inability to walk or stand for long hours Skin conditions / dermatitis which could predispose skin loss Skin ulcers especially near the ankle, usually referred to as venous ulcers Development of carcinoma or sarcoma in longstanding venous ulcers. Over 100 reported cases of malignant transformation have been reported at a rate reported as 0.4% to 1% Severe bleeding from minor trauma, of particular concern in the elderly Blood clotting within affected veins, termed superficial thrombophlebitis. These are frequently isolated to the superficial veins, but can extend into deep veins, becoming a more serious problem. Acute fat necrosis can occur, especially at the ankle of overweight people with varicose veins. 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. 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