Intermittent claudication caused by compression of tibial vessels as a result of calf muscle hypertrophy: Case report Angela Mailis, M D , MSc, F R C P C , Alan Lossing, BSc, M D , F R C S C , Peter Ashby, M B , M D , M R C P ( L o n d ) , F R C P ( E d ) , F R C P C , and Jacob Abarbanel, M D , Toronto, Ontario, Canada
We present a case with findings suggestive of popliteal artery entrapment in a patient with intermittent claudication and localized muscle hypertrophy in the calf muscles after removal of a herniated disk. Angiography failed to demonstrate popliteal artery entrapment but instead revealed compression of the tibial vessels caused by calf muscle hypertrophy. The concept of muscle hypertrophy caused by denervation is also discussed. (J VASC SURG 1992;16:116-20.)
We present the case o f a 50-year-old man in w h o m severe right calf hypertrophy and pain developed after a diskectomy.
CASE REPORT In 1982 back pain developed in a 50-year-old man and included right sciatica with hypoesthesia of the lateral foot and calf weakness and atrophy. Six months later he underwent L5-$1 diskectomy and decompression of the right S-1 root, which completely relieved back and leg pain, but the hypoesthesia remained. Two months after operation he returned to his job. Over the next 12 to 15 months he noticed gradual increase in his right calf size, and by that time he started having calf pressure primarily below the knee level. In 1985 he noted rippling of the calfmuscles. An extensive calf muscle biopsy showed marked fiber hypertrophy with central migration of nuclei, with type 1 fiber predominance as well as areas of atrophy with type grouping. The patient thought that after the extended muscle biopsy the calf hypertrophy was accelerated. Electtomyography of the right calf in 1985 showed chronic neurogenic changes with significant fasciculations and fibrillations. The patient underwent numerous orthopedic, neurologic, and neurosurgical consultations. He was told that his pain and his calf hypertrophy were caused by irritation of his S-1 root, and no surgical intervention was possible. By 1988 the patient became permanently disabled. By the summer of 1989 he was referred to the Pain Investigation Unit, at the Toronto Western Hospital. At the time of admission he complained mainly of From the Departments of Medicine and Surgery, University of Toronto, Toronto, Ontario, Canada. Reprint requests: AngelaMailis, MD, Director,Pain Investigation Unit, 328-11MP, Toronto WesternHospital, 399 Bathurst St., Toronto, Ontario M5T 2S8 Canada. 24/4/35439 116
constant moderate boring tight calf pain localized behind the knee as well as at the calf and severe numbness at the posterior calf, the lateral foot, and the toes. The discomfort was severely aggravated by walking. There was intermittent hyperalgesia, and contact with the bed clothes was unbearable. He reported spasms of the right leg and visible rippling of the right calf. He had some back pain intermittently, which he thought was a minimal complaint, and it was aggravated by bending or lifting. He had no other complaints. Past medical history was only positive for hypertension and kidney stones 12 years previously. There was a strong family history of diabetes, but the patient was not diabetic. On examination the right calf only appeared impressively hypertrophic (Fig. 1). There were no color or temperature changes, and the peripheral pulses were strongly palpable. There was loss of right ankle jerk and hypoesthesia in the tight S-1 root distribution. Muscle strength was normal in both legs except for minimal weakness in the right toe plantar flexion. Straight leg raising both in the sitting and supine position to the right side at 70 degrees produced pulling and tingling across all toes. There was no detectable hyperalgesia or allodynia, and deep calf palpation did not alter his constant deep-seated calf discomfort. Back examination revealed local midline lumbosacral tenderness and pain aggravated by back extension. Investigations in the hospital Relevant investigations were as follows: radiographs o f the lumbosacral spine showed mild lumbosacral disk degeneration. Lumbosacral spine C r scanning showed mild spinal stenosis at the L4-5 level as a result o f facet joint hypertrophy and increased soft tissue density at the L5-$1 level causing deviation o f the thecal sac to the right. This was
