Regarding “The effect of long saphenous vein stripping on deep venous reflux” by MacKenzie RK, Allan PL, Ruckley CV, and Bradbury AW. Eur J Vasc Endovasc Surg 28, 104–107 (2004)

Abstract

Ms. MacKenzie and her colleagues have reported a very interesting finding that ‘incomplete stripping [of the Great Saphenous Vein] appears to be associated with the development of new deep reflux in a significant proportion of limbs.’ This phenomenon has never been reported before, thus deserves discussion. Unfortunately, careful reading of the manuscript left me with little information regarding this subject, as well as regarding the patient population studied by the authors. Multiple studies performed before reported prevalence of Deep Venous Reflux (DVR) in patients with primary chronic venous disease (CVD) as 10% or lower. Yet, 32 of 77 limbs (42%), in this study demonstrated DVR. Possible explanation of this difference may be that authors included patients with secondary (post-thrombotic) CVD. This may also explain the unusually high prevalence of severe disease in these patients: 31 limb (40%) had open or healed ulcers; additional 18 limbs (23%) had skin changes. In post-thrombotic limbs, deep venous reflux often co-exists with more proximal obstructions. Perhaps this explains another interesting finding on this paper: more frequent development of isolated popliteal reflux. Figs. 1 and 2 show that 2 years after stripping, 10 limbs appeared to have new reflux in popliteal vein, but only 7 in femoral vein. Presence of proximal obstruction is often associated with development of collateral outflow including re-connection between deep and superficial system and enlargement of pre-existing accessory saphenous veins. This leads to another question: what were those ‘incompletely stripped’ limbs which constituted 63% of studied population? Unfortunately, authors only provide the estimated length of the open segments, but not their exact location or connection to incompetent perforators and other veins. Many of these questions would be answered if the authors adhere to CEAP classification, and reported not only the clinical class, but also aetiology ‘E’ as primary and secondary CVD (not primary and recurrent varicose veins as in Table 1), more detailed anatomy ‘A’ (only four segments were studied providing no information on proximal or perforator veins), and pathophysiology ‘P’ (reporting both reflux and obstruction).