eMedicine Specialties > Dermatology > Diseases of the Vessels

Varicose Veins and Spider Veins

Author: Robert Weiss, MD, Associate Professor, Department of Dermatology, Johns Hopkins University School of Medicine,
Coauthor(s): Craig F Feied, MD, FACEP, FAAEM, FACPh, Professor of Emergency Medicine, Georgetown University School of Medicine; General Manager, Microsoft Enterprise Health Solutions Group
Contributor Information and Disclosures

Updated: Nov 15, 2009

Introduction

Background

Varicose veins and telangiectasia (spider veins) are the visible surface manifestations of an underlying problem with reverse venous flow, which is also termed venous insufficiency syndrome. Venous insufficiency syndromes describe venous blood deviating from a normal flow path and flow in a retrograde direction so that fluid accumulates, causing a "congested" leg.

Mild forms of venous insufficiency are merely uncomfortable, annoying, or cosmetically disfiguring, but severe venous disease can produce serious systemic consequences and can lead to loss of life or limb.

Most patients with venous insufficiency have subjective symptoms that may include pain, soreness, burning, aching, throbbing, cramping, muscle fatigue, and restless legs. Over time, chronic venous insufficiency leads to cutaneous and soft tissue breakdown that can be debilitating.

Chronic venous insufficiency eventually produces chronic skin and soft tissue changes that begin with mild swelling and then progress to include discoloration, inflammatory dermatitis, recurrent or chronic cellulitis, cutaneous infarction, ulceration, and even malignant degeneration.

Pathophysiology

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.

Frequency

United States

The incidence and prevalence of venous insufficiency disease depend on the age and sex of the population. Varicosities were observed in 72% of women aged 60-69 years but in only 1% of men aged 20-29 years in the Tecumseh community health study.

International

The prevalence of venous disease is higher in Westernized and industrialized countries, most likely due to alterations in lifestyle and activity.

Mortality/Morbidity

Death can occur because of bleeding from friable varicose veins,¹ but the mortality associated with varicose veins is almost entirely due to the association of this condition with venous thromboembolism. When treating a patient with varicose veins, the possibility of associated deep venous thrombosis must always be considered because the mortality rate of unrecognized and untreated thromboembolism is 30-60%.

• Patients with varicose veins are at increased risk of deep vein thrombosis because venous stasis and injury often cause superficial phlebitis that can pass through perforating vessels to involve the deep venous system.
• Varicose veins may arise after an unrecognized episode of deep vein thrombosis that causes damage to venous valves. Such patients have some underlying risk factor for thromboembolism and are at especially high risk for recurrence.
• Varicose veins may sometimes serve as an important pathway for venous return in a patient with acute blockage of the deep venous system from any cause. This most often occurs after an episode of deep vein thrombosis, but it may also be a response to tumor growth or to impaired portal flow through a cirrhotic liver.

Sex

Because of hormonal factors, varicosities and telangiectasia are more common in women than in men at any age.²

Age

• Most varicose and spider veins in adults have their genesis in childhood. Serial examinations of children aged 10-12 years and again 4 and 8 years later showed that symptoms are experienced (and venous test results are abnormal) before any abnormal veins are visible at the surface of the skin.
• When abnormal veins do become visible, reticular veins usually appear first and are followed after several years by incompetent perforators. Smaller telangiectatic webs and large varicose veins usually become visible only in adulthood, many years after the true onset of disease.
• Although varicosities continue to worsen and to recruit new areas of involvement throughout life, only a small number of new cases appear after the childbearing years.

Clinical

History

Patients with varicose veins may present with acute varicose complications, including variceal bleeding, new onset of dermatitis, thrombophlebitis, cellulitis, and ulceration. Patients may also consult a physician because of worsening chronic symptoms or for a variety of other reasons. Some are seeking advice on the medical implications of varicose veins. Others have purely aesthetic concerns.

