Venous disease may range from simple varicose veins which may be quite asymptomatic to severe chronic venous insufficiency with associated ulcers or wounds.
Incidence varicose veins are common; in fact, some people consider them normal since they are so common. The older the people being examined, the more common varicose veins are seen. Most people over the age of 60 have some form of varicose veins. In many patients, there is a familial tendency (genetic basis) with their mother or father having varicose veins. The problem is more common in women than in men. Being overweight, pregnant and/or having to stand for long periods of time may increase the risk of having varicose veins. There are three kinds of varicose vein: varicose veins of the saphenous or just off the largest superficial veins (trunk varices), reticular veins, and telangiectasis (spider veins). The typical varicose veins that most people think of are the trunk varices. These are directly part of the large superficial veins of the leg including the great saphenous vein (the largest vein going from groin to ankle in the fat just under the skin) or the small saphenous vein (the largest superficial vein going from the ankle to just behind the knee). These veins are almost ½ inch in size and may be larger. They can usually be easily felt especially when the person is standing. Reticular veins are small blue veins seen under the skin. They are usually < 4 millimeters in size (less than a tenth of an inch). They usually cannot be felt through the normal skin. Up to 80% of adults may have reticular veins. Telangiectasis or spider veins are very near to the surface of the skin. These veins are usually bright red or purple. They are < 1mm in size, so very small. More than 90% of adults have reticular veins.
Most people with varicose veins do not have any symptoms or so little problems that they chose not to seek treatment. Patients who want to get rid of the varicose veins are usually unhappy with the look of their legs, they have problems they think are due to the varicose veins, or they are worried that they will develop a worse problem if they do not care for the varicose veins.
In general complaints noted with varicose veins may be seen in 50% of adults. Symptoms commonly seen with varicose veins include:
However, these complaints are not only seen in patients with varicose veins and are not described as more or less common or worse the larger the veins seen on examination (these symptoms are noted related to severity) Also, the worse the reflux (backward flow of blood in the vein) does not mean that the patient will have worse complaints (that is, no relationship between the severity of reflux on ultrasound study and the presence of symptoms). Therefore it can be difficult to know which patients will have relief from their symptoms after surgery or other treatments for the varicose veins. In addition only a small number of patients will go on to have those complaints seen with chronic venous insufficiency when they only have varicose veins.
Patients with chronic venous insufficiency (CVI) develop skin changes resulting from high pressures in the veins that then affect the fat and skin most often around the ankle. It is seen as chronic swelling, more severe skin changes of thickening or fibrosis (lipodermatosclerosis) or dark color changes called hyperpigmentation, or with the most severe condition, venous stasis ulcers (open wounds). Usually patients with CVI have more than just varicose veins. They may have other reasons for the skin changes such as high pressures in the veins from heart failure or damage of the vessels that remove protein from the leg called lymphedema. Severe pain associated with CVI is unusual and should make your doctor look for other causes such as poor blood supply to the leg (arterial disease) or infection.
The signs of CVI may include: corona phlebectatica, lipodermatosclerosis or open ulcers. Corona phlebectatica is a fan-shaped flare of reticular veins and telangiectasias around the inside of the foot and ankle. Lipodermatosclerosis is thickening and fibrosis (scar formation) of the skin of the lower leg. This may begin suddenly and be mistaken for an infection or for a blood clot. After having CVI for a long time, the skin of the lower leg becomes shiny, hard and has a darker color than the surrounding skin. The skin is fixed or anchored to the underlying tissues making the skin tenser and less flexible. The skin may be very dry (dermatitis). White scar tissue (atrophie blanche) may also be present.
The CEAP classification consensus document was written by the American Venous Forum in 1994 to provide a comprehensive objective classification. It was universally accepted and endorsed, with most published papers now using all or portions of the CEAP system. It was comprised of two parts: classification and severity scoring.
As a result of now meaningful scientific communication of venous disease, improvements in diagnosis and treatment followed. This naturally led to the need to update and refine CEAP. Based on international consensus recommendations the AVF published a revised CEAP document in 2004.
C- clinical manifestation
E- etiologic factors
A- anatomic distribution
P- pathophysiologic dysfunction
1. Number of anatomic segments affected
2. Grading of signs and symptoms
C0: no visible or palpable signs of venous disease.
C1: telangiectasies or reticular veins.
C2: varicose veins.
C4a: pigmentation and eczema.
C4b: lipodermatosclerosis and atrophie blanche.
C5: healed venous ulcer.
C6: active venous ulcer.
S: symptoms including ache, pain, tightness, skin irritation, heaviness, muscle cramps, as well as other complaints attributable to venous dysfunction.
ETIOLOGIC CLASSIFICATION (No change)
Es: secondary (postthrombotic).
ANATOMIC CLASSIFICATION (No change)
s: superficial veins.
p: perforator veins.
d: deep veins.
Pr,o: reflux and obstruction.
Pn: no venous pathophysiology identifiable. Due to the various types of venous diseases and lymphatic diseases please consult a physician for proper diagnosis and treatment.
Original authors: Andrew W. Bradbury, Andrew D. Lambert, Robert B. McLafferty, and C. Vaughan Ruckley
Abstracted by Teresa L. Carman