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Subclavian Vein Thrombosis

  • Author: Shabir Bhimji, MD, PhD; Chief Editor: Mary C Mancini, MD, PhD, MMM  more...
 
Updated: Aug 03, 2015
 

Background

The subclavian vein courses over the first rib and posterior to the clavicle; the artery lies superior and posterior to the vein (see the image below). Sir James Paget first described thrombosis of the subclavian veins in 1875.[1] He coined the name gouty phlebitis to describe the spontaneous thrombosis of the veins draining the upper extremity. Paget noted that the syndrome was accompanied by pain and swelling of the affected extremity, but he incorrectly attributed the syndrome to vasospasm. In 1884, von Schrötter postulated that this syndrome resulted from occlusive thrombosis of the subclavian and axillary veins.[2] In 1949, in recognition of the work of these pioneers, Hughes coined the term Paget–von Schrötter syndrome.[3]

This figure shows the area where the subclavian ve This figure shows the area where the subclavian vein is obstructed in the neck area. The vein is usually compressed by the first rib, clavicle, and serratus anterior muscle.

A related condition is thrombosis of the subclavian vein that is induced by the presence of indwelling catheters. The incidence of this condition has increased remarkably over the past two decades because of the extensive use of central venous catheters in patients with cancer and other chronic medical conditions.

The demand for a more standardized treatment of subclavian vein thrombosis is growing. However, until randomized data from well-designed trials are available, absolute statements about treatments cannot be made. Linked medical records using administrative healthcare data sets may provide information (ie, readmission rate or level of outpatient services) on the results of treatment of large numbers of patients with subclavian vein thrombosis or significant risk factors such as central venous cannulation. Until such information is obtained, the best way of treating subclavian vein thrombosis is to prevent it by limiting the use of central venous catheters for extended periods.

For patient education resources, see Phlebitis.

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Pathophysiology

During long-term venous catheterization of the subclavian vein and internal jugular vein in cancer patients, the risks of complications appear to be similar. However, for short-term catheterization, subclavian vein catheterization is recommended because of the decreased risks of thrombotic complications and catheter colonization by skin flora. For patients requiring hemodialysis, the femoral and internal jugular veins appear to have similar thrombotic complications. However, the risk of mechanical complications via the internal jugular vein appear to be higher. The subclavian vein should be avoided for both long- and short-term hemodialysis because the risk of thrombosis is very high.[4]

Differentiating catheter-associated subclavian vein thrombosis and Paget–von Schrötter syndrome is important because they appear to have different natural histories.

Paget–von Schrötter syndrome

This syndrome sometimes is referred to as spontaneous axillary-subclavian vein thrombosis (ASVT) to express the usually dramatic unexpected presentation of the disorder in otherwise healthy, generally young individuals. Over the past two decades, there has been growing recognition that the disorder can occur equally in both sexes and can affect all age groups. In the 1960s, the term effort-induced thrombosis was applied to this disease to acknowledge that it often follows unusually strenuous use of the arm or shoulder on the affected side.

The pathophysiology of effort-induced thrombosis is multifactorial. It involves compressive changes in the vessel wall, stasis of blood, and hypercoagulability. External compression of the axillary-subclavian vein has been suggested to contribute to the stasis of blood that engenders thrombosis. The factors that cause external compression include the following:

  • Anomalous subclavius or scalenus anterior, long transverse process of cervical spine, cervical rib, abnormal insertion of the first rib, congenital fibromuscular bands, or narrowing of the costoclavicular space from depression of the shoulder
  • Stress from exercise temporarily causing hypercoagulability
  • Repetitive shoulder-arm motion causing microscopic intimal tears in the vessel wall

These factors, taken together, satisfy the classic Virchow triad for thrombosis. Furthermore, coexistent hematologic abnormalities that can contribute to thrombosis include protein C deficiency, antithrombin III deficiency, factor V Leiden mutation, and prothrombin 20210A mutation.

Catheter-induced subclavian vein thrombosis

Introducing catheters and transvenous pacemakers in to the subclavian vein alters the venous flow and increases turbulence. This results in platelet aggregation, release of procoagulants, and, ultimately, fibrin deposition. This causes a further reduction in the lumen of the vessel due to thrombus formation, which eventually culminates in total vessel occlusion. Intravenous (IV) medications and even parenteral nutrition have been known to cause thrombophlebitis. In patients with cancer, an additional contributing factor is that the tumor may generate procoagulant factors, predisposing to thrombosis at sites remote from the tumor.

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Etiology

The primary etiology is referred to as effort-induced thrombosis or Paget–von Schrötter syndrome. It usually results from the excessive use of the involved arm by predisposed individuals. The secondary etiology is subclavian vein catheterization, especially in patients with cancer. (For detailed descriptions of catheterization techniques, see Central Venous Access, Subclavian Vein, Subclavian Approach and Central Venous Access, Subclavian Vein, Supraclavicular Approach.)

