Effort Thrombosis of the Subclavian Vein in Athletes

Upper-extremity deep venous thrombosisis is a potentially life-threatening condition. There are several predisposing factors, including thrombophilic states, malignancy and indwelling of central venous catheters, pacemakers and different kinds of ports. Cruveilhier described spontaneous axillary-subclavian vein thrombosis in 1816. The first detailed data on axillary-subclavian vein thrombosis originated from Sir James Paget in 1875. Vascular trauma from muscle strain was identified as a potential risk factor in 1894 by Von Schroetter. In 1948, Hughes came up with the term Paget-Schroetter syndrome (PSS), which he described in his review of 320 cases of subclavian vein thrombosis1. Paget-Schroetter syndrome or effort thrombosis is a relatively rare condition that affects young and healthy athletes, with an incidence of approximately 1 in 50,000 people per year. It occurs through vigorous repetitive activity of the upper limbs, as seen in wrestling, swimming or playing basketball. Although it was first described in a viola player who suddenly increased his practice time 10-fold, today it is most frequently seen in young athletes. Extension, hyperabduction and retroversion of the arm are believed to be the causes of Paget-Schroetter syndrome. These movements lead to strain on the subclavian vein which causes microtrauma to the endothelium, triggering coagulation mechanisms. Furthermore, the anatomic abnormalities of the upper thoracic outlet facilitate PSS. There is substantial evidence that abnormalities such as cervical rib, abnormal insertion of the costoclavicular ligament, hypertrophy of scalene tendons and congenital bands (Figure 1) predispose to the development of PSS2,3. The compression of these anatomical elements on the subclavian vein leads to stasis in the blood flow. As described by Rudolf Virchow, three elements contribute to thrombosis: haemodynamic changes (stasis, turbulence), endothelial injury (or dysfunction) and hypercoagulability4. In his study, Cassada showed that approximately two-thirds of patients with PSS had concomitant thrombophillia5. Other studies have shown that there is a higher frequency of Factor V Leidin and mutations of the prothrombin gene6-8. All these pathological changes lead to perivenular or endothelial inflammation, which progresses to fibrosis and adhesions of the subclavian vein. This can lead to intimal hyperplasia and thrombosis and EFFORT THROMBOSIS OF THE SUBCLAVIAN VEIN IN ATHLETES