Varicose Veins

Basics

Varicose veins (VV), or varicosities, are dilated subcutaneous veins of at least 3 mm in diameter, measured with patient in upright position. They are part of a spectrum of chronic venous disorders ranging from telangiectasias to chronic venous insufficiency. Ovarian vein failure can also cause pelvic VV and subsequently pelvic congestion syndrome.

Description

  • Lower extremities venous drainage is accomplished via a network of superficial veins > small perforator veins > deep veins; diseases in any of these systems may result in VV.
  • VV usually form in the greater and lesser saphenous veins and sometimes their branches.

Geriatric Considerations

  • Surgeries have low morbidity and mortality in patients aged >60 years, with significant self-reported improvement despite more advanced disease on presentation.
  • High-risk geriatric patients should avoid hybrid procedures and general anesthesia when possible.

Pregnancy Considerations
External compression is the first-line treatment in pregnant female.

Epidemiology

Treatment of VV late complications such as chronic venous ulcerations results in an estimated 3 billion per year to treat in the United States.

Prevalence

  • Approximately 23% of U.S. adult have VV.
  • VV affect an estimate of 22 million women and 11 million men between 40 and 80 years old; of which, 2 million will develop symptom.

Etiology and Pathophysiology

Exact pathophysiology is debated, but it involves venous hypertension, valves dysfunction, structural changes in the vessel wall, inflammation, alteration of shear wall stress, and genetic disposition.

  • Venous hypertension is caused by reflux from valvular incompetence, outflow obstruction, calf muscle failure, or increased intra-abdominal pressure from pregnancy, obesity, chronic constipation, tumor, or other proximal obstruction.
  • Valve dysfunction may be due to deformation, tearing, thinning or adhesion of the valve leaflets, the vein wall stiffening with failure of the leaflet to fit together, trauma, deep thrombophlebitis, and congenital valvular incompetence.
  • Structural changes in the vein wall (disruption of smooth muscle cells and elastic fibers, etc.) leads to vessels weakening and dilation.
  • Turbulent flow, reflux, and increases in shear stress promote inflammatory and prothrombotic changes that further contribute to the loss of wall and leaflet integrity.
  • Deep venous insufficiency can lead to secondary VV via enlarging collaterals.

Genetics
VV is highly polygenic; a cohort study of >500,000 individuals has generated a list of genetic associations that include 30 new loci, with the strongest associations occurring in intron region CASZ1 (implicated in blood pressure) and 16q24 (contains genes that encode a vascular mechanosensory channel).

Risk Factors

  • Inherited: tall height (>180 cm), congenital syndromes
  • Acquired: age, deep vein thrombosis (DVT), pregnancy, decreased leg impedance
  • Lifestyle: prolonged standing and/or sitting, tobacco use, obesity
  • Hormonal: female gender (high estrogen state)
  • Socioeconomic: lower education level

General Prevention

  • Maintain a healthy body mass index.
  • Avoid sitting or standing for prolonged periods of time.
  • Wear compression stockings.

Commonly Associated Conditions

  • Stasis dermatitis
  • Lipodermatosclerosis
  • Venous ulceration (usually near medial malleolus/gaiter area)

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