| Primary Venous Disease: Epidemiology and Sequelae
copyright 2001 Craig F. Feied, MD, FACEP, FAAEM
Incidence & prevalence
Estimates of the prevalence of primary venous diseases are varied. Published estimates of the prevalence of varicosities range from 7% to 60% in the adult population of the United States, while the incidence of deep venous thrombosis is believed to be nearly 1% per year.
The incidence and the prevalence of deep and superficial venous disease depends on the age and sex of the population. In the Tecumseh community health study, for example, varicosities were observed in 72% of women aged 60 to 69 but in only 1% of men aged 20 to 29.(1)
| Age |
Female |
Male |
| 20 - 29 |
8% |
1% |
| 40 - 49 |
41% |
24% |
| 60 - 69 |
72% |
43% |
Reticular veins occur or are noticed earlier in life, with only a small number of new cases developing after the childbearing years. Truncal varicosities and telangiectatic webs, on the other hand, are relatively less common in youth, and continue to appear throughout life.
Studies in children have shown that symptoms are experienced (and venous tests are abnormal) before any abnormal veins are visible at the surface. The Basle study (1978) showed that abnormal reticular veins are the first to appear, and are followed after several years by incompetent perforators and by truncal varicosities.(2)
| Age |
Reticular veins |
Incompetent perforators |
Large varicosities |
| 10 - 12 |
10.2% |
0 |
0 |
| 14 - 16 |
30.3% |
4% |
2% |
Subjective symptoms of venous disease
Subjective symptoms are typically more severe early in the progression of disease, then less severe in the middle phases, and finally worse again with advancing age. Episodic pain and other symptoms associated with superficial venous disease may also be temporally related to hormonal changes, both physiologic and pharmacologic.
Pain due to spider veins
Even small telangiectasias are often symptomatic. 53% of patients presenting with telangiectasias less than 1mm in diameter complained of symptoms which abated after treatment. Symptoms included burning, swelling, throbbing, cramping and leg fatigue.(3)
Pain due to varicose veins
Subjective complaints are also common in patients with truncal varices. 18% of patients with varicosities report frequent or continuous symptoms, while almost 50% complain of episodic symptoms.(4)
Objective signs of venous disease
Besides the subjective complaints of the patient, there are a number of objectively verifiable medical problems related to superficial venous disease. The most common physical signs are those which are attributed to the progressive syndromes of chronic venous stasis and chronic venous hypertension. Death can occur in connection with superficial venous problems, as thrombophlebitis of the superficial varicose veins often accompanies or leads to a serious deep vein thrombosis, and bleeding from ruptured varicose veins can also be life-threatening.
Venous insufficiency syndrome
There are several mechanisms by which this syndrome develops. The normal pressure in the venous system of the lower leg during ambulation is near zero, and the early standing pressure in the normal leg is at most the hydrostatic pressure of a column of blood as high as the nearest competent valve. Failed valves serve to increase this hydrostatic pressure. Failure of the calf muscle pump increases it more. High venous pressure is directly responsible for many aspects of this syndrome, including edema, protein deposition, fibrin cuffing, and red cell extravasation. The progression of this syndrome is approximately as follows:
- Edema
- Hyperpigmentation
- Chronic venous dermatitis
- Chronic cellulitis
- Cutaneous infarction (atrophie blanche)
- Ulceration
- Malignant degeneration
Venous hypertension accounts for many of the sequelae of peripheral venous disease, but not for all. For example, not all patients with venous hypertension will develop ulceration, and some patients with venous ulceration do not have marked venous hypertension. Poor clearance of lactate, CO2, and other products of cellular respiration also contributes to the development of the syndrome. A defect in clearance of extraneous substances can be quantified: if we inject albumin labeled with a radioactive tracer into the foot tissues, the clearance rate is markedly slowed by deep venous obstruction or by deep or superficial venous incompetence.
Local venous recirculation
Although we often refer to this effect as 'venous stasis', reduced clearance of cellular metabolites is not always due to true venous stasis: in many cases the venous blood is moving at a normal speed. It is a local recirculation of venous blood that prolongs the average transit time for blood to pass from the heart and lungs through the legs and back to the central circulation.
The concept of blood aliquot transit time is similar to the cardiac output measure used for the heart. We inject a tracer substance into the femoral artery and record the tracer as it is cleared through the femoral vein. In the normal patient a bolus of tracer makes a rapid transit of the leg and is cleared as a slightly spread out bolus. In a patient with venous reflux and venous recirculation the first appearance of the tracer is very slightly slowed, but the remainder of the tracer is cleared very slowly, as a low level of tracer over very prolonged period of time. The time required for an aliquot of radiolabeled blood to pass from the femoral artery through the leg and back to the central circulation correlates extremely well with the development of leg ulcers.
