Vascular Reflux Testing - SD

Introduction

Good afternoon.
I'm Phillip Bendick, the technical director
of the Peripheral Vascular Laboratory at William Beaumont
Hospital in Royal Oak, Michigan, a suburb just
outside Detroit in the southeastern part of the state.
Today I'm gonna be talking
to you about venous reflux testing, the technique
and interpretation of those studies.

Venous Thromboembolic Disease

I'm going to talk about venous reflux testing today,
but with a short introduction on venous thromboembolic
disease because as history has shown,
it is not a trivial problem.
There is a lot of death
and disability caused secondary due to the problem
of acute deep vein thrombosis when it does embolize into the
lungs and disrupt the pulmonary circulation.
And again, it can be a fatal problem. Most definitely.
If you look at the epidemiology of this problem each year,
there are roughly a million venous thromboembolic events
and about 30% of these are fatal,
leaving over 600,000 non-fatal events to contend with.
If you look at this compared
to other commonly thought about diseases,
if you look at heart attacks for example,
there are more venous thromboembolic events than heart
attacks every year, and more venous thromboembolic
events than total strokes that occur each year.
If you look at the mortality statistics, again,
the related deaths from venous thromboembolic disease
exceeds that of myocardial infarction
or heart attacks, as well
as stroke related deaths almost equal in those two
combined in their annual mortality rate.
Another way to look at that is each year,
venous thromboembolic related deaths exceed the population
of the entire state of Alaska.
One way we look at such things in Michigan
and I'm near the Ann Arbor where the University
of Michigan is housed as their football stadium,
which houses or which holds approximately
113,000 spectators.
If you fill that place up for eight home games,
you're talking about approximately the number
of people in the United States who come down
with venous thromboembolic disease every year.
If you eliminate three of those stadium attendances,
you basically account for the number of people
who die related to venous thromboembolic disease every year.
It just gives you a slightly different perspective on the
significance of the disease.
But the other factor that must be considered is the 600,000
plus survivors who then are at risk
for chronic venous insufficiency
or some form of post-thrombotic syndrome,
and that's the group we wish to address primarily today.

Prevalence of Chronic Venous Insufficiency

If you look for example at the annual incidence
and overall prevalence
of common diseases in the United States,
coronary heart disease leads the pack at this point
with a roughly 13 point a half million
peripheral arterial disease, congestive heart failure,
stroke, et cetera.
But venous reflux disease supersedes all
of these dramatically with approximately 25 million people
currently affected in the United States by some form
of chronic venous insufficiency, abbreviated CVI.
Again, deep vein thrombosis is the attention gitter.
It provides the glamor and the glitz in this process
and it's the one that gets people very nervous and worried,
but one should not lose sight of the big picture,
and that is really chronic venous disease as
that involves so many people.
It also is a complex diagnostic problem in
that involves the deep venous system,
the superficial venous system,
and the perforating veins that connect these two systems.
And these can be alone
or in any combination adding more
complexity to the diagnosis.
For this, it comes in a lot of shapes and forms.
If you talk simply about varicose veins,
you're talking roughly 25 million
people in the United States.
Certainly significant clinically significant swelling
affects approximately 6 million.
There are chronic skin changes in a million patients in the
United States and about half
of these have actual skin breakdown
and ulceration during any one year.

CEAP Classification System

The venous disease we're talking about is classified
by the so-called CEAP system where C is the clinical side,
is their pain, edema, ulceration,
varicose, veins, et cetera.
E is the etiology, is it congenital primary or secondary?
A is the anatomic,
is it involved the superficial deep perforator systems
or some combination And P is the pathophysiology.
Is it a problem of reflux disease or venous obstruction
or a combination of these two pathophysiologic phenomenon?
And this then lets us standardize our discussions about
chronic venous insufficiency.

Pathophysiology of Chronic Venous Insufficiency

But if you look at the underlying pathophysiology,
it is all basically a result of
what is called chronic ambulatory venous hypertension.
That is to say when we are upright
and ambulatory, the venous pressure is chronically elevated
to the point that the veins cannot tolerate it any longer
and the stasis changes start to occur.
Another way to think of it is a simple quote from,
I'm not sure whom, but man made a big
mistake when he stood up.
And this is not a new phenomenon.
Venus varicose veins have
been recognized for a long time.
This is an old Greek sculpture over in Athens in one
of the older buildings over there
and the there is actually a saint
for varicose vein Saint Peregrine.

