A 16-yr-old, right-hand dominant boy presented to the athletic training room complaining of right hand numbness and pain. Despite not seeking medical treatment, he admitted that his symptoms began approximately 4 wk earlier. His symptoms commenced after he caught a pass during a varsity football game and sustained a direct helmet blow to the medial aspect of his right elbow. He had immediate pain, ecchymosis, and swelling at that site in the days after the injury. After the injury, he had pain at rest; however, over the next week, his symptoms improved, and he had no pain at rest but did continue to experience pain with activity. One week after the initial injury, he returned to play and noticed that his fingers became cold, and he admitted to numbness and tingling in the middle three fingers of his right hand. These symptoms were associated with the change in color of his fingers: the fingertips would “turn white and purple at the very tip.” The football season ended, and his symptoms appeared to resolve. After a 2-wk rest period, he resumed basketball and, after shooting approximately 10 free throws, the symptoms had returned. Upon presentation, he rated his pain as a 0/10 at rest.
He denied any previous injury to the arm and had no family history of any similar injury or condition. He had been treated with ipratropium/albuterol inhaler for asthma but had no other medical conditions. He denied tobacco consumption.
On physical examination, he had no ecchymosis or tenderness about the right elbow region. While he had no discoloration of the digits, his right hand was cooler to the touch than the left hand. He had symmetric brisk capillary refill and brachial pulse near the axilla but diminished radial pulse and brachial pulse at the elbow compared with the contralateral limb. He had full extension in the elbow and flexion to 140 degrees. He had full forearm pronation and supination. He had 5/5 strength with wrist extension, thumb IP flexion, finger abduction, forearm supination, elbow flexion and extension, and his light touch was grossly intact and symmetric to contralateral limb in the median, radial, and ulnar nerve distributions.
No bony abnormalities were visualized on anteroposterior (AP) and lateral views of the right elbow. Arterial duplex imaging demonstrated occlusion of the proximal and midbrachial artery and reconstitution of flow in the distal brachial artery above the antecubital fossa (Fig. 1).
After a lengthy discussion with two vascular surgeons, he and his parents decided to continue playing sports and delay any consideration of revascularization until the conclusion of the basketball season. He would undergo serial arterial duplexes throughout the season and was maintained on antiplatelet therapy with aspirin.
Over the course of the basketball season, his symptoms slowly improved. He was able to tolerate increasing activity duration without pain. Repeat arterial duplex imaging obtained midway through the season revealed partial recanalization of the proximal brachial artery, a brachial pressure of 82 mm Hg (compared with 102 mm Hg on the contralateral limb), and wrist-brachial index of 0.69 (compared with 0.87 on the contralateral limb). At the conclusion of the season, a season in which he led his league-championship team in scoring, he underwent reevaluation. On examination, his right forearm had atrophied noticeably, and its circumference was 0.5 cm less than his nondominant left forearm. However, given his demonstrated ability to perform a high-functional level and mild improvement of symptoms, he elected to continue with nonoperative management. Aspirin regimen was discontinued. That spring, he competed in javelin, achieved personal best distances, and finished within the top 10 in the state competition.
He returned for follow-up 5 months later and before the upcoming football season. His radial pulse was barely palpable but his symptoms remained minimal. Arterial duplex imaging showed recanalization of the midbrachial artery (Fig. 2), a brachial pressure of 84 mm Hg (compared with 108 mm Hg on the contralateral limb), and wrist-brachial index of 0.70 (compared with 0.92 on the contralateral limb). He starred offensively and defensively for his football team in the fall and was reevaluated after the season, 14 months after the initial injury. He denied any symptoms at rest but admitted to mild symptoms with exertion in cold temperatures. His radial pulse, though diminished, was more readily palpable. Arterial duplex imaging revealed recanalization of the midbrachial artery with near-normal flow (Fig. 3), a brachial pressure of 98 mm Hg (compared with 102 mm Hg on the contralateral limb), and wrist-brachial index of 1.02 (compared with 0.94 on the contralateral limb). He completed his senior basketball season and signed an athletic scholarship at a division one university.
