Abstract
Thoracic outlet syndrome (TOS) is caused by compression of peripheral nerves and vascular structures along their course through the upper thoracic aperture to the axilla. The aim of our study was to analyze long-term outcomes of different treatments stratified by symptom severity. We performed a retrospective analysis of a cohort of 73 consecutive patients treated at our institution presenting with TOS-associated venous thrombotic events. Treatment strategies and immediate outcome analysis were completed by long-term follow-up with duplex ultrasound controls 6–12 months after the initial clinical event. Conservative therapy was started in mildly symptomatic patients (n = 32), of which 12 required endovascular procedures because of treatment failure. Endovascular treatment was attempted in all highly symptomatic patients and in those with conservative treatment failure (n = 53), of which 12 required acute surgical intervention. Elective surgical treatment was indicated in 30 other patients because of persistent symptoms. Surgery was associated with a significantly lower rate of the ultrasound-detected signs of persisting vascular compression. However, the rate of persisting clinical symptoms was comparable to those treated only by endovascular or conservative therapy. Our data demonstrate that initial endovascular treatment proposed as first line therapy to highly symptomatic subjects and in those with conservative treatment failure improves the symptoms in 77% of patients avoiding the need of acute surgery. Acute and elective surgical decompression leads to lower rates of vascular compression signs without significant amelioration of persisting clinical symptoms as compared to endovascular or conservative therapy.
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Skalicka, L., Lubanda, JC., Jirat, S. et al. Endovascular treatment combined with stratified surgery is effective in the management of venous thoracic outlet syndrome complications: a long term ultrasound follow-up study in patients with thrombotic events due to venous thoracic outlet syndrome. Heart Vessels 26, 616–621 (2011). https://doi.org/10.1007/s00380-010-0112-2
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DOI: https://doi.org/10.1007/s00380-010-0112-2