Lower Extremity Venous Duplex Ultrasound: Chronic Venous Insufficiency - SD

Introduction to Chronic Venous Insufficiency

Good afternoon.
I'm Philip Bendick from William Beaumont 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 venous insufficiency.

Good afternoon. This afternoon we're gonna be talking about the lower extremity venous duplex ultrasound examination for chronic venous insufficiency.
People are well aware of the problems of acute venous disease, the deep venous thrombosis problem and the risk of pulmonary embolism, and that is actually the clinical problem that gets a lot of the glitz, glamor and colorful attention.
But it is not really the big picture of venous disease and one should always keep in mind the large picture of venous disease brought about by chronic changes associated with acute episodes of thrombophlebitis and other chronic changes in the venous system.
This big picture is the one that affects many people in the United States today.

Prevalence of Chronic Venous Insufficiency

If you look at prevalence of vascular diseases, when you talk about carotid 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 venous 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 venous insufficiency and a small fraction of these have active venous stasis ulceration secondary to their chronic venous 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.

Pathophysiology: Chronic Ambulatory Venous Hypertension

But it all comes down to the very fundamental principle that these changes directly result from elevated pressures within the venous system in a chronic sense or so-called chronic ambulatory venous 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 venous system.

If you look at pressures within the venous system when we are supine, they're very, very low.
By going through the arterials and the capillary bed, there's a significant pressure drop.
So typically throughout the venous system in the body, when the patient is supine, they're about five to 10 millimeters 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 a hundred millimeters of mercury or more because of the gravitational and hydrostatic pressures that are exerted on the venous system.
And under those pressures chronically the veins become very dilated.
There is leakage throughout the endothelial lining in 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 the lower extremities where we see the significant physical findings and a lot of the symptoms present related to chronic venous insufficiency.
So it is these chronically elevated pressures that lead to many of the problems normally in the venous system, the hemodynamic responses are basically slow.
Nothing happens quickly in the venous system.
There is evidence of resting spontaneous pressure, they are low velocities and they change slowly with the respiratory cycle.
When you inhale 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 cava, so you see on inspiration the velocities in the venous system and the femoral vein is shown here, slow down significantly and when the patient exhales, the flow speeds up again in response 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 venous 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 venous system.
So the augmented flow is a significant component of the examination for chronic venous insufficiency.

CEAP Classification for Chronic Venous Disease

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 venous 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 in discolorations associated with chronic venous hypertension and then the skin changes associated with an ulceration, whether they are healed or in the active state.

Etiologic, Anatomic, and Pathophysiologic Classification

The etiologic classification for chronic venous disease, is the disease process a congenital one, are there primary varicose veins or is the venous 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 venous 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 venous clinical severity score which will assign a numeric grade to the severity of the chronic venous 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 venous changes, particularly in association with ulceration.

Abnormal Hemodynamics and Valvular Incompetence

Now, abnormal hemodynamics with chronic ambulatory venous 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 venous 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 venous stasis.
If you want to objectively assign a grade to valvular closure insufficiency, then numerically the textbook answers show in the primary deep veins of the leg less than one second is a normal valve closure time in the calf veins and great saphenous and small saphenous veins less than 0.5 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 venous system as a 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 saphenous 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 saphenous vein, 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 venous insufficiency.
Individual valve closure times will not give you terribly useful information as they address only a single site in your interested more in systemic insufficiency and what the effects are.

