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Axillary block complicated by hematoma and radial nerve injury
RegionalAnesthesia and Pain Medicine 24(3): 264-266, 1999
Axillary Block Complicated by Hematoma and Radial Nerve Injury Bruce Ben-David, M.D.,* and Shalom Stahl, M.D. t
Background and Objectives. Hematoma is typically cited as one mechanism of nerve injury following axillary block. However, documented cases of this are lacking. Methods. A healthy 38-year-old man was scheduled for surgical removal of a tumor of the hand. A transarterial axillary block was performed with a 22-gauge short-bevel needle using 40 mE of a mixture of equal volumes of 1.5% lidocaine and 0.5% bupivacaine containing 1:200,000 epinephrine. No paresthesias were reported. Postoperative, the patient developed a large axillary hematoma accompanied by paresthesias and radial nerve weakness. Results. With conservative management, nerve recovery was complete in 6 months. Conclusions. Hematoma complicating axillary block may result in nerve dysfunction. Reg Anesth Pain Med 1999: 24: 264-266. Key words" regional anesthesia and pain management, brachial plexus block, neurologic complications.
Nerve injury resulting f r o m axillary block has a reported incidence of as high as 19% (1) and as low as less t h a n 1% (2,3). Other investigators h a v e indicated a 2-3 % incidence of n e r v e dysfunction lasting b e y o n d the early postoperative period (4,5). Most of these n e r v e injuries are transient dysesthesias w h i c h resolve within weeks; h o w e v e r , m o t o r i n v o l v e m e n t , prolonged recovery, or p e r m a n e n t injury m a y occur. There are several possible m e c h anisms of n e r v e injury following axillary block, including direct n e r v e transection, intraneural injection with p r e s s u r e - i n d u c e d ischemic injury, ischemia caused by vasoconstrictors, direct toxicity of agents, e n d o n e u r a l herniation, fibrosis, a n d hema~ t o m a d e v e l o p m e n t w i t h n e u r o v a s c u l a r compression. This report details a case of brachial plexus injury
associated with a large axillary h e m a t o m a following axillary block anesthesia.
Case Report A 38-year-old m a n with no significant medical history and taking no chronic medications was scheduled for r e m o v a l of a giant cell t u m o r located on the p a l m a r aspect of the wrist. He denied a n y prior history of bleeding a b n o r m a l i t y and denied recent use of nonsteroidal a n t i - i n f l a m m a t o r y drugs. Preoperative, his h e m o g l o b i n was 14.2 g/dL and platelet count was 280,000. No other preoperative studies w e r e p e r f o r m e d . For surgery, the patient was administered an ax M illary block several m i n u t e s after sedation with int r a v e n o u s 2 m g midazolam. The block was perf o r m e d with a 22-gauge short-bevel needle using a transarterial technique, w i t h o u t report of p a r e s t h e sias. A m i x t u r e of equal v o l u m e s of 1.5% lidocaine a n d 0.5% bupivacaine, containing 1:200,000 epin e p h r i n e was i n j e c t e d - - 2 0 mL posterior and 20 m L anterior to the axillary artery. The block was perf o r m e d w i t h o u t difficulty, a n d the artery was ap-
From the *Department of Anesthesia, EIerzlia-Haifa (Horev) Medical Center, Haifa, Israel, and the tHand Surgery Unit, Ram~ ham Medical Center, Haifa, Israel. Accepted for publication October 12, 1998. Reprint requests: Bruce Ben-David, M.D., Medical Director, Herzlia-Haifa (Horev) Medical Center, Haifa, Israel. Copyright © 1999 by the American Society of Regional Anesthesia. 0146-521Xl9912403-001655.0010
264
Axillary Block, Hematoma, and Nerve Injury
•
Ben-David and Stahl
265
might be lost because of fibrosis) and active physiotherapy to strengthen functional muscles. Nerve conduction and electromyographic studies at 4 weeks postsurgery demonstrated signs of neuropraxia. By 10 weeks postsurgery, the patient's weakness had resolved. Dysesthesias, however, persisted for 6 months. At 6 m o n t h s after surgery, the patient had achieved complete recovery with no residual neurologic deficit.
