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Thrombosis of the Axillary Artery Secondary to Compression by the Pectoralis Minor Muscle
Thrombosis of the Axillary Artery Secondary to Compression by the Pectoralis Minor Muscle Joel A. Finkelstein, MD, and K. Wayne Johnston, MD, FRCS(C), Toronto, Ontario, Canada
This case presentation reports the second case of axillary artery thrombosis secondary to pectoralis minor compression. Evidence to explain this etiology is presented from arteriographic and intraoperative clinical findings. Management includes division of the pectoralis minor muscle and local arterial repair if the vessel is severely damaged. (Ann Vasc Surg 1993;7:287-290.)
In t h e s p e c t r u m of t h o r a c i c o u t l e t s y n d r o m e , arterial c o m p r e s s i o n occurs in less t h a n 5 % of all p a tients. ~ C o m p r e s s i o n of t h e s u b c l a v i a n a r t e r y is p r i m a r i l y in t h e c o s t o s c a l e n e p a s s a g e w h e r e b o n y a b n o r m a l i t i e s , i n c l u d i n g cervical ribs a n d fibrous bands, h a v e b e e n r e c o g n i z e d . 2 Less f r e q u e n t l y , c o m p r e s s i o n m a y o c c u r at t h e c o s t o c l a v i c u l a r space. ~ The i m p o r t a n c e of t h e . h y p e r a b d u c t i o n s y n d r o m e a n d t h e p e c t o r a l i s m i n o r t e n d o n as a cause of axillary a r t e r y c o m p r e s s i o n h a s also b e e n well described. 4-6 H o w e v e r , to o u r k n o w l e d g e , o n l y o n e case of a x i l l a r y a r t e r y t h r o m b o s i s s e c o n d a r y to pectoralis m i n o r c o m p r e s s i o n h a s b e e n reported. ~ W e r e p o r t a case of a x i l l a r y a r t e r y t h r o m bosis s e c o n d a r y to c o m p r e s s i o n b y t h e p e c t o r a l i s m i n o r w i t h t h r o m b o e m b o l i s m o c c l u d i n g t h e radial a n d u l n a r arteries.
CASE R E P O R T This 56-year-old right-handed w o m a n had experienced coolness, paleness, and pain in her right hand and forearm for 3 days prior to presentation. There was associated numbness of the fingertips. For several months
From the Division of Vascular Surgery, The Toronto Hospital, University of Toronto, Toronto, Ontario, Canada. Reprint requests: K. W. Johnston, MD, TorontoHospital, General Division, 9th Floor, Eaton Wing North, 200 Elizabeth St., Toronto, Ontario, Canada MSG 2C4.
she also noted rapid fatigue of her right arm with activity. The patient was a nonsmoker, had no cardiac history, and was not a diabetic. Her only medication was estrogen replacement. Examination revealed a cold right hand and forearm up to the elbow. Radial, ulnar, and brachial pulses were not palpable in the right arm, although the supraclavicular subclavian artery and the axillary artery pulses were normal. Faint monophasic Doppler signals were present at the brachial and ulnar arteries but no blood pressure was obtained. All pulses were present in the left arm and blood pressure in the left a r m was 140/80 m m Hg. The ECG demonstrated a normal sinus rhythm. A chest x-ray film showed no evidence of a cervical rib. An arteriogram of the right arm showed patent subclavian and proximal axillary arteries and a nonocclusive intravascular filling defect in the second part of the axillary artery (Fig. 1). The radial artery at the midforearm and the proximal ulnar artery were occluded and distal filling was not demonstrated. Because of severe ischemia with sensory symptoms the patient was taken to the operating room. At this stage the presumptive diagnosis was embolism. Brachial arteriotomy was used because we believed that the major technical problem would be to clear her occluded distal arteries and not the partially occluding axillary artery lesion. With the use of a Fogarty catheter, thromboric material was retrieved from the axillary artery and excellent arterial inflow was established. The radial artery was also successfully cleared of white thrombotic and/or embolic material. The site of the axillary artery thrombus shown in Fig. 1 was not explored at the initial 287
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Fig. 1. Arteriogram showing nonocclusive mural thrombus present at the second portion of the axillary artery (arrow).