Evaluation of the Deep Venous System

So we need to evaluate three venous systems when we look at venous insufficiency.
First is the deep venous system.
Is there obstruction from a previous episode of thrombophlebitis and or is there deep venous valvular incompetence associated with that?
In this case you see a femoral vein in approximately mid thigh just below the femoral artery in this case and with probe compression on the skin, you can see complete collapse of that vein indicating the absence of any venous obstruction.
On the other hand, in this popliteal 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 venous caliber whatsoever indicating a occlusion of this popliteal vein clearly an obstructive problem which is going to inhibit venous emptying and cause elevated venous pressures in the lower leg.
In a more chronic sense, you may see some evidence of recanalization in a small channel which is open in this case in a popliteal 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 popliteal vein, the thrombus is going to prevent it from working properly.
So while there may be venous emptying through this recanalized channel, there will also be reflux flow when the patient stands up in the pressures increase in the lower extremity venous system.
Similarly in this long axis view of a recanalized popliteal vein, you can see the very irregular channel with evidence of venous emptying back towards the heart, but the minute the patient stands up and gravitational pressure 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 venous system because of the old thrombotic episode evidenced here you also doing augmentation maneuvers in the venous system.
We'll look for reflux flow.
Here is a normal popliteal 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 popliteal vein from a previous episode of phlebitis, you have an augmentation which augments flow into the popliteal 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 popliteal vein.
So this would be a case of valvular incompetence not associated with any deep venous 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.

Superficial Venous System

We talk about the great saphenous and the small saphenous veins and I bring that up because we've had a terminology problem over the years, but there's been an international consensus conference that hopefully has solved that problem in the United States.
Previously we had a greater saphenous and a lesser saphenous vein, the lesser saphenous being the one along the posterior calf in the superficial system in the United Kingdom for example, they had a long saphenous vein, which is what we called the greater saphenous vein, and they had a short saphenous vein, which we called the lesser saphenous vein.
You can see the problem in the United States we used LSV to refer to lesser saphenous vein in the United Kingdom.
They used LSV to refer to long saphenous vein and we could never communicate properly with one another.
So the International Consensus Conference decided we will now use the terminology of a great saphenous vein along the medial thigh calf and a small saphenous vein along the posterior calf abbreviated GSV and SSV the acronym LSV should no longer exist and it is no longer used when we're properly discussing the superficial venous system.

So in the superficial veins we have a great saphenous 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 popliteal vein somewhere in the popliteal space, a small saphenous vein and that's the anatomy that we are dealing with at this point.
The other thing to remember about the saphenous venous 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 saphenous system in this case, the great saphenous 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 saphenous vein properly.
It is a branch of the great saphenous vein 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 saphenous vein itself?
So we need to pay particular attention to the presence or absence of this fascial sheath that will surround the true saphenous vein and the absence of this when we're dealing with branch vessels.
Likewise, the same applies to the small saphenous vein along the posterior calf.
You see the near and far fascial planes distinguished from intramuscular branches, the gastrocnemius veins which also empty directly into the popliteal vein, but they remain within the muscular compartment.
The small saphenous 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 venous insufficiency.

The Calf Muscle Pump and Its Role

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 venous system and cause emptying.
It's 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 in the veins will prevent reflux 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 venous system back towards 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 venous system at the ankle from as much as a hundred millimeters mercury to less than 20 millimeters mercury without any difficulty whatsoever.
And this large drop in so-called ambulatory venous pressure abbreviated AVP here, will restore basically normal pressures or pressures within the venous 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 venous hypertension.
So think of walking as a good thing and the exercise in the face of a normal calf muscle pump will enhance venous emptying and inhibit the chronic ambulatory venous hypertension that sometimes can develop

Primary Varicose Veins and Their Impact

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're directly under the skin.
The problem with primary varicose veins is when we ambulate the calf muscle pump can still do its job emptying into the deep system, but the superficial venous 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 venous pressure in the presence of primary varicose veins, we may only decrease our venous ankle pressure from a hundred millimeters mercury to 50 millimeters mercury or so.
This is an elevation in pressure that will keep the veins dilated.
Eventually there may be some breakdown in 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 venous pressure enough to prevent those chronic changes from occurring.
What we look at with duplex ultrasound is evidence of normal resting flow in a saphenous vein, but now when we compress proximally above the vein, we are able to force reflux flow back down into the calf passed incompetent valvular sites.
When we release that proximal compression, we then get augmented flow, but again, we see the reflux flow recurring very quickly.
So we have evidence by duplex ultrasound of systemic valvular incompetence in the great saphenous system in this particular case, which will then lead to that ambulatory venous hypertension and the changes associated with chronic venous insufficiency.
The same applies to any branches we might see off the saphenous vein.
This is a large varicose branch coming over the anterolateral aspect of the left thigh and again, you can see with proximal compression above the site of Doppler interrogation that sustained reflux flow for as long as you're willing to use that augmentation maneuver and inducing reflux flow in that vein again indicating the incompetence in that particular large varicosity.
In this case a branch vein off the great saphenous, not the great saphenous vein itself.