Discussion
Fig. l. The patient's axilla and splinted arm 1 week after surgery. The hematoma is now much less prominent in the axilla but has dissected as far as the elbow.
patently penetrated only once. Digital pressure was not applied to the axilla or artery following injection. Anesthesia and surgery proceeded u n e v e n t fully. A t o u r n i q u e t carefully positioned over padding on the operative proximal arm was inflated to 240 m m Hg for 70 minutes. The arm was positioned during surgery to avoid abduction greater than 90 ° . Intraoperative blood pressures ranged from 150/80 to 170/90 m m Hg, compared with a preoperative blood pressure of 140/75 m m Hg. During the postoperative visit the following day, the patient complained of sensory changes and pain in the dorsum of his h a n d and evidenced weakness of wrist and finger extension (radial nerve distribution). Median and ulnar nerve examinations were w i t h o u t sensory or m o t o r impairment. The axilla was tender to percussion (positive Tinel's sign) with p r o m i n e n t swelling and h e m a t o m a (Fig. 1). At this time, p r o t h r o m b i n time and partial thromboplastin time were normal, and no further laboratory investigations were clone to rule out the possibility of other occult coagulopathy. The patient was observed for progression of his h e m a t o m a and for neurologic deterioration. H e m a t o m a expansion was assessed using a circumferential m e a s u r e m e n t at a fixed distance (10 cm) from the lateral epicondyle and with close observation. Because neither of these worsened, it was decided to not surgically explore the axilla for clot evacuation, decompression, and control of bleeding. Further m a n a g e m e n t included elevation, splinting, and both passive physiotherapy to maintain range of m o t i o n (as
The most c o m m o n l y e n c o u n t e r e d vascular complications of axillary block include intravascular injection, vasospasm, and local bruising and tenderness. Hematomas are infrequently n o t e d and are typically small and inconsequential. Stan et al. (3) reported a series of 1,000 axillary brachial plexus blocks using the transarterial approach. In their series, there were only two cases of h e m a t o m a , both small and both uncomplicated by neural dysfunction. Pearce et al. (4) reported a 3% frequency (6 of 200 patients) of h e m a t o m a d e v e l o p m e n t using a "first indicator of sheath entry" technique. Two of these six patients experienced dysesthesias on abduction of the arm; however, symptoms disappeared promptly in both patients with no medical intervention. Neural dysfunction associated with p s e u d o a n e u r y s m of the axillary artery has been reported following axillary block (6,7). Cases of large h e m a t o m a s causing nerve injury have b e e n reported following axillary angiography (8); however, our literature review failed to reveal a single case of significant nerve injury caused by h e m a toma following axillary block. It is regrettable in this case that we have n o clear explanation for the severity of the patient's hematoma. The needle used for the axillary block was a standard 22-gauge short-bevel block needle. We do not believe there were multiple punctures of the artery. The patient denied having taken nonsteroidal anti-inflammatory agents, and he received no anticoagulants perioperatively. It is possible that the patient suffers from a subclinical coagulopathy (e.g., von Willebrand's, factor XI deficiency), but further testing was not done to examine this possibility. The mild rise in blood pressure intraoperatively and the failure to apply digital pressure following the block m a y have contributed, t h o u g h this is speculative. Although ultrasound m a y be valuable in assessing the progression of a h e m a t o m a , it was not used here because the peripheral location of the hematoma made the simple m e t h o d of observation prac-
266
RegionalAnesthesia and Pain Medicine Vol. 24 No. 3 May-June 1999
tical. There is no well-defined fascial c o m p a r t m e n t in the axilla or u p p e r a r m as, for example, in the forearm, so an axillary h e m a t o m a will easily exp a n d in size t h e r e b y m a k i n g the observation of its progression easier. Because the h e m a t o m a did not continue to e x p a n d and because there was no bruit, we h a d no reason to suspect a false a n e u r s y m w h i c h w o u l d h a v e also w a r r a n t e d u l t a s o u n d evaluation. Some authors r e c o m m e n d p r o m p t surgical evacuation and decompression of an axillary h e m a t o m a to avoid pressure-induced ischemia of the brachial plexus. Some theorize that pressure injury m a y be possible as a result of the potential closed space of the axillary