Varicose Veins

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Varicose veins (VV), or varicosities, are dilated, tortuous, subcutaneous veins of at least 4 mm in diameter, measured with the patient in the upright position. VV is 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 extremity 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 great and small saphenous veins and 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 first-line treatment in pregnant females.

Epidemiology

Treatment of late complications of VV, such as chronic venous ulcerations, costs an estimated $3 billion per year in the United States.

Prevalence

Approximately 23% of US adults have VV, affecting an estimated 22 million women and 11 million men between 40 and 80 years old; 2 million will develop symptoms.

Etiology and Pathophysiology

Exact pathophysiology is debated, but involves: venous hypertension, valve 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, increased intra-abdominal pressure from pregnancy, obesity, chronic constipation, tumors, or other proximal obstruction.
  • Valve dysfunction may be due to deformation, tearing, thinning, adhesion of the valve leaflets, vein wall stiffening with failed leaflet fit, trauma, deep thrombophlebitis, and congenital valvular incompetence.
  • Structural changes in the vein wall (disruption of smooth muscle cells and elastic fibers, etc.) leads to vessel dilation and weakening.
  • Turbulent flow, reflux, and increases in shear stress, promotes 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 linked genetic associations with 30 new loci, the strongest occurring in intron region CASZ1 (implicated in blood pressure) and 16q24 (genes encoding a vascular mechanosensory channel).

Risk Factors

  • Inherited: gender, 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, and wear compression stockings.

Commonly Associated Conditions

  • Stasis dermatitis
  • Lipodermatosclerosis (chronic inflammation and fibrosis causing skin hyperpigmentation and underlying fat hardening)
  • Venous ulceration (usually near medial malleolus/gaiter area)

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