Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3834_Библиотеки_им_академика_М_И_Перельмана

signicant venous reux, to then remove the venous reux and nally to remove the varicosi­ties themselves, in order to prevent thrombosis and painful thrombophlebitis in the redundant venous dilations (varices).

1. Failure to treat the correct vein or veins—the

allowvaricosities to recur.

3. The underlying reux was successfully and

permanently treated, but new reux develops

in previously normal veins in the same limb—

The second problem with this old understand­ing of venous disease is that sources of venous reux causing varicose veins are many and varied and not related only to the great and small saphe­nous vein. It is now readily recognised that sig­nicant varicose veins can be associated with venous reux in anterior accessory saphenous veins [

If during this venous duplex ultrasonography venous reux is found to be arising from veins coming from the pelvis, then pelvic vein imaging will be suggested. In women, this will be a trans­vaginal venous duplex ultrasound scan performed using the Holdstock protocol [14], with the patient positioned at 45°, and using Valsalva for venous stimulation. In females unable or unwill­ing to undergo this, and inmen, an MRV is per­formed in the rst instance understanding that venous diameter alone is not adequate to diag­nose venous reux [15].

16], and there are very clear descriptions in

such models as to how veins heal after being divided. A divided vein produces a haematoma and thrombus within the end of the vein, pre­venting exsanguination. Provided the subject survives, endothelium buds out of the cut ends of the vein, producing solid cords of endothe­lial cells that branch into the haematoma. The haematoma appears to stimulate this process, and some studies have suggested that rather than the endothelial cells growing out of the ends of the damage vein, these endothelial cords may well arise from broblasts [ even bone marrow-derived stem cells in the haematoma itself [18].

process is called “neovascularisation”.For many years, surgeons refused to believe that this occurred.

When a great saphenous vein is stripped, there is haematoma between the saphenofemoral junc­tion stump and the bottom end of the stripped vein. There is endothelium at both of these points that is free and quite able to be involved in the process of neovascularisation. However, what makes the process easier to occur is the fact that neovascularisation does not happen just between these two ends. Any surgeon who has ever har­vested a great saphenous vein for bypass will know that there are any number of tributaries and perforators that have junctions with the great saphenous vein in the thigh. During the stripping process, all of these become contributing veins to the formation of the haematoma but also contrib­uting points to the process of neovascularisation. However, when we talk about the regrowth of a stripped truncal vein, we tend to call it “strip tract revascularisation” rather than neovascularisation, keeping this latter word for the small serpiginous veins usually seen local to the site of the surgical incision.

It became clear that the major advantage of endovenous surgery was not of reduced pain, improved mobility and return to work, nor better cosmetic result but was actually a reduction in the risk of recurrence of the treated vein. Having understood how veins healed again by neovascu­larisation and strip tract revascularisation after stripping, endovenous thermoablation with radio­frequency was clearly causing a different healing process in the treated vein. I treated a segment of exvivo great saphenous vein with a VNUS clo­sure catheter so that I can see the effect that the radiofrequency ablation was having on the vein wall directly. The white vein with a mild pink hue from being freshly removed shrivelled and con­tracted on the VNUS Closure catheter, turning beige as the protein constricted and burned.

devices now have segmental radiofrequency devices of xed treatment length, bipolar and monopolar radiofrequency devices. Endovenous laser stretches across many wavelengths, many bre diameters and many tips giving different dis­tributions of the laser energy once inside the vein.

I have discussed elsewhere the difference between the individual devices, but in principle, all of the thermoablation devices are currently catheter based and are placed within the vein lumen under ultrasound control. They all need some form of anaesthesia, whether in the form of tumescence directly around the vein or regional/ general anaesthesia with or without compression such as an Esmarch bandage on the leg. In today’s world, it is hard to justify anything but tumes­cence and a walk-in walk-out procedure. Some doctors still give sedation or other forms of anaes­thesia for a variety of reasons ranging from fund­ing through to traditional organised pathways of treatment, perceived patient preference and their own condence (or lack of)in cannulating veins.