sheath; on the other hand, h o w e v e r , there is no risk of a c o m p a r t m e n t s y n d r o m e in the axilla or u p p e r arm. In this case, the injury was a partial a n d not a complete radial palsy, thus indicating some radial n e r v e function. Conservative t r e a t m e n t is advisable in m a n y cases of radial palsy. For example, in closed fracture of the h u m e r u s associated w i t h radial n e r v e injury, it is advisable to p o s t p o n e surgical exploration because typically the radial n e r v e fully recovers. Similarly, w e anticip a t e d full recovery in this case. Moreover, it is a surgical principle that caution should be used in evacuating h e m a t o m a s (they will absorb over time a n y w a y ) , because doing so increases the risk of infection and abscess formation. Surgical drainage w o u l d h a v e b e e n done in this case if (a) the h e m a t o m a h a d c o n t i n u e d to expand, (b) the neural dysfunction did not i m p r o v e w i t h resolution of the h e m a t o m a , (c) there was deterioration of n e u r o logic status, or (d) there was evidence of vascular or l y m p h a t i c obstruction. In this case, careful observation and a conservative a p p r o a c h a p p e a r to h a v e b e e n justified. A l t h o u g h it is not clear w h a t impact surgical i n t e r v e n t i o n w o u l d h a v e h a d on the course of our patient's recovery, it w o u l d certainly h a v e exposed the patient to other potential complications. We a c k n o w l e d g e that there in no proot ot a causal connection b e t w e e n the h e m a t o m a a n d the neural dysfunction. That is, it is possible that the h e m a t o m a and the n e r v e injury w e r e m e r e l y coincidental. However, the radial n e r v e dysfunction h e r e differs f r o m the usual p a t t e r n ot n e r v e injury following axillary block (which is typically of the m e d i a n or ulnar nerves) (5). Also, s o m e believe that n e r v e injury is m o r e likely to occur in the presence of elicited paresthesia w h e t h e r intentional or not (5,9), a n d o u r patient reported no paresthesia during block p l a c e m e n t . It is unlikely that the
light level of sedation in this patient obscured the elicitation of a paresthesia. Last, the h e m a t o m a in this case was so p r o m i n e n t that this alone m a k e s a compelling a r g u m e n t . Therefore, we are confident t h a t a causal link exists b e t w e e n the h e m a t o m a a n d the neural dysfunction. Perhaps one m i g h t expect n e r v e injury caused b y h e m a t o m a to equally affect all n e r v e roots. However, this presupposes an e v e n distribution of pressure within or a b o u t the axillary s h e a t h - - a n a s s u m p t i o n w h i c h is p r o b a b l y not valid and thus does n o t contradict o u r conclusion regarding etiology of the n e u r o p a t h y . In s u m m a r y , w e present a case w h e r e an axillary block was complicated by a large axillary h e m a t o m a and radial n e r v e dysfunction. The presence of a h e m a t o m a should alert one to carefully evaluate neurologic function. A l t h o u g h the association of n e r v e injury requires that due consideration be given to surgical decompression and e v a c u a t i o n of the h e m a t o m a , conservative m a n a g e m e n t m a y be appropriate in specific cases.
References 1. Urban MK, Urquhart B. Evaluation of brachial plexus anesthesia for upper extremity surgery. Reg Anesth 1994: 19: 175-182. 2. Winchell SW, Wolfe R. The incidence of neuropathy following upper extremity nerve blocks. Reg Anesth 1985: 10: 135-142. 3. Stan TC, Krantz MA, Solomon DL, Poulos JG, Chaouki K. The incidence of neurovascular complications following axillary brachial plexus block using a transarterial approach. A prospective study of 1000 consecutive patients. Reg Anesth 1995: 20: 486-492. 4. Pearce H, Lindsay D, Leslie K. Axillary brachial plexus block in two hundred consecutive patients. Anaesth Intens Care 1996: 24: 453-458. 5. Selander D, Edshage S, Wolff T. Paresthesiae or no paresthesiae? Nerve lesions after axillary blocks. Acta Anaesth Scand 1979: 23: 27-33. 6. Groh GI, Gainor BJ, Jeffries JT, Brown M, Eggers GWN. Pseudoaneurysm of the axillary artery with median-nerve deficit after axillary block anesthesia. J Bone Joint Surg 1990: 72A: 1407-1408. 7. Zipkin M, Backus WW, Scott B, Poppers PJ. False aneurysm of the axillary artery folowing brachial plexus block. J Clin Anesth 1991: 3: 143-145. 8. Dudrick S, Masland W, Mishkin M. Brachial plexus injury following axillary artery puncture. Radiology 1967: 88: 271-273. 9. Auroy Y, Narchi P, Messiah A, Litt L, Rouvier B, Samii K. Serious complications related to regional anesthesia. Anesthesiology 1997: 87: 479-486.