operation because we were not certain if this represented embolic material from a proximal source or a primary arterial abnormality and believed that further investigation was warranted. Postoperatively arterial perfusion and pulses were normal and the patient was asymptomatic. Brachial blood pressures were equal in both arms and arterial duplex Doppler studies showed normal symmetric waveforms from the brachial, radial, and ulnar arteries. An echocardiogram showed no abnormalities of the heart. A repeat arteriogram showed an eccentric irregularity in the axillary artery at the site of previous thrombus (Fig. 2, A). Because of the unusual site of the original arterial lesion, another arteriogram was obtained with the shoulder and arm in different positions. With hyperabduction of the arm, focal narrowing was present at the second part of the axillary artery in the region of the pectoralis minor muscle (Fig. 2, B). We thought this was the most likely explanation for her arterial injury and thrombus formation. She was taken to the operating room a second time, and through a subclavicular transverse skin incision,
the pectoralis minor was divided from its insertion into the coracoid process. Scarring of the adventitia of the axillary artery under the pectoralis muscle was apparent. Movement of the shoulder showed that with elevation above shoulder level the artery was pulled proximal and anterior in such a manner that it was compressed by the pectoralis minor musde. The artery was not opened to inspect the extent of the intimal injury because the arteriogram showed no major defect, clinical examination of the artery did not reveal significant mural thickening or other abnormalities apart from the obvious adventitiaI scarring, and we believed that the vessel would heal after relief of the initiating cause. The patient made a good postoperative recovery and was discharged on oral anticoagulants for 6 months. The follow-up vascular examination and noninvasive assessment were normal at 9 months.
DISCUSSION T h e r e h a v e b e e n several reports of n e u r o v a s c u l a r c o m p r e s s i o n r e q u i r i n g release of the pectoralis
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Thrombosis of axillary artery 289
A
B
Fig. 2. A, Following axillary artery thrombectomy, repeat arteriograms revealed a small irregularity present at the site of the previous thrombus (arrow). B, Abduction of the arm caused focal narrowing of the second portion of the axillary artery by the pectoralis m i n o r muscle (arrow).
minor tendon. 5.e' McCarthy et al. 8 reported three athletes with axillary artery compression by the pectoralis minor, none of w h o m had arterial thrombosis. Tullos et a17 reported the only previous case of axillary artery thrombosis due to compression by the pectoralis minor muscle in a baseball pitcher. W h e n a nonocclusive axillary artery thrombosis is present, signs and s y m p t o m s can include claudication, rapid fatigue, decreased distal pulses, pallor, and diminished skin temperature. Arterial complications of thoracic outlet syndrome are always secondary to long-standing compression. The pathophysiology of arterial t h r o m b o e m b o lism secondary to thoracic outlet syndrome has
been well described. 9Extrinsic compression on the axillary artery leads to arterial injury, intimal ulceration, platelet thrombus, and peripheral embolization, which can cause occlusion of the radial and ulnar arteries, as likely occurred in our patient. Occlusion of the arteries of the upper extremities due to atherosclerosis is relatively u n c o m m o n . W h e n present, however, the usual site is in the proximal part of the subclavian artery, most often involving the arch of the aorta on the left and the innominate artery on the right.~° In our patient, e v e n though the circulation to her limb was satisfactorily reestablished following t h r o m b e c t o m y and embolectomy, a postoperative
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arteriogram established a cause for the arterial occlusion. The arteriogram revealed the location of the arterial narrowing (Fig. 2, A) and d e m o n strated partial obstruction with hyperabduction, which suggested the etiology (Fig. 2, B). Further, at operation u n d e r direct vision and with the arm freely draped to allow m o v e m e n t of the shoulder, the offending pectoralis minor muscle proved to be the cause. After the pectoralis minor was detached from the coracoid process, significant scarring of the adventitia of the axillary artery b e n e a t h the muscle was apparent. The artery was not damaged e n o u g h to warrant repair; however, the patient was anticoagulated for 6 m o n t h s to minimize the risk of t h r o m b o e m b o l i s m while the artery was healing.
