[Treatment of the thoracic outlet vascular syndrome]

The title "Thoracic Outlet Syndrome" (TOS) was introduced by Peet in 1956 [1]. In 1958 Charles Rob defined TOS as a "set of symptoms that may exist due to compression on the brachial plexus and on subclavian vessels in the region of the thoracic outlet" [2]. Compression due to cervical rib was first described by Galenus and Veaslius in the 2nd century A.D. The first unsuccessful resection of the cervical rib in patients with TOS was performed by Coote in 1861 [4]. In 1905 Murphy first made a successful resection of the cervical rib in patients with TOS and subclavian artery aneurysm [5]. He also removed the normal first rib in patients with TOS using the supraclavicular approach for the first time [6]. In 1920 Law described ligaments and other structures originating in soft tissue associated with TOS [8], while Adson and Coffey in 1927 emphasized the role of the scalene anticus muscle in TOS [3]. Ochsner, Gage and DeBakey in 1935 named it the "scalenus anticus syndrome", and made the first successful resection of the anterior scalene muscle [9]. In 1966 David Ross introduced the transaxillary resection of the first rib to relieve TOS [11]. The aim of the paper is to describe the treatment of patients with vascular TOS.

Over a six-year-period (1990-1997) 12 patients with vascular TOS were evaluated at our Centre. Seven (58%) were female and 5 (42%) male patients, average age 33.1 years. Eleven of them had congenital TOS, and one acquired TOS after trauma at neck-shoulder region. Seven patients had arterial and 5 venous TOS. Two patients with arterial TOS had ischaemia of the upper extremity due to embolism of the brachial artery. In one of them axillary artery was completely thrombosed, and in the other postenotic dilatation of the subclavian artery was present. The other 5 patients with arterial TOS demonstrated only hand pain and radial puls during hyperabduction of the arm. One of our patients with venous TOS had also symptoms and signs of hand oedema during hyperabduction, while four patients had axillary-subclavian deep venous thrombosis (DVT). All patients underwent CW-Doppler and Duplex-ultrasonographic examination. The results were positive in all patients with arterial TOS. The angiographic (selective arteriography of the subclavian artery) examination showed the same results. Diagnostic procedures were performed in normal position of the arm and during hyperabduction. The angiography also revealed: one aneurysm of the subclavian artery, one poststenotic dilatation of the subclavian artery with brachial artery embolization, and one thrombosed axillary artery with brachial artery embolization (Figure 1). In five patients the angiogram was normal in normal position of the arm, but showed arterial flow obstruction at the thoracic outlet during hyperabduction (Figures 2a and 2b). In patients with venous TOS Duplex ultrasonographic examination was performed. The cervical rib caused TOS in four of our patients and clavicle fracture calus in one case. In 7 patients bone anomalies were not found (Figure 3). The operative treatment was carried out in 3 patients with venous and 7 patients with arterial TOS. In two patients with DVT of the axillary-subclavian segment, 6 months after standard anticoagulant therapy, decompressive procedures were performed (one resection of the cervical rib, and one transauxillary resection of the first rib). In the case of venous TOS without DVT, a supraclavicular resection of the first rib was performed immediately after diagnosis. In 5 patients with arterial TOS without morphologic changes on the arterial system, a decompressive procedure was done. The following procedures were carried out: one scalenotomy, one supraclavicular and three transaxillary resections of the first rib. (ABSTRACT TRUNCATED)