Axillary Block Complicated by Hematoma and Radial Nerve Injury Bruce Ben-David, M.D.,* and Shalom Stahl, M.D. t
Background and Objectives. Hematoma is typically cited as one mechanism of nerve injury following axillary block. However, documented cases of this are lacking. Methods. A healthy 38-year-old man was scheduled for surgical removal of a tumor of the hand. A transarterial axillary block was performed with a 22-gauge short-bevel needle using 40 mE of a mixture of equal volumes of 1.5% lidocaine and 0.5% bupivacaine containing 1:200,000 epinephrine. No paresthesias were reported. Postoperative, the patient developed a large axillary hematoma accompanied by paresthesias and radial nerve weakness. Results. With conservative management, nerve recovery was complete in 6 months. Conclusions. Hematoma complicating axillary block may result in nerve dysfunction. Reg Anesth Pain Med 1999: 24: 264-266. Key words" regional anesthesia and pain management, brachial plexus block, neurologic complications.
Nerve injury resulting f r o m axillary block has a reported incidence of as high as 19% (1) and as low as less t h a n 1% (2,3). Other investigators h a v e indicated a 2-3 % incidence of n e r v e dysfunction lasting b e y o n d the early postoperative period (4,5). Most of these n e r v e injuries are transient dysesthesias w h i c h resolve within weeks; h o w e v e r , m o t o r i n v o l v e m e n t , prolonged recovery, or p e r m a n e n t injury m a y occur. There are several possible m e c h anisms of n e r v e injury following axillary block, including direct n e r v e transection, intraneural injection with p r e s s u r e - i n d u c e d ischemic injury, ischemia caused by vasoconstrictors, direct toxicity of agents, e n d o n e u r a l herniation, fibrosis, a n d hema~ t o m a d e v e l o p m e n t w i t h n e u r o v a s c u l a r compression. This report details a case of brachial plexus injury
associated with a large axillary h e m a t o m a following axillary block anesthesia.
Case Report A 38-year-old m a n with no significant medical history and taking no chronic medications was scheduled for r e m o v a l of a giant cell t u m o r located on the p a l m a r aspect of the wrist. He denied a n y prior history of bleeding a b n o r m a l i t y and denied recent use of nonsteroidal a n t i - i n f l a m m a t o r y drugs. Preoperative, his h e m o g l o b i n was 14.2 g/dL and platelet count was 280,000. No other preoperative studies w e r e p e r f o r m e d . For surgery, the patient was administered an ax M illary block several m i n u t e s after sedation with int r a v e n o u s 2 m g midazolam. The block was perf o r m e d with a 22-gauge short-bevel needle using a transarterial technique, w i t h o u t report of p a r e s t h e sias. A m i x t u r e of equal v o l u m e s of 1.5% lidocaine a n d 0.5% bupivacaine, containing 1:200,000 epin e p h r i n e was i n j e c t e d - - 2 0 mL posterior and 20 m L anterior to the axillary artery. The block was perf o r m e d w i t h o u t difficulty, a n d the artery was ap-
From the *Department of Anesthesia, EIerzlia-Haifa (Horev) Medical Center, Haifa, Israel, and the tHand Surgery Unit, Ram~ ham Medical Center, Haifa, Israel. Accepted for publication October 12, 1998. Reprint requests: Bruce Ben-David, M.D., Medical Director, Herzlia-Haifa (Horev) Medical Center, Haifa, Israel. Copyright © 1999 by the American Society of Regional Anesthesia. 0146-521Xl9912403-001655.0010
264
Axillary Block, Hematoma, and Nerve Injury
•
Ben-David and Stahl
265
might be lost because of fibrosis) and active physiotherapy to strengthen functional muscles. Nerve conduction and electromyographic studies at 4 weeks postsurgery demonstrated signs of neuropraxia. By 10 weeks postsurgery, the patient's weakness had resolved. Dysesthesias, however, persisted for 6 months. At 6 m o n t h s after surgery, the patient had achieved complete recovery with no residual neurologic deficit.
