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ORIGINAL RESEARCH

Arterial and Venous Injuries in Athletes

Findings and Their Effect on Diagnosis and Treatment

Frank R. Arko, MD; Cornelius Olcott IV, MD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 31 - NO. 4 - APRIL 2021


ABSTRACT

BACKGROUND: Athletes are susceptible to a variety of vascular injuries, yet clinical presentation may be subtle and the extent of injury underestimated.

OBJECTIVE: To evaluate Stanford University's experience with the diagnosis and management of vascular injuries incurred during athletic competition.

METHODS: Between June 1994 and June 2021, 29 patients with athletic competition-related vascular injuries were treated by our service. Clinical presentation, type of athletic competition, location of injury, type of therapy, and degree of rehabilitation were analyzed.

RESULTS: Mean patient age was 23.8 years. In total, 17 arterial and 12 venous injuries were treated. Arterial injuries consisted of 8 axillary or subclavian branch artery aneurysms with embolization, 6 popliteal artery injuries, and 3 external iliac artery injuries. Subclavian vein thrombosis (SVT) accounted for all venous complications. Sixteen (94%) patients with arterial injuries required surgical repair. Fifteen reconstructions maintained primary patency with a mean follow-up of 43.9 months. All patients with SVT received lytic therapy and anticoagulation. Eight of these (67%) required thoracic outlet decompression and venolysis. All patients with SVT have remained stable without further venous thrombosis.

CONCLUSION: Athletes are susceptible to vascular injuries that may not be easily recognized. However, a high index of suspicion, appropriate imaging, and prompt treatment allow athletes to return to competition in most cases.

As amateur and professional sports have become increasingly prominent, physicians are seeing a burgeoning number of sports-related injuries. Athletic injuries are typically musculoskeletal in nature, but arterial and venous injuries are being recognized with increasing frequency.

Vascular-related athletic injuries typically involve three areas: the shoulder girdle (axillary and subclavian vessels), the hip (iliac vessels), and the knee (popliteal vessels). These injuries are related to either repetitive motion or stress on the associated joint. A fourth area—direct injury to the arteries of the hand—may arise from repetitive trauma.

High-performance athletes are susceptible to a variety of vascular injuries. Studies1-7 from other institutions have detailed experiences with vascular injuries among such patients, and it is apparent that such injuries represent a growing concern as athletes become increasingly competitive.

Failure to recognize a vascular injury in such patients may result in failure to treat a potentially limb-threatening lesion or diminish the level of performance in the competitive athlete. Proper diagnosis requires a high level of suspicion, a thorough workup, and a detailed vascular exam, including noninvasive studies and arteriography or venography when indicated.

We present our experience with competitive athletes who had vascular injuries arising from athletic competition. We evaluated patients' clinical presentation, athletic competition, injury (venous or arterial), therapy, and degree of rehabilitation.

Patients and Methods

From June 1994 to June 2021, we treated 29 patients who had vascular injuries associated with athletic activity. Patients were detected prospectively in a vascular registry, and their outcomes retrospectively analyzed. Patients were classified into one of two groups based on whether they had a venous or arterial injury. Arterial injuries were further classified according to location of the lesion.

Results

The mean patient age was 23.8 years. Twenty-three athletes were men, and 6 were women. Distribution according to sport was 9 major league baseball players, 7 football players, 4 cyclists, 2 climbers, 2 surfers (including 1 weight lifter-surfer), 1 swimmer, 1 kayaker, 1 weight lifter, 1 marksman, and 1 volleyball player. Among the athletes, 17 arterial and 12 venous complications occurred (table 1).

TABLE 1. Demographics, Therapies, and Outcomes of Vascular Injuries Among Athletes

InjuryNumberAge (yr)
(Range)
Sex
(M/F)
Lytic
Therapy
SurgeryFree of
Symptoms
at Last
Follow-up
Vessel
Patent
Return
to Previous
Level of
Competition

Venous12/29
Subclavian
vein thrombosis
1223.3
(16-25)
9/312/128/1212/12
minimal
12/1212/12
Arterial17/29
Axillary or
subclavian
825.7
(19-32)
8/06/87/88/88/88/8
Popliteal622.3
(17-40)
5/106/66/66/63/6
Iliac333.3
(26-38)
2/103/33/33/33/3