• A careful history exposes the patient's underlying concerns and guides further workup and treatment planning.
  • Treatment that does not properly address the patient's primary concerns cannot result in a satisfactory overall outcome.
  • Patients who have become acclimatized to their chronic disease may not volunteer information about symptoms. Common symptoms that should be elicited include leg heaviness, exercise intolerance, pain or tenderness along the course of a vein, pruritus, burning sensations, restless legs, night cramps, edema, skin changes, and paresthesias.
  • Subjective symptoms usually are more severe early in the progression of disease, less severe in the middle phases, and worse again with advancing age.
  • Symptoms do not correlate with the size or extent of visible varices or with the volume of reflux.
  • Not all symptomatic patients are aware of their symptoms because the onset may be extremely gradual. After treatment, patients are often surprised to realize how much chronic discomfort they had accepted as normal.
  • Common symptoms of telangiectasia include burning, swelling, throbbing, cramping, and leg fatigue. Pain associated with larger varicose veins usually is a dull ache that is worse after prolonged standing.
  • Pain caused by venous insufficiency is often improved by walking or by elevating the legs in contrast to the pain of arterial insufficiency, which is worse with ambulation and elevation.
  • Pain and other symptoms may worsen with the menstrual cycle, with pregnancy, and in response to exogenous hormonal therapy (eg, oral contraceptives).
  • A small number of women regularly experience pain associated with their varicose veins after sexual intercourse.
• The venous history should also include the following elements:
  • History of venous insufficiency (eg, date of onset of visible abnormal vessels, date of onset of any symptoms, any known prior venous diagnoses, any history of pregnancy-related varices)
  • Presence or absence of predisposing factors (eg, heredity, trauma to the legs, occupational prolonged standing, sports participation)
  • History of edema (eg, date of onset, predisposing factors, site, intensity, hardness, modification after a night's rest)
  • History of any prior evaluation of or treatment for venous disease (eg, medications, injections, surgery, compression)
  • History of superficial or deep thrombophlebitis (eg, date of onset, site, predisposing factors, sequelae)
  • History of any other vascular disease (eg, peripheral arterial disease, coronary artery disease, lymphedema, lymphangitis)
  • Family history of vascular disease of any type

Physical

The physical examination of the venous system is fraught with difficulty. In most areas of the body, the deep venous system cannot be inspected, palpated, ausculted, or percussed. Examination of the superficial venous system must serve as an indirect guide to the deep system.

Veins and their connections become gradually better defined through inspection, palpation, percussion, and hand-held Doppler examination to form a venous map that later guides treatment. The courses of all the dilated veins that are identified may be marked along the leg with a pen and later transcribed into the medical record as a map of all known areas of superficial reflux.

