Initially, endovenous ablation procedures were directed to the greater saphenous and lesser saphenous veins addressing pathologic venous reflux.

Anyone who has completed endovenous ablation procedures for very long, will agree that many other pathways exist that contribute to superficial venous hypertension of the lower extremities other than the greater/lesser saphenous vein circuits.

Perforator veins allow communication between the superficial venous system and deep venous system of the legs in conjunction or independent of the greater/lesser saphenous circuits. Perforator veins, as their name implies, (which perforate the aponeurosis fascial tissues along with accompanying arteries and nerves) are typically 1-3mm in diameter at the fascial junction and have one to three valves.

 These bicuspid valves of the perforator veins are oriented to allow blood to go in one direction, from the superficial veins to the deep veins. The unidirectional blood flow in these perforator veins is also maintained by the oblique course of the perforator veins through the muscle groups associated. The average number of perforator veins per extremity is highly variable and reported to be as many as 155 perforator veins per lower limb.

Obviously, not all of these are clinically important, but some can cause significant morbidity as they are thought to play a fundamental role in the development of superficial varicose veins in the lower extremities. The distribution of perforator veins increases in density as one approaches the distal calf/ankle regions. The perforator veins occur in a ratio of 8:1, with 8 times more perforator veins in the lower leg, ankle and foot than in the thigh. Perforator veins are considered to be pathologic when they reach diameters of >4 mm and have large volume flow, venous reflux, feeding an array of superficial varicose veins above the fascial layer of the muscles.

The gaiter areas of the lower extremities are the areas where skin changes and venous stasis ulcers are most likely to occur; these areas are where the most prominent perforator veins are likely to be found.

Perforator vein incompetence in these gaiter areas have been shown to increase ambulatory venous pressures above 100 mm Hg (venous hypertension), a phenomenon that has also been referred to as “ankle blow-out” syndrome in the gaiter areas.

The combination of incompetent perforator veins and resultant superficial venous hypertension over time causes damage to capillaries in the skin and  subcutaneous capillaries, allowing protein rich fluid and red blood cells to escape into the subcutaneous tissue around the ankle. Thus, the subcutaneous tissues becomes fibrotic with skin pigmentation resulting from hemosiderin deposition.

With superficial venous hypertension, there is an increased capacity for blood volume to be expelled down a pressure gradient through both dilated low-resistance incompetent perforators and the incompetent greater saphenous vein or lesser saphenous vein circuits.

This gives an added degree of complexity to an already complex network of veins that result in perforator-based venous reflux disease. As such, if endovenous ablation procedures are limited to the greater and lesser saphenous systems alone, treatment would be insufficient. Unfortunately, some insurance providers have limited reimbursement coverage for any veins outside the greater saphenous and lesser saphenous vein circuits. It is hoped that in the near future codes will be designated for endovenous ablation procedures directed at pathologic perforator veins.

Perforator surgery should be added when patients have obvious perforator venous reflux disease related to superficial venous hypertension.

 The clinically important perforator veins are in the thigh (along Hunter’s canal), calf (soleus and gastrocnemius types), medial leg below knee (Boyd’s), lateral (outer) leg (peroneal) and Cockett’s. The Cockett’s type is the most recognized and occurs within 18-20 cm superior to the medial ankle. New anatomic designations have been given, but most us still know the familiar names associated with pioneers in phlebology.

Perforator veins exit the fascia at various levels within 3 cm along the line previously described by Linton. An experienced phlebologist can locate these important perforators for targeted ultrasound review.

Initial attempts at endovenous laser ablation of the pathologic perforator veins using 810 diode lasers were associated with paraesthesias and permanent superficial nerve damage.

A majority of the perforator veins exit through the fascia accompanied by a cutaneous nerve branch and artery. As the 810nm laser generates significant heat during ablation, the nerve could sustain collateral heat damage by conduction. Newer laser wave lengths target water as a chromophore and not blood. To that end, endoluminal temperatures are lower and collateral damage are significantly reduced. We present techniques to address pathologic perforator veins of the lower extremities using a 980nm diode laser.

Primarily endovenous ablation is completed to the greater and lesser saphenous circuits as clinically indicated. Then the pathologic perforator veins are addressed during the same intervention.

Ultrasound guidance is mandatory; requiring steady hands of the ultrasonographer and the endovascular physician. Single hand access approach is nearly impossible. The perforator veins are marked at the surface with permanent skin markers. The entire extremity is prepped and draped.
Venous reflux in the greater saphenous and lesser saphenous vein circuits are addressed by ablation.

Many times the pathologic perforator veins will go into a state of venous spasm due to intervention in the greater or lesser saphenous circuits. Two percent Nitropaste is placed topically over the individual perforator vein and is usefully to avoid obstacles by procedure venospasm. Using a 7-10 Mhz linear array ultrasound transducer, the pathologic perforator vein is again imaged according to previous skin marks. The needle access can be longitudinal with the vessel wall or semi-transverse using a modified Seldinger technique.