Blunt vascular injuries involving the upper extremity have been widely reported in athletes (1,2,6,8,12,13,18,21–24,26,28,30,33). However, most reports have focused on those participating in sports involved with repetitive overhead activity, such as baseball (6,8,13,21,24,28,30), volleyball (18), swimming (1), and tennis (21). While most proximal arteriopathies involve compression of the subclavian artery or axillary artery by the scalene and pectoralis minor muscles (21,22,28), humeral head (22,24), or cervical ribs (21), distal arterial occlusion occurs as a result of repetitive microtrauma to the superficial palmar arch (6,18,23). Arterial injury at sites other than the hand and shoulder girdle has received scant attention among the athletic population. Kostianen and Orava (18) reported two cases of arterial injury in the distal forearm caused by repetitive microtrauma sustained by volleyball players. Five cases of brachial artery injury were identified in a registry study of winter sport injuries but no information was available to determine the nature (blunt versus penetrating) of these injuries (10). To our knowledge, there have been no reported cases of brachial arteriopathy sustained as a result of blunt trauma during participation in American football. Furthermore, upper extremity arterial thrombosis caused by a single traumatic event has been previously unreported within the athletic population.
Traumatic brachial artery injuries constitute a large proportion of upper extremity peripheral arterial injuries because of the superficial position of the vessel in the arm (7). In one study of 189 upper extremity arterial injuries, 55% of cases involved the brachial artery (7). Most arterial injuries to the upper extremity are secondary to penetrating trauma; however, those injuries sustained via blunt trauma are more likely to lead to eventual amputation (7).
Because of its anatomic location and close proximity to nervous and osseous structures, brachial artery injury is combined with nerve and skeletal injuries in 65% (7). The brachial artery represents a continuation of the axillary artery, begins at the lower border of the teres major muscle, and terminates approximately 3 to 5 cm below the elbow skin crease, where the artery divides into the radial and ulnar arteries (32). Once the artery exits the axilla, the brachial artery is a relatively superficial structure and is covered only by skin, subcutaneous tissue, and deep fascia. Proximally, the artery is flanked by the humerus and median nerve laterally and ulnar and radial nerves medially. As it nears the elbow, the brachial artery courses anteriorly and is crossed by the median nerve, which assumes a position medial to the artery. These anatomic relationships render the brachial artery vulnerable to traumatic injury often associated with distal humerus fractures, elbow dislocations, and neurologic injury (7). Often, the severity and outcomes of injuries to these adjacent structures will govern the ultimate outcome after blunt vascular trauma to the brachial artery (29).
Despite its vulnerable superficial location, injury to the brachial artery, the major artery in the arm, does not always produce distal ischemia. The brachial artery has three main branches (profundi brachii, superior ulnar collateral, and inferior ulnar collateral arteries), which afford a collateral circulation that can maintain distal perfusion in cases of traumatic injury to the brachial artery (32) (Fig. 4). The profunda brachii artery, the most proximal branch, is accompanied by the radial nerve, courses posteriorly between the medial and long heads of the triceps muscle and participates in two important collateral anastomoses involving (a) axillary artery through its posterior circumflex humeral branch and (b) the radial recurrent artery via the profunda brachii's anterior branch. The superior ulnar collateral artery travels with the ulnar nerve posterior to the medial epicondyle and forms an anastomosis with the posterior ulnar recurrent artery, while the inferior ulnar collateral artery combines with the ulnar artery’s anterior recurrent branch to create a rich collateral network around the elbow.
Traumatic brachial artery injury can often be diagnosed clinically with a thorough history and physical exam (7). Many with brachial artery injury may have minimal symptoms particularly at rest. However, pain, numbness, and tingling of the distal extremity crescendos with increasing repetitive activity. Insensitivity to cold temperatures, especially when performing vigorous activity, is another common presenting symptom.
Physical examination should focus on not only identifying the injury but also determining if there is enough collateral flow to allow for adequate perfusion. When performing a vascular examination, the side of suspected injury should be compared with the uninjured limb. Physical examination signs of injury include absent or diminished radial, ulnar, and/or radial pulses; skin color changes; delayed capillary refill; palpable thrill or audible bruit; or, in the case of penetrating trauma, expanding or pulsatile hematoma (11). Of these, brachial artery injuries can be uncovered most reliably with pulse deficit. Assuming the contralateral limb is normal, the wrist-brachial index can be another useful test to provide objective evidence of arterial compromise. A threshold of less than 0.9 is an indication for invasive studies or operative exploration in equivocal cases.
