started on range of motion exercises. He had a complete return of both sensory and motor functions within I week. At 3-month follow-up, he had a full range of motion of both knee and ankle and had normal motor and sensory function of the right leg. DISCUSSION
In 1943 Volt17 first described an acute exertional anterior tibial compartment syndrome induced by marching. In 1957 Blandy and Fuller’ reported two cases of the acute syndrome with lateral compartment involvement. Reneman,15 in his literature review, notes that the anterior compartment has been involved in 46 cases, the lateral alone in 6 cases, and the combination of anterolateral in 6 acute syndromes. Except for the present case, an acute form of the exertional syndrome involving either the superficial posterior to deep posterior compartment has not been described previously. In 1956 Mavor9 presented the first case report of a chronic anterior compartment syndrome brought on by exertion. Since then, more than 60 other documented chronic cases involving either the anterior or a combination of the anterior and lateral compartments have been reported. 15 In 1970 Kirby’ described a case with bilateral chronic superficial posterior compartment syndromes; the symptoms were relieved by fasciotomies. Three additional cases of chronic syndromes in the su-
perficial posterior compartment were reported by Snook. 16 Eleven cases of exertional syndromes involving the deep posterior tibial compartment were reported in 1974 by Puranen.l4 The exact pathogenesis of the exertional tibial compartment syndrome is unknown. Muscle and nerve ischemia caused by elevated compartment pressure appears to be the immediate cause of pain and disability. Studies of this group of patients in 15 our laboratory and by others3, 6. have shown elevated pressures in the involved compartments at rest, and even higher pressures after exertion sufficient to precipitate symptoms. The factors responsible for the prolonged elevation of compartment pressures in certain individuals following exercise remain speculative. Ex-
plained simply, a compartment syndrome is a mechanical problem occurring when a mass of soft tissue (primarily muscle) is too large for the rigid
osseofascial compartment in which it is contained. It is known that once a critical level is reached, a very small increase in volume results in a very large increase in pressure.4 Individual variations in the relationship of muscle bulk to compartment volume may account for the susceptibility of certain individuals to development of the exertional syndromes. It is also of interest that a majority of the cases of exertional syndromes have occurred in well-trained athletes. This suggests that their hypertrophic muscle may decrease the space available for swelling within the relatively fixed volume
compartment.
Wrighe8 stated that muscle increases in bulk by 20%
following exercise. The swelling brought on by acute exercise may be sufficient in these susceptible individuals to raise pressures to critical levels&dquo; and cause muscle and nerve ischemia with
subsequent pain. Cessation of activity before muscle fiber and capillary wall necrosis occur can result in resorption of excess fluid volume, and decrease in compartment pressure with consequent relief of ischemia and pain. Hemorrhage from muscle rupture in either normal or ischemic muscle may also add to the volume and therefore the pressure. Hemorrhage occurred in the soleus in this case and has been reported by others.’, 5,
13
The combination of hemorrhage which is not rapidly absorbed and continuation of the exercise for a prolonged period may produce swelling and elevated pressure above end-arteriolar filling. This results in ischemia of sufficient duration to cause necrosis of capillary walls and muscle. This in turn leads to extravasation of additional edema fluid,&dquo; initiating a self-perpetuating cycle resulting in increasing myonecrosis. Attempts at this stage to decrease the volume of the muscle mass and edema within the compartment by elevation, ice, and other various measures have been uniformly unsuccessful. The only alternative is therefore to increase the size of the compartment by decom-
pressive fasciotomy. This