Discussion
Fig. l. The patient's axilla and splinted arm 1 week after surgery. The hematoma is now much less prominent in the axilla but has dissected as far as the elbow.
patently penetrated only once. Digital pressure was not applied to the axilla or artery following injection. Anesthesia and surgery proceeded u n e v e n t fully. A t o u r n i q u e t carefully positioned over padding on the operative proximal arm was inflated to 240 m m Hg for 70 minutes. The arm was positioned during surgery to avoid abduction greater than 90 ° . Intraoperative blood pressures ranged from 150/80 to 170/90 m m Hg, compared with a preoperative blood pressure of 140/75 m m Hg. During the postoperative visit the following day, the patient complained of sensory changes and pain in the dorsum of his h a n d and evidenced weakness of wrist and finger extension (radial nerve distribution). Median and ulnar nerve examinations were w i t h o u t sensory or m o t o r impairment. The axilla was tender to percussion (positive Tinel's sign) with p r o m i n e n t swelling and h e m a t o m a (Fig. 1). At this time, p r o t h r o m b i n time and partial thromboplastin time were normal, and no further laboratory investigations were clone to rule out the possibility of other occult coagulopathy. The patient was observed for progression of his h e m a t o m a and for neurologic deterioration. H e m a t o m a expansion was assessed using a circumferential m e a s u r e m e n t at a fixed distance (10 cm) from the lateral epicondyle and with close observation. Because neither of these worsened, it was decided to not surgically explore the axilla for clot evacuation, decompression, and control of bleeding. Further m a n a g e m e n t included elevation, splinting, and both passive physiotherapy to maintain range of m o t i o n (as
The most c o m m o n l y e n c o u n t e r e d vascular complications of axillary block include intravascular injection, vasospasm, and local bruising and tenderness. Hematomas are infrequently n o t e d and are typically small and inconsequential. Stan et al. (3) reported a series of 1,000 axillary brachial plexus blocks using the transarterial approach. In their series, there were only two cases of h e m a t o m a , both small and both uncomplicated by neural dysfunction. Pearce et al. (4) reported a 3% frequency (6 of 200 patients) of h e m a t o m a d e v e l o p m e n t using a "first indicator of sheath entry" technique. Two of these six patients experienced dysesthesias on abduction of the arm; however, symptoms disappeared promptly in both patients with no medical intervention. Neural dysfunction associated with p s e u d o a n e u r y s m of the axillary artery has been reported following axillary block (6,7). Cases of large h e m a t o m a s causing nerve injury have b e e n reported following axillary angiography (8); however, our literature review failed to reveal a single case of significant nerve injury caused by h e m a toma following axillary block. It is regrettable in this case that we have n o clear explanation for the severity of the patient's hematoma. The needle used for the axillary block was a standard 22-gauge short-bevel block needle. We do not believe there were multiple punctures of the artery. The patient denied having taken nonsteroidal anti-inflammatory agents, and he received no anticoagulants perioperatively. It is possible that the patient suffers from a subclinical coagulopathy (e.g., von Willebrand's, factor XI deficiency), but further testing was not done to examine this possibility. The mild rise in blood pressure intraoperatively and the failure to apply digital pressure following the block m a y have contributed, t h o u g h this is speculative. Although ultrasound m a y be valuable in assessing the progression of a h e m a t o m a , it was not used here because the peripheral location of the hematoma made the simple m e t h o d of observation prac-
266
RegionalAnesthesia and Pain Medicine Vol. 24 No. 3 May-June 1999
tical. There is no well-defined fascial c o m p a r t m e n t in the axilla or u p p e r a r m as, for example, in the forearm, so an axillary h e m a t o m a will easily exp a n d in size t h e r e b y m a k i n g the observation of its progression easier. Because the h e m a t o m a did not continue to e x p a n d and because there was no bruit, we h a d no reason to suspect a false a n e u r s y m w h i c h w o u l d h a v e also w a r r a n t e d u l t a s o u n d evaluation. Some authors r e c o m m e n d p r o m p t surgical evacuation and decompression of an axillary h e m a t o m a to avoid pressure-induced ischemia of the brachial plexus. Some theorize that pressure injury m a y be possible as a result of the potential closed space of the axillary