Volume 16 Number 1 July 1992
Compression of tibial vesselscaused by muscle hypertrophy 117
Fig. 1. Posterior view of both calves. Scar in right calf is a result of large muscle biopsy site after which the patient thought his hypertrophy progressed further. consistent with fibrosis. Arterial Doppler study of the legs demonstrated an ankle-brachial index (ABI) of 1.0 in both legs. However, on dorsiflexion of the right ankle the index dropped to 0.52. There was no change with flexion of the right knee. Furthermore, there was no change in the ABI on the left side with dorsiflexion of the ankle. Posterior compartment opening pressures after exercise were 5 to 7 mm Hg (normal). CT scanning with intravenous contrast and magnetic resonance imaging of the extremity revealed hypertrophy of the right gastrocnemius/soleus muscle with some diffuse fatty infiltration in the distal third of the calf. No asymmetry of the popliteal artery was seen. Concentric needle electromyography studies showed spontaneous activity in the right leg of two types: fibrillations and complex repetitive discharges present only in the soleus and medial/lateral gastrocnemius. Voluntary activity included many long-duration polyphasic potentials, some of them up to 10 mV in amplitude. Venous blood gases were tested from the left and right foot before and after walking. Within 5 to 10 minutes of stair climbing the patient complained of his familiar severe cramping pain, and the right dorsal pedal pulse became nonobtainable. At that time the venous blood 0 2 saturation to the right foot fell dramatically indicating considerable ischemia. Finally, femoral angiography demonstrated the following: With the right leg in neutral position (Fig. 2) no abnormalities were noted. With the right knee flexed and the ankle
Fig. 2. Angiography: Right calf with ankle and knee joints in neutral position.
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Fig. 3. Angiography: Anteroposterior view of right knee with dorsiflexed ankle.
Fig. 4. Angiography: Lateral view of right knee with dorsiflexed ankle.
dorsiflexed or plantaffiexed anterior (Fig. 3) and lateral (Fig. 4), popliteal artery views were normal. However, with the ankle dorsiflexed, views of peroneal and posterior tibial arteries showed severe attenuation of those vessels (Fig. 5). A high-flow torque control cobra visceral catheter (Cook Inc., Bloomington, Ind.) was inserted and same views in the left side (Fig. 6) did not demonstrate similar findings. Lumbar sympathetic blocks failed to relieve both the resting discomfort and the severely exacerbated leg pain on walking.
of marked fiber hypertrophy and areas of fiber atrophy. Although wasting is the most common pathologic reaction to denervation, rarely do the denervated muscles become hypertrophic instead of atrophic. This has been reported in disorders of peripheral nerves, 1,2 roots, 36 and anterior horn cellsf 9 All the reported cases of denervation hypertrophy were associated with longstanding "partial denervation." The complex repetitive discharges with low jitter in the electromyography (also seen in myopathies) indicate a muscle cell of origin. The current hypothesis is that one fiber serves as a pacemaker initiating the activity which propagates ephaptically in neighboring fibers) ° The second issue is calf pain. The patient's calf cramping pain (on walking) was considered to be primarily ischemic, arising from compression of the tibial vessels within the bulk of the hypertrophic gastrosoleus muscle. The resting pain was primarily attributed to nerve root fibrosis (neuropathic pain)
DISCUSSION There are several interesting issues with this patient's appearance: The first is that of calf hypertrophy. After the L5-$1 disk removal the previously wasted calf changed behavior and became hypertrophied with rippling contractions of the gastrocnemius muscle. Pathologic examination of the muscle showed areas
Volume 16 Number 1 JuJy 1992
Compression of tibial vessels caused by muscle hypertrophy 119
Fig. 5. Angiography: Anteroposterior view of right calf with dorsiflexed ankle. Severe narrowing of tibial and peroneal vessels (arrow).
Fig. 6. Angiography: Anteroposterior view of left calf with dorsiflexed ankle. Tibial and peroneal vessels are normal in caliper.