case
demonstrates both the subacute and
types of the exertional compartment syndrome. For 3 weeks prior to admission, the patient had symptoms in the posterior leg which were acute
relieved by rest, indicating that the phenomenon reversible. The run on the day of admission precipitated edema and hemorrhage sufficient to produce the self-perpetuating edema-ischemia cycle. The physical fmdings of tenseness over the involved muscles and the marked pain on passive was
289
stretch of the gastrosoleus are consistent with the muscle ischemia and necrosis. Sensory deficit was present in the sural nerve that traverses the involved compartment. This case presented in 1973 prior to initiating clinical use of the wick catheter (July 1, 1974).l0 Since then we have used the wick to diagnose and treat acute and chronic compartment syndromes. Normal intracompartment pressure is 4 t 4 mm Hg. A pressure of 30 mm Hg or greater seems to be the critical level for immediate fasciotomy, based on our evaluation of more than 50 patients with suspected acute compartment syndromes.&dquo; Our preliminary data on chronic syndromes indicate that their resting and postexercise compartment pressures are significantly elevated compared with normals. The details of this data will be the subject of a future publication. SUMMARY
This
case
report of
an
acute
exertional compart-
syndrome involving predominantly the superficial posterior compartment emphasizes several important facts: ( 1 ) The subacute recurring syndromes, if left untreated, may develop into an acute syndrome. (2) The diagnostic findings separating the acute syndrome from the chronic forms are marked pain with passive stretch of the involved muscles, paresis, and sensory deficit. 8, 12, 15 (3) In the acute form, immediate fasciotomy is mandatory and often results in full recovery. (4) All four major compartments of the leg are susceptible to chronic or acute compartment syndromes initiated by exertion. These compartments can be decompressed as necessary through a limited skin incision as recently reported.&dquo; (5) The need for an easily obtainable and reproducible method for measuring intracompartment pressures (e.g., the wick catheter technique) is indicated. ment
REFERENCES 1.
Blandy JP, Fuller R: March gangrene. J Bone Joint Surg 39B: 679-693, 1957
290
2. Carter AB, Richards RB, Zachary B: The anterior tibial syndrome. Lancet 2: 928-934, 1949 3. French EB, Price WH: Anterior tibial pain. Br Med J 2: 1290-1296, 1962 4. Hargens AB, Akeson WH, Mubarak SJ, et al: Fluid balance within canine anterolateral compartment and its relationship to compartment syndromes. J Bone Joint Surg 60A: 499-505, 1978 5. Horn CE: Acute ischaemia of the anterior tibial muscle and the long extensor muscles of the toes. J Bone Joint Surg 27: 615-622, 1945 6. Kennelly BM, Blumberg L: Bilateral anterior tibial claudication. JAMA 203: 487-491, 1968 7. Kirby NG: Exericse ischaemia in the fascial compartment of soleus. J Bone Joint Surg 52B: 738-740, 1970 8. Leach RE, Hammond G, Stryker WS: Anterior tibial compartment syndrome. Acute and chronic. J Bone Joint Surg 49A: 45462, 1967 9. Mavor GE: The anterior tibial syndrome. J Bone Joint Surg 38B: 513-517, 1956 10. 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 58A: 1016-1020, 1976 11. Mubarak SJ, Owen CA: Double incision fasciotomy of the leg for decompression in compartment syndromes. J Bone Joint Surg 59A: 184-187, 1977 12. Mubarak SJ, Owen CA, Hargens AR, et al: Acute compartment syndromes: diagnosis and treatment with the aid of wick catheter. J Bone Joint Surg (in
press) 13. Pearson C, Adams RD, Denny-Brown D: Traumatic necrosis of pretibial muscles. N Engl J Med 231:
213-217, 1948 14. Puranen J: The medial tibial syndrome. J Bone Joint Surg 56B: 712-714, 1974 15. Reneman RS: The Anterior and the Lateral Compartment Syndrome of the Leg. Hague, Mouton and Co, 1968 16. Snook GA: Intermittent claudication in athletes. J Sports Med 3: 71-75, 1975 17. Vogt PR: Ischemic muscular necrosis following marching. Unpublished paper, Oregon State Medical Society Meeting, September 4, 1943. Cited by CE Horn (1945) 18. Wright S: Applied Physiology. Tenth edition. London, Oxford University Press, 1961