Conversely endovenous laser emits photons of electromagnetic radiation, either in the visible

It is quite clear that for most truncal veins, a LEED over 60J/cm is required to cause ablation (i.e. transmural death) [32]. “Closure” can be obtained at lower values, but this often leads to recanalisation in the future, as can be seen in reports where the success rate drops as the fol­low- up continues over the rst year or two. Successful ablation should lead to atrophy and no chance of any reopening. There have been argu­ments from clinical practice that the microwave lasers that use water as a chromophore can reach the same clinical end-point at a lower LEED than the visible light lasers using haemoglobin as a chromophore. Our invitro studies [33–35] have shown that there is certainly some evidence to support this view, although our review on the subject suggests that any LEED under 60J/cm is likely to have a signicant chance of recanalisa­tion and keeping to the higher range of LEED is probably safer in terms of atrophy and permanent ablation of the vein [32].

In a series of 3studies, we showed that if the power was reduced and the time of treatment was increased, the same LEED could be reached but with a better thermal spread through tissue and without carbonisation at the point of contact. Initially, we proved this point in an invitro por­cine liver model, checked our theory in exvivo great saphenous vein and nally showed 100% success in closing great saphenous veins using a protocol derived from this work [33, 34, 38].

Hence, it is clear that to reduce the risk of recurrent varicose veins after endovenous ther­moablation, it is not which device you use, but it is the understanding of the total energy that is reaching the vein wall and over what time period the energy is applied, ensuring that adequate pen­etration throughout the vein wall is achieved— which of course means ensuring transmural death of the vein wall.

Traditionally, sclerotherapy has been thought to damage the endothelial layer of the vein, allowing the vein to be “stuck” together after compression. However, this does not follow the principles of transmural death of the vein wall and also doesn’t help us understand why sclero­therapy is so effective in small veins with thin walls but less effective in large veins with thick walls. This observation lends more credence to the idea that sclerotherapy also works by causing transmural death.

Hence, it is likely that this is the mechanism of failure in the current clinical studies showing high recanalisation rates after the treatment of truncal veins with foam sclerotherapy [44].

gators have suggested a direct effect of the wire on the endothelium [45, 46], our own research has suggested that the mechanism is actually a shearing stress produced in the vein wall from the rotating wire, creating channels in the vein wall like a “Swiss cheese” which allows the scle­rosant to penetrate the vein wall itself [47]. This allows sclerotherapy to enter the vein wall, allowing the effect of the sclerosant to penetrate deep inside the wall and achieving transmural death. Not surprisingly, the results of closure of a treated GSV from MOCA appear to be far higher than foam sclerotherapy alone in truncal veins at 1year [48, 49].

We can now nally turn to some of the latest techniques that are being used without tumes­cence. The rst are the cyanoacrylate glues and the second area group of combination techniques using low-power laser with sclerotherapy.

The cyanoacrylate glue is a relatively new treatment that has not been available for the treatment of varicose veins as long as endove­nous laser and radiofrequency, and so it has not been studied to the same extent. The mechanism of action on the vein wall has been studied in the swine supercial epigastric vein model which suggests that the lumen is lled with the adhe­sive, occluding it (occasionally mixing with the blood), and over 30 and 60days, inammatory processes affect the intima and project into the media of the vein [50, 51]. In addition, at 60days, brous tissue was seen to project into the lumen [51].

75.7 and 92.9% [50–52]. As such, although there are clear advantages in terms of ease of use and lack of tumescence, long-term studies need to be done to show that the lack of transmural death of the vein wall doesn’t result in failures and recanalisation.

proven. Enthusiasts suggest that the low-power lasers can either cause constriction of the vein which they seem to think will help the action of the foamed sclerosant [53] or interact with the sclerosant making it more active [54].

3.0–4.5% chance of developing new varicose veins in that leg per year. Such varicose veins