CONCLUSION To our knowledge, this is only the second report of axillary artery thrombosis secondary to compression by the pectoralis minor. The pathology in this case was complicated by severe distal embolization causing complete occlusion of the radial and ulnar arteries. Although compression of the artery is rare at this site, recognition that the pectoralis minor muscle is a potential cause of axillary artery compression is important. Division of this tendon from
Commentary Richard J. Sanders, MD, and Michael A. Cooper, MD
This is indeed a rare condition that raises two controversial questions of management. First, the initial operation could have been pectoralis minor t e n o t o m y and open axillary artery thrombectomy. At that time, if there was intimal ulceration, the artery could have been replaced. Experience has s h o w n that this will usually restore the hand to normal even t h o u g h the ulnar and radial arteries remain occluded. Distal thrombectomy, which is fraught with m a n y hazards, can thus be avoided. This view is championed by the French surgeon Cormier. The second controversial area is w h e t h e r or not to open the axitlary artery routinely, particularly w h e n thrombosis has occurred here, even t h o u g h the arteriogram is normal. It is reasonable to as-
the coracoid process will prevent further arterial damage. If the arterial wall is severely damaged, arterial repair will be necessary; however, as illustrated by this case, healing of the arterial injury is possible after removal of the initiating cause. REFERENCES 1, E t h e r e d g e S, Wilbur B, Stoney RJ. Thoracic outlet s y n d r o m e . A m J Surg 1979;138:175-181. 2, Roos DB. Congenital a n o m a l i e s associated with thoracic outlet s y n d r o m e - - A n a t o m y , s y m p t o m s , diagnosis, a n d treatm e n t . A m J Surg 1976;132:771-778. 3. Roos DB. Experience with first rib resection for thoracic outlet s y n d r o m e . A n n Surg 1971;173:429-442. 4. W r i g h t IS. The n e u r o v a s c u l a r s y n d r o m e p r o d u c e d by h y p e r a b d u c t i o n of the arms. A m Heart J 1945;29:1-19. 5, Stallworth JM, Q u i n n G J, A i k e n AF, Is rib resection necessary for relief of thoracic outlet s y n d r o m e ? A n n Surg 1977; 185:581 589. 6. McIntyre DI. Subcoracoid n e u r o v a s c u l a r e n t r a p m e n t . Clin Orthop 1975; 108:27-30. 7. Tullos HS, Erwin WD, W o o d s W, et al. U n u s u a l lesions of the pitching arm. Clin O r t h o p 1972;88:169-182. 8. M c C a r t h y W J, Yao JST, Schafer MF, et al. Upper extremity arterial injury in athletes. J Vasc Surg 1989;9:317-327. 9~ Haimovici H. Arterial t h r o m b o e m b o l i s m of t h e upper e x t r e m ity associated with thoracic outlet s y n d r o m e . J Cardiovasc Surg 1982;23:214-220. 10. J u e r g e n s JL, Bernatz PE. Atherosclerosis of the extremities. In J u e r g e n s JL, Spittell JA, Fairbairn JF, eds. Peripheral Vascular Diseases,, 5th ed. Philadelphia: WB Saunders, 1980, p 257.
s u m e that for t h r o m b u s to form in the axillary artery at the point of muscular compression the intima must be damaged. Therefore the artery should probably be replaced. Although the risk of axillary artery rethrombosis is u n k n o w n , some risk exists. We have seen one instance of recurrent thrombosis with distal emboli occurring 5 years following resection of an anomalous first rib and subclavian artery thrombectomy. Only w h e n the hand became severely ischemic was the artery replaced with a saphenous vein graft. Routine exploration of all arteries that contain t h r o m b u s is the more conservative and probably the safest approach. The risk of rethrombosis in a vessel that was once the source of thrombus is probably greater than the risk of late complications from exploring and closing a normal axillary artery.