Venous Anatomy

If we look at the venous anatomy,
we have the superficial system right under the skin
and this is primarily the saphenous vein in its some
of its branches and then we have the
saphenous vein in its own compartment
and then we have the deep venous system
and then the connecting veins that go there.
The two superficial systems
of primary interest are the great saphenous vein,
which runs along the medial aspect of the thigh and calf
and the small saphenous vein which runs along the posterior
calf in both legs.
There are a number of important branches
and tributaries, too many to go into a name at this point,
but they do exist and any
of these can become involved in chronic
venous insufficiency.
The perforating veins penetrate the deep fascia
and connect the deep veins to the superficial compartments.
The major perforating veins tend
to be anatomically consistent In in the old formatting there
was cocke group, which were the predominant ones just
above the medial maus
and the, at the level of the ankle,
the so-called gator zone, there are Boyds perforators just
below the level of the knee
and Dodds perforators in the distal thigh near the adductor
hiatus and hunter's canal.
Those were the three primary groups
people used to talk about.
Now they talk about perforators
of the thigh in the new classification system of the knee
and popliteal space, calf
and ankle, anterior, posterior, medial
and lateral to give a more precise definition
of the location of the perforator veins.
And there are complicated maps that you can draw out
of the lower extremities which demonstrate
where these veins occur.
But again, the prominent point
to remember is the important major groups are anatomically
fairly consistent and those are the ones
that if any play a role,
they're the ones most likely to be involved.

Types of Perforating Veins

In terms of the perforating veins, they come in two types.
There is the direct perforating vein, which goes
directly from the superficial system to the deep system,
and then there are the indirect perforating veins which
connect via the saphenous system to the deep venous system.
Normally there are valves at this level
and layer of fascia right in through here,
and the valves in the perforating veins are designed
to only allow flow in a normal setting from the superficial
into the deep system, not
to allow flow out from the deep into the superficial system.
And that's an important consideration
to keep in mind when we return to the hemodynamics
of the perforating veins.
Their size is also a consideration.
This is the deep fascial plane,
this is the deep venous compartment.
Here's the superficial compartment,
and when you measure the diameter of the perforating vein at
that fascial plane, they should be in the neighborhood
of two to two and a half millimeters.
If they were all this large
and this easy to see, they would all be incompetent normally
because they are small and have a limited amount of flow.
Color doppler is the best way to look at them
and we'll return to this point later on in the talk.

Venous Physiology

Venous physiology itself is also interesting.
It is very different obviously from arterial physiology in
that things don't happen very quickly.
There's not a lot of heart rate puls ity,
but there are other variations in venous flow
that one must consider.
Importantly, the way the veins are designed
with their valve structure is they are designed
to allow blood to flow back to the heart,
but if flow tries to go back down the leg, for example,
into the lower leg, the valve closes
and prevents that return or reflux flow into the lower leg.
These valves are very small, delicate, fragile structures,
however, and they can be damaged very easily leading
to chronic venous insufficiency when reflux flow
is allowed distally.
This is a short video clip that shows in real time
a normally functioning venous valve.
You can see it's snap shut when when pressure is increased
in this region trying to force flow back down the leg,
but normally they are open permitting the rapid egress
of flow from the lower extremity back towards the heart.
That's a normal functioning valve as it should appear.

The Calf Muscle Pump

The other important consideration in venous physiology
is the calf muscle pump.
Normally when the calf muscle contracts,
it will constrict the deep veins within the calf compartment
and it will force blood flow dramatically
and forcefully back to the heart.
When the muscles relax
and the veins are no longer compressed, the valves close
and do not allow reflux flow back down into the lower leg,
but the veins then have to fill
through capillary filling in their normal channel,
which is provides a good effort from the calf muscle pump.
If you look at it schematically,
when the calf contracts a few times, you get a large degree
of emptying the valves function properly.
There's no reflux flow
and the actual pressure in the venous system can drop 80
to 90% during that type of ambulation, just taking two
or three steps if you were to stand perfectly still
and upright, normal adult would have approximately a hundred
millimeters mercury pressure at the level of the ankle,
but by just the the motion of taking a few steps,
the calf muscle pump empties that compartment,
it fills up very slowly through the capillary bed.
So during ambulation in a normal venous system,
your pressure at the ankle is roughly in the neighborhood
of 10 to 20 millimeters of mercury instead
of a hundred millimeters of mercury.
And the ankle
and the venous system can tolerate
these pressures very nicely.
So again, ambulation
and walking is a good thing when the calf muscle pump
and the valves are working properly.