Other causes include transvenous pacemakers, factor V Leiden mutation, protein C deficiency, protein S deficiency, antithrombin III deficiency, and prothrombin 20210A mutation. Long-term parenteral nutrition[5] and use of hemodialysis catheters[6] account for some cases of subclavian vein thrombosis. Trauma is only rarely associated with this syndrome.

In a few cases, the diagnosis remains unknown. However, routine follow-up with these patients has revealed the development of lung cancer within 1 year of follow-up. The most common lung malignancy associated with subclavian thrombosis has been the Pancoast tumor.

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Epidemiology

Before 1967, thrombosis of the axillary or subclavian vein accounted for 1-2% of all cases of deep vein thrombosis (DVT). Since then, the incidence has risen as a consequence of more frequent use of central venous access for multiple clinical conditions. Among patients with effort-induced thrombosis with subclavian vein stenosis, the thrombosis occurs in the dominant arm in 80% of cases.

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Prognosis

Case fatality rates for untreated ASVT-related pulmonary embolism (PE) may be as high as 10%, a figure comparable to that seen with PE originating from the lower extremity. The long-term consequences of venous occlusion cause substantial morbidity related to persistent pain and swelling for protracted periods of time. These symptoms occasionally are severe and can be exacerbated by physical activity, particularly with extended use of the affected arm. Consequently, this syndrome can lead to occupational disability and can adversely impact the patient's quality of life.

Conservative treatment consisting of bed rest, limb elevation, and anticoagulation is associated with a worse outcome. Some reports suggest that as many as 74% of patients treated with these conservative measures have residual disability as compared with those who are treated with thrombolysis.

With advances in endovascular technology, there is more supporting evidence that these techniques are the modality of choice when encountering a patient with upper-extremity thrombosis. Anticoagulation or thrombolytic therapy alone has proved inadequate. Today, both benign and malignant causes of upper-extremity thrombosis can be managed with endovascular stenting. This technique allows much faster recovery while giving rise to less morbidity and fewer complications in the long run.[7]

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Contributor Information and Disclosures
Author

Shabir Bhimji, MD, PhD Cardiothoracic and Vascular Surgeon, Saudi Arabia and Middle East Hospitals

Shabir Bhimji, MD, PhD is a member of the following medical societies: American Cancer Society, American College of Chest Physicians, American Lung Association, Texas Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

Chike Magnus Nzerue, MD, FACP Professor of Medicine, Associate Dean for Clinical Affairs, Meharry Medical College

Chike Magnus Nzerue, MD, FACP is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Society of Nephrology, National Kidney Foundation

Disclosure: Nothing to disclose.

Steven Ugbarugba, MD, MD 

Steven Ugbarugba, MD, MD is a member of the following medical societies: American College of Physicians

Disclosure: Received none from none for none.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Vincent Lopez Rowe, MD Professor of Surgery, Program Director, Vascular Surgery Residency, Department of Surgery, Division of Vascular Surgery, Keck School of Medicine of the University of Southern California

Vincent Lopez Rowe, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, Society for Vascular Surgery, Vascular and Endovascular Surgery Society, Society for Clinical Vascular Surgery, Pacific Coast Surgical Association, Western Vascular Society

Disclosure: Nothing to disclose.

Chief Editor

Mary C Mancini, MD, PhD, MMM Professor and Chief of Cardiothoracic Surgery, Department of Surgery, Louisiana State University School of Medicine in Shreveport

Mary C Mancini, MD, PhD, MMM is a member of the following medical societies: American Association for Thoracic Surgery, American College of Surgeons, American Surgical Association, Society of Thoracic Surgeons, Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

William H Pearce, MD Chief, Division of Vascular Surgery, Violet and Charles Baldwin Professor of Vascular Surgery, Department of Surgery, Northwestern University, The Feinberg School of Medicine

William H Pearce, MD is a member of the following medical societies: American College of Surgeons, American Heart Association, American Surgical Association, Association for Academic Surgery, Association of VA Surgeons, Central Surgical Association, New York Academy of Sciences, Society for Vascular Surgery, Society of Critical Care Medicine, Society of University Surgeons, Western Surgical Association

Disclosure: Nothing to disclose.

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This figure shows the area where the subclavian vein is obstructed in the neck area. The vein is usually compressed by the first rib, clavicle, and serratus anterior muscle.
A venogram in a patient with subclavian vein obstruction. Long-standing obstruction causes development of collaterals.
Recanalization after thrombolytic therapy and stent placement. Patient underwent first rib resection and scalenectomy later.
 
 
 
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