Guía de la American Heart Association (1996)


La frecuencia de las trombosis de las extremidades superiores afectando a las venas axilar y/o subclavia ha aumentado en los últimos años con el aumento de la implantación de catéteres. La trombosis de las extremidades superiores se clasifica como primaria y secundaria. La trombosis primaria puede ser ocasionada por la compresión venosa local producida por movimientos o posturas poco usuales del brazo (trombosis de esfuerzo) mientras que la segunda es producida por la presencia de dispositivos implantados (204, 205).La trombosis primaria ha sido descrita después de levantar pesos, deportes de raqueta, o directamente por una presión prolongada en la axila. La trombosis de la vena axilar puede ser también una manifestación del síndrome de estrechamiento torácico, un trauma o compresión debida a un tumor (206)



The frequency of upper-extremity venous thrombosis involving the axillary and/or subclavian veins has increased in the last decade with the increasing use of long-term indwelling catheters. Upper-extremity venous thrombosis is classified as primary and secondary. Primary upper extremity thrombosis can be caused by local venous compression produced by unusual movements or positions of the arm ("effort thrombosis"), whereas secondary thrombosis is usually caused by indwelling intravenous devices.204,205 Effort thrombosis has been described following weight-lifting, pole-vaulting, racquet sports, or direct and prolonged pressure to the axilla. Axillary vein thrombosis can also be a manifestation of the thoracic inlet syndrome or can be caused by direct trauma or compression by tumor.206 Axillary or subclavian vein thrombosis has been described in AT-III deficiency, protein S deficiency, hypoplasminogenemia, and antiphospholipid syndrome.207,208,209,210 T

hrombosis secondary to the use of long-term indwelling catheters, often used in administration of chemotherapy, is now a much more common cause of upper-extremity thrombosis than effort thrombosis. Upper-extremity venous thrombosis can be complicated by PE211 and rarely by massive PE.212,213 The most important complications are long-term disability caused by venous hypertension and loss of venous access in patients requiring long-term chemotherapy. Venous hypertension can produce swelling, fatigability, aching, and weakness of the affected arm, particularly following activity. The symptoms can be disabling in athletes or manual laborers during and after activity involving the affected arm. The reported frequency of disabling upper-extremity venous hypertension after spontaneous axillary/subclavian vein thrombosis varies from 25% to 47%.214-216 Lower rates (12%) have been reported in a series of patients treated with thrombolysis,217 but no randomized trials have been reported comparing anticoagulants with thrombolysis.

The diagnosis of upper-extremity vein thrombosis is usually suspected on clinical grounds and confirmed by venography. Optimal visualization of the thrombosed axillary/subclavian veins is best achieved by injecting the radiographic contrast into the median basilic vein. Injection of contrast material into a distal vein in the hand or wrist will demonstrate an obstruction and the presence of collateral vessels but does not usually outline the thrombus. Imaging studies in which color flow duplex ultrasound was used lack the sensitivity of venography for upper-extremity thrombosis.218 Various treatments have been advocated for primary upper-extremity thrombosis. Resolution of acute symptoms can usually be obtained with either anticoagulant or lytic agents.145-147 Anticoagulant therapy is not usually associated with anatomic resolution of the thrombus and clinical improvement because collaterals develop and bypass the obstruction.

Thrombolytic therapy appears to be more effective than anticoagulants in producing early resolution.219,220 Local therapy administered through a small catheter introduced through the basilic vein and advanced into the clot has been advocated. A loading dose of 250 000 IU urokinase infused into the clot over 1 hour and then continued at a lower dose of 1000 IU/min for up to 24 hours has been used successfully.221 The patient is then treated with heparin for 5 days, followed by warfarin for 3 months. Surgical removal of the first rib has been advocated by some if symptoms of venous obstruction persist after a course of conservative treatment. However, the effectiveness of this invasive approach has never been evaluated in an appropriately designed clinical trial. Long-term venous access through a central venous catheter is required for treatment of long-term disorders requiring chemotherapy, antibiotics, or hyperalimentation. Thrombosis of the subclavian/axillary vein is a common complication of central venous catheterization. These thrombi may be asymptomatic,222,223 although spontaneous resolution is uncommon when long-term venographic follow-up studies are performed.224 The standard treatment of secondary axillary/subclavian vein thrombosis has been removal of the catheter, limb elevation, and anticoagulation. This approach usually results in rapid improvement of symptoms, but on follow-up 70% of patients have been reported to have some pain and/or swelling in the affected arm.225 Of greater importance, the venous lumen is obliterated and cannot be used again for venous access.

Thrombolytic therapy has been used successfully to treat secondary upper-extremity thrombosis.226-228 Initial reports used high-dose systemic therapy. More recently local catheter-directed thrombolytic therapy has been used with apparent success.229 A dosage regimen of urokinase has been established, empirically consisting of 250 000 IU/h for 2 hours followed by 60 000 IU/h until clot lysis has been achieved. Heparin can be given in full doses either during or after completion of thrombolytic therapy and anticoagulation with heparin, followed by warfarin for ~3 months. With this approach, a 78% lysis rate has been reported in a small study of 31 patients.229 Successful lysis is more common with fresh thrombi.230