and could contribute to a degree to the walking discomfort as well. Originally the diagnosis of chronic compartment syndrome or popliteal artery entrapment syndrome was questioned. The patient's posterior compartment pressures, however, were normal. We recognize the fact that measurement error may be a possibility. Given the size of the patient's muscle compartment, we found it unusual that the posterior compartment was not involved. As far as the popliteal artery entrapment syndrome is concerned, it has been identified in detail. 11 Reported cases and series focus on the popliteal fossa as the site of the abnormality. H13 Some authors have reported on the validity of noninvasive testing in the diagnosis of popliteal entrapment. 1~,1s Angiography in our patient did not support the diagnosis of popliteal artery entrapment syndrome. Actually, the popliteal artery in all views, including anterior and
medial aspects both in neutral and dorsiflexed position, was normal. In contrast, the tibial and peroneal arteries were severely narrowed on dorsiflexion of the ankle only in the involved hypertrophied leg. From the arterial point of view, the only treatment we thought indicated was a fasciotomy. From the neuropathic point of view the only available treatment was a trial of spinal stimulator. The patient refused all offered treatments. REFERENCES
1. Walenstein E, Watson RT, Parker LJ. Myokymiamuscle hypertrophy and percussion myotonia in chronic recurrent polyneuropathy.Neurology1978;28:1130-4. 2. Visser M, Hodjedijk JE, Visser BWO, Verbeeten B. Calf enlargement in hereditary motor and sensory neuropathy. Muscle Nerve 1990;13:40-5. 3. Bernat JL, Ochoa JL. Muscle hypertrophy after partial denervation. A human case. J Neurol Neurosurg Psychiatry 1978;41:719-25.
120
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Wlailis et al.
4. Mielke U, Richer K, Emser W, Boxier K. Unilateral calf enlargement following S1 radiculopathy. Muscle Nerve 1982; 5:434-8. 5. Montagna P, Martinelli P, Rasi F, Cirignotta F, Govoni E, Lugaresi E. Muscular hypertrophy after chronic radiculopathy. Arch Neurol 1984;41:397-8. 6. Visser M, Verbeeten B, Lyppens KCH. Pseudohypertrophy of the calf following $1 radiculopathy. Neuroradiology 1986;28:279-80. 7. Pearn J, Hudgson P. Anterior horn cell degeneration and gross calf hypertrophy with adolescent onset. Lancet 1978; 2:1059-61. 8. Fetell MR, Smallnerg J, Lewis LD, Lovelace RE, Hays AP, Rowland LP. A benign motor neuron disorder: delayed cramps and fasciculations after poliomyelitis or myelitis. Ann Neurol 1982;11:423-7. 9. D'Alessandro R, Montagna P, Govoni E, Pazzaglia P. Benign familial spinal muscular atrophy with hypertrophy of the calves. Arch Neurol 1982;39:656-60. 10. Trontelj J, Stalberg E. Bizarre repetitive discharges recorded
11. 12. 13. 14. 15.
with single fiber EMG. J Neurol Neurosurg Psychiatry 1983;46:310-6. Bouhoutsos J, Daskalakis E. Muscular abnormalities affecting the popliteal vessels. Br J Surg 1981;68:501-6. Delaney TA, Gonzales LL. Occlusion of popliteal artery due to muscular entrapment. Surgery 1971;69:97-101. Inada K, Hirose Y, Iwashima Y, Matsumoto K. Popliteal artery entrapment syndrome: a case report. Br )" Surg 1978;65:613-5. Miles S, Roedeger W, Cooke P, et al. Doppler ultrasound in the diagnosis of popliteal entrapment syndrome. Br J Surg 1977;64:883-4. Bouhoutsos J, Argyropoulos G, Papadiamantopoulos P. Doppler records at the ankle in the diagnosis of popliteal artery entrapment. Presented at Fifth Panhellenic Congress of the Medical Societies, October 1979, Athens, Greece.
Submitted July 30, 1991; accepted Nov. 29, 1991.
LIEBIG FOUNDATION AWARD FOR VASCULAR SURGICAL RESEARCH, 1993 The Liebig Foundation announces the eleventh annual competitive award of $10,000 for the best essay on a problem in general vascular surgery. The investigative work shall be: 1. Clinical or experimental research 2. Original and unpublished (not submitted elsewhere for publication) 3. Performed by a house officer in the United States, Canada, or Mexico, with senior collaborators acting in a consultive capacity 4. Submitted in English (6 copies of typed manuscript and 6 copies of glossy prints of illustrations) 5. Accompanied by a signed letter from the essayist's superior confirming the status of the essayist and complying with "Information for Authors" of the JOURNAL The submitted manuscripts will be evaluated by a select committee of vascular surgeons. The manuscript judged best will be submitted to the Program Committee of the Southern Association for Vascular Surgery for consideration for inclusion on its 1993 scientific program and publication in the JOURNALOF VASCULARSURGERY. Further inquiries may be directed to the same address to which the essays must be sent, postmarked no later than Sept. 15, 1992. Dr. Richard Turner Award Committee Secretary 112 Bauer Dr. Oakland, NJ 07436 USA (201)337-6126
We present a case with findings suggestive of popliteal artery entrapment in a patient with intermittent claudication and localized muscle hypertrophy in the calf muscles after removal of a herniated disk. Angiography failed to demonstrate popliteal artery entrapment but instead revealed compression of the tibial vessels caused by calf muscle hypertrophy. The concept of muscle hypertrophy caused by denervation is also discussed. (J VASC SURG 1992;16:116-20.)