While angiography is generally considered the criterion standard for the diagnosis of arterial injuries, other modalities, such as Doppler ultrasound, computed tomography angiography, and magnetic resonance arteriography, are gaining traction as equivalent testing in evaluating arterial flow (3,11). Doppler ultrasound is relatively inexpensive, readily available, and can provide flow data without injection of a contrast agent or radiation. In addition, Doppler ultrasonography provides a relatively inexpensive method of serially monitoring arterial flow on successive examinations. Computed tomography angiography has the advantage of being quick and providing detailed information but generally requires administration of an iodine-containing contrast agent and exposure to irradiation. Magnetic resonance arteriography eliminates irradiation exposure and risk of renal insult from contrast agent but is the most time-consuming and costly imaging modality (11).
Acutely, the primary aim in treating those sustaining a traumatic brachial artery injury is the prevention of limb ischemia due to inadequate blood flow to support tissue oxygen and nutrient requirements. Cell death and irreversible changes can be seen in peripheral nerves and skeletal muscle within 6 h of arterial obstruction. Therefore, acute limb ischemia is a serious medical emergency and requires emergent therapy for limb salvage (9). The extent of ischemic injury depends on the duration and location of the arterial blockage, the amount of collateral flow, and the previous health of the involved limb (25). Prolonged limb ischemia beyond 12 h is associated with increased rates of amputation (7).
Because of a robust collateral circulation around the elbow, upper limb arterial occlusions are not usually limb-threatening like similar lower-limb injuries, which often require immediate thrombectomy and/or reconstruction to prevent end-tissue damage (5). The origin of the deep brachial artery is the key branching point in determining acuity of the upper extremity vascular insult: occlusions occurring proximal to the origin of the deep brachial artery result in distal limb ischemia due to lack of collateral supply, whereas those occlusions distal to the origin of the deep brachial artery produce less distal damage because of abundant antecubital collateral blood supply. Upper extremity congenital vascular variations exist in 20% to 30% of the population and may alter the expected clinical presentation of the injury (27).
While there is general consensus that acute injuries resulting in distal ischemia require prompt intervention, debate persists over the aggressiveness of treatment required for acute brachial artery injury in a viable arm. Because of the rich collateral flow, most of these injuries are presumably relatively asymptomatic and can be treated nonoperatively. However, it has been reported that delayed treatment of upper limb occlusions carries an 8% potential risk for amputation and residual functional impairment (4). It is worth noting that symptoms can exist in the setting of normal resting hemodynamics. In high-performance athletes, very high levels of activity may be necessary to elicit abnormal findings on exercise vascular laboratory testing (19). Indications for vascular reconstruction in these patients must be tailored to each individual’s symptoms. In this patient, the lack of symptoms even at high levels of activity obviated any need for intervention.
While penetrating trauma may prompt more urgent treatment, blunt trauma often represents a more complex problem because of the extent of injury to the vessel and adjacent soft-tissue injury (7,15). Options to treat arterial thrombosis caused by blunt trauma are based on the chronicity of the thrombosis, location and length of blocked segment, and magnitude of symptoms. If operative management is contemplated, surgical options include thrombectomy, bypass grafting, and/or excision of diseased segment with primary repair or interpositional grafting (9,16). Thrombectomy with or without angioplasty has limited utility, because of associated injury to arterial walls in traumatic cases (20), while excision of the disease segment may be too extensive to allow for direct end-to-end repair. Bypass grafting affords the ability to excise the injured artery and reestablish flow without creating any undue tension on the reconstruction. While this may often require an additional incision to harvest a vein conduit, excision of the injured segment combined with vein interposition grafting has become the mainstay of treatment to allow for adequate debridement of the injured artery wall, a tension-free anastomosis, and restoration of arterial flow (7,19,31). According to the results of a study of 89 patients undergoing grafting after blunt upper-extremity arterial injury, interposition grafts have an early patency of 93% and long-term patency of 98.6% among those followed up at 6 yr (14,19). Despite these promising results, grafting is limited by donor-site morbidity from vein harvest, potential need for prolonged anticoagulation in an athletic population prone to contact, and continued cold intolerance in up to 40% (17).