Measuring Venous Physiology

Venous physiology can measure all of this.
You quantitatively using some type of plethysmography,
you empty the leg with the patient's supine, stand them up,
and you look at venous filling time
and the amount of flow that it takes to fill the calf.
You then take a emptying, a single emptying maneuver
of the calf to see what the emptying volume is,
and then you can take repetitive emptying maneuvers to see
what the residual volume in the calf is,
and again, then look at venous refilling with the patient
or subject upright.
This gives you a quantitative look physiologically at the
function of the calf muscle pump in the
valves simultaneously.
This has been done historically with photo plethysmography.
This is an example of normal emptying of the calf
and a slow refilling through the capillary bed.
The upper trace shows an abnormal response when you do not
get as good an emptying
and you have a more rapid refilling
of the calf in an abnormal setting indicating valvular
incompetence and some dysfunction of the calf muscle pump.
This test in this day
and age can be somewhat automated through different types
of testing tables
and beds where the patient lies supine for emptying
and then the patient is just tipped upright very quickly.
Computer monitoring of the diameter of the calf
and the volume of the lower leg in terms of venous filling
and capacitance, it can all go wrong,
however very clearly by the number of patients involved
with chronic venous insufficiency out there,
and when it does, we need to make that diagnosis
as accurately as possible.

Diagnosis of Venous Insufficiency

This is a normal vein with the valve open and closed.
If you have a leaky valve,
the valve leaflets cannot close properly
or they have been damaged for some reason.
Then you're going to have reflux flows back down the calf.
And here is where things get complicated in terms
of diagnosis because you have to evaluate
for deep venous insufficiency,
superficial venous involvement, perforator involvement,
obstruction in the venous outflow track
and is the venous calf pump working properly.
All of those things go into a study and they can occur alone
or in any combination.

Patient Examination

The first thing to do when a patient presents
for a possible venous insufficiency test though,
is basically turn on the lights in the examination room,
stand the patient up
to put their veins under gravitational pressure
and look at the legs to see if there are prominent varicose
veins that stand out.
This will be a guideline for where you need
to use your duplex ultrasound system
to actually get a complete and thorough diagnosis,
and it may not just be the site of the great saphenous
or small saphenous vein.
It may be one or more of these tributaries
and branches that we mentioned earlier.
So standing the patient up
and actually physically examining the leg
and using a marker on the leg if you need to
to mark the path of these obvious varicose veins can be
very, very helpful as the examination continues.
The other trick in this is if you're going to test
for venous insufficiency, it's best done later in the day
after the patient has been ambulatory for some time.
We did a study a number of years ago and looked at the size
and the number of perforating veins
that were readily apparent with duplex ultrasound
and found that later in the afternoon we could see on
average two more perforating veins in each calf
with an average diameter approximately half a millimeter
larger than it was at rest early in the day.
So the perforating veins
and the venous insufficiency will be more prominent later in
the day after a day of normal activity,
and that is the best time to do testing for insufficiency.