This case presentation reports the second case of axillary artery thrombosis secondary to pectoralis minor compression. Evidence to explain this etiology is presented from arteriographic and intraoperative clinical findings. Management includes division of the pectoralis minor muscle and local arterial repair if the vessel is severely damaged. (Ann Vasc Surg 1993;7:287-290.)
In t h e s p e c t r u m of t h o r a c i c o u t l e t s y n d r o m e , arterial c o m p r e s s i o n occurs in less t h a n 5 % of all p a tients. ~ C o m p r e s s i o n of t h e s u b c l a v i a n a r t e r y is p r i m a r i l y in t h e c o s t o s c a l e n e p a s s a g e w h e r e b o n y a b n o r m a l i t i e s , i n c l u d i n g cervical ribs a n d fibrous bands, h a v e b e e n r e c o g n i z e d . 2 Less f r e q u e n t l y , c o m p r e s s i o n m a y o c c u r at t h e c o s t o c l a v i c u l a r space. ~ The i m p o r t a n c e of t h e . h y p e r a b d u c t i o n s y n d r o m e a n d t h e p e c t o r a l i s m i n o r t e n d o n as a cause of axillary a r t e r y c o m p r e s s i o n h a s also b e e n well described. 4-6 H o w e v e r , to o u r k n o w l e d g e , o n l y o n e case of a x i l l a r y a r t e r y t h r o m b o s i s s e c o n d a r y to pectoralis m i n o r c o m p r e s s i o n h a s b e e n reported. ~ W e r e p o r t a case of a x i l l a r y a r t e r y t h r o m bosis s e c o n d a r y to c o m p r e s s i o n b y t h e p e c t o r a l i s m i n o r w i t h t h r o m b o e m b o l i s m o c c l u d i n g t h e radial a n d u l n a r arteries.
CASE R E P O R T This 56-year-old right-handed w o m a n had experienced coolness, paleness, and pain in her right hand and forearm for 3 days prior to presentation. There was associated numbness of the fingertips. For several months
From the Division of Vascular Surgery, The Toronto Hospital, University of Toronto, Toronto, Ontario, Canada. Reprint requests: K. W. Johnston, MD, TorontoHospital, General Division, 9th Floor, Eaton Wing North, 200 Elizabeth St., Toronto, Ontario, Canada MSG 2C4.
she also noted rapid fatigue of her right arm with activity. The patient was a nonsmoker, had no cardiac history, and was not a diabetic. Her only medication was estrogen replacement. Examination revealed a cold right hand and forearm up to the elbow. Radial, ulnar, and brachial pulses were not palpable in the right arm, although the supraclavicular subclavian artery and the axillary artery pulses were normal. Faint monophasic Doppler signals were present at the brachial and ulnar arteries but no blood pressure was obtained. All pulses were present in the left arm and blood pressure in the left a r m was 140/80 m m Hg. The ECG demonstrated a normal sinus rhythm. A chest x-ray film showed no evidence of a cervical rib. An arteriogram of the right arm showed patent subclavian and proximal axillary arteries and a nonocclusive intravascular filling defect in the second part of the axillary artery (Fig. 1). The radial artery at the midforearm and the proximal ulnar artery were occluded and distal filling was not demonstrated. Because of severe ischemia with sensory symptoms the patient was taken to the operating room. At this stage the presumptive diagnosis was embolism. Brachial arteriotomy was used because we believed that the major technical problem would be to clear her occluded distal arteries and not the partially occluding axillary artery lesion. With the use of a Fogarty catheter, thromboric material was retrieved from the axillary artery and excellent arterial inflow was established. The radial artery was also successfully cleared of white thrombotic and/or embolic material. The site of the axillary artery thrombus shown in Fig. 1 was not explored at the initial 287
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Fig. 1. Arteriogram showing nonocclusive mural thrombus present at the second portion of the axillary artery (arrow).
