[Music] good afternoon I'm Philip bendick uh from William Bowmont Hospital technical director and director of surgical research in the peripheral vascular laboratory there and we'll be talking to you this afternoon about chronic Venus insufficiency good afternoon this afternoon we're going to be talking about the lower extremity Venus duplex ultrasound Examination for chronic Venus insufficiency people are well aware of the problems of acute Venus disease the Deep Venus thrombosis problem and the risk of pulmonary embolism and that is actually the clinical problem that gets a lot of the glitz Glamour and color attention but it is not really the big picture of Venus disease and one should always keep in mind the large picture of Venus disease brought about by chronic changes associated with acute episodes of thrombolites and other chronic changes in the Venus system this big picture is is the one that affects many people in the United States today if you look at prevalence of vascular diseases when you talk about cored atherosclerotic disease there are approximately 3 million Americans running around with clinically significant disease if you talk about Peripheral arterial disease in the lower extremities there are 5 million plus Americans with that particular problem coronary artery disease the number one killer of people in this country the leading cause of death there are approximately 12 million adults with this problem but if you look at Chronic Venus insufficiency there are roughly 25 million adults in the United States with this problem today again those are predominantly patients that have varicose veins but a significant percentage have edema in the lower extremities that may limit lifestyle and activities again about 10% of these patients have permanent skin changes and dermal changes associated with The Chronic Venus insufficiency and a small fraction of these have active Venus stasis ulceration secondary to their chronic Venus disease so medically this is obviously a very large problem and economically it's an expensive problem it is not however a new problem the ancient Greeks even recognize this in their statuary as you can see here but it all comes down to the very fundamental principle that these changes directly result from elevated pressures within the Venus system in a chronic sense or so-called chronic ambulatory Venus hypertension this is what it looks like the patient with varicose veins in today's age and you can sum all this up very succinctly by simply saying man made a big mistake when he stood up because that is what puts the excessive pressure on the peripheral Venus system if you look at pressures within the Venus system when we are Suppy they're very very low by going through the arterials and the capillary bed there's a significant pressure drop so typically throughout the Venus system in the body when a patient is sepine there about 5 to 10 mm of mercury and the veins are pretty much collapsed under these very low pressures and behave very well however when we stand up we can Elevate the pressure at the level of the ankles very quickly to as much as 100 millimeters of mercury or more because of the gravitational and hydrostatic pressures that are exerted on the Venus system and under those pressures chronically the veins become very dilated there is leakage throughout the endothelial lining in the the walls of the veins into the surrounding tissue and it is then that these chronic changes build up particularly at the ankle regions and in in the lower extremities where we see the significant physical findings and a lot of the symptoms present related to Chronic Venus insufficiency so it is the are these chronically elevated pressures that lead to many of the problems normally in the Venus system the hemodynamic uh responses are basically slow nothing happens quickly in the Venus system there is evidence of resting spontaneous pressure they are low velocities and they change slowly with the respiratory cycle when you inhale slows flow down flows slow down when you exhale then flows will speed up again and in response to the changing abdominal pressures and extrinsic compression of the inferior vena so you see on inspiration the velocities in the Venus system and the femoral vein as shown here slow down significantly and when the patient exhales the flow speeds up again in response resp to those changes in intraabdominal pressure we can also augment flow with manual compression of the limb in this case you see in the femoral vein the normal resting spontaneous flow very early on in the cycle that you see right here and then with manual compression of the calf there's enhanced Venus emptying through the Deep veins which shows this augmentation response and when you release that manual compression of the calf you go back to restoring normal respiratory change flows in the Venus system so the augmented flow is a significant P component of the Examination for chronic Venus insufficiency clinically the disease can be classified using the ceap classification scheme and this is a great Aid when you're looking at patient populations to make sure when you come up with strategies to treat chronic Venus disease you're talking about the same types of patients the ceap classification is a function of clinical signs the important ones being grades four five and six which relate to permanent changes in the skin the dermal changes and discolorations associated with chronic Venus hypertension and then the skin changes associated with an ulceration whether they are healed or in the active State the ideologic classification for chronic Venus disease is the disease process A congenital one are there primary varicose veins or is the Venus disease secondary to some other underlying problem for example a previous episode of deep vein thrombosis anatomically we are