What causes varicose veins and spider veins (telangiectasia)?

Updated: Feb 28, 2018
  • Author: Robert Weiss, MD; Chief Editor: William D James, MD  more...
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Answer

Intrinsic pathological conditions and extrinsic environmental factors combine to produce a wide spectrum of varicose disease.

Most varicose disease is due to elevated superficial venous pressures, but some people have an inborn weakness of vein walls and can develop varicosities even in the absence of elevated venous pressures. Some patients with varicose veins of the legs also have abnormally distensible veins in the forearm and hand veins.

Heredity is important in determining susceptibility to primary valvular failure, but the specific genetic factors responsible for varicosities have not yet been elucidated. Reflux at the saphenofemoral junction (where the superficial greater saphenous vein joins the deep common femoral vein) is twice as likely when a parent had a similar condition. Monozygotic twins are concordant with regard to varicose veins in 75% of cases. The prevalence of varicose veins is 43% in female relatives of patients with varicose veins but is only 19% in male relatives.

Prolonged standing leads to increased hydrostatic pressures that can cause chronic venous distention and secondary valvular incompetence anywhere within the superficial venous system. If proximal junctional valves become incompetent, high pressure passes from the deep veins into the superficial veins and the condition rapidly progresses to become irreversible. Women are particularly susceptible to this type of varicose problem because vein walls and valves periodically become more distensible under the influence of cyclic increases in progesterone.

Pregnancy is a common cause of varicosities. During pregnancy, circulating hormonal factors increase the distensibility of vein walls and soften valve leaflets. At the same time, the veins must accommodate a greatly expanded circulating blood volume. Late in pregnancy, the enlarged uterus compresses the inferior vena cava, causing further venous hypertension and secondary distension of leg veins. Depending on the relative contributions of these mechanisms, varicose veins of pregnancy may or may not spontaneously regress after delivery. Treatment of existing varicose veins prior to pregnancy has been shown to prevent the progression of disease and reduce the recruitment of other veins during pregnancy.

Age is an independent risk factor for varicosities. With advancing age, the elastic lamina of the vein becomes atrophic and the smooth muscle layer begins to degenerate, leaving a weakened vein that is more susceptible to dilatation.

Wherever a venous outflow obstruction exists, varicose veins may arise as a bypass pathway. Such veins are an important pathway for venous return and must not be ablated.


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