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Current Trends in the Treatment of Venous Thoracic Outlet Syndrome: a Comprehensive Review

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Current Trends in the Treatment of Venous Thoracic Outlet Syndrome: a Comprehensive Review REVIEW Current trends in the treatment of venous thoracic outlet syndrome: a comprehensive review Venous thoracic outlet syndrome (TOS) is a less common presentation than neurogenic TOS. It is caused by venous obstruction due to axillosubclavian venous thrombosis or, less frequently, nonthrombotic external compression. Thrombotic venous TOS is commonly known as Paget–Schroetter syndrome and primarily involves axillosubclavian vein thrombosis. Patients with nonthrombotic forms of venous TOS typically have normal venography at rest, but arm abduction generates a positional venous compression resulting in arm swelling and pain. This paper reviews the anatomy and pathophysiology associated with venous TOS and suggests an approach for diagnostic workup and treatment. Controversies exist as to the most appropriate treatment and, in particular, the timing of treatment during the natural course of the disease. Here we describe treatment options and suggest an algorithm for appropriate, safe and effective patient management. 1 KEYWORDS: axillosubclavian venous thrombosis n effort thrombosis n nonthrombotic Nikos Tsekouras venous thoracic outlet syndrome n Paget–Schroetter syndrome n thoracic outlet 1 syndrome & Anthony J Comerota* 1Jobst Vascular Institute, 2019 Hughes Drive, Suite 400, Toledo, OH 43606, USA The term ‘thoracic outlet syndrome’ (TOS) Nonthrombotic venous TOS represents an *Author for correspondence: represents a variety of disorders caused by the intermittent/positional venous obstruction usu- Tel.: +1 419 291 2080 Fax: +1 419 479 6980 compression of nerves, arteries and veins as ally due to external compression, without the [email protected] they exit the thorax and enter the axilla. Three presence of intraluminal thrombus. Patients basic syndromes are reported according to the generally have normal venograms at rest, but involved anatomic structures: neurogenic, develop varying degrees of extrinsic compres- venous and arterial. Occasionally, the neuro- sion and venous collateral drainage with the logical and arterial syndromes may coexist in arm abducted [6]. The natural history of these the same patient. However, for ease of under- patients is not clear; however, some believe it may standing, each of these syndromes should be be a precursor of Paget–Schroetter syndrome. conceptualized as distinct clinical entities for This review focuses on the anatomy and they have characteristic differences in clinical pathophysiology associated with venous TOS, presentation, diagnostic workup and treat- the diagnostic workup and proposed treatment. ment. Venous TOS, which is the topic of this The venous variant of TOS in many ways is less review, can be further divided into two cat- controversial than the neurogenic variety and egories, the thrombotic and the less common can be objectively identified by clinical exami- nonthrombotic venous TOS. nation, ultrasonography or venography. How- Thrombotic venous TOS, also known as ever, controversies remain regarding the most Paget–Schroetter syndrome, specifically refers appropriate treatment, the need for thoracic to primary axillosubclavian vein thrombosis outlet decompression, the role of thrombolytic [1] . Another term for this syndrome is ‘effort therapy, and the indications for balloon angio- thrombosis’, as it is frequently associated with plasty or stenting. Most importantly, significant repetitive activities of arm elevation or exertion controversy exists regarding the timing of treat- over a long period of time [2]. Sir James Paget ment during the natural course of the disease. first described a spontaneous thrombosis of the We describe treatment options and suggest an subclavian vein in 1875 [3], and in 1884 von algorithm for appropriate, safe and effective Schroetter correlated this entity with direct patient management. damage of the vein caused by muscular strain [4]. The eponym ‘Paget–Schroetter syndrome’ Epidemiology, anatomy first appeared in 1948 when it was coined by & pathophysiology Hughes, an English surgeon who described this Venous TOS accounts for approximately 5% clinical condition in more detail [5]. of all TOS syndromes [7]. Axillosubclavian part of 10.2217/ICA.13.91 © 2014 Future Medicine Ltd Interv. Cardiol. (2014) 6(1) , 10 3 –115 ISSN 1755 -5302 103 REVIEW Tsekouras & Comerota venous thrombosis is seen more often than autorepair) or in athletes, such as baseball pitch- nonthrombotic obstruction. Interestingly, only ers and swimmers [1] . More specifically, all of three reports have been published addressing the these activities are characterized by repetitive or nonthrombotic clinical entity since 1973 [6,8,9]. prolonged