Patient Positioning and Testing Techniques

Positioning of the patient is also very important.
You need to have them in a relaxed position.
A degree of reverse trendelenberg is often sufficient.
The patient does not often have to stand up
to complete this test, but it should be at least
15 to 20 degrees.
The head of the stretcher raised
that leg in a relaxed externally rotated position.
In the olden days, we used to do a lot of Valsalva maneuvers
as well, but this has been found relatively difficult
to explain to many patients there's a variable amount
of patient effort and that those lead
to very poor reproducibility of Valsalva.
It is much better if you can just have the patient take in a
small breath and hold it
and then use manual compression either proximal
or distal to achieve your augmentation responses
for insufficiency testing.
This type of instruction for the patient,
just taking a breath and hold it is easily understood.
The patient is not required to put much
of any effort into this process
and you get excellent reproducibility
because the operator is now in control of the degree
of augmentation response that they're looking
for in the extremity.
When you do look at venous flows, you want
to establish again distal augmentation, which shows
that there is flow back towards the heart
and then when you release that augmentation,
there is reflux flow indicated flow going back down
towards the lower leg.
This indicates valvular incompetence in this case in the
popliteal vein, in the deep venous system.
Similar testing is done in the saphenous system.
This is the great saphenous vein above the knee,
which again shows distal augmentation
and when that augmentation is released,
there is significant reflux flow down into the lower leg
because of valvular incompetence
also applies when you see those very complex varicose veins
that often occur as tributaries to the saphenous
and again, showing the results
of gravitational forces causing reflux flow throughout.
In this case, an anterolateral branch off the great
saphenous vein in the left lower extremity.

Valve Closure Times

If you think about valve closure times the the data out
there, it very clearly suggests
that in the deep venous system it should take less than one
second to completely close a valve in the calf veins.
In the saphenous venous system,
it should take less than half a second
and in the perforating veins, because they're small
and relatively short,
it should take less than approximately a third of a second.
These are the textbook valve closure times
and any reflux flow measured longer than these times would
be considered indicative of valvular incompetence.
However, if you're talking clinical significance,
basically an incompetent valve is going
to allow persistent reflux flow that basically persists
as long as the augmentation maneuver is maintained.
In a case like this,
you have distal augmentation in this particular vein,
and when you release it, you can see the long extended five
to six second degree of reflux flow indicating severe
and clinically important valvular incompetence in this
particular venous system
or certainly chronic venous insufficiency.
Likewise, in the great saphenous vein,
you can see the extended reflux flow here
with proximal compression
and when that is released,
there's flow back towards the heart, but the to
and fro flow in the venous system indicates
that incompetence,

Impact on Calf Muscle Pump

the calf muscle pump is an interesting
phenomenon when this occurs.
When you have primary varicose veins,
just the saphenous vein is involved,
but the deep system is normal.
The calf muscle pump empties properly,
but the incompetence in the saphenous system allows reflux
flow to come back down into the calf in
more rapid refilling.
So even with ambulation, you only get a 40
to 70% pressure drop.
So in a patient with primary varicose veins,
the ambulatory venous pressure at the level
of the ankle instead of being 10 to 20 millimeters,
mercury is approximately 50 millimeters of mercury.
And this is what leads to a lot
of the chronic venous changes, swelling at the ankle,
changes in skin,
and ultimately in many patients,
outright venous stasis ulceration.
There's an old method of treating this going back
to the European days in the 17th and 18th, 18th
and 19th century called the RIN Flesh Procedure,
which clearly effectively isolates the saphenous vein from
the rest of the circulation,
but we have much better ways to treat this disease now,
which are cosmetically, superior.

Hemodynamic Forces in Venous Disease

I would like to refer back to this quote from Ruckle
who is an investigator in the United Kingdom
when he talks about venous disease
and he says that evidence-based medicine has not been
so far a strong free feature
of phlebological practice in that.
Much of what has been done historically in treating
and managing chronic venous insufficiency
is based on past experience,
but not necessarily on evidence and data.
We do know for certain
that the hemodynamic forces involved are first
gravitational reflux.
When you stand up, gravity wants to push
that fluid back down towards the lower leg.
Ideally the valves prevent that,
but not in all cases when there has been valvular damage.
There are also cases of the perforator valves failing,
allowing reflux flow from the deep system
as you can see in this case out into the superficial system
instead of the proper normal flow
directed flow into the deep system.
So these two factors hemodynamically combine in many cases
in chronic venous insufficiency.