We present the case o f a 50-year-old man in w h o m severe right calf hypertrophy and pain developed after a diskectomy.
CASE REPORT In 1982 back pain developed in a 50-year-old man and included right sciatica with hypoesthesia of the lateral foot and calf weakness and atrophy. Six months later he underwent L5-$1 diskectomy and decompression of the right S-1 root, which completely relieved back and leg pain, but the hypoesthesia remained. Two months after operation he returned to his job. Over the next 12 to 15 months he noticed gradual increase in his right calf size, and by that time he started having calf pressure primarily below the knee level. In 1985 he noted rippling of the calfmuscles. An extensive calf muscle biopsy showed marked fiber hypertrophy with central migration of nuclei, with type 1 fiber predominance as well as areas of atrophy with type grouping. The patient thought that after the extended muscle biopsy the calf hypertrophy was accelerated. Electtomyography of the right calf in 1985 showed chronic neurogenic changes with significant fasciculations and fibrillations. The patient underwent numerous orthopedic, neurologic, and neurosurgical consultations. He was told that his pain and his calf hypertrophy were caused by irritation of his S-1 root, and no surgical intervention was possible. By 1988 the patient became permanently disabled. By the summer of 1989 he was referred to the Pain Investigation Unit, at the Toronto Western Hospital. At the time of admission he complained mainly of From the Departments of Medicine and Surgery, University of Toronto, Toronto, Ontario, Canada. Reprint requests: AngelaMailis, MD, Director,Pain Investigation Unit, 328-11MP, Toronto WesternHospital, 399 Bathurst St., Toronto, Ontario M5T 2S8 Canada. 24/4/35439 116
constant moderate boring tight calf pain localized behind the knee as well as at the calf and severe numbness at the posterior calf, the lateral foot, and the toes. The discomfort was severely aggravated by walking. There was intermittent hyperalgesia, and contact with the bed clothes was unbearable. He reported spasms of the right leg and visible rippling of the right calf. He had some back pain intermittently, which he thought was a minimal complaint, and it was aggravated by bending or lifting. He had no other complaints. Past medical history was only positive for hypertension and kidney stones 12 years previously. There was a strong family history of diabetes, but the patient was not diabetic. On examination the right calf only appeared impressively hypertrophic (Fig. 1). There were no color or temperature changes, and the peripheral pulses were strongly palpable. There was loss of right ankle jerk and hypoesthesia in the tight S-1 root distribution. Muscle strength was normal in both legs except for minimal weakness in the right toe plantar flexion. Straight leg raising both in the sitting and supine position to the right side at 70 degrees produced pulling and tingling across all toes. There was no detectable hyperalgesia or allodynia, and deep calf palpation did not alter his constant deep-seated calf discomfort. Back examination revealed local midline lumbosacral tenderness and pain aggravated by back extension. Investigations in the hospital Relevant investigations were as follows: radiographs o f the lumbosacral spine showed mild lumbosacral disk degeneration. Lumbosacral spine C r scanning showed mild spinal stenosis at the L4-5 level as a result o f facet joint hypertrophy and increased soft tissue density at the L5-$1 level causing deviation o f the thecal sac to the right. This was
Volume 16 Number 1 July 1992
Compression of tibial vesselscaused by muscle hypertrophy 117
Fig. 1. Posterior view of both calves. Scar in right calf is a result of large muscle biopsy site after which the patient thought his hypertrophy progressed further. consistent with fibrosis. Arterial Doppler study of the legs demonstrated an ankle-brachial index (ABI) of 1.0 in both legs. However, on dorsiflexion of the right ankle the index dropped to 0.52. There was no change with flexion of the right knee. Furthermore, there was no change in the ABI on the left side with dorsiflexion of the ankle. Posterior compartment opening pressures after exercise were 5 to 7 mm Hg (normal). CT scanning with intravenous contrast and magnetic resonance imaging of the extremity revealed hypertrophy of the right gastrocnemius/soleus muscle with some diffuse fatty infiltration in the distal third of the calf. No asymmetry of the popliteal artery was seen. Concentric needle electromyography studies showed spontaneous activity in the right leg of two types: fibrillations and complex repetitive discharges present only in the soleus and medial/lateral gastrocnemius. Voluntary activity included many long-duration polyphasic potentials, some of them up to 10 mV in amplitude. Venous blood gases were tested from the left and right foot before and after walking. Within 5 to 10 minutes of stair climbing the patient complained of his familiar severe cramping pain, and the right dorsal pedal pulse became nonobtainable. At that time the venous blood 0 2 saturation to the right foot fell dramatically indicating considerable ischemia. Finally, femoral angiography demonstrated the following: With the right leg in neutral position (Fig. 2) no abnormalities were noted. With the right knee flexed and the ankle
Fig. 2. Angiography: Right calf with ankle and knee joints in neutral position.