interested in whether the Deep superficial and or perforator Venus systems are involved either alone or in combination and pathophysiologically are we worried about obstruction reflux flows or both in some circumstances there's also a Venus clinical severity score which will assign a new grade to the severity of the chronic Venus disease and this is based on allowing points for the various signs and symptoms associated as seen here on the scoring scale this can be found in the literature and is a relatively easy scale to use and keep track of and it allows one to track the clinical progress of the healing of chronic Venus changes particularly in association with ulceration now abnormal hon anemics with chronic ambul at Venus hypertension are primarily related to valvular incompetence normally the valves in the veins are there to allow flow back to the heart but prevent reflux flow back into the lower extremity so when we have chronic ambulatory Venus hypertension this can lead to excess pressure on the veins and dilation as pointed out earlier and this will lead ultimately to valvular incompetence and reflux flow creating Venus stasis if you want to objectively assign a grade to valvular closure insufficiency then numerically the textbook answerers show in the primary deep veins of the leg less than one second is a normal valve closure time and the calf veins and great saffin and small sainis veins less than 05 seconds and in the Perforating veins less than approximately a third of a second but as I say those are textbook answers and they only address individual valves not the overall Venus system as a whole whole clinically significant or clinically important valvular incompetence is going to imply that you will see reflux flows for the duration of any augmentation maneuver that you may perform and this is a classic example where you see spontaneous flow in the great sainis vein in this case with a little distal augmentation there's augmented flow back towards the heart but the instant that is released there is sustained reflux flow basically for the duration of that augmentation maneuver in a retrograde fashion in this case in the great saffin vean this would be clinically important reflux flow and you would not need to measure a precise or quantitative valve closure time in this case to know that this was clinically important and this is what you're going to find when testing for Venus insufficiency individual valve closure times will not give you terribly useful information as they address only a single site and you're interested more in systemic insufficiency and what the effects are so we need to evaluate three Venus systems when we look at Venus insufficiency first is the Deep Venus system is there obstruction from a previous episode of thrombol fitis and or is there deep Venus valvular incompetence associated with that in this case you see a femoral vein in the approximately mid thigh just below the femoral artery in this case and with prox with probe compression on the skin you can see complete collapse of that vein indicating the absence of any Venus obstruction on the other hand in this poal vein you see echogenic filling of the Lumen and you see with probe compression at the level of the skin there is no change in the Venus caliber whatsoever indicating a an occlusion of this poal vein clearly an obstructive problem which is going to inhibit Venus emptying and cause elevated Venus pressures in the lower leg in a in a more chronic sense you may see some evidence of recanalization in a small Channel which is open in this case In aaal Vein with a heterogeneous thrombus there indicating a chronic disease process but as you can imagine even if there were at one point a valve at this point in the poal vein the thrombus is going to prevent it from working properly so while there may be Venus emptying through this recanalized channel there will also be reflux flow when the patient stands up and the pressures increase in the lower extremity Venus system similarly in this long axis view of a recanalized Pomo vein you can see the very irregular Channel with evidence of Venus emptying back towards the heart but the minute the patient stands up and gravitational pressure uh exerts itself this flow will be allowed to flow directly back into the lower leg because there is no chance there will be any kind of a competent valve in this portion of the Venus system because of the old thrombotic episode evidenced here you also when doing augmentation Maneuvers in the Venus system will'll look for reflux flow here is a normal poal vein where we see the respiratory variations and then with a augmentation maneuver in the calf we can see that distal augmentation of flow and then an absence of flow as the calf is emptied and there is no evidence of reflux flow down into the calf on the other hand when there is an incompetent in this case clearly evident fibrotic valve in the palal vein from a previous episode of fitis you have an augmentation which augments flow into the poal vein but when released you can see that there is significant reflux flow to the magnitude there is even aliasing in the Doppler signal this all represents reflux flow back down into the calf in a grossly incompetent poal vein so this would be a case of valvular incompetence not associated with any deep Venus obstruction because the vein itself the Lumen is wide open but there's no valve to prevent reflux flow when looking at The Superficial veins we talk about the Great saffin and the small saffin veins and I bring that up because we've had a terminology problem over the over the years but there's been an international consensus conference that hopefully has solved that problem in the United States previous ly we had a greater sainis and a lesser sainis vein the Lesser sainis being the one along the posterior