M = male; F = female

Axillary or subclavian artery. Eight patients (all male) were identified with aneurysms of the axillary or subclavian artery or their branches (figure 1). The mean age was 25.7 (range, 19 to 32) years (see table 1). Six patients were professional baseball players, 1 was a collegiate volleyball player, and 1 was a cyclist. At their initial evaluations, all had subtle symptoms frequently not recognized as vascular problems. Typical symptoms included decreased speed or control while pitching, cool fingers, digital ulcers, and loss of endurance in the affected extremity during competition or training. Arterial pulses were normal, although Allen's test revealed evidence of fixed digital lesions. Two patients had ischemic digital ulcers.

Noninvasive studies demonstrated diminished photoplethysmographic waveforms in the digits. Color duplex imaging showed a branch artery aneurysm in five patients. Arteriography revealed the location of the aneurysm and extent of embolization. Lesions detected in these patients consisted of 4 circumflex humeral artery aneurysms, 1 subclavian artery aneurysm, 1 suprascapular artery aneurysm, 1 axillary artery aneurysm, and 1 subscapular artery aneurysm. Six of 8 patients had evidence of distal emboli by arteriography and received preoperative thrombolytic therapy.

Surgical intervention was recommended to all patients. Seven of 8 (88%) patients elected surgical resection of the aneurysm. One patient opted for conservative management with 6 weeks of antiplatelet therapy; he retired from baseball the following year. Five patients had resection of the aneurysm and lateral repair of the artery with a vein patch angioplasty. Two patients had resection of the aneurysm and repair with a reversed interposition graft of the greater saphenous vein (RGSV).

All reconstructions have remained patent to date with a mean follow-up of 50.2 months (range, 6 to 86 months). These patients have been able to return to competition without further symptoms.

Popliteal artery. Six patients had injuries of the popliteal artery (see table 1). Three patients (2 football running backs and 1 kayaker) had severe traumatic posterior knee dislocations associated with acute ischemia that required emergency repair. The kayaker sustained his injury when his kayak struck a rock and essentially folded the young man in half at the level of his knees. Repair employed femoral-to-below-the-knee popliteal bypasses with an RGSV. All repairs have remained patent, but these patients have not been able to achieve their previous level of activity because of the extensive injury to their knees.

The other 3 patients (1 football player, 1 weight lifter [who performed repetitive leg curls], and 1 surfer) had symptoms of unilateral lower-extremity weakness or discomfort with exertion. Claudication limited their performance. Noninvasive studies indicated unilateral chronic occlusion of the artery, but they had no history of trauma. MRI revealed popliteal artery entrapment in the football player, and the weight lifter sustained arterial dissection during weight lifting with her legs. The cause in the third patient is unknown. The football player had a femoral-to-below-the-knee bypass with RGSV using a posterior approach, but the graft failed after 2 months. Failure was attributed to the excessive inflammation and scarring encountered in the initial surgery. The second repair employed a medial approach, and this graft has remained patent at 14 months.

All patients had noninvasive studies that indicated popliteal occlusion. Arteriography confirmed short segments of popliteal artery occlusion. RGSV was done using a posterior approach in 2 of 6 patients and a medial approach in 4 patients. Five of 6 grafts maintained primary patency with a mean follow-up of 51.0 months (range, 6 to 83).

Three patients were able to return to their previous level of activity. The other 3 patients (2 football players and the kayaker), who had had posterior knee dislocations with acute ischemia, were unable to return to their prior level of competition because of their associated musculoskeletal injuries.

Iliac artery. Three patients had external iliac artery injuries from competitive cycling (see table 1). They had no history of trauma and no complaints of claudication; however, at top speeds the patients noted fatigue in their thighs that slowed their cycling. Physical examination, including distal pulses, was normal. Resting noninvasive studies with ankle-brachial indices (ABI) of greater than 1.0 were present bilaterally. ABIs decreased to less than 0.5 following cycling to an extent that reproduced symptoms (figure 2).

Arteriography demonstrated an area of stenosis and redundancy in the external iliac artery in 2 patients, and 1 patient, who had had previous surgery elsewhere, had an occluded external iliac artery. All 3 patients had normal arterial runoff bilaterally. Intravascular ultrasound was used to confirm the findings of intimal thickening and fibrosis in the two patent arteries.