118
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lOUrllal of VASCUI_.AR SURGERY
Fig. 3. Angiography: Anteroposterior view of right knee with dorsiflexed ankle.
Fig. 4. Angiography: Lateral view of right knee with dorsiflexed ankle.
dorsiflexed or plantaffiexed anterior (Fig. 3) and lateral (Fig. 4), popliteal artery views were normal. However, with the ankle dorsiflexed, views of peroneal and posterior tibial arteries showed severe attenuation of those vessels (Fig. 5). A high-flow torque control cobra visceral catheter (Cook Inc., Bloomington, Ind.) was inserted and same views in the left side (Fig. 6) did not demonstrate similar findings. Lumbar sympathetic blocks failed to relieve both the resting discomfort and the severely exacerbated leg pain on walking.
of marked fiber hypertrophy and areas of fiber atrophy. Although wasting is the most common pathologic reaction to denervation, rarely do the denervated muscles become hypertrophic instead of atrophic. This has been reported in disorders of peripheral nerves, 1,2 roots, 36 and anterior horn cellsf 9 All the reported cases of denervation hypertrophy were associated with longstanding "partial denervation." The complex repetitive discharges with low jitter in the electromyography (also seen in myopathies) indicate a muscle cell of origin. The current hypothesis is that one fiber serves as a pacemaker initiating the activity which propagates ephaptically in neighboring fibers) ° The second issue is calf pain. The patient's calf cramping pain (on walking) was considered to be primarily ischemic, arising from compression of the tibial vessels within the bulk of the hypertrophic gastrosoleus muscle. The resting pain was primarily attributed to nerve root fibrosis (neuropathic pain)
DISCUSSION There are several interesting issues with this patient's appearance: The first is that of calf hypertrophy. After the L5-$1 disk removal the previously wasted calf changed behavior and became hypertrophied with rippling contractions of the gastrocnemius muscle. Pathologic examination of the muscle showed areas
Volume 16 Number 1 JuJy 1992
Compression of tibial vessels caused by muscle hypertrophy 119
Fig. 5. Angiography: Anteroposterior view of right calf with dorsiflexed ankle. Severe narrowing of tibial and peroneal vessels (arrow).
Fig. 6. Angiography: Anteroposterior view of left calf with dorsiflexed ankle. Tibial and peroneal vessels are normal in caliper.
and could contribute to a degree to the walking discomfort as well. Originally the diagnosis of chronic compartment syndrome or popliteal artery entrapment syndrome was questioned. The patient's posterior compartment pressures, however, were normal. We recognize the fact that measurement error may be a possibility. Given the size of the patient's muscle compartment, we found it unusual that the posterior compartment was not involved. As far as the popliteal artery entrapment syndrome is concerned, it has been identified in detail. 11 Reported cases and series focus on the popliteal fossa as the site of the abnormality. H13 Some authors have reported on the validity of noninvasive testing in the diagnosis of popliteal entrapment. 1~,1s Angiography in our patient did not support the diagnosis of popliteal artery entrapment syndrome. Actually, the popliteal artery in all views, including anterior and
medial aspects both in neutral and dorsiflexed position, was normal. In contrast, the tibial and peroneal arteries were severely narrowed on dorsiflexion of the ankle only in the involved hypertrophied leg. From the arterial point of view, the only treatment we thought indicated was a fasciotomy. From the neuropathic point of view the only available treatment was a trial of spinal stimulator. The patient refused all offered treatments. REFERENCES
1. Walenstein E, Watson RT, Parker LJ. Myokymiamuscle hypertrophy and percussion myotonia in chronic recurrent polyneuropathy.Neurology1978;28:1130-4. 2. Visser M, Hodjedijk JE, Visser BWO, Verbeeten B. Calf enlargement in hereditary motor and sensory neuropathy. Muscle Nerve 1990;13:40-5. 3. Bernat JL, Ochoa JL. Muscle hypertrophy after partial denervation. A human case. J Neurol Neurosurg Psychiatry 1978;41:719-25.
