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.