• Inspection: Inspection is performed in an organized manner, usually progressing from distal to proximal and from front to back. The perineal region, pubic region, and abdominal wall must also be inspected.
  • Inspection may reveal such findings as ulceration, telangiectasias, atrophie blanche, interdigital mycosis, acrocyanosis, eczematous lesions, microulcers, stasis dermatitis, flat angiomata, prominent varicose veins, scars from a prior surgical operation, or evidence of previous sclerosant injections. Measuring and photographing lesions is recommended because patients undergoing treatment for varicose and spider veins often forget the original appearance of their legs and feet and may report that preexisting lesions were caused by treatment.
  • Normal veins typically are visibly distended at the foot and ankle and occasionally in the popliteal fossa. For other regions of the leg, visible distension of superficial veins usually implies disease. Translucent skin may allow normal veins to be visible as bluish subdermal reticular pattern, but dilated veins above the ankle usually are evidence of venous pathology.
  • Discolored skin often is a sign of chronic venous stasis, particularly if it is localized along the medial ankle and the medial aspect of the lower leg. Nonhealing ulcers in this area are most likely due to underlying venous stasis. Skin changes or ulcerations that are localized only to the lateral aspect of the ankle are more likely to be related to prior trauma or to arterial insufficiency than to pure venous insufficiency.
• Palpation: The entire surface of the skin is lightly palpated with the fingertips because dilated veins may be palpable even where they are not readily observed. Palpation helps to locate both normal and abnormal veins. After light palpation to identify superficial vascular abnormalities, deeper palpation helps to elucidate the causes and sources of the superficial problems.
  • Palpation begins with the anteromedial surface of the lower limb (the territory of the long saphenous vein), proceeds to the lateral surface (collateral varicose veins of large trunks and nonsaphenous varicose veins), and finally focuses on the posterior surface (territory of the short saphenous vein) of both lower limbs. The location, size, shape, and course of all varicosities are noted, and the diameter of the largest vessel is measured as accurately as possible.
  • Both distal and proximal arterial pulses should be palpated. An ankle-brachial index is useful if any suspicion of arterial insufficiency exists.
  • The arch of the long saphenous vein may be palpable in some patients who do not have varicose veins, but it is particularly well appreciated in patients with truncal reflux at the saphenofemoral junction. It is best palpated 2 fingerbreadths below the inguinal ligament and just medial to the femoral artery. If reflux is present, a forced coughing maneuver may produce a palpable thrill or sudden expansion at this level.
  • The short saphenous vein may be palpable in the popliteal fossa in some slender patients. Other normal superficial veins above the foot usually are not palpable even after prolonged standing.
  • Palpation of an area of leg pain or tenderness may reveal a firm, thickened, thrombosed vein. These palpable thrombosed vessels are superficial veins, but an associated deep vein thrombosis may exist in up to 40% of patients with superficial phlebitis. When completely thrombosed, the popliteal vein (a continuation of the femoral vein as it passes behind the knee and into the calf) may sometimes be palpated in the popliteal fossa, and the same is true of the common femoral vein at the groin. Palpation for deep thrombosis is not reliable because the vast majority of cases of deep vein thrombosis do not produce any palpable abnormality.
  • Varices of recent onset are easily distinguished from chronic varices by palpation. Newly dilated vessels sit on the surface of the muscle or bone; chronic varices erode into underlying muscle or bone, creating deep boggy or spongy pockets in the calf muscle and deep palpable bony notches, especially over the anterior tibia.
  • Palpation often reveals fascial defects in the calf along the course of an abnormal vein at sites where superficial tributaries emerge through openings in the superficial fascia. Incompetent perforating veins may connect the superficial and deep venous systems though these fascial defects, but the finding is neither sensitive nor specific for perforator incompetence.
• Percussion: Venous percussion is useful to determine whether different venous segments are directly interconnected. Percussion can be used to trace the course of veins already detected on palpation, to discover varicose veins that could not be palpated, and to assess the relationships between the various varicose vein networks.
  • With the patient in a standing position, a vein segment is percussed at one position while an examining hand feels for a pulse wave at another position. The propagation of a palpable pulse wave demonstrates a patent superficial venous segment with open or incompetent valves connecting the 2 positions. The examination findings can be misleading because prolonged standing causes even a normal vein to become distended. If valves have floated open, a pulse wave may be propagated even in a normal vein. The technique is most valuable when a bulging venous cluster in the lower leg has no obvious connection with veins in the upper thigh, yet a palpable pulse wave demonstrates the existence of an unseen connection.
  • Percussion can be used to elucidate the course of any significant superficial vein. With the patient standing, the lowest portion of the vein is percussed while the opposite hand searches above for a percussion wave. The procedure is repeated along the entire course of the vein and then along every identifiable superficial vein until a clear anatomic picture has been elucidated.
• Perthes maneuver: The Perthes maneuver is a traditional technique intended to distinguish antegrade flow from retrograde flow in superficial varices. Antegrade flow in a variceal system indicates that the system is a bypass pathway around deep venous obstruction. This is critically important because, if deep veins are not patent, superficial varices are an important pathway for venous return and must not be sclerosed or surgically removed.
  • To perform the Perthes maneuver, a Penrose tourniquet is placed over the proximal part of the varicose leg in such a way as to compress superficial varicose veins but not the deep veins. The patient walks or performs toe-stands to activate the calf muscle pump. The calf muscle pump normally causes varicose veins to be emptied, but if deep system obstruction exists, then the varicose veins paradoxically become more congested.
  • If the result of the Perthes maneuver is positive (ie, distal varices have become engorged), then the patient is placed supine with the tourniquet in place and the leg elevated (Linton test). If varices distal to the tourniquet do not drain after a few seconds, deep venous obstruction must be suspected. These maneuvers are not consistently reliable and are of primarily historical interest.
• Trendelenburg test: The Trendelenburg test can often be used to distinguish patients with superficial venous reflux from those with incompetent deep venous valves.
  • The leg is elevated until the congested superficial veins have all collapsed. An examining hand is used to occlude a varicose vein just below the saphenofemoral junction or at another point of suspected reflux from the deep system into the superficial varicosity. The patient stands with the occlusion still in place.
  • If the distal varicosity remains empty or fills very slowly, the principal entry point of high pressure into the superficial system has been identified. Rapid filling despite manual occlusion of the suspected high point of reflux means that some other reflux pathway is involved.
• Doppler auscultation: The physical examination as described thus far cannot differentiate dilated veins of normal function from true varicosities that carry venous blood in a retrograde direction. Doppler examination is an adjunct to the physical examination that can directly show whether flow in a suspect vein is antegrade, retrograde, or to-and-fro.
  • When used as part of the physical examination, a Doppler transducer is positioned along the axis of a vein with the probe at an angle of 45° to the skin. Gentle tapping on the underlying vessel produces a strong Doppler signal and confirms the correct positioning of the transducer.
  • An augmentation maneuver is performed by compressing and then releasing the underlying veins and muscles below the level of the probe. Compression causes forward flow in the direction of the valves. Release of compression causes backward flow through incompetent valves, but no Doppler signal is noted if the valves are competent and the blood cannot flow backwards.
  • These compression-decompression maneuvers are repeated while gradually ascending the limb to a level where the reflux can no longer be appreciated.
  • Each superficially visible or palpable is investigated in this way. If no visible or palpable dilated varices exist, the presence or absence of retrograde flow is documented at the top, middle, and bottom of long and short saphenous veins on each leg.
  • Doppler flow assessment adds a great deal of information to the physical examination findings, but patients with significant varicosities should also be evaluated by duplex ultrasonography, which combines Doppler flow detection with 2-dimensional ultrasound imaging.

Causes

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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