These long-term effects are difficult to establish in clinical trials focusing on groups with existing artery decline. Klippel–Trenaunay syndrome and Parkes Weber syndrome are relevant for differential diagnosis.Another cause is chronic alcohol consumption due to the vasodilatation side effect in relation to gravity and blood viscosity. Diagnosis
Clinical test
Clinical tests that may be used include:
Trendelenburg test–to determine the site of venous reflux and the nature of the saphenofemoral junction

Investigations
Traditionally, varicose veins were investigated using imaging techniques only if there was a suspicion of deep venous insufficiency, if they were recurrent, or if they involved the saphenopopliteal junction. This practice is now less widely accepted. People with varicose veins should now be investigated using lower limbs venous ultrasonography. The results from a randomised controlled trial on patients with and without routine ultrasound have shown a significant difference in recurrence rate and reoperation rate at 2 and 7 years of follow-up. Stages
The CEAP (Clinical, Etiological, Anatomical, and Pathophysiological) Classification, developed in 1994 by an international ad hoc committee of the American Venous Forum, outlines these stages
C0 – no visible or palpable signs of venous disease
C1 – telangectasia or reticular veins
C2 – varicose veins
C2r - recurrent varicose veins
C3 – edema
C4- changes in skin and subcutaneous tissue due to Chronic Venous Disease
C4a – pigmentation or eczema
C4b – lipodermatosclerosis or atrophie blanche
C4c- Corona phlebectatica
C5 – healed venous ulcer
C6 – active venous ulcer
C6r- recurrent active ulcerEach clinical class is further characterized by a subscript depending upon whether the patient is symptomatic (S) or asymptomatic (A), e.g. C2S.
Females have a higher tendency of being affected than males

Causes
Varicose veins are more common in women than in men and are linked with heredity. Other related factors are pregnancy, obesity, menopause, aging, prolonged standing, leg injury and abdominal straining. Varicose veins are unlikely to be caused by crossing the legs or ankles. Less commonly, but not exceptionally, varicose veins can be due to other causes, such as post-phlebitic obstruction or incontinence, venous and arteriovenous malformations.Venous reflux is a significant cause. Research has also shown the importance of pelvic vein reflux (PVR) in the development of varicose veins. Varicose veins in the legs could be due to ovarian vein reflux. Both ovarian and internal iliac vein reflux causes leg varicose veins. This condition affects 14% of women with varicose veins or 20% of women who have had vaginal delivery and have leg varicose veins. In addition, evidence suggests that failing to look for and treat pelvic vein reflux can be a cause of recurrent varicose veins.There is increasing evidence for the role of incompetent perforator veins (or "perforators") in the formation of varicose veins. and recurrent varicose veins.Varicose veins could also be caused by hyperhomocysteinemia in the body, which can degrade and inhibit the formation of the three main structural components of the artery: collagen, elastin and the proteoglycans. Homocysteine permanently degrades cysteine disulfide bridges and lysine amino acid residues in proteins, gradually affecting function and structure. Simply put, homocysteine is a corrosive of long-living proteins, i.e. collagen or elastin, or lifelong proteins, i.e. fibrillin.