Historical Background of Varicose Veins

Now historically actually varicosities have a little bit of an interesting background.
It started in from the Latin terminology for twisted and swollen vein.
Thanks to Hippocrates approximately 2,500 years ago.
We still see those terms today and what better definition of a varicose vein than a twisted and swollen vascular system.
Galen, who's well known in medical circles too about 1800 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.
Anita, 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 pare actually noted the association of ulceration with these varicose veins and made that association of chronic venous changes associated with large varicosities.
This is just an old European procedure called the Rindfleisch procedure, for treating lower leg varicose veins and basically just by making a corkscrew like incision was able to exclude the varicose veins completely from the rest of the circulation.
Though obviously this left a large very unsightly scar in treating this problem of primary varicose veins.
We do a much better job with the various ablation 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, that we have to deal with and you can see the difference between simple ablation of the great saphenous vein shown here just at the site of the saphenofemoral junction at the level of the groin versus this old procedure as say, which left a rather nasty looking scar in the lower leg.

Secondary Varicose Veins and Post-Thrombotic Syndrome

The third consideration for chronic venous disease are those not primary but secondary varicose veins, 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 venous system or there is valvular incompetence because of the previous thrombosis in the deep venous 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 oftentimes lead to ulceration in the lower leg.
And this is that classic venous 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 venous stasis ulcer, which makes healing of that wound a 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 popliteal 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 contracts you get venous emptying when the calf muscle relaxes, you get venous refilling through the same route.
So you end up basically with a two and fro flow from the calf and no significant venous 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 venous pressure in cases like this, not any decrease at all.
So you would go from a hundred millimeters mercury to 110 millimeters mercury when you're ambulating in a case like this, which will simply make matters worse as you've now increased the presence of venous hypertension in this particular system.
When we talk then about the thrombotic patient particularly or secondary venous 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 venous insufficiency.

Perforating Veins in Chronic Venous Insufficiency

The primary perforating veins of interest are the so-called cockett group, which are just above the medial malleolus in the lower leg in that so-called gaiter zone in the lower leg.
Important perforators also are Boyd's perforator in the upper calf and Dodd's perforator at approximately the level of the adductor hiatus in the lower medial thigh.
But hemodynamically typically the important perforator veins are the cockett's perforators as there is where you will see the chronic venous changes and potential ulceration.
Dr. Cockett started all this approximately 50 years ago when 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 type syndrome which led to degradation of the skin and ultimate ulceration, particularly in this gaiter zone as shown here.
The problem in chronic venous insufficiency in cases like this is a combination of the gravitational reflux 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 venous examination as a rule, and they all have valves which are designed to allow venous 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 color coded 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.
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. Burnand saying they really had no clinical importance.
That controversy actually is still ongoing.
The debate still rages and it really becomes a function of individualizing each patient and looking at the underlying cause of their chronic venous 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 doppler imaging their valvular competence.
It is interesting to note a number of studies have shown that if you look at primary varicose veins in these patients with chronic venous 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 two millimeters in lumen diameter is going to be competent and anything greater than three and a half millimeters is probably going to be incompetent between two and 3.5 millimeters.
In lumen diameter is the transition zone, but with color doppler imaging, these are large enough to readily identify and established valvular competence with simple augmentation maneuvers of the calf.
This is an example of a very large dilated perforating vein, the deep venous 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, 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 coating blue being away from the probe red back towards, and then by simply simultaneously while imaging and 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 doppler is perfectly adequate and sensitive documentation for the presence or absence of perforator vein incompetence.