calf in The Superficial system in the United Kingdom for example they had a long saffin vein which is what we call the greater saffin vein and they had a short saffin vean which we called the Lesser saffos vean you can see the problem in the United States we used lsv to refer to lesser saffin fan in the United Kingdom they used lsv to refer to Long saffin fan and and we could never communicate properly with one another so the international consensus conference decided we will now use the terminology of a great sainis vein along the medial th calf and a small saffin vein along the posterior calf abbreviated gsv and SSV the the acronym lsv should no longer exist and it is no longer used when we're properly discussing the superficial Venus system so in The Superficial veins we have a great saffin vein coming off approximately mid common femoral vein running along the medial thigh and the medial calf down to the level of the ankle and along the posterior calf typically emanating from or emptying into the poal vein somewhere in the poal space a small sainis vein and that's the anatomy that we are dealing with at this point the other thing to remember about the saffin Venus systems is they are contained within a fascial sheath there is a fascial plane close to the probe near the skin a superficial and a deep fascial plane the saffin system in this case the great saffos vein is contained within that fascial sheath if you see a superficial vein such as this small one out here outside of that fascial sheath it is no longer the great saffin vein properly it is a branch of the great safos vean and it is very important to identify specifically particularly in cases of primary varicose veins when they're going to be treated are we dealing with a varicose Branch or are we dealing with the great sainis vein itself so we need to pay particular attention to the presence or absence of this fascial sheath that will surround the true sainis vein and the absence of this when we're dealing with Branch vessels likewise the same applies to the small saffin vein along the posterior calf you see the near and far fascial Plaines distinguished from intramuscular branches the gastrus veins which also empty directly into the poao vein but they remain within the muscular compartment the small savus vein very quickly becomes a superficial vein again constrained by that fascial sheath here we are interested in not only obstruction and valvular competence or incompetence but the presence of these varicosities and Associated branches as they can contribute to significant Venus in efficiency this also brings up the concept and the importance of the calf muscle pump when the calf muscles contract and for example as when we take a step the muscles bulge they will put extrinsic pressure on the Venus system and cause emptying is basically an inherent augmentation maneuver and increase flow back towards the heart when the calf muscle relaxes and the extrinsic pressure on the veins is removed normally the valves and the veins will prevent reflx flow from occurring down into the calf and you'll have then refilling of these veins which when the calf muscle contracts again will cause augmented flow back towards the heart in a nice rhythmic fashion when a patient is ambulating what this means in terms of pressures is pressure relief on the Deep veins in the lower leg particularly we will see with a calf muscle contraction we will have augmented flow into the deep Venus system back to WS the heart and with competent valves there can be no reflux flow so with in a matter of taking just a few short steps one can reduce pressures in the Venus system at the ankle from as much as 100 millimet Mercury to less than 20 Millers Mercury without any difficulty whatsoever and this large drop in so-called ambulatory Venus pressure abbreviated AVP here will restore basically normal pressures or pressure within the Venus system that it can easily tolerate and withstand so the calf muscle pump is a very important functional system that allows us to prevent ambulatory Venus hypertension so think of walking as a good thing and the exercise in the face of a normal calf muscle pump will enhance Venus emptying and inhibit The Chronic ambulatory Venus hypertension that sometimes can develop when we have primary varicose veins this all changes now the calf muscle pump may still work but we may have these superficial veins that become very tortuous and look like small ropes underneath the skin with flow going in all possible directions obviously or in this three-dimensional representation you can see the tortuous path that these varicose veins ultimately do take and when you look at a patient's leg you see the same thing as they are directly under the skin the problem with primary varicose veins is when we ambulate the C muscle pump can still do its job emptying into the deep system but the superficial Venus insufficiency allows reflux flows to come right back down and through our Perforating veins very quickly refill the calf compartment that means as we're ambulating instead of an 80% decrease in ambulatory Venus pressure in the presence of primary varicose veins we may only decrease our Venus ankle pressure from 100 Mill 100 millim Mercury to 50 50 mm Mercury or so this is an elevation and pressure that will keep the veins dilated eventually there may be some breakdown and development of chronic edema and some tissue changes and ultimately possibly ulceration at the level of the ankle in these patients simply because we cannot when we're ambulating decrease our Venus pressure enough to prevent those chronic changes from occurring what we look at with duplex ultrasound is evidence of normal resting flow in a sainis vein but now when we compress proximately above the vein we are able to force reflux flow back down into the calf past incompetent