Abstract
Obstruction of the Subclavian Vein at the thoracic inlet is caused by compression in a vise mechanism between the tendons of the subclavius muscle and the costal clavicular ligament superiorly, the anterior scalene muscle posteriorly, and the first rib inferiorly (Fig. 13.1a, b). Thrombosis of the vein at that level is generally classified as either acute or chronic. The latter is a consequence of repeated pinching of the vein causing gradual fibrosis of its walls and, ultimately, progressive stenosis. When the process gets to a critical point, the vein finally obstructs causing an acute thrombosis at that level (Fig. 13.2a, b). This may rapidly propagate distally into the axillary vein or even down into the arms. Acute thrombosis on the other hand is due to a sudden unusual effort involving arms which damages the intima of the subclavian vein and precipitates acute thrombosis. The vein usually retains its normal caliber once the clot is removed and the compression mechanism around the vessel is relieved. In the case of recurrent chronic pinching of the vein causing gradual stenosis and fibrosis, the patient develops collateral circulation. Initially this may not be noticeable until total occlusion occurs and the collateral veins around the shoulder and the axillary vein become very prominent very rapidly (Fig. 13.3a, b). The arm may become significantly edematous, and frequently develops a blue hue (Fig. 12.1a, b). The illustration that Von Schroetter displayed in his original contribution [1] shows obvious advanced collateralization, which suggests that the obstruction has been present for a considerable period of time. In our own series of over 200 cases treated, only about 3% were seen during the acute event in a perfectly normal individual with no previous episodes of compression of the vein; the rest presented in the chronic stage of the obstruction. We call the thrombosis acute if this condition is diagnosed within the first 2 weeks of the original occurrence; beyond 2 weeks we consider the thrombosis chronic because we have seen some patients even that within that period of time who demonstrated a substantial amount of fibrosis extending distally into the axillary vein, sometimes into the arm, which of course renders any possibility of surgical intervention impossible (Fig. 13.4).
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsReference
Schroetter VL. Erkrankungen der Gefasse. Northnagel Handbuch der Pathologie und Therapie. Wien: Alfred Holder; 1884.
Author information
Authors and Affiliations
Rights and permissions
Copyright information
© 2013 Springer Science+Business Media New York
About this chapter
Cite this chapter
Molina, J.E. (2013). Etiology. In: New Techniques for Thoracic Outlet Syndromes. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-5471-7_13
Download citation
DOI: https://doi.org/10.1007/978-1-4614-5471-7_13
Published:
Publisher Name: Springer, New York, NY
Print ISBN: 978-1-4614-5470-0
Online ISBN: 978-1-4614-5471-7
eBook Packages: MedicineMedicine (R0)