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Noninvasive Vascular Diagnosis pp 515–524Cite as

Overview of Venous Disorders

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Abstract

Venous disorders are among the most common conditions in the Western world. To understand the various venous disorders, it is important to understand the normal anatomy. Venous disorders can be divided into acute and chronic.

Acute venous disorders are entirely thrombotic. The physiology of the acute thrombotic events can be ascribed to Virchow’s triad: hypercoagulability, hemodynamic changes (venous stasis), and endothelial injury/dysfunction. Examples are superficial thrombophlebitis, acute deep venous thrombosis, acute axillary-subclavian venous thrombosis, and portal vein system thrombosis. Novel therapeutic strategies for lower extremity acute vein thrombosis, such as catheter-directed thrombolysis, may be associated with a reduction of post-thrombotic syndrome risk.

Chronic venous disorders are dominated by reflux through incompetent valves. It is thought that the development of all the clinical manifestations of chronic venous insufficiency (CVI) can be ascribed to a blood flow-driven inflammatory process. All the clinical manifestations of primary and secondary CVI may be conducted by this basic pathogenic mechanism. Telangiectasias and reticular varicosities are to be considered miniature varicose veins. Skin changes, such as atrophie blanche, lipodermatosclerosis, and venous ulcers, are to be considered advanced manifestations and therefore part of the pathologic spectrum of CVI.

Thermal and chemical ablations for axial reflux have almost completely replaced high ligation and stripping of the great saphenous vein and short saphenous vein. In patients with post-thrombotic syndrome, iliac vein recanalization, angioplasty, and stenting have been shown to aid time to ulcer healing.

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Author information

Authors and Affiliations

  1. Department of Surgery, University of Iowa Hospitals and Clinics, 1524 JCP, 200 Hawkins Dr., Iowa City, IA, 52242, USA

    Luigi Pascarella MD

  2. Surgery, Duke University Hospital, DUMC 3538, Durham, NC, 27710, USA

    Cynthia K. Shortell MD, FACS

Authors
  1. Luigi Pascarella MD
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  2. Cynthia K. Shortell MD, FACS
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Corresponding author

Correspondence to Luigi Pascarella MD .

Editor information

Editors and Affiliations

  1. Charleston, West Virginia, USA

    Ali F. AbuRahma

Review Questions

Review Questions

  1. 1.

    In the current nomenclature of the vein of the lower extremity, the acronym GSV refers to:

    1. a.

      Greater saphenous vein

    2. b.

      Great saphenous vein

    3. c.

      Grand saphenous vein

    4. d.

      Groin saphenous vein

  2. 2.

    What is the treatment of choice of superficial thrombophlebitis of the great saphenous vein with thrombus within 3 cm from the saphenofemoral junction?

    1. a.

      Nonsteroidal anti-inflammatory drugs, leg elevation, and compression stockings

    2. b.

      Anticoagulation for 3 months

    3. c.

      Aspirin 81 mg daily

    4. d.

      High ligation of the great saphenous vein

  3. 3.

    What is thought to be the most important basic pathogenic mechanism involved in the development of varicose veins?

    1. a.

      Venous stasis

    2. b.

      Venous hypertension

    3. c.

      Blood flow-driven inflammatory process

    4. d.

      Thrombosis

Answer Key

  1. 1.

    b. In the new nomenclature of the veins of lower limb, the acronym GSV refers to the great saphenous vein, opposed to greater saphenous vein, long saphenous vein, or vena saphena magna.

  2. 2.

    b. The current guidelines for the treatment of thrombophlebitis of the great saphenous vein include low molecular weight heparin at prophylactic dose for 45 days, in addition to nonsteroidal anti-inflammatory drugs, leg elevation, and compression stockings. If thrombus is detected within 3 cm from the saphenofemoral junction, full anticoagulation for 3 months is recommended. Patients with recurrence or contraindications for anticoagulation may be recommended for high ligation of the great saphenous vein.

  3. 3.

    c. It is thought that the development of all the clinical manifestations of chronic venous insufficiency can be ascribed to a blood flow-driven inflammatory process. Leukocytes are activated and marginalized. Adhesion to the endothelium is prompted by the expression of adhesion molecules, such as ICAM-1, VCAM-1, and L and P selectins. Ultimately, they infiltrate the venous wall. Lytic and extracellular matrix enzymes are released (MMP1, MMP2, MMP9) and activated. The extracellular matrix is degraded and the venous wall and valves undergo remodeling [18]. The loss of the venous wall’s most intimal architecture leads to dilation, tortuosity, and the formation of varicose veins.

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Pascarella, L., Shortell, C.K. (2017). Overview of Venous Disorders. In: AbuRahma, A. (eds) Noninvasive Vascular Diagnosis. Springer, Cham. https://doi.org/10.1007/978-3-319-54760-2_38

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  • DOI: https://doi.org/10.1007/978-3-319-54760-2_38

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  • Publisher Name: Springer, Cham

  • Print ISBN: 978-3-319-54758-9

  • Online ISBN: 978-3-319-54760-2

  • eBook Packages: MedicineMedicine (R0)

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