valvular sites when we release that proximal compression we then get augmented flow but again we see the reflx flow recurring very quickly so we have evidence by duplex ultrasound of systemic valvular incompetence in the great saffin system in this particular case which will then lead to that ambulatory Venus hypertension and the changes associated with chronic Venus insufficiency the same applies to any branches we might see off the sainis vein this is a large varicose Branch coming over the anal lateral aspect of the left thigh and again you can see with proximal compression above the sight of Doppler interrogation that sustained reflex flow for as long as you're willing to use that augmentation maneuver and inducing refle flux flow in that vein again indicating the incompetence in that particular large varicosity in this case a branch vein off the great safis not the great saffin vein itself now historically actually varicosities have a little bit of an an interesting background uh it started in from the Latin terminology for Twisted and swollen vein thanks thanks to hypocrates approximately 2500 years ago uh we still see those terms today and what better definition of a varicose vein than a twist twisted and swollen vascular system Galen who is well known in medical circles too about 1,800 years ago actually was recommended the first vein stripping when he said that these varicosities should just be torn out by the use of a Sharp hook which sounds somewhat brutal but that's what a vein stripping is even today under it's just done under more sterile surgical conditions aunita about 1500 years ago actually described the ligation and excision of these varicose veins again a direct surgical approach somewhat more civilized than what Galen proposed with just a sharp hook and it wasn't until about 500 years ago that Ambrose paray actually noted the association of ulceration with these varicose veins and made that Association of chronic Venus changes associated with large varicosities this is just an old European procedure called the renli procedure uh for treating lower leg varicose veins and basically just by making a cork screw like incision was able to exclude the varicose veins completely from the rest of the circulation though obviously this this left a large very unsightly scar in treating this problem of primary varicose veins we do a much better job with the various a oblation techniques be they radio frequency or laser ablation and also some ultrasound guided sclerotherapy techniques with foam agents which are used to ablate superficial varicosities as well so again a little bit more civilized treatment of the problem but it does remain a significant problem uh that we have to deal with and you can see the difference between simple oblation of the great saffos vein shown here just at the site of the saffo femoral Junction at the level of the groin versus this old procedure as say which left a rather nasty looking scar in the lower leg the third consideration for chronic Venus disease are those not primary but secondary varicose vein particularly in patients who have what we call the Post thrombotic syndrome they have had an episode of previous deep vein thrombosis and now the residual effects of that are felt either because there is chronic obstruction in the Deep Venus system or there is valvular incompetence because of the previous thrombosis in the Deep Venus system or worst case scenario both exist It's a combination of insufficiency and obstruction these are patients who very frequently have significant stasis changes and which often times lead to ulceration in the lower leg and this is that classic Venus stasis ulcer it's a very superficial type of ulceration it's a very wet weepy wound very difficult to heal because of the chronic skin changes surrounding the site of ulceration that are frequently seen and there's very poor circulation and oxygenation to the tissue at the site of a venostasis ulcer which makes healing of that wound significant clinical challenge the problem here again goes back to that we saw with the calf muscle pump if you look at the function of the calf muscle pump in light of either for example a poal occlusion or combination occlusion and reflux flow when the calf muscle contracts in the case of obstruction the only source of emptying is out through the perforator veins into the superficial system both of these very quickly dilate and become incompetent so the calf muscle contract you get Venus emptying when the calf muscle relaxes you get Venus refilling through the same route so you end up basically with a two and fro flow from the calf and no significant Venus emptying towards the heart when in fact a patient ambulates and walks aggressively over a period of time this actually will increase arterial inflow into the calf and you can see a small increase in ambulatory Venus pressure in cases like this not any decrease at all so you would go from 100 millim Mercury to 110 mm Mercury when you're ambulating in a case like this which will simply make matters worse as you've now increased the the presence of Venus hypertension in this particular system when we talk then about the post thrombotic patient particularly or secondary Venus insufficiency obviously then the Perforating veins become an important player so we have to look at them very carefully as well when we're considering chronic Venus insufficiency the primary Perforating veins of Interest are the so-called cocket Group which are just above the mediom malus in the lower leg in that so-called Gator Zone in the lower leg important perforators also are boy's perforator in the upper calf and Dodge perforator at approximately the level of the adductor Hiatus in the lower medial thigh but hemodynamically typically the important perforator veins are the cocket perforators as