Historical description and evolution of treatment įigure 2: Dilated tortuous incompetent perforators as seen on duplex ultra sound. Some authors have even described PVI as ‘normal’ allowing the blood from the refluxing superficial veins to return back to the superficial venous system (Figure 2). However, the role of PVI as a cause of CVI is not universally conclusive. Stuart and colleagues (2000) demonstrated that the number and diameter of incompetent perforator veins was directly related to the eventual disease severity in CVI. Increased ambulatory venous pressure causes further incompetence of perforators resulting in a vicious cycle of events that result in CVI and ulceration. It is postulated that once these perforator veins become incompetent, it results in reflux of blood from the deep veins to the superficial veins, contributing to superficial venous hypertension. Recent studies that attempted to define the anatomy of PVI have described that approximately 45% of all incompetent perforators are located within 10-15 cm of the medial malleolus and are located as medial perforators communication with the lower GSV. Direct perforator veins are the classical perforators that connect superficial to deep veins while indirect perforators are more variable in their location and connect superficial veins to muscular veins. More recent studies by Mozes and colleagues have identified these perforator veins to be more anatomically complex than the original descriptions and thus have been categorized as direct and indirect.
Historically, these perforators have been classified according to their anatomical location, being named after their founders such as Hunter, Dodd, Boyd and Cockett. In physiology, perforator veins carry blood from the superficial to deep veins.
Perforator veins traverse the deep fascia of the leg while forming communication channels between the superficial and deep venous systems.
C) Early relaxation phase: muscles relex (black arrows) causing relative low pressure in the deep system promoting flow from superficial to deep direction. B) Contraction phase: muscualr compressin (black arrows) of the deep veins empties the veins and closes the fascial gate perventing excess retrograde perforator flow. A) Resting phase of pump cycle: blood is filling the deep veins, and deep venous pressure is increasing. Red arrows denote flow direction, superficial vein is on the left, deep vein on the roght in each image.
Relux suite 2014 plus#
Plus and minus signs denote relative pressure differential between deep and superficial systems. Schematic representation of normal perforator function. Venous ulceration is the end result of CVI and chronic ambulatory venous hypertension causing overlying local tissue destruction (Figure 1).įigure 1: Perforator veins in physiology and pathology (Adapted from ‘How I decide to ablate a refluxing perforator’ Chieh-Min fan). Junctional reflux may occur at the sapheno-femoral junction or sapheno-popliteal junction while the truncal reflux may affect either the great saphenous vein (GSV) or small saphenous vein (SSV). While this may involve either the superficial venous system, deep venous system or both, the vast majority of such CVI results from junctional or truncal insufficiency of the superficial veins. However, while the role of definitive management for junctional and truncal venous reflux in symptomatic CVI is well-established, the exact indications for management of PVI in isolation remains somewhat unclear.ĬVI is the result of lower extremity venous valvular incompetence causing inadequate venous return and eventual venous hypertension in the legs. The importance of PVI in the manifestation of CVI and ulceration has since been well-recognized and widely studied. Homan in his landmark publication of 1917 described the pathophysiology of CVI caused by superficial and deep venous incompetence along with the importance of perforator incompetence in venous ulceration. Nevertheless, its morbidity and health care economic burden remain universal. The wide variation in global prevalence results from the wide variability in reporting, diagnosis and risk factors. Global prevalence rates of CVI are variable but may be as high as 40% among females and 17% among males. Apart from the chronic physical and psychological disability caused to the individual, it also results in an enormous economic burden to the health care administration. Chronic Venous Insufficiency (CVI) and venous ulceration is a common health problem causing significant patient morbidity.
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