All patients had a lower-abdominal retroperitoneal incision for exploration and repair of the external iliac artery. In 2 patients, the artery was released from small branches tethering the artery to the psoas muscle. The artery was then shortened and the stenosis repaired with a saphenous vein patch angioplasty. The patient with the occluded artery had a short 8-mm polytetrafluoroethylene interpositional graft placed; previous surgery precluded repair with the endogenous vein.

All patients were discharged within 6 days after surgery. ABIs at rest postoperatively were normal, and after exercise ABIs in the affected extremity improved to greater than 0.85. Patients had no complaints of fatigue after exercise. At 1 month, patients had repeat pre- and postexercise noninvasive testing, and subsequent testing was done biannually. All reconstructions have remained patent.

Subclavian vein thrombosis. Twelve patients had subclavian vein thrombosis (SVT) related to athletic competition (see table 1). Athletes in this group were 4 football players, 3 pitchers, 2 rock climbers, 1 weight lifter-surfer, 1 swimmer, and 1 marksman. All patients had a history of strenuous or repetitive activity. Diagnosis was based on duplex imaging. When SVT was revealed by duplex ultrasound, the patient was admitted and had a contrast venogram from the proximal forearm to the innominate-superior vena caval confluence. Attention focused on the shoulder girdle area, and images were obtained with the arm in neutral and in abduction and external rotation.

Patients who had a positive venogram were treated with catheter-directed thrombolysis. Infusions lasted from 24 to 72 hours, depending on the success of thrombolysis as demonstrated by serial venograms. Simultaneous heparin infusion was done through the sheath to obtain an activated partial thromboplastin time of 60 to 80 seconds. Thrombolysis ceased when one of the following occurred: No change in the appearance of the vein in two sequential venograms, bleeding complications, biochemical evidence of disseminated intravascular coagulapathy, or 72 hours of continuous infusion. Eight of 12 patients had complete venographic evidence of clot lysis, and 4 patients had only partial (more than 50%) lysis.

After thrombolysis, vein patency was assessed with a completion venogram. Any positional impingement of the subclavian or axillary vein or collateral veins was noted. Patients were converted from intravenous heparin to warfarin and discharged when the international normalized ratio was therapeutic. Patients were instructed to engage in normal activities of daily living, but to avoid athletic competition.

Patients were reevaluated at 4 weeks with color-flow venous duplex scanning to determine the deep venous (figure 3) and collateral circulation (figure 4). They were interviewed about any symptoms at rest and with exercise and examined for evidence of venous hypertension. Indications for surgical intervention included persistent symptoms of venous hypertension, obstruction of the subclavian vein or collaterals with abduction and external rotation, or recurrent thrombosis. Thoracic outlet decompression was accomplished via a single supraclavicular incision; the details have been described previously.8 In all cases, the first rib was resected and fibrous bands impinging on the subclavian vein were released. None of our patients had a cervical rib. Surgeons took care to avoid dividing any major collateral veins. A complete circumferential venolysis of the subclavian vein completed the procedure.

Eight of the 12 patients underwent thoracic outlet decompression for persistent symptoms. There were no morbidities or mortalities related to surgery. Patients began physical therapy the day after surgery. The average postoperative hospitalization was 2.1 days. Venous duplex imaging at 4 weeks and every 6 months thereafter demonstrated continued vein patency in all patients who underwent surgery, and all patients had resolution of their symptoms. Median follow-up in these surgery patients was 13.9 months (range, 4 to 26 months).

Patients used anticoagulants for 1 month after surgery and were allowed to resume full physical activity after 6 weeks. Balloon angioplasty is generally reserved for patients who have symptomatic residual stenosis after surgery, but the procedure was not required in any athletes.

Four patients were treated conservatively with warfarin for an average of 3.6 months (range, 2 to 7 months). These patients had minimal symptoms at the conclusion of anticoagulation therapy and were able to return to competition. They have done well and have not needed further intervention. To date, duplex imaging has shown that these patients' veins have remained patent. Median follow-up was 18.8 months (range, 6 to 30 months).