they're is where you will see the chronic Venus changes and potential ulceration Dr cockett started all this approximately 50 years ago when he very he wrote the paper very aptly titled the ankle blowout syndrome because he was able to associate incompetent perforators and the Jets of flow with calf muscle contraction impinging on the skin and basically causing a blowout tight syndrome which led to degradation of the skin and ultimate ulceration particularly in this Gator Zone as shown here the problem in chronic Venus insufficiency in cases like this is a combination of the gravitational reflex we saw with primary varicose veins as well as failed perforator valves normally these perforator veins tend to be fairly small you don't see them on a normal resting Venus examination as a rule and they all have valves which are designed to allow Venus emptying from The Superficial into the deep system when these valves break down and you have perforator valvular incompetence that allows flow from the deep out into the superficial system and this is what leads to The Chronic problems in the post thrombotic syndrome and ulceration with color Doppler it's easy to identify you see the Deep system you see The Superficial system and colorcoded red which means in this case flow is towards the probe or from the deep into the superficial system you're able to readily identify incompetence of the perforator vein and breakdown of the valve that's normally present there is some debate still ongoing about the importance of perforator vein incompetence uh in the mid 1980s a couple well-noted clinicians in the United Kingdom both wrote papers about the clinical importance one claiming they were very important and Dr Bernard saying they really had no clinical importance so that controversy actually is still ongoing the debate still rages and it really Bec comes a function of individualizing each patient and looking at the underlying cause of their chronic Venus insufficiency and what are the clinical changes associated with that duplex ultrasound is an excellent means of identifying the location of Perforating veins we can measure their Lumen diameter or caliber and we can readily assess with color doler Imaging their valvular competence it is interesting to note a number of Studies have shown know that if you look at primary varicose veins in these patients with chronic Venus insufficiency approximately 20% of the limbs in these patients do in fact have incompetent Perforating veins if you look at the Lumen size it can give you insight into whether or not the valve is going to be competent pretty much any Perforating vein that is less than 2 millimet in Lumen diameter is going to be competent and anything greater than three and a half millimeters is probably going to be incompetent between 2 and 3.5 mm in Lumen diameter is the transition zone but with color Doppler Imaging these are large enough to readily identify and establish valvular competence with simple augmentation maneuvers of the calf this is an example of a very large dilated Perforating Vein The Deep Venus system The Superficial system measuring the Lumen diameter where it crosses the fascial plane this is where the valve normally exists and looking at the diameter at that point point you can classify it fairly readily just based on anatomic considerations into likely competent likely incompetent or transition region using Color Doppler Imaging it's a very easy way to determine the competence of these by just Imaging the Perforating vein turning color Doppler on using your standard color coding blue being away from the probe red back towards and then by simply simultaneously while Imaging in color Doppler squeezing the calf to augment flow look for the presence of reflux flow in that Perforating vein and if you do see it you then identify that as an incompetent Perforating vein such as shown here again the example going from the deep system flow going out to The Superficial system and at the level of the fascial plane here that valve has become incompetent allowing that reflux flow you can do document the same thing with spectral Doppler Imaging and spectral Doppler displays if you like but it is complicated because you're using two hands for this maneuver you have to keep everything very stable color doler is perfectly adequate and sensitive documentation for the presence or absence of perforator vein incompetence so why do Perforating veins become incompetent in the first place there are two theories that have been proposed out there the first one is because of calf muscle contraction you get that increased pressure on the Deep Venus system which dilates the Perforating veins at which point they become in incompetent uh you could call that sort of the Tigger syndrome if you like because of the increase deep calf pressures in invoked by the contraction of that calf muscle the second theory is because there is incompetence in the saffin system there is a pressure Overload at their entry point through Perforating veins into the deep system and it is this chronic pressure overload that leads to Perforating vein in com competence well there are two theories both sound fairly likely and possible what we do know is that Perforating vein incompetence is pretty much always associated with superficial Venus insufficiency it is extremely rare to find a per an incompetent Perforating vein isolated without any evidence of any saffin superficial Venus insufficiency so when you see something like this great saffos insufficiency it would not be surprising to find an incompetent Perforating vein if the great saffin system were in fact competent throughout it would be very surprising at that point to find an incompetent Perforating vein we've also learned through Natural History studies and serial duplex ultrasound evaluations that Perforating veins