Paget-Schroetter Syndrome in Nonathletic31-Year-Old Female Without Hypercoagulopathy
Thomas B. Rehder III, DO ; and Kevin Casey, MD
Abstract
Paget-Schroetter syndrome is an infrequent event in which an upper-extremity thrombosis forms typically after strenuous overhead activities, such as weight-lifting, swimming, pitching, and wrestling. This occurs most frequently in athletic men in their second or third decade of life and may be associated with thoracic outlet anatomical abnormalities that result in venous compression and increased risk for repetitivemicrotrauma leading to thrombosis. An atypical presentation in a 31-year-old nonathletic woman information technology worker without hypercoagulability is presented here.
Background
Paget-Schroetter syndrome (PSS), or “effort vein thrombosis,” refers to subclavian and axillary vein thrombosis often associated with repetitive, strenuous, upper-extremity (UE) activities, such as weightlifting, swimming, pitching, and wrestling. The typical patient demographic is an active man in his second or third decade of life. Symptoms aremore frequent in the dominant arm (1, 2). The pathology is fromrecurrent microtrauma to the subclavian and axillary veins sustained with hyperabduction or extension of the arm intensified bymechanical compression of the vein by adjoining muscle, bone, or ligamentous structures (3, 4). Chronic scarring then eventually leads to blood stasis and thrombosis. PSS is an infrequent occurrence with approximately 1 to 2 per 100 000 people yearly and accounts for 1% to 4% of all venous thromboembolic events (2). The thoracic outlet consists of the spinal column, first ribs, and sternum. The subclavian vein (SCV), as it passes through the thoracic outlet, has 2 distinct areas of external compression: the costoclavicular space between the first rib inferiorly, clavicle superiorly, anterior scalene muscle posteriorly, and costoclavicular ligament anteriorly; and the pectoralis minor space between the rib cage and pectoralis minormuscle. Evidence has shown that anatomical abnormalities
of the thoracic outlet, such as hypertrophy of the scalenes, congenital lateral insertion of the costoclavicular ligament, and cervical ribs, contribute to the pathogenesis of effort thrombosis (4, 5). The narrowing of the costoclavicular space can compress the vein and result in stasis in blood flow. It may also restrict themobility of the SCV, thereby increasing the risk for intimal vessel trauma fromoverexertion of the UE (1, 4).
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