There is limited data regarding return to play after arterial injury. When treated nonoperatively, athletes traditionally have been allowed to return to play immediately provided they are not taking anticoagulants and avoid the inciting agent if a repetitive activity, such as volleyball “bump,” was thought to cause the occlusion (18). While no data exist on return to play after surgical treatment of brachial artery injury, Todd et al. reported on two major league pitchers who were allowed to begin range of motion at 6 wk, light throwing at 3 months, and full return to play 4 months after interpositional grafting of the axillary artery (30). Similarly, Duwayri et al. (8) permitted a cohort of overhead athletes who underwent axillary artery repair to begin vigorous upper-extremity physiotherapy after discontinuing anticoagulation and antiplatelet therapy and undergoing routine reimaging the anastomosis 6 wk postoperatively; most returned to full, unrestricted activity within 2 to 3 months after the procedure.
We presented the case of a football player who suffered blunt trauma to his arm causing occlusion of the brachial artery. Because of the late presentation and his limited symptomatology, he was treated nonoperatively and was able to continue to reach high levels of athletic success. This injury is rarely reported among athletes. A history of trauma, pain with repetitive activity, and/or cold intolerance combined with diminished or absent distal pulses should raise suspicion for this rare injury. Doppler ultrasonography can provide an inexpensive, noninvasive, and reliable method of detecting the location and severity of the occlusion. Due to the rich, collateral flow around the elbow, most brachial artery injuries, especially those distal to the take-off of the profunda brachii artery, can be managed nonoperatively, and, in fact, may recanalize with return of normal hemodynamics. In those with ischemia or persistent symptoms that necessitate surgical intervention, interposition vein grafting is the procedure of choice. Interposition grafting has a high (>90%) success rate and can be expected to allow athletes to return to play by 3 months after surgery.
None of the researchers or an affiliated institute has received (or agreed to receive) from a commercial entity something of value (exceeding the equivalent of US $500) related in any way to this manuscript or research. None of the researchers have any conflicts of interest related to this manuscript.
1. Arko FR, Harris EJ, Zarins CK, Olcott C 4th. Vascular complications in high-performance athletes. J. Vasc. Surg
. 2001; 33:935–42.
2. Arko FR, Olcott C 4th. Arterial and venous injuries in athletes: findings and their effect on diagnosis and treatment. Phys. Sportsmed
. 2003; 31:41–8.
3. Bynoe RP, Miles WS, Bell RM, et al. Noninvasive diagnosis of vascular trauma by duplex ultrasonography. J. Vasc. Surg
. 1991; 14:346–52.
4. Coskun S, Soylu L, Coskun PK, Bayazit M. Short series of upper limb acute arterial occlusions in 4 different etiologies and review of literature. Am. J. Emerg. Med
. 2013; 31:1719.e1–4.
5. Deguara J, Ali T, Modarai B, Burnand KG. Upper limb ischemia: 20 years experience from a single center. Vascular
. 2005; 13:84–91.
6. De Monaco D, Fritsche E, Rigoni G, et al. Hypothenar hammer syndrome. Retrospective study of nine cases. J. Hand. Surg. Br
. 1999; 24:731–4.
7. Dragas M, Davidovic L, Kostic D, et al. Upper extremity arterial injuries: factors influencing treatment outcome. Injury
. 2009; 40:815–9.
8. Duwayri YM, Emery VB, Driskill MR, et al. Positional compression of the axillary artery causing upper extremity thrombosis and embolism in the elite overhead throwing athlete. J. Vasc. Surg
. 2011; 53:1329–40.
9. Ekim H, Tuncer M. Management of traumatic brachial artery injuries: a report on 49 patients. Ann. Saudi Med
. 2009; 29:105–9.
10. Eun JC, Bronsert M, Hansen K, et al. Vascular injury is associated with increased mortality in winter sports trauma. Ann. Vasc. Surg
. 2015; 29:109–13.
11. Grasu BL, Jones CM, Murphy MS. Use of diagnostic modalities for assessing upper extremity vascular pathology. Hand Clin
. 2015; 31:1–12.
12. Jackson MR. Upper extremity arterial injuries in athletes. Semin. Vasc. Surg
. 2003; 16:232–9.