Superficial varicosities always produce venous recirculation, and can result in prolonged clearance that may be very localized or may affect the whole leg. As a practical matter, if the peak retrograde flows in the greater and short saphenous veins and in the popliteal vein add up to less than 10 cc/sec then progressive 'stasis dermatitis' and ulceration will not occur. If their sum is greater than 15 cc/sec, then the incidence of ulceration will be very high.(5) In some cases a local reflux that is purely superficial and is more than 7 cc/sec may produce local ulceration.(6)
Ulcers
Chronic nonhealing leg ulceration can be debilitating. Approximately 1 million persons in the United States have an ulceration due to superficial venous disease, and approximately 100,000 of these persons are classified as 'disabled' due to their condition.(1)
Although there are many different potential causes for nonhealing wounds, at the Center for Wound Care about two-thirds of our patients have a venous etiology for their chronic ulcers. Approximately two-thirds of these have venous disease which is purely or largely confined to the superficial venous system, while the other one-third are the result of chronic DVT or of whole-leg deep venous valvular insufficiency of unproven etiology.
The syndromes of venous hypertension and reduced venous clearance are important causes of morbidity and disability in patients with varicose venous disease, but they rarely result in death. Death from superficial venous disease is not unheard of, however, and may result either from hemorrhage or from superficial thrombophlebitis which progresses to cause pulmonary thromboembolism.
Variceal hemorrhage
Bleeding from lower extremity varicosities can be fatal: there were 23 such fatalities reported from England and Wales in 1971.(8) Although this is not a rare problem, it is one that rarely is seen by office-based phlebologists; patients usually present to an emergency department where the traditional management involves oversewing of the involved vessel. Patients who have had a significant blood loss are sometimes admitted to the service of a vascular surgeon, particularly if the bleeding varicosity is extensive and the overlying tissue is friable.
We have successfully managed a number of these patients in our emergency department by primary sclerotherapy using sotradecol, following the experience of Tretbar, who reported a series of 12 such cases treated successfully by compression sclerotherapy over a three year period.(7)
Superficial thrombophlebitis
The lifetime incidence of superficial thrombophlebitis in patients with untreated varicose veins has been estimated at 20% - 50%. This is not a benign condition: unrecognized deep vein thrombosis may cause or may follow an obvious superficial phlebitis. One study found that approximately 10% of hospitalized patients with superficial thrombophlebitis progress to develop pulmonary thromboembolism, with a 20% death rate in the group with PE.(9-11)
Ascending superficial thrombophlebitis may propagate into the deep veins via perforating veins at any level, but is most worrisome when it progresses along the greater saphenous vein and threatens to approach the level of the saphenofemoral junction at the groin. The literature strongly suggests surgical interruption of the saphenofemoral junction and removal of the phlebitic saphenous vein in such cases.(12)
Even if pulmonary embolism does not occur, progression of superficial thrombophlebitis into the deep veins may result in permanent deep venous valvular insufficiency, with a 60% to 90% subsequent incidence of venous leg ulceration.(13)
Summary
Primary superficial venous disease is neither uncommon nor benign. Patients presenting with complaints referable to the venous system should be taken seriously, and treatment should be aimed at ameliorating the symptoms and, whenever possible, at correcting the underlying abnormality.
References
1. Coon WW, Willis PW, Keller JB: Venous thromboembolism and other venous disease in the Tecumseh Community Health Study Circulation 1973;48:839-846.
2. Schultz-Ehrenburg U, et al: Prospective epidemiological investigations on early and preclinical stages of varicosis, in Davy A, Stemmer R (eds): Phlebologie 89. Montrouge, France, John Libby Eurotext Ltd.; 1992:
3. Weiss RA, Weiss MA: Resolution of pain associated with varicose and telangiectatic leg veins after compression sclerotherapy. J Dermatol Surg Oncol 1990;16:333-336.
4. Wilder CS: Prevalence of selected chronic circulatory conditions. Vital Health Stat 1974;94:1
5. Nicolaides A, Christopoulous D, Vasdekis S: Progress in the investigation of chronic venous insufficiency. Ann Vasc Surg 1989;3(3):278
6. Christopoulos D, Nicolaides AN, Szendro G: Venous reflux: quantitation and correlation with the clinical severity of chronic venous disease. Brit J Surg 1988;75:352
7. Tretbar LL: Bleeding from varicose veins, treatment with injection sclerotherapy, in Davy A, Stemmer R (eds): Phlebologie '89. France, John Libby Eurotext; 1989:
8. Evans GA, Evans DM, Seal RM, Craven JL: Spontaneous fatal haemorrhage caused by varicose veins. Lancet 1973;2:1359-1361.
9. Zollinger RW, Williams RD, Briggs DO: Problems in the diagnosis and treatment of thrombophlebitis. Arch Surg 1962;85:18
10. Guilmot J-L, Wolman F, Lasfargues G: Thromboses veineuses superficielles. Rev Prat 1988;38:2062
11. Zollinger RW: Superficial thrombophlebitis. Surg Gynecol Obstet 1967;124:1077
12. Lofgren EP, Lofgren KA: The surgical treatment of superficial thrombophlebitis. Surgery 1981;90:49
13. Hirsh J, Genton E, Hull RD: Venous thromboembolism, New York, Grune & Stratton; 1981:
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