operation because we were not certain if this represented embolic material from a proximal source or a primary arterial abnormality and believed that further investigation was warranted. Postoperatively arterial perfusion and pulses were normal and the patient was asymptomatic. Brachial blood pressures were equal in both arms and arterial duplex Doppler studies showed normal symmetric waveforms from the brachial, radial, and ulnar arteries. An echocardiogram showed no abnormalities of the heart. A repeat arteriogram showed an eccentric irregularity in the axillary artery at the site of previous thrombus (Fig. 2, A). Because of the unusual site of the original arterial lesion, another arteriogram was obtained with the shoulder and arm in different positions. With hyperabduction of the arm, focal narrowing was present at the second part of the axillary artery in the region of the pectoralis minor muscle (Fig. 2, B). We thought this was the most likely explanation for her arterial injury and thrombus formation. She was taken to the operating room a second time, and through a subclavicular transverse skin incision,
the pectoralis minor was divided from its insertion into the coracoid process. Scarring of the adventitia of the axillary artery under the pectoralis muscle was apparent. Movement of the shoulder showed that with elevation above shoulder level the artery was pulled proximal and anterior in such a manner that it was compressed by the pectoralis minor musde. The artery was not opened to inspect the extent of the intimal injury because the arteriogram showed no major defect, clinical examination of the artery did not reveal significant mural thickening or other abnormalities apart from the obvious adventitiaI scarring, and we believed that the vessel would heal after relief of the initiating cause. The patient made a good postoperative recovery and was discharged on oral anticoagulants for 6 months. The follow-up vascular examination and noninvasive assessment were normal at 9 months.
DISCUSSION T h e r e h a v e b e e n several reports of n e u r o v a s c u l a r c o m p r e s s i o n r e q u i r i n g release of the pectoralis
Vol, 7, No. 3 1993
Thrombosis of axillary artery 289
A
B
Fig. 2. A, Following axillary artery thrombectomy, repeat arteriograms revealed a small irregularity present at the site of the previous thrombus (arrow). B, Abduction of the arm caused focal narrowing of the second portion of the axillary artery by the pectoralis m i n o r muscle (arrow).
minor tendon. 5.e' McCarthy et al. 8 reported three athletes with axillary artery compression by the pectoralis minor, none of w h o m had arterial thrombosis. Tullos et a17 reported the only previous case of axillary artery thrombosis due to compression by the pectoralis minor muscle in a baseball pitcher. W h e n a nonocclusive axillary artery thrombosis is present, signs and s y m p t o m s can include claudication, rapid fatigue, decreased distal pulses, pallor, and diminished skin temperature. Arterial complications of thoracic outlet syndrome are always secondary to long-standing compression. The pathophysiology of arterial t h r o m b o e m b o lism secondary to thoracic outlet syndrome has
been well described. 9Extrinsic compression on the axillary artery leads to arterial injury, intimal ulceration, platelet thrombus, and peripheral embolization, which can cause occlusion of the radial and ulnar arteries, as likely occurred in our patient. Occlusion of the arteries of the upper extremities due to atherosclerosis is relatively u n c o m m o n . W h e n present, however, the usual site is in the proximal part of the subclavian artery, most often involving the arch of the aorta on the left and the innominate artery on the right.~° In our patient, e v e n though the circulation to her limb was satisfactorily reestablished following t h r o m b e c t o m y and embolectomy, a postoperative
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arteriogram established a cause for the arterial occlusion. The arteriogram revealed the location of the arterial narrowing (Fig. 2, A) and d e m o n strated partial obstruction with hyperabduction, which suggested the etiology (Fig. 2, B). Further, at operation u n d e r direct vision and with the arm freely draped to allow m o v e m e n t of the shoulder, the offending pectoralis minor muscle proved to be the cause. After the pectoralis minor was detached from the coracoid process, significant scarring of the adventitia of the axillary artery b e n e a t h the muscle was apparent. The artery was not damaged e n o u g h to warrant repair; however, the patient was anticoagulated for 6 m o n t h s to minimize the risk of t h r o m b o e m b o l i s m while the artery was healing.