vigorous hyperabduction or external In a 15-year review, 66 out of 87 patients oper- rotation of the shoulder joint [19] . ated on for TOS had subclavian vein thrombosis The exact mechanism of venous injury associ- and 21 had obstruction without thrombosis [6]. ated with the syndrome is not very well known. Effort thrombosis is more widely reported. Its In the case of thrombosis, it is also unclear if incidence in Sweden has been estimated at 2.03 thrombus is the result of a single insult or the per 100,000 people per year [10] and accounts for cumulative effects of chronic injury to the vein. approximately 1–4% of all episodes of venous It has been hypothesized that repetitive and pro- thrombosis [11,12] . The male-to-female ratio is longed focal venous injury results in repeated approximately 2:1 and the mean age of presenta- trauma to both the intima and the wall of the tion is the early 30s [10] . The right upper extrem- vein itself. The intimal trauma results in intimal ity is more commonly involved owing to the hypertrophy [20] and activation of the coagula- higher incidence of right-hand dominance and tion cascade [21], predisposing to thrombosis. 60–80% of patients have a history of vigorous The perivascular tissue develops inflammation, exercise of the involved extremity, such as heavy which in turn leads to fibrosis and scar tissue lifting, repetitive overhead motion or strenuous formation by dense collagen with persistent vein athletic activity [13] . compression [22,23]. Lack of vein mobility due The thoracic outlet is defined anatomically to the surrounding scar tissue increases the risk as two distinct spaces, the interscalene triangle of vein trauma, producing a cycle of progres- (demarcated by the anterior and middle scalene sive injury whenever the diameter of the costo- muscles and the first rib) and the costoclavicular clavicular space changes. Perivenous fibrosis can space (between the first thoracic rib and the clav- be identified during the operative procedure to icle) [14] . The interscalene triangle contains the decompress the subclavian vein [1] . brachial plexus and the subclavian artery. The It seems that there is an initial phase of the costoclavicular space contains the subclavian syndrome that is characterized by intermittent vein alone. The subclavian vein crosses anterior venous outflow obstruction prior to vein injury. to the anterior scalene muscle, passing adjacent Patients may be asymptomatic due to the devel- to the junction of the clavicle and the first rib[15] . opment of first rib collateral veins that facilitate A third muscle, the subclavius, can also provide drainage of the upper extremity. This condition ‘bulk’ and narrow the costoclavicular space. has been described as nonthrombotic venous Theoretically, the subclavian vein can be TOS and can be confirmed by a venogram compressed in this narrow passageway between showing the obstructed subclavian vein and its bony structures (first rib and clavicle), muscu- collateral veins when the arm is abducted [1] . On lar structures (hypertrophied anterior or middle occasion, nonthrombotic TOS can progress to scalene and subclavius muscle) or a bony and severe symptoms requiring decompression. This a muscular structure. Reported abnormalities generally occurs as a result of the loss of collateral include venous compression between the clavicle venous drainage, illustrated by FIGURE 1. Between and first rib, between a hypertrophied scalene the nonthrombotic state and the acute throm- or subclavian tendon and first rib, between a botic condition (Paget–Schroetter syndrome) scalene and a subclavian tendon, or by a con- is another condition characterized by recurrent genital web [15] . However, it is not quite clear if partial thrombosis followed by recanalization the external compression of the subclavian vein [16] . The alternation between thrombosis and originates from a narrow costoclavicular space, recanalization causes local inflammation and an abnormal bony structure, a hypertrophied scar formation leading to the development of muscle or from a combination of all of these venous webs and fibroelastic structures in the since it has been demonstrated that the vein can venous lumen. Eventually thrombus occludes the be easily compressed even in normal individu- narrow segment of the subclavian vein due to als [16] . Nevertheless, whichever abnormality is stagnant flow. Propagation of the clot into the responsible for the subclavian vein compres- axillary vein compromises subclavian venous col- sion, the compression occurs or worsens when laterals, resulting in the acute symptoms of effort the arm is abducted [17,18]. Interestingly, this thrombosis. When the thrombus is acute, it can syndrome is often present in patients where the be lysed, restoring patency to the central veins arm is overhead (painting, weight training and and first
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