tend to develop in two ways one is in a descending manner as you get great saffin vein proceeding or propagating down the leg at some re-entry point where the saffos re-enters through a Perforating vein into the deep system if the superficial Venus incompetence is ascending in the saffos vein and going up the leg in some manner you then tend to find incompetent Perforating veins at the extension the proximal extension of that superficial Venus insufficiency we also have discovered through surgical trials and other and followup studies that if in many cases particularly primary varicose veins if you treat the saffin vein insufficiency this significantly decreases es the number of Limbs who do in fact then have after surgery incompetent Perforating veins and these are just a few of the the series using large numbers of patients that have shown a significant reduction in the percentage of Limbs pre-operative versus post postoperative versus preoperative in the percentage of Limbs with incompetent perforator Venus involvement so treating the great saffos insufficiency also in many cases effectively treats perforator Venus insufficiency so what we have surmised from this basically is that theory 2 seems to hold the most weight that incompetent Perforating veins appear to be secondary to saffin Venus incompetence and a result of that saffin insufficiency there is that final group of post thrombotic patients who develop ulceration however that do deserve a little bit of special consideration if you look at Venus ulceration and stasis ulceration about 50% of these patients have their ulceration related to primary varicose veins which may have Associated incompetent perforator veins but as mentioned earlier if you look at the ceap classifications the clinically important ones grades four through six perforator incompetence alone is an extremely rare finding and again if you treat the V the venostasis ulceration whether you do it surgically or with compression therapy you're able to achieve good healing of the ulcer both at 12 months and at 36 months but again surgical correction which does tend to decrease the number of perforators involved has a much lower Venus stasis recurrence rate and looking at 15 versus 34% recurrence rate then compression therapy which did nothing to treat the underlying perforator veins so again we can say that incompetent Perforating veins certainly appear to be secondary to saphenous Venus incompetence and they probably play a minimal role in the Venus ulceration in patients with primary Venus insufficiency since fixing the saffos veins takes care of many of the Perforating veins if you do not fix the saffin system you do get multiple recurrence of ulcerations that again leads us however to the postthrombotic patient a patient who may have chronic Venus obstruction in the Deep Venus system or may have recanalization and then chronic Venus reflux in the Deep Venus system with a with or without a small component of obstruction and if you look at the natural history of Venus ulceration particularly you will see that if the Deep Venus system is normal you have primary varicose veins you treat the Venus ulcer appropriately and treat The Superficial Venus system you have a very low recurrence rate of ulcers in the post thrombotic patient where you cannot directly treat the Venus system you have a much higher recurrence rate of Venus ulceration likewise primary incompetence versus post thrombotic incompetence looking at the recurrence of Venus ulceration after treatment of Just The Superficial and perforator systems a much higher recurrence rate in the post thrombotic group hypothetically the reason for this is if you look at the presence of a dilated incompetent Perforating vein in the presence of Venus is ulceration approximately 70% of these venostasis ulcers will be directly associated with an underlying incompetent Perforating vein so if you just treat the saffin system and do not treat this underline source of pressure you are unable basically to treat the Deep Venus system the obstruction is going to remain chronically so as the calf muscle pump then works even after treatment and obliteration of the saffin system you have not treated the perfect ating veins so you still have that blowout effect that cockett described almost 50 years ago which will lead to recurrence of skin breakdown and recurrent Venus ulceration so what can we conclude from all of this well first and foremost duplex ultrasound provides an excellent means of documenting the patterns of Venus insufficiency whether it involved the Deep system The Superficial saffin systems and or the perforator Venus systems alone or or in combinations we can also conclude that if we treat the sainis Venus system in patients with primary vericose veins that plays a large role in the prevention of Venus stasis ulcer recurrence and we also know that by treating the saffin system in these patients we will effectively treat a number of incompetent Associated perforator veins in treat treatment however of incompetent perforans alone has shown to have very little effect on the healing or recurrence of Venus ulceration they do not appear to be the primary source of the problem it may be however important to treat Associated incompetent Perforating veins directly in those patients who have venostasis ulceration in patients with the postthrombotic syndrome so that one can prevent the occurrence of this so-called blowout syndrome described by cockett so long ago and help prevent the recurrence of ulcer this is not level one evidence this is hypothetical at this point but in patients that are where the superficial and perforator veins are treated directly in patients with postthrombotic disease this has been effective in preventing the recurrence of many Venus ulcerations thank you for your time and attention