CONCLUSION To our knowledge, this is only the second report of axillary artery thrombosis secondary to compression by the pectoralis minor. The pathology in this case was complicated by severe distal embolization causing complete occlusion of the radial and ulnar arteries. Although compression of the artery is rare at this site, recognition that the pectoralis minor muscle is a potential cause of axillary artery compression is important. Division of this tendon from
Commentary Richard J. Sanders, MD, and Michael A. Cooper, MD
This is indeed a rare condition that raises two controversial questions of management. First, the initial operation could have been pectoralis minor t e n o t o m y and open axillary artery thrombectomy. At that time, if there was intimal ulceration, the artery could have been replaced. Experience has s h o w n that this will usually restore the hand to normal even t h o u g h the ulnar and radial arteries remain occluded. Distal thrombectomy, which is fraught with m a n y hazards, can thus be avoided. This view is championed by the French surgeon Cormier. The second controversial area is w h e t h e r or not to open the axitlary artery routinely, particularly w h e n thrombosis has occurred here, even t h o u g h the arteriogram is normal. It is reasonable to as-
the coracoid process will prevent further arterial damage. If the arterial wall is severely damaged, arterial repair will be necessary; however, as illustrated by this case, healing of the arterial injury is possible after removal of the initiating cause. REFERENCES 1, E t h e r e d g e S, Wilbur B, Stoney RJ. Thoracic outlet s y n d r o m e . A m J Surg 1979;138:175-181. 2, Roos DB. Congenital a n o m a l i e s associated with thoracic outlet s y n d r o m e - - A n a t o m y , s y m p t o m s , diagnosis, a n d treatm e n t . A m J Surg 1976;132:771-778. 3. Roos DB. Experience with first rib resection for thoracic outlet s y n d r o m e . A n n Surg 1971;173:429-442. 4. W r i g h t IS. The n e u r o v a s c u l a r s y n d r o m e p r o d u c e d by h y p e r a b d u c t i o n of the arms. A m Heart J 1945;29:1-19. 5, Stallworth JM, Q u i n n G J, A i k e n AF, Is rib resection necessary for relief of thoracic outlet s y n d r o m e ? A n n Surg 1977; 185:581 589. 6. McIntyre DI. Subcoracoid n e u r o v a s c u l a r e n t r a p m e n t . Clin Orthop 1975; 108:27-30. 7. Tullos HS, Erwin WD, W o o d s W, et al. U n u s u a l lesions of the pitching arm. Clin O r t h o p 1972;88:169-182. 8. M c C a r t h y W J, Yao JST, Schafer MF, et al. Upper extremity arterial injury in athletes. J Vasc Surg 1989;9:317-327. 9~ Haimovici H. Arterial t h r o m b o e m b o l i s m of t h e upper e x t r e m ity associated with thoracic outlet s y n d r o m e . J Cardiovasc Surg 1982;23:214-220. 10. J u e r g e n s JL, Bernatz PE. Atherosclerosis of the extremities. In J u e r g e n s JL, Spittell JA, Fairbairn JF, eds. Peripheral Vascular Diseases,, 5th ed. Philadelphia: WB Saunders, 1980, p 257.
s u m e that for t h r o m b u s to form in the axillary artery at the point of muscular compression the intima must be damaged. Therefore the artery should probably be replaced. Although the risk of axillary artery rethrombosis is u n k n o w n , some risk exists. We have seen one instance of recurrent thrombosis with distal emboli occurring 5 years following resection of an anomalous first rib and subclavian artery thrombectomy. Only w h e n the hand became severely ischemic was the artery replaced with a saphenous vein graft. Routine exploration of all arteries that contain t h r o m b u s is the more conservative and probably the safest approach. The risk of rethrombosis in a vessel that was once the source of thrombus is probably greater than the risk of late complications from exploring and closing a normal axillary artery.