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.
Samoyed - More severe disease than the Husky. Dominant PRA
Bullmastiff - Inherited as an autosomal dominant trait due to a mutation in the gene for rhodopsin. Feline PRA
Abyssinian - Two forms exist. One is inherited as an autosomal dominant trait and has an early age onset. The other is inherited as an autosomal recessive trait and has a middle age onset. Early onset PRA has also been reported in the domestic shorthaired cat and Persian. The Siamese also likely has a hereditary form of PRA. Despite belief among breeders to the contrary, there is apparently no link between coat color in Persians and the development of PRA. Central progressive retinal atrophy (CPRA)
CPRA is also known as retinal pigment epithelial dystrophy (RPED). The cause of this condition is the loss of the retinal pigment epitheliums ability to effectively process the photoreceptor outer segment (POS) and subsequent accumulation of POS material in the RPE and loss of function. The loss of function of the RPE leads to photoreceptor degeneration. Vitamin E deficiency may play a role in the development of CPRA. It is characterized by accumulation of pigment spots in the retina surrounded by retinal atrophy and a mottled appearance of the pigmented nontapetal fundus. The pigmented spots eventually coalesce and fade as the atrophy of the retina increases. It is an inherited condition (in the Labrador Retriever it is inherited as an autosomal dominant trait with variable penetrance). CPRA occurs in older dogs. Peripheral vision is retained for a long time.