Journal of Vascular and Endovascular Therapy

Description

Chronic venous insufficiency of the lower limbs (CVI) is characterized by symptoms or signs produced by venous hypertension as a result of structural or functional abnormalities of veins. Symptoms may include aching, heaviness, leg-tiredness, cramps, itching, sensations of burning, swelling, the restless leg syndrome, dilatation or prominence of superficial veins, and skin changes. Signs may include telangiectasia, reticular or varicose veins, edema, and skin changes such as pigmentation, lipodermatosclerosis, eczema, and ulceration. The most frequent causes of CVI are primary abnormalities of the venous wall and the valves and secondary changes due to previous venous thrombosis that can lead to reflux, obstruction, or both. Congenital malformations are rare causes of CVI. Because the history and clinical examination will not always indicate the nature and extent of the underlying abnormality (anatomic extent, pathology, and cause), a number of diagnostic investigations have been developed that can elucidate whether there is calf muscle pump dysfunction and can determine the anatomic extent and functional severity of obstruction or reflux. The difficulty in deciding which investigations to use and how to interpret the results has stimulated the development of this consensus document.

Anatomic Extent

Because the history and clinical examination will not always indicate the nature and extent of the underlying abnormality (anatomic extent, pathology, and cause), a number of diagnostic investigations have been developed that can elucidate whether there is calf muscle pump dysfunction and determine the anatomic extent and severity of obstruction or reflux. The difficulty in deciding which investigations to use and how to interpret the results has stimulated the development of this consensus document. The aim of this document was to provide an account of these tests, with an outline of their usefulness and limitations and indications of which patients should be subjected to the tests and when and of what clinical decisions can be made. This document was written primarily for the clinician who would like to learn the latest approaches to the investigation of patients with CVI and the new applications that have emerged from recent research, as well as for the novice who is embarking on venous research.

Venous Hypertension

The aim of this document was to provide an account of these tests, with an outline of their usefulness and limitations and indications of which patients should be subjected to the tests and when and of what clinical decisions can be made. It is believed that they are usually due to abnormal distensibility of connective tissue in the vein wall. Early work has suggested that veins from patients with varicosities are more distensible than those from patients with normal veins,38 indicating a probable systemic basis for the abnormality. Varicosities usually start at points where superficial veins communicate with deep veins, particularly at the saphenofemoral and saphenopopliteal junctions and in the perforating system, because of valvular incompetence. Primary varicose veins result from venous dilatation without previous thrombosis. Secondary varicose veins are caused by valvular damage after deep vein thrombosis (DVT) and recanalization that gives rise to incompetent deep and perforating veins. Sometimes, varicose veins may be associated with reflux through vulvar varices without any relation to the saphenofemoral junction or other deep-to-superficial reflux in the lower limb. Such varices also may be associated with clinical symptoms and signs suggestive of pelvic congestion, including uterine retroversion and dyspareunia. They are more common in women who have had several pregnancies and had had hemorrhoids and vulvar varicosities during and after pregnancy.394041 Poor venous drainage and resulting venous hypertension increase transmural pressure in postcapillary vessels, producing skin capillary damage, fluid exudation, edema, and tissue malnutrition, which favors inflammation, infection, thrombosis, and tissue necrosis with lipodermatosclerosis and eventual ulceration.