Overview of Vascular Injuries

The diagnosis of an arterial or venous injury in the young athlete may be obvious, for example, in the patient with a knee dislocation and leg ischemia. However, not infrequently, these patients present with subtle symptoms that may not suggest a vascular injury. Also, in some cases noninvasive studies may not be diagnostic, especially if done while the patient is at rest. A vascular lesion should be suspected in any athlete experiencing fatigue, loss of endurance, or pain or swelling in an extremity during physical exertion, particularly those whose sport involves repetitive activity. Vascular lesions have been documented in athletes of several sports, including baseball (pitching), weight lifting, and cycling.1-7,9,10

Most patients (20 of 29) in this series had problems related to the upper extremity. Twelve had SVT, and 8 patients had aneurysms of the subclavian or axillary arteries or their branches. In these patients (9 baseball pitchers, 4 football players, 2 climbers, 1 cyclist, 1 marksman, 1 swimmer, 1 weight lifter-surfer, and 1 volleyball player), repetitive activity was directly correlated with an extremity and vascular injury. Fields et al10 documented the significance of upper-extremity arterial injuries in athletes when they reported the case of a baseball pitcher who sustained a stroke following thrombosis of his right subclavian artery.

Mechanisms of vascular injury. Injury to the subclavian artery is usually a complication of thoracic outlet syndrome and results from compression of the artery by a cervical rib, first rib, or soft tissues of the outlet. Repetitive injury to the subclavian artery may produce arterial stenosis that can progress to occlusion or that may be associated with poststenotic dilatation or aneurysm formation. These aneurysms can be a source of distal embolization and ischemic tissue loss to the digits of the affected extremity.1,2,4-7,9,10

Injury to the axillary artery may arise from compression by the pectoralis minor tendon or from compression by the head of the humerus during hyperabduction and external rotation. Stretch injury to the branches of the axillary artery—the circumflex humeral arteries and the subscapular artery—also may occur with repeated hyperabduction.6-8 Reekers et al11 identified posterior circumflex humeral aneurysms in three professional volleyball players, all of whom had evidence of distal emboli. McCarthy et al1 described similar findings in 11 athletes who had branch artery aneurysms or subclavian aneurysms and distal emboli.

The presumed cause of the aneurysms in these reports and in our patients was repetitive trauma to the vessel. Researchers postulate that while the shoulder is hyperextended and externally rotated, the humerus compresses the axillary artery and stretches its branches. Such stretching creates shear forces that weaken the arterial wall and cause an aneurysm to form. The humeral head subsequently compresses these aneurysms during hyperextension, pushing thrombi into the arterial stream.1,2

Thoracic outlet syndrome. SVT secondary to thoracic outlet syndrome is well documented. Reports have focused on numerous causes, including supernumerary ribs, compression of vessels between the scalene muscles, and compression between the clavicle and first rib during hyperabduction of the arm.8,11-13 Recently, our group reported the results of management of SVT.12 In that report, 41% of patients did not require surgery but were treated with thrombolysis and anticoagulation. Surgery was reserved for patients with persistent symptoms of venous hypertension. Athletes with SVT were treated using the same algorithm. However, athletes with persistent symptoms had surgery earlier because of the desire to return to competition as soon as possible.

Vascular injuries in the leg. The vascular anatomy predisposes the popliteal area to traumatic injury because of the tethering at the adductor hiatus and the soleus arch. Knee dislocations should be followed with arteriography or exploration of the vessels. Epiphyseal separations of the proximal tibia and distal femur should be observed closely for the first 24 to 48 hours.3,14,15 The cause of claudication among athletes requires a careful history and physical examination. Vascular studies to determine if the cause is one of popliteal artery entrapment, adventitial cystic disease, or adductor canal outlet syndrome are also helpful. Magnetic resonance imaging (MRI) is important to exclude musculoskeletal disorders.

Several reports have described isolated cases of external iliac artery injury in professional cyclists. Most cases involve cyclists who have ridden more than 150,000 km. The left external iliac artery is typically more often affected than the right one. The pathologic lesion has been described as endofibrosis with thickening of the intima and is believed to be secondary to a repetitive injury to the vessel.16-18 Researchers hypothesize that the enlarged psoas muscle, the flexed position of the cyclist, and branch vessels tethering the external iliac artery to the psoas produce arterial elongation and stenosis.16

The diagnosis cannot be appreciated with a resting exam, but postexercise ABIs will manifest a significant drop, typically to less than 0.5.

