INTRODUCTION
Paget-Schroetter syndrome (PSS) is a thrombosis of the axillary-subclavian vein (SV), due to repetitive use of the arm associated with ‘the presence of one or more compressive elements in the thoracic outlet’.1 The condition mainly affects young males and is relatively uncommon for those with thoracic outlet syndrome, accounting for 1-4% of all cases of venous thrombosis. The incidence of PSS is estimated to be between 1 to 2 per 100000 population.2 The SV is the most anterior structure traversing the first rib out of the thoracic cavity. The first rib is the most curved and usually the shortest of all the ribs and furthermore it is broad and flat. The head of the rib is small and rounded whilst the neck is narrow with the tubercle on the outer border. The upper surface has two shallow grooves with a ridge between them and is prominent medially as a bony prominence. This is the scalene tubercle where the scalenus anterior muscle inserts. The anterior groove is where the SV course whilst the subclavian artery and the lowest trunk of the brachial plexus runs in the posterior groove (Figure 1).
Apart from surrounding anatomical structures, intrinsic vascular factors exist that may dramatically increase the risk PSS. Chronic stenosis of the SV resulting from repeated motion-induced compression and paraneoplastic pro-thrombotic states are examples of documented intrinsic lesions that impede flow in the SV independent of surrounding structures, and lead to PSS.3
Current optimum management for PSS is immediate catheter-directed thrombolysis (CDTL) followed by surgical decompression of the SV.4 Such a hybrid approach would involve endovascular thrombolysis, perhaps via CDTL or mechanical thrombectomy, followed by open surgical decompression of local structures. These may then be followed by adjunctive angioplasty in acute settings or venous bypass in chronic cases. Proceeding with both endovascular and open surgical interventions ensures that intrinsic and extrinsic insults are dealt with, and could help to further mitigate the risk of recurrent thromboses – the combined approach has been noted to allow 100% of patients to regain preoperative function in the affected upper limb.4
Successful extravascular management of PSS depends on a thorough understanding of the anatomical structures that may impinge on SV and cause extrinsic compression. The subclavius muscle and tendon are located medially at the thoracic outlet and can potentially cause nutcracker-like compression of the SV with very minimal movement (Figures 1 and 2). The costoclavicular ligament inserts inferiorly to the upper medial aspect of the cartilage of the first rib and proceeds posterolaterally to the costal tuberosity on the inferior aspect of the medial clavicle. Rigberg in 2006 described the ‘scissoring’ effect between the clavicle and first rib with arm movement, to explain the potential for compression of neurovascular structures at the thoracic outlet.5
This review seeks to evaluate the roles of endovascular intervention against open surgical decompression for the management of PSS. Existing literature was reviewed to determine the significance of adopting both intervention modalities for the successful treatment of PSS. In addition, data gathered over 15 years in a tertiary referral centre in South Wales concerning the surgical approaches to anatomical resection are included. The outcomes scrutinised after thrombolysis, surgical decompression and venoplasty included vein patency, adjunctive measures performed at first admission and symptom relief.