Risk factors for deep venous thrombosis of the upper extremity include venous compression by a cervical rib and the Paget-Schroetter, or “effort,” syndrome, whereby recurrent exertion of the arm results in endothelial damage that predisposes to clot formation. Most series of upper-extremity deep venous thrombosis have included patients with localized tumor or a subclavian catheter. Ellis and colleagues investigated the risk factors and clinical outcomes of upper extremity thrombosis in 18 patients with spontaneous axillosubclavian thrombosis.
Patients in this retrospective study were 22 to 70 years of age (median age: 38 years). They were seen from 1989 to 1997. Axillosubclavian thrombosis was suggested clinically by the presence of erythema, pain and swelling of the affected arm. The presence of thrombosis was confirmed by color duplex ultrasonography or venography. Excluded from the study were patients with a history of trauma or a subclavian catheter on the affected side. Patients in the study were compared with age- and sex-matched patients hospitalized because of thrombosis of the popliteal or iliofemoral vein.
Risk factor assessment after diagnosis included obtaining a detailed history and laboratory tests for protein C antigen, protein S antigen and activity, activated protein C resistance (APCR), antithrombin III activity, lupus anticoagulant and anticardiolipin antibodies (aCL-Abs). Computed tomography of the thoracic inlet region was performed to detect any anatomic abnormalities.
An exogenous risk factor for venous thrombosis was identified in 14 of the 18 patients. These included pregnancy (four patients), estrogen ingestion (four patients), effort syndrome (five patients) and malignancy (one patient). No patient was found to have an anatomic abnormality of the thoracic inlet.
Thrombophilia was found in 11 (61 percent) of the 18 patients. These included APCR in nine patients (50 percent), aCL-Abs in 4 patients (22 percent) and both abnormalities in two patients (11 percent). No patients were found to have protein C, protein S or antithrombin III deficiency. Thirteen of the 18 patients had more than one risk factor for venous thrombosis.
Treatment in 13 patients consisted of unfractionated intravenous heparin followed by three to six months of warfarin therapy. One patient was given intravenous streptokinase, followed by heparin and warfarin. The four patients who were pregnant were given low-molecular weight heparin during the pregnancy and then warfarin for six weeks following delivery of the infant.
Symptoms of deep venous thrombosis resolved by 12 to 72 hours after institution of therapy. None of the patients had chest pain, tachypnea, tachycardia, hypotension or dyspnea suggestive of a pulmonary embolism. During a median follow-up of 15 months, three patients were found to have postphlebitic syndrome manifested by pain and prominence of the superficial veins of the affected arm. Two other patients experienced recurrent venous thrombosis, one at the same site and the other in the lower extremity.
The authors conclude that most patients with deep venous thrombosis of the upper extremity have an underlying thrombophilic disorder. Detection of an underlying hypercoagulable state is important because of prognostic and therapeutic implications for patients considering pregnancy, surgery or prolonged immobilization. Because the clinical outcome in most patients with axillary or subclavian thrombosis is good and the incidence of pulmonary embolism and postphlebitic complications is low, a conservative approach to treatment, essentially limited to anticoagulation, is recommended.