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(BQ) Part 2 book Phlebology, vein surgery and ultrasonography presents the following contents: Perforator veins, upper deep vein disease, lower deep vein disease, ultrasound for thrombosis, superficial venous thrombophlebitis, deep vein thrombosis, venous leg ulcers, vein anesthesia,...
Part IV Non-Superficial Veins 14 Perforator Veins Elna M Masuda and Darcy M Kessler Abstract Contents 14.1 Introduction 191 14.2 History 192 14.3 Anatomy 192 14.4 Pathophysiology 194 14.5 Evidence in Favor of Importance of PVs 194 14.6 Evidence Against the Importance of IPVs 196 14.7 Fate of IPVs After Surgery 197 14.8 Diagnosis 197 14.9 14.9.1 14.9.2 14.9.3 14.9.4 Treatment Options and Techniques SEPS Percutaneous Ablation Thermal Ablation Techniques Ultrasound-Guided Sclerotherapy Techniques 198 198 198 199 200 14.10 Influence of Postthrombotic Syndrome on Outcomes 203 14.11 Suggested Indications for PV Treatment 203 References 203 E.M Masuda, MD (*) • D.M Kessler, RVT Division of Vascular Surgery, Straub Clinic and Hospital, John A Burns School of Medicine, Honolulu, HI, USA e-mail: emasuda@straub.net; dkessler@straub.net Perforator veins (PVs) are one of three major venous systems in the leg directly linked to serious manifestations of chronic venous disease (CVD) including venous ulceration Although its anatomical details are clearly defined, the physiology and clinical importance of PVs continue to remain less explicit This chapter will review the evidence to support the diagnosis, indication for treatment, noninvasive and invasive options for management of PVs 14.1 Introduction Nearly 100 years ago, Homans presented a comprehensive description of the relationship between perforator veins and leg ulceration [1] Despite its long history and the fact that perforator veins are frequently identified in the “gaiter area” beneath ulcers and areas of venous stasis dermatitis, controversy still prevails over its clinical significance and role in producing the pathologic state Additionally, choices for treatment are highly variable and range from invasive eradication by long calf incisions to simple ablation by direct injections This chapter will attempt to clarify the role of PVs in CVI and discuss the optimal diagnostic and therapeutic strategies E Mowatt-Larssen et al (eds.), Phlebology, Vein Surgery and Ultrasonography, DOI 10.1007/978-3-319-01812-6_14, © Springer International Publishing Switzerland 2014 191 E.M Masuda and D.M Kessler 192 14.2 History Perforator veins were first identified by Russian anatomist von Loder in 1803 then linked to skin changes by John Gay in 1868 who discussed the varicose disease of the leg and its “allied disorders” consisting of skin discoloration, induration and ulcers [2, 3] In 1917, John Homans published a landmark paper describing the anatomic and pathophysiologic relationship of PVs to venous ulceration and proposed treatment, based solely on his astute clinical skills and careful physical examination [1, 4] In 1938, Linton followed with a method of treating perforator veins to correct venous ulceration using extensive calf incisions, often through compromised skin, a technique associated with a high rate (up to 58%) of wound complications, which led to other proposed treatment approaches including limited incisions directly over the perforator [5–7] Cockett and Jones, like Homans and Linton, reported in 1953 their findings that non-healing ulcers were associated with the post-thrombotic syndrome, PV’s were important in the production of ulcers in the “gaiter” area or the “ankle blow out syndrome”, and that ligation of the perforators promoted healing [8] The high incidence of wound complications associated with the Linton procedure gave way to less invasive methods with multiple parallel incisions made along the natural skin lines plus skin grafting popularized by Ralph De Palma [9] Hauer from Germany in 1985 [10] introduced and promulgated the use of endoscope and hence the emergence of SEPS (subfascial endoscopic perforator surgery) in reducing post op wound complications and decreased hospital length of stay SEPS was the mainstay of therapy for PVs from 1985 to the mid-2000’s and has proven to be less invasive than open surgery, and equally effective in eliminating PV’s with lower wound complication rates More recently, other less invasive techniques such as endovenous radiofrequency ablation, laser ablation, and ultrasound guided sclerotherapy have evolved, many of which can be performed under local anesthesia in an office setting, although outcomes have not been validated by controlled studies 14.3 Anatomy Perforator veins connect the superficial veins with the deep system and penetrate the deep fascia There are more than 60–150 perforating veins in the normal leg, 20 of which are most commonly involved with pathology [11, 12] In normal limbs, the direction of flow is unidirectional from the superficial to the deep system through one to two bicuspid valves, although outward flow has been found in up to 21 % of normal limbs [13] When associated with chronic venous disease (CVD), the reflux can be outward from the deep to superficial alone (unidirectional) or both deep to superficial and superficial to deep (bidirectional) New terms have been suggested to replace numerous eponyms and are detailed in Table 14.1 [14] The majority of clinically important perforators are found along the mid to distal medial calf (Fig 14.1) The posterior tibial perforators connect the posterior accessory great saphenous vein of the leg (formerly called posterior arch or Table 14.1 Suggested changes in anatomic terms for leg veins Previous terms and eponyms Superficial femoral vein Greater or long saphenous vein Lesser or short saphenous vein Saphenofemoral junction Giacomini vein Posterior arch vein or Leonardo’s vein Cockett perforators (I, II, III) Boyd’s perforator Sherman’s perforators “24 cm” perforators Hunter’s and Dodd’s perforators May’s or Kuster’s perforators Replaced by newer terms Femoral vein Great saphenous vein (GSV) Small saphenous vein (SSV) Confluence of the superficial inguinal veins Intersaphenous vein Posterior accessory great saphenous vein of the leg Posterior tibial perforators (lower, middle, upper) Paratibial perforator (proximal) Paratibial perforators Paratibial perforators Perforators of the femoral canal Ankle perforators Reproduced with permission from Gloviczki and Mozes [14] 14 Perforator Veins 193 Fig 14.1 Anatomy of the major perforator veins in the lower limb Leonardo’s vein) to the paired deeper posterior tibial veins The posterior tibial perforators lower, middle, and upper were previously referred to as Cockett veins I, II, and III The lower posterior tibial perforator is usually found posterior to the medial malleolus and is not usually accessible by SEPS The paratibial perforators connect the great saphenous vein to the posterior tibial veins Multiple paratibial perforators are found 2–4 cm posterior to the medial edge of the tibia or “Linton’s Lane” and are particularly important for conducting a proper SEPS procedure The perforators of the femoral canal (previously referred to as Dodd and Hunterian perforators) connect the great saphenous and femoral veins Ankle perforators include the former May’s or Kuster’s perforators In the foot, there are dorsal plantar, medial, and lateral foot perforators where the normal direction of flow is outward, distinctly opposite from PVs in the calf The large perforator in the foot arises between the first and second metatarsal bones and connects the pedal vein to the superficial dorsal venous arch E.M Masuda and D.M Kessler 194 14.4 Pathophysiology PVs alone not appear to be the primary cause of venous ulcers Instead, they are almost always accompanied by local or axial superficial and/ or deep venous reflux or obstructive disease Although PVs are frequently found in areas of intense inflammation, pre-ulcerative skin changes or in the vicinity of ulcers, they are not found as isolated abnormalities in venous ulcers [15] Frequently, the most recalcitrant ulcers are associated with reflux in all three systems (deep, superficial and PVs) Neither isolated perforator nor isolated deep venous reflux is commonly found associated with severe CVD [16] Usually two or more venous systems are abnormal in advanced CVD PVs appear to act as reentry points between two axial systems allowing blood to flow from incompetent superficial to deep or vise versa [17] If the primary problem is deep venous obstruction or reflux, the elevated venous pressure produced by deep venous obstruction or reflux during calf muscle contraction is transmitted to the connecting perforators and into the superficial veins The blood under the calf muscle pump is forced to escape via the PVs and “yo-yos” up and down the deep system [17] This may result in enlargement of the dermal capillary bed and release of proteins into the interstitial space including fibrinogen, which may eventually result in ulceration [18, 19] In primary venous insufficiency with no prior DVT, the pathology is likely a refluxing saphenous system causing dilatation of the PVs, rendering the valves incompetent and often referred to as a “reentry perforator” This is supported by the findings of Stuart and Campbell who found that in cases of combined PVs and saphenous reflux, by abolishing the superficial saphenous vein alone PVs were no longer detectable or became competent [20, 21] In a prospective study by Labropoulos and colleagues, new perforator incompetence always occurred with reflux in the superficial veins [22] If the clinical state worsened, outcomes could not be attributed to development of PVS alone because of the inevitable presence of superficial disease [22] Increasing size and numbers of PVs are associated with increasing severity of CVD [23, 24] Size of PVs play an important role since larger diameters of PVs are more likely to be incompetent [25] Diameters of >3.5mm are associated with reflux in 90% of cases [26] PVs with diameters >3.9mm possess a high specificity of 96%, but lower sensitivity of 73% for incompetence with the lower sensitivity attributable to one third of incompetent PVs possessing diameters of