Seldinger technique describes vessel access as a through and through vessel wall approach. Diseased perforator veins under pressure over time develop arterialized thickened walls. Thus, venopuncture can be difficult. Once aligned by ultrasound, a thrusting technique is used to quickly puncture the wall of the vein, limiting vein roll. Access is completed with a 16g Angiocatheter with a retractable safety needle. The angiocatheter needle has a convenient window to identify venous blood return upon entering the vein.

 
Access of the vessels with micro access kits have been tried with attempts at sheath exchange to accommodate the 600 micron laser fiber. Often times the sheath will not advance unless the micro access wire can be secured sufficiently into the perforator vein below the fascial junction. This is not always possible with short tortuous perforator veins.

Needle access of perforator veins is usually a one shot deal. If the vein is not accessed on the first attempt, one will likely not get a second attempt due to venospasm and or hematoma at the site. A longitudinal approach is preferred; but, many times access by the longitudinal route is not possible due to the vessel position and topography of the surface of the limb. If the modified Seldinger technique is used, vein access is obtained with the vein in an obtuse fashion to allow more contact of the laser fiber with the intima of the vessel wall.

The laser fiber is extended to the fascial junction and the angiocatheter is then pulled back 2-3cm. Once the laser fiber is in place, either in the vessel lumen or in the juxtapose position (through and through the vessel wall), tumescent anesthetic solutions are infiltrated using ultrasound guidance. Ultrasound images are maintained on the laser fiber without movement from this stable view. This is important as the tumescent solution will distort the topography. Enough tumescent solution is routinely placed to allow for a 1cm heat sink in all directions from the laser fiber. Laser ablation is completed in two different formats depending on the position of the laser fiber.

If the laser fiber is within the vessel wall for a significant longitudinal distance; laser ablation is completed with the fiber stationary at 9-10 watts continuous wave delivering 100j of energy using the 980nm diode laser. Steam bubbles are evident at the site of ablation with extension proximal and distal to the laser tip.

Slowly the tip is pulled back 1mm per second producing an estimated 50j per centimeter of vessel treated. If the laser fiber is in the juxtaposed position to the vessel wall; laser ablation is completed at 9-10 watts continuous wave with the fiber actively being pulled back 1mm per second until steam bubbles are evident in the lumen of the vein. Again, steam bubbles are evident at the site of ablation with extension proximal and distal to the laser tip by ultrasound review.  

Once the fiber has attained an intraluminal position, it is held stationary to deliver 100j of energy using the 980nm diode laser at 9 -10 watts continuous wave to the site.

Slowly the tip is pulled back 1mm per second producing an estimated 50j per centimeter of vessel treated. Average ablation energy delivered to pathologic perforator veins is approximately 300j of energy by the 980nm laser. The laser ablation is continued until the fiber exits the vein wall. Fiber exit of the vein wall is usually evident by ultrasound view of a sudden sap of the vessel wall as the active fiber tends to stick to the vein wall by coagulation. Once the fiber has exited the vein wall, laser excitation is ceased and the laser fiber removed.

Routinely, patients are asked to notify for any sensation of burning or stinging sensations with radicular patterns down the extremity. If sensations are noted, additional tumescent solutions are infiltrated or the laser fiber is pulled back 1-2mm and laser ablation tested again for sensations. Immediate thrombosis of the target vein is usually noted by ultrasound review during the laser ablation. Small associated reticular veins 1-4mm can be addressed by ultrasound guided foam sclerotherapy using sclerant solutions.

Advanced Surgical Concepts vein center in Chattanooga,Tenn., has utilized these perforator techniques using the 980nm diode laser since January. Approximately 900 pathologic perforator vein ablations have been completed. Of the 900, 400 perforator veins have been followed by ultrasound review for more than 6 months. Two perforator veins were noted to recanulize of the 400 reviewed for more than 6 months.

Complications included: three of 400 reported paraesthesias at or below the perforator ablation site. These paraesthesias were self limiting and resolved within 6 weeks of the ablation procedure. One skin entrance burn was sustained and identified at the initial procedure. This burn was addressed with immediate elliptical skin excision and layered skin closure at the site. The site healed without incident with excellent cosmetic effect. Multiple patients with chronic venous stasis ulcerations have been treated by these techniques, many of whom have already had endovenous ablation techniques or surgical vein stripping of the greater saphenous/lesser saphenous circuits years prior.

In our experience, patients with venous ulcers almost always have perforator reflux and can be screened by clinical and verified by an ultrasound and duplex venous study. Minimally invasive laser ablation techniques can accomplish laser ligation of these perforators to help heal stasis ulcers and aid in the reduction of superficial venous hypertension.

It has been estimated that in patients who develop chronic venous insufficiency, 4 percent will progress to develop venous stasis ulcers. That is a high number, signifying that one in 25 people who have chronic venous insufficiency will develop these venous stasis ulcers due to venous reflux related to pathologic perforator veins independent of the greater saphenous or lesser saphenous vein circuits.

James E. White, MD, FACS, is the owner of Advanced Surgical Concepts of Chattanooga, Tenn.