Assessing Perforating Veins

The best way to determine competence
of the perforating veins is using color doppler imaging
with flow augmentation maneuvers
with the legs hanging in some type of dependent position.
Again, this is showing normally directed flow from the
superficial system into the deep system
through this perforating vein here clearly demonstrated
with color doppler.
This is another example of a competent perforating vein
with normally directed flow,
and you can see clearly the difference between a competent
and an incompetent perforating vein
just by the change in color.
Here red indicates flow from the deep system out
through the fascial plane into the superficial compartment
indicating valvular incompetence in
that particular perforating vein.
You can use spectral doppler
to compliment this showing flow into the deep system
and then out into the superficial compartment,
but this is usually not necessary.
The color doppler imaging tells the story very nicely.
The spectral doppler it is can be difficult doing
augmentation maneuvers to maintain position of
that spectral sample volume in exactly the right position.
To get this kind of spectral trace
and I say it is usually not necessary.
The color doppler is certainly adequate.
You will also get a feeling
for whether the perforating vein is going to be competent
or incompetent just
by measuring its size at the fascial plane looking
at its diameter.
If it's less than approximately two millimeters,
there's a extremely high probability that it's competent.
If it's greater than 3.5 millimeters,
an equally high probability that it is incompetent
between two and 3.5 millimeters is the transition zone.
And there the vein does need to be assessed carefully
and looked at with color doppler imaging particularly
to determine the status of the valve function.
Again, this measurement should be taken right at the fascial
plane where the vein goes from the deep into the superficial
compartment right at this level, looking at the diameter
to get some insight as to whether it is competent
or incompetent and then complemented
with color doppler imaging.

Etiology of Perforating Vein Incompetence

One thing we do know based on secondary
to primary varicose veins
that perforator vein incompetence may develop over a very
short period of time.
You may see a patient today
and they do not have an incompetent perforating vein in
three months they might return
and the perforating vein may have developed incompetence in
that very short period of time.
Also, approximately 20% of patients
with chronic venous insufficiency do have incompetent
perforating veins involved
with their primary varicose veins.
It is also strongly associated
with worsening clinical classifications using the CEAP
system, particularly the classification going from
varicose veins to stasis dermal changes to ulceration
as the perforating vein incompetence becomes more
and more involved in this process, whether
or not these failed perforator valves are truly clinically
important is up to debate.
In 1985 in the United Kingdom and a writer came out
and said they were clinically important,
three years later another author came out
and said, no, they're not clinically important,
and the debate is still ongoing today.
They again, remember Ruckle's admonition about
evidence-based medicine and how we do or do not practice it.
So what is the etiology of perforating vein incompetence?
Because that could tell us whether they do have a
significant role In this entire process
of chronic venous insufficiency,
two mechanisms have been proposed
with increased deep venous pressure
during calf muscle contraction, utilization
of the calf muscle pump that increased deep venous pressure,
dilates the perforating veins
and causes them to become incompetent.
The second theory is there is a volume
and pressure overload at the entry point
that is involving the saphenous,
the incompetent saphenous vein, and
because of the incompetence there, the volume and pressure
and the in the superficial compartment overloads,
the perforating veins and causes them to dilate
and become incompetent.
So is it the deep system pressure increase
or is it the superficial VE vessel system pressure increase
that causes that incompetence?
Those are the two theories that have been proposed.
Well, Nicos Lois has done a lot of research in this
and I think has provided us with some very good answers
to to these questions.
The first thing he showed that perforator vein incompetence
was always associated with superficial venous insufficiency,
particularly in the case of primary varicose veins.
So when you see this type of primary varicose veins,
there is going to be perforating vein incompetence
oftentimes associated with that.
He also showed in in some studies
that the perforating vein incompetence tends to develop,
and again, over a short period of time, in many cases,
either in a descending manner at a reentry point
where the per where the saphenous incompetence enters back
the flow enters back into the deep system
or as the superficial venous insufficiency extends
proximally in an ascending manner following that extension
of the saphenous insufficiency.
Also, we have seen in a number of published studies
for treating primary saphenous insufficiency
that the number and severity
of perforator vein incompetence decreases dramatically
simply by treating the incompetent saphenous vein.
And these are just a few of the studies
that have demonstrated
that effect showing a dramatic decrease in perforator vein
incompetence just
by treating the great saphenous vein in its insufficiency.
So we do know incompetent perforator veins appear
to be secondary to saphenous vein incompetence as
as best we can tell,
and saphenous vein surgery
for insufficiency improves the calf muscle pump function
for when the surgery is for primary varicose veins,
and again, it will improve all of the findings
that we get objectively using plethysmography when we look
at that calf muscle pump function.

