What is the pathophysiology of 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

Varicose veins and spider veins are normal veins that have dilated under the influence of increased venous pressure.

In healthy veins, one-way valves direct the flow of venous blood upward and inward. Blood is collected in superficial venous capillaries, flows into larger superficial veins, and eventually passes through valves into the deep veins and then centrally to the heart and lungs. Superficial veins are suprafascial, while deep veins are within the muscle fascia. Perforating veins allow blood to pass from the superficial veins into the deep system.

Within muscle compartments, muscular contraction compresses deep veins and causes a pumping action that can produce transient deep venous pressures as high as 5 atmospheres. Deep veins can withstand this pressure because of their construction and because their confining fascia prevents them from becoming excessively distended. In contrast to deep veins, the venous pressure in superficial veins normally is very low. Exposure to high pressures causes superficial veins of any size to become dilated and tortuous.

Perfectly normal veins dilate and become tortuous in response to continued high pressure, as is observed in patients with dialysis shunts or with spontaneous arteriovenous malformations. In a subset of patients with hereditary vein wall weakness, even normal venous pressures produce varicose changes and venous insufficiency.

Elevated venous pressure most often is the result of venous insufficiency due to valve incompetence in the deep or superficial veins. Varicose veins are the undesirable pathways by which venous blood refluxes back into the congested extremity. Ablation of the varicose pathways invariably improves overall venous circulation.

Chronically increased venous pressure can also be caused by outflow obstruction, either from intravascular thrombosis or from extrinsic compression. In patients with outflow obstruction, varicosities must not be ablated because they are an important bypass pathway allowing blood to flow around the obstruction. Specific diagnostic tests can distinguish between patients who will benefit from ablation of dilated superficial veins and those who will be harmed by the same procedure.

Deep vein thrombosis initially produces an obstruction to outflow, but in most cases the thrombosed vessel eventually recanalizes and becomes a valveless channel delivering high pressures from above downward.

Most commonly, superficial venous valve failure results from excessive dilatation of a vein from high pressure of reverse flow within the superficial venous system. Valve failure can also result from direct trauma or from thrombotic valve injury. When exposed to high pressure for a long enough period, superficial veins dilate so much that their delicate valve leaflets no longer meet.

In the most common scenario, a single venous valve fails and creates a high-pressure leak between the deep and superficial systems. High pressure within the superficial system causes local dilatation, which leads to sequential failure (through over-stretching) of other nearby valves in the superficial veins. After a series of valves have failed, the involved veins are no longer capable of directing blood upward and inward. Without functioning valves, venous blood flows in the direction of the pressure gradient: outward and downward into an already congested leg.

As increasing numbers of valves fail under the strain, high pressure is communicated into a widening network of dilated superficial veins in a recruitment phenomenon. Over time, large numbers of incompetent superficial veins acquire the typical dilated and tortuous appearance of varicosities.

Varicose veins of pregnancy most often are caused by hormonal changes that render the vein wall and the valves themselves more pliable. The sudden appearance of new dilated varicosities during pregnancy still warrants a full evaluation because of the possibility that these may be new bypass pathways related to acute deep vein thrombosis.

The sequelae of venous insufficiency are related to the venous pressure and to the volume of venous blood that is carried in a retrograde direction through incompetent veins. Unfortunately, the presence and size of visible varicosities are not reliable indicators of the volume or pressure of venous reflux. A vein that is confined within fascial planes or is buried beneath subcutaneous tissue can carry massive amounts of high-pressure reflux without being visible at all. Conversely, even a small increase in pressure can eventually produce massive dilatation of an otherwise normal superficial vein that carries very little flow.


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