sheath; on the other hand, h o w e v e r , there is no risk of a c o m p a r t m e n t s y n d r o m e in the axilla or u p p e r arm. In this case, the injury was a partial a n d not a complete radial palsy, thus indicating some radial n e r v e function. Conservative t r e a t m e n t is advisable in m a n y cases of radial palsy. For example, in closed fracture of the h u m e r u s associated w i t h radial n e r v e injury, it is advisable to p o s t p o n e surgical exploration because typically the radial n e r v e fully recovers. Similarly, w e anticip a t e d full recovery in this case. Moreover, it is a surgical principle that caution should be used in evacuating h e m a t o m a s (they will absorb over time a n y w a y ) , because doing so increases the risk of infection and abscess formation. Surgical drainage w o u l d h a v e b e e n done in this case if (a) the h e m a t o m a h a d c o n t i n u e d to expand, (b) the neural dysfunction did not i m p r o v e w i t h resolution of the h e m a t o m a , (c) there was deterioration of n e u r o logic status, or (d) there was evidence of vascular or l y m p h a t i c obstruction. In this case, careful observation and a conservative a p p r o a c h a p p e a r to h a v e b e e n justified. A l t h o u g h it is not clear w h a t impact surgical i n t e r v e n t i o n w o u l d h a v e h a d on the course of our patient's recovery, it w o u l d certainly h a v e exposed the patient to other potential complications. We a c k n o w l e d g e that there in no proot ot a causal connection b e t w e e n the h e m a t o m a a n d the neural dysfunction. That is, it is possible that the h e m a t o m a and the n e r v e injury w e r e m e r e l y coincidental. However, the radial n e r v e dysfunction h e r e differs f r o m the usual p a t t e r n ot n e r v e injury following axillary block (which is typically of the m e d i a n or ulnar nerves) (5). Also, s o m e believe that n e r v e injury is m o r e likely to occur in the presence of elicited paresthesia w h e t h e r intentional or not (5,9), a n d o u r patient reported no paresthesia during block p l a c e m e n t . It is unlikely that the
light level of sedation in this patient obscured the elicitation of a paresthesia. Last, the h e m a t o m a in this case was so p r o m i n e n t that this alone m a k e s a compelling a r g u m e n t . Therefore, we are confident t h a t a causal link exists b e t w e e n the h e m a t o m a a n d the neural dysfunction. Perhaps one m i g h t expect n e r v e injury caused b y h e m a t o m a to equally affect all n e r v e roots. However, this presupposes an e v e n distribution of pressure within or a b o u t the axillary s h e a t h - - a n a s s u m p t i o n w h i c h is p r o b a b l y not valid and thus does n o t contradict o u r conclusion regarding etiology of the n e u r o p a t h y . In s u m m a r y , w e present a case w h e r e an axillary block was complicated by a large axillary h e m a t o m a and radial n e r v e dysfunction. The presence of a h e m a t o m a should alert one to carefully evaluate neurologic function. A l t h o u g h the association of n e r v e injury requires that due consideration be given to surgical decompression and e v a c u a t i o n of the h e m a t o m a , conservative m a n a g e m e n t m a y be appropriate in specific cases.
References 1. Urban MK, Urquhart B. Evaluation of brachial plexus anesthesia for upper extremity surgery. Reg Anesth 1994: 19: 175-182. 2. Winchell SW, Wolfe R. The incidence of neuropathy following upper extremity nerve blocks. Reg Anesth 1985: 10: 135-142. 3. Stan TC, Krantz MA, Solomon DL, Poulos JG, Chaouki K. The incidence of neurovascular complications following axillary brachial plexus block using a transarterial approach. A prospective study of 1000 consecutive patients. Reg Anesth 1995: 20: 486-492. 4. Pearce H, Lindsay D, Leslie K. Axillary brachial plexus block in two hundred consecutive patients. Anaesth Intens Care 1996: 24: 453-458. 5. Selander D, Edshage S, Wolff T. Paresthesiae or no paresthesiae? Nerve lesions after axillary blocks. Acta Anaesth Scand 1979: 23: 27-33. 6. Groh GI, Gainor BJ, Jeffries JT, Brown M, Eggers GWN. Pseudoaneurysm of the axillary artery with median-nerve deficit after axillary block anesthesia. J Bone Joint Surg 1990: 72A: 1407-1408. 7. Zipkin M, Backus WW, Scott B, Poppers PJ. False aneurysm of the axillary artery folowing brachial plexus block. J Clin Anesth 1991: 3: 143-145. 8. Dudrick S, Masland W, Mishkin M. Brachial plexus injury following axillary artery puncture. Radiology 1967: 88: 271-273. 9. Auroy Y, Narchi P, Messiah A, Litt L, Rouvier B, Samii K. Serious complications related to regional anesthesia. Anesthesiology 1997: 87: 479-486.