Perforating Veins in Venous Ulceration

The other question remains is what is the role
of perforator veins when there's ulceration when we reach
stage five and six in the CEAP classification system,
either active or healed ulceration?
Are those patients different in some manner than simple
primary varicose veins and stasis dermal changes?
Well, about 50% of venous ulceration is related
to primary varicose veins,
and again, it is rarely a complication
of perforator incompetence only.
So 45 to 50% of the
CEAP classifications four through six,
which are the worst changes associated
with chronic venous insufficiency
or saphenous vein incompetence, the primary varicose veins
lead to incompetent perforating veins.
And it's very likely
because so many
of the perforating veins do become competent when the
saphenous vein is treated that these veins have any kind
of significant role in venous ulceration when it is
secondary to primary varicose veins.
However, there is another class of patients
with venous ulceration, the other half of those patients
that have, venous ulceration secondary
to chronic venous insufficiency, which is often a result
of the post-thrombotic syndrome.
So when we look at the consequences
of acute deep vein thrombosis, not
so much worried about pulmonary embolism in this case,
but what happens chronically when these veins start to heal?
Well, then you have a combination
of events going on in the post thrombotic syndrome.
You have not only valvular incompetence,
but you have an obstructive component.
And here when the calf compartment contracts,
the muscles contract
and put pressure on the veins within the calf.
The emptying cannot occur in a normal channel,
and it is quite likely here
that theory one kicks in the increased calf pressure in the
deep system dilates the perforating veins to the point
that they become incompetent.
It leads to secondary incompetence in the great saphenous
and superficial venous system.
And now when a patient ambulates
and walks briskly, there is very poor emptying.
There is reflux flow because of the incompetence
and the flow in the calf tends to be a back
and forth phenomenon.
And because now you're ambulating
and exercising arterial flow increases
and you can get actually an increase in ambulatory,
venous pressure at the level of the ankle.
So instead of a hundred millimeters of mercury,
it might go up to 110 millimeters of mercury.
And this is what can lead to these venous stasis ulcerations
that everybody has problems dealing with.
It's also interesting to note,
if you look directly at the bed
of an ulceration in these patients, approximately 70 to 75%
of them will have very clearly an underlying associated
incompetent perforating vein indicating some degree
of involvement in that perforating vein in
the entire process.
If you also look at management of these problems,
if you have a normal deep venous system
and you get venous ulceration, which does heal,
and you have surgery to treat the superficial insufficiency,
the recurrence of ulceration is extremely low.
If on the other hand,
it is post-thrombotic in the deep venous system
and there is some degree of obstruction you treat the
superficial insufficiency with, with saphenous surgery,
there is a high rate of recurrence
of venous ulceration in these patients,
even though you have treated the superficial component
of the problem if you have not treated
the perforating veins.

Treatment and Evidence-Based Medicine

So how can we make all of this right?
We have to keep in mind R'S admonition
about evidence-based medicine.
So we do know in primary venous insufficiency saphenous vein
surgery is associated very strongly with the prevention
of venous ulcer recurrence
and there is very strong clinical evidence
that this is the case.
We also know that in primary venous insufficiency,
saphenous vein surgery will eliminate much
of the perforator vein incompetence
that we do commonly see in this problem.
We also know that treatment
of the incompetent perforating veins alone has very little
effect on healing
or recurrence of venous ulceration in patients
with primary venous insufficiency.
Though again, the level of evidence is not quite as strong
for these particular patients.
The treatment of associated incompetent perforating veins
may be important to decrease venous ulceration in patients
with post-thrombotic syndrome.
However, we do not have a lot of evidence
to support this contention,
but the association of incompetent perforating veins
with ulceration in post thrombotic syndrome, the fact
that ulcers tend to recur at a high degree in patients
with post thrombotic syndrome when the saphenous system is
treated is very different behavior than is seen in primary
venous insufficiency.
So there is evidence to at least suspect that treatment
of associated perforating veins may be an important factor
in eliminating the recurrence
of venous ulceration in these patients.

Conclusion

Well, I suspect my time is pretty much up at this point,
so I'll be happy to stop and answer any questions.
Thank you.