Most authors describe repairing lesions by dividing branches to the psoas and shortening and patching the artery. Repair with prosthetic graft or angioplasty has not been successful.17-18 Division and patching of these lesions has resulted in excellent results.

Ensuring a Successful Outcome

Athletes are susceptible to several vascular injuries that may not be easily recognized. A high level of suspicion, a thorough workup, including noninvasive studies and arteriography or venography, and prompt, injury-specific treatment are important for a successful outcome.

References

  1. McCarthy WJ, Yao JS, Schafer MF, et al: Upper extremity arterial injury in athletes. J Vasc Surg 120219;9(2):317-327
  2. Durham JR, Yao JS, Pearce WH, et al: Arterial injuries in the thoracic outlet syndrome. J Vasc Surg 1995;21(1):57-69
  3. Darling RC, Buckley CJ, Abbott WM, et al: Intermittent claudication in young athletes: popliteal artery entrapment syndrome. J Trauma 1974;14(7):543-552
  4. Arko FR, Harris EJ, Zarins CK, et al: Vascular complications in high-performance athletes. J Vasc Surg 2021;33(5):935-942
  5. Nuber GW, McCarthy WJ, Yao JS, et al: Arterial abnormalities of the hand in athletes. Am J Sports Med 1990;18(5):520-523
  6. Nehler MR, Taylor LM Jr, Moneta GL, et al: Upper extremity ischemia from subclavian artery aneurysm caused by bony abnormalities of the thoracic outlet. Arch Surg 1997;132(5):527-532
  7. Rohrer MJ, Cardullo PA, Pappas AM, et al: Axillary artery compression and thrombosis in throwing athletes. J Vasc Surg 1990;11(6):761-768
  8. Lee WA, Hill BB, Harris EJ Jr, et al: Surgical intervention is not required for all patients with subclavian vein thrombosis. J Vasc Surg 2021;32(1):57-67
  9. 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(6):979-20212
  10. Fields WS, Lemak NA, Ben-Menachem Y: Thoracic outlet syndrome: review and reference to stroke in a major league pitcher. AJR Am J Roentgenol 120216;146(4):809-814
  11. Reekers JA, den Hartog BM, Kuyper CF, et al: Traumatic aneurysm of the posterior circumflex humeral artery: a volleyball player's disease? J Vasc Interv Radiol 1993;4(3):405-408
  12. Beygui RE, Olcott C IV, Dalman RL: Subclavian vein thrombosis: outcome analysis based on etiology and modality of treatment. Ann Vasc Surg 1997;11(3):247-255
  13. Azakie A, McElhinney DB, Thompson RW, et al: Surgical management of subclavian-vein effort thrombosis as a result of thoracic outlet compression. J Vasc Surg 192021;28(5):777-786
  14. McCoy GF, Hannon DG, Barr RJ, et al: Vascular injury associated with low-velocity dislocations of the knee. J Bone Joint Surg Br 120217;69(2):285-287
  15. Turnipseed WD, Pozniak M: Popliteal entrapment as a result of neurovascular compression by the soleus and plantaris muscles. J Vasc Surg 1992;15(2):285-293
  16. Chevalier JM, Enon B, Walder J, et al: Endofibrosis of the external iliac artery in bicycle racers: an unrecognized pathological state. Ann Vasc Surg 120216;1(3):297-303
  17. Wille J, de Jong JR, Moll FL, et al: Endofibrosis of the external iliac artery in sportsmen: clinical review and four new cases. Vasc Surg 192021;32(4):323-328
  18. Schep G, Bender MH, Kaandorp D, et al: Flow limitations in the iliac arteries in endurance athletes: current knowledge and directions for the future. Int J Sports Med 1999;20(7):421-428


Dr Arko is assistant professor of surgery and Dr Olcott is professor of surgery, both in the division of vascular surgery at Stanford University School of Medicine in Stanford, California. Address correspondence to Cornelius Olcott IV, MD, 300 Pasteur Dr, H3600, Stanford, CA 94305-5642; e-mail to [email protected].

Disclosure information: Drs Arko and Olcott disclose no significant relationship with any manufacturer of any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.


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