Theories on Perforator 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 venous system which dilates the perforating veins at which point they become incompetent.
You could call that sort of the Tigger syndrome if you like, because of the increased deep calf pressures invoked by the contraction of that calf muscle.
The second theory is because there is incompetence in the saphenous 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 incompetence.
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 venous insufficiency.
It is extremely rare to find a incompetent perforating vein isolated without any evidence of any saphenous superficial venous insufficiency.
So when you see something like this great saphenous insufficiency, it would not be surprising to find an incompetent perforating vein.
The great saphenous 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 in serial duplex ultrasound evaluations that perforating veins tend to develop in two ways.
One is in a descending manner as you get great saphenous vein proceeding or propagating down the leg at some reentry point where the saphenous reenters through a perforating vein into the deep system.
If the superficial venous incompetence is ascending in the saphenous 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 venous insufficiency.
We also have discovered through surgical trials and other and follow up studies that if in many cases it particularly primary varicose veins, if you treat the saphenous vein insufficiency, this significantly decreases the number of limbs who do in fact then have after surgery incompetent perforating veins.
And these are just a few of the series using large numbers of patients that have shown a significant reduction in the percentage of limbs, preoperative versus postoperative versus preoperative in the percentage of limbs with incompetent perforator venous involvement.
So treating the great saphenous insufficiency also in many cases effectively treats perforator venous insufficiency.
So what we have surmised from this basically is that theory two seems to hold the most weight that incompetent perforating veins appear to be secondary to saphenous venous incompetence and a result of that saphenous insufficiency.

Perforators in Post-Thrombotic Ulceration

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 venous 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 one's, grades four through six, perforator incompetence alone is an extremely rare finding.
And again, if you treat the venous stasis 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 venous stasis recurrence rate and looking at 15 versus 34% recurrence rate than 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 venous incompetence and they probably play a minimal role in the venous ulceration in patients with primary venous insufficiency.
Since fixing the saphenous veins takes care of many of the perforating veins.
If you do not fix the saphenous system, you do get multiple recurrence of ulcerations.
That again leads us, however, to the post thrombotic patient, a patient who may have chronic venous obstruction in the deep venous system or may have recanalization, and then chronic venous reflux in the deep venous system with a, with or without a small component of obstruction.
And if you look at the natural history of venous ulceration, particularly you will see that if the deep venous system is normal, you have primary varicose veins, you treat the venous ulcer appropriately and treat the superficial venous system, you have a very low recurrence rate of ulcers in the post-thrombotic patient where you cannot directly treat the venous system.
You have a much higher recurrence rate of venous ulceration.
Likewise, primary incompetence versus post-thrombotic incompetence looking at the recurrence of venous 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 venous stasis ulceration, approximately 70% of these venous stasis ulcers will be directly associated with an underlying incompetent perforating vein.
So if you just treat the saphenous system and do not treat this underlying source of pressure, you are unable basically to treat the deep venous system, the obstruction is going to remain chronically.
So as the calf muscle pump then works even after treatment and obliteration of the saphenous system, you have not treated the perforating vein.
So you still have that blowout effect that cockett described almost 50 years ago, which will lead to recurrence of skin breakdown and recurrent venous ulceration.

Conclusions

So what can we conclude from all of this?
Well, first and foremost, duplex ultrasound provides an excellent means of documenting the patterns of venous insufficiency, whether it involved the deep system, the superficial saphenous systems, and or the perforator venous systems alone or in combinations.
We can also conclude that if we treat the saphenous venous system in patients with primary varicose veins, that plays a large role in the prevention of venous stasis ulcer recurrence.
And we also know that by treating the saphenous system in these patients, we will effectively treat a number of incompetent associated perforator veins.
In treatment. However, of incompetent perforating alone has shown to have very little effect on the healing or recurrence of venous 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 venous stasis ulceration in patients with the post-thrombotic 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 post-thrombotic disease, this has been effective in preventing the recurrence of many venous ulcerations.
Thank you for your time and attention.