120
Journal of VASCULAR SURGERY
Wlailis et al.
4. Mielke U, Richer K, Emser W, Boxier K. Unilateral calf enlargement following S1 radiculopathy. Muscle Nerve 1982; 5:434-8. 5. Montagna P, Martinelli P, Rasi F, Cirignotta F, Govoni E, Lugaresi E. Muscular hypertrophy after chronic radiculopathy. Arch Neurol 1984;41:397-8. 6. Visser M, Verbeeten B, Lyppens KCH. Pseudohypertrophy of the calf following $1 radiculopathy. Neuroradiology 1986;28:279-80. 7. Pearn J, Hudgson P. Anterior horn cell degeneration and gross calf hypertrophy with adolescent onset. Lancet 1978; 2:1059-61. 8. Fetell MR, Smallnerg J, Lewis LD, Lovelace RE, Hays AP, Rowland LP. A benign motor neuron disorder: delayed cramps and fasciculations after poliomyelitis or myelitis. Ann Neurol 1982;11:423-7. 9. D'Alessandro R, Montagna P, Govoni E, Pazzaglia P. Benign familial spinal muscular atrophy with hypertrophy of the calves. Arch Neurol 1982;39:656-60. 10. Trontelj J, Stalberg E. Bizarre repetitive discharges recorded
11. 12. 13. 14. 15.
with single fiber EMG. J Neurol Neurosurg Psychiatry 1983;46:310-6. Bouhoutsos J, Daskalakis E. Muscular abnormalities affecting the popliteal vessels. Br J Surg 1981;68:501-6. Delaney TA, Gonzales LL. Occlusion of popliteal artery due to muscular entrapment. Surgery 1971;69:97-101. Inada K, Hirose Y, Iwashima Y, Matsumoto K. Popliteal artery entrapment syndrome: a case report. Br )" Surg 1978;65:613-5. Miles S, Roedeger W, Cooke P, et al. Doppler ultrasound in the diagnosis of popliteal entrapment syndrome. Br J Surg 1977;64:883-4. Bouhoutsos J, Argyropoulos G, Papadiamantopoulos P. Doppler records at the ankle in the diagnosis of popliteal artery entrapment. Presented at Fifth Panhellenic Congress of the Medical Societies, October 1979, Athens, Greece.
Submitted July 30, 1991; accepted Nov. 29, 1991.
LIEBIG FOUNDATION AWARD FOR VASCULAR SURGICAL RESEARCH, 1993 The Liebig Foundation announces the eleventh annual competitive award of $10,000 for the best essay on a problem in general vascular surgery. The investigative work shall be: 1. Clinical or experimental research 2. Original and unpublished (not submitted elsewhere for publication) 3. Performed by a house officer in the United States, Canada, or Mexico, with senior collaborators acting in a consultive capacity 4. Submitted in English (6 copies of typed manuscript and 6 copies of glossy prints of illustrations) 5. Accompanied by a signed letter from the essayist's superior confirming the status of the essayist and complying with "Information for Authors" of the JOURNAL The submitted manuscripts will be evaluated by a select committee of vascular surgeons. The manuscript judged best will be submitted to the Program Committee of the Southern Association for Vascular Surgery for consideration for inclusion on its 1993 scientific program and publication in the JOURNALOF VASCULARSURGERY. Further inquiries may be directed to the same address to which the essays must be sent, postmarked no later than Sept. 15, 1992. Dr. Richard Turner Award Committee Secretary 112 Bauer Dr. Oakland, NJ 07436 USA (201)337-6126