13. Kee ST, Dake MD, Wolfe-Johnson B, et al. Ischemia of the throwing hand in major league baseball pitchers: embolic occlusion from aneurysms of axillary artery branches. J. Vasc. Interv. Radiol
. 1995; 6:979–82.
14. Klocker J, Bertoldi A, Benda B, et al. Outcome after interposition of vein grafts for arterial repair of extremity injuries in civilians. J. Vasc. Surg
. 2014; 59:1633–7.
15. Klocker J, Falkensammer J, Pellegrini L, et al. Repair of arterial injury after blunt trauma in the upper extremity—immediate and long-term outcome. Eur. J. Vasc. Endovasc. Surg
. 2010; 39:160–4.
16. Klocker J, Fraedrich G. Traumatic injury of upper extremity arteries. In: Liapis CD, Balzer K, Benedetti-Valentini F, Fernandes e Fernandes J (Eds.), European Manual of Medicine—Vascular Surgery
, Berlin: Springer; 2007. p. 257–61.
17. Klocker J, Peter T, Pellegrini L, et al. Incidence and predisposing factors of cold intolerance after arterial repair in upper extremity injuries. J. Vasc. Surg
. 2012; 56:410–4.
18. Kostianen S, Orava S. Blunt injury of the radial and ulnar arteries in volley ball players. A report of three cases of the antebrachial-palmar hammer syndrome. Br. J. Sports Med
. 1983; 17:172–6.
19. Kral CA, Han DC, Edwards WD, et al. Obstructive external iliac arteriopathy in avid bicyclists: new and variable histopathologic features in four women. J. Vasc. Surg
. 2002; 36:565–70.
20. Lönn L, Delle M, Karlström L, Risberg B. Should blunt arterial trauma to the extremities be treated with endovascular techniques? J. Trauma
. 2005; 59:1224–7.
21. McCarthy WJ, Yao JS, Schafer MF, et al. Upper extremity arterial injury in athletes. J. Vasc. Surg
. 1989; 9:317–27.
22. Nuber GW, McCarthy WJ, Yao JS, et al. Arterial abnormalities of the shoulder in athletes. Am. J. Sports Med
. 1990; 18:514–9.
23. Nuber GW, McCarthy WJ, Yao JS, et al. Arterial abnormalities of the hand in athletes. Am. J. Sports Med
. 1990; 18:520–3.
24. Rohrer MJ, Cardullo PA, Pappas AM, et al. Axillary artery compression and thrombosis in throwing athletes. J. Vasc. Surg
. 1990; 11:761–8; discussion 768–9.
25. Sachatello CR, Ernst CB, Griffen WO Jr. The acutely ischemic upper extremity: selective management. Surgery
. 1974; 76:1002–9.
26. Schneider K, Kasparyan NG, Altchek DW, et al. An aneurysm involving the axillary artery and its branch vessels in a major league baseball pitcher. A case report and review of the literature. Am. J. Sports Med
. 1999; 27:370–5.
27. Sultan S, Evoy D, Eldin AS, et al. Atraumatic acute upper limb ischemia: a series of 64 patients in a Middle East tertiary vascular center and literature review. Vasc. Surg
. 2001; 35:181–97.
28. Takach TJ, Kane PN, Madjarov JM, et al. Arteriopathy in the high-performance athlete. Tex. Heart Inst. J
. 2006; 33:482–6.
29. Thompson PN, Chang BB, Shah DM, et al. Outcomes following blunt vascular trauma of the upper extremity. Vascular
. 1993; 1:248–50.
30. Todd GJ, Benvenisty AI, Hershon S, Bigliani LU. Aneurysms of the mid axillary artery in major league baseball pitchers—a report of two cases. J. Vasc. Surg
. 1998; 28:702–7.
31. van der Sluis CK, Kucey DS, Brenneman FD, et al. Long-term outcomes after upper limb arterial injuries. Can. J. Surg
. 1997; 40:265–70.
32. Wong VW, Katz RD, Higgins JP. Interpretation of upper extremity arteriography: vascular anatomy and pathology. Hand Clin
. 2015; 31:121–34.
33. Yao JS. Upper extremity ischemia in athletes. Semin. Vasc. Surg
. 1998; 11:96–105.