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Although the role of perforator veins (PVs) in the development of signs and symptoms remains unclear, the number of incompetent PVs and the size of both competent and incompetent PVs have been shown to increase with worsening chronic venous disease (CVD). Furthermore, it was recently reported that the duration of outward flow in these veins was longer in patients with ulcers compared with those in lower classes of CVD.
Clinical practice guidelines of the Society for Vascular Surgery and the American Venous Forum (2014) recommend treatment of perforating veins with reflux greater than 500 ms and a vein diameter greater than 3.5 mm located near healed or active venous ulcers (clinical, etiology, anatomy, and pathophysiology [CEAP] class 5 and class 6). In contrast, these guidelines recommend against perforator treatment in CEAP class 1 and class 2 patients. The value of perforator treatment in CEAP class 3 and class 4 disease remains unclear.
Reflux in PVs is defined as outward flow from the deep to the superficial veins. It has been suggested that high flow from the deep veins during muscular contraction eventually renders the PVs incompetent. The etiology of venous reflux in superficial veins and PVs is unknown. The most predominant theory is that the weakening of the venous wall eventually leads to valve failure. During early stages of the disease, reflux is most prevalent in the superficial veins. Others have also suggested that reflux in the PVs is caused by volume overload at the reentry points of incompetent superficial veins. However, direct evidence for both theories is lacking because most investigations have been cross-sectional, population studies without sufficient longitudinal study regarding disease progression.
Labropoulos et al. identified two other patterns by which previously competent PVs become incompetent; these were ascending development and new sites becoming incompetent. The ascending development of reflux into PVs from previously competent segments of superficial veins was more prevalent. A smaller number of incompetent PVs were detected in new locations that previously did not have reflux in any system. PV reflux was always associated with reflux in an adjacent superficial vein and underscores the important role of superficial vein reflux in the development of PV incompetence. Because most limbs in the early stages of CVD exhibit reflux in the superficial veins only, it can be assumed that one of the mechanisms for development of PV insufficiency involves the presence of reflux in an adjacent, superficial vein segment that acts as a capacitor for the refluxing PV. As local hemodynamic conditions change, and as intravenous pressure increases, the diameter of the PV increases, and the PV valve becomes incompetent. This may be in combination with, or separate from, primary venous wall disease.
Deep vein reflux is not required for development of PV incompetence in primary venous disease. Rather, deep vein reflux can develop as a result of increased flow from the incompetent superficial veins through the PV, the diameter of which has increased. Labropoulos et al. showed that only five new incompetent PVs were seen in association with juxtaposed reflux in the deep vein. At all five sites, deep vein reflux was not present at the time of the initial duplex study when the adjacent PV was still competent; the deep venous incompetence developed simultaneously with PV incompetence. Superficial vein reflux was present at all sites.
Finally, this study also suggested that the development of reflux in previously normal PVs was seen in association with worsening of the clinical stage of CVD in 40% of limbs. Although the worsening of the clinical stage cannot be attributed to extension of reflux in the PVs alone, one can assume that the natural history of long-standing reflux in the superficial veins is that of progressive deterioration, with extension of reflux to other previously competent segments of the superficial veins and their associated PVs.
In general, PVs should be reserved for specific situations:
When they are found in continuity with the areas of axial (or neovascular) reflux in recurrent varicose vein cases
When found beneath an ankle ulcer
When there are large incompetent midthigh PVs serving as escape points and represent the highest point of reflux
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