A PERSONAL HISTORY
W.G. Fegan MB MCh, FRCSI
Emeritus Professor of Surgery, Trinity College Dublin
Dictated 2005
This is a story of the technique, which is evolved in the last 50 years and how
situations and people influenced the technique.
I was born on the 27th of March 1921 in a small town in Ireland; two days after I
was born my mother developed a deep vein thrombosis. As I grew up I was
constantly reminded of my responsibility for nearly killing the person who was
so dear to many people. I grew up. My father was a relatively rich man and he
expected me to follow in his footsteps as head of a prosperous company. But I
was quite certain that I wanted to become a doctor and I refused his generous
offer.
I started medicine in Dublin in 1939; I qualified in 1945 and became a doctor in
the Royal Northern Hospital in London in 1946. One of my jobs there was at the
varicose vein clinic. It was a clinic in which hundreds of people with varicose
veins were injected. They walked up a ramp, they stood in front of me and I
injected their veins standing up. This was an established tradition in a very old
established hospital. The technique used at the Royal Northern was widely used
throughout the world. The result of this technique, of injecting the full vein
standing up, was the production of a clotted vein. I did not know the follow up
results, but I followed in the footsteps of many distinguished surgeons and I
never questioned the correctness of the procedure.
I subsequently became aware of the work of Agrifoglio and Edwards in Boston,
where they surveyed large numbers of people whose veins had been injected
with a similar technique. They found the recurrence rate to be 85%. As the result
of their work many people around the world gave up the injection technique.
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The next job I was offered on my return to Dublin was the management of the
varicose vein clinic in the Rotunda Hospital in Dublin. By this time I had
acquired a fellowship and a mastership in surgery and I was if anything a
dedicated surgeon. The treatment in the clinic that I was offered was the
injection of varicose veins. As a result of the work of Edwards I was very
dubious about this technique, but I did not have the right to beds in the hospital
so I could not take the patients to the hospital to operate on and I was therefore
compelled to use a discredited injection treatment. I felt very unhappy about
those things and did my best to advise people on the foolishness of standing, the
importance of walking, the wisdom of resting and the use of an elastic stocking.
I started the clinic on a Saturday morning and I arrived in this large hospital with
20 patients waiting to see me. A formidable medical nursing sister gave me a
white coat and introduced me to my patients. She had a trolley loaded with
syringes and she obviously expected me to start injecting the varicose veins. The
patients were lying on couches and I tried to advise them on a conservative
treatment. After the third patient was advised by me and I did not use any of her
injections she almost accused me of being unable to do the injection treatment.
With a great sense of guilt I injected the fourth patient. I finished the clinic and a
week later I was due to see these patients again.
One patient whom I injected stands out clearly in my mind. She had a large
bunch of varicose veins and when I examined her on her returned visit she had
no veins. I questioned her as to what she did after my injection. She told me that
I had kept her late to meet her children from school and so she had to run after
the injection the whole way to school. I carefully examined the area where the
veins had been, there were no veins but I could feel a hard cord like a vein.
Thinking about this patient led me to the conclusion that perhaps there was a
technique of injection of varicose veins that was different from the discredited
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thrombosing technique. By running after the injection she reduced the pressure
in her superficial veins to near zero. When she got home she lay down with her
feet up. These factors led me to the conclusion that if I injected an empty vein
and kept compression on it the result might be different. And instead of 85%
recurrence I might have found a technique that was 85% successful.
In the next couple of years I injected many people emptying their veins before
injection and putting on compression immediately afterwards and I advised them
to walk as soon as possible. In the following 2 years I concentrated my activities
very much on examining the possibility of an alternative technique of the
treatment of varicose veins.
After treating these people I took sections out of their veins and I compared the
situation of the empty vein with the full vein. The vein is a living tube and when
the wall of the vein is damaged clot formation starts in the damaged area. The
damaged lining of the vein allows the large fibroblast to come into the thrombus
to affect organisation of it. But in many cases before the organisation is
complete many veins reopen and the patient is as bad as before, if not worse.
The compressed empty vein leaves very little work to be done by the fibroblast
and the vein does not reopen before the fibrosis is complete. This could be
compared to a wound healing by primary intention and a wound in which you
get a hematoma and healing does not take place and the wound often opened. As
a result of these histological examinations I was satisfied that this technique
could change the results of Agrifoglio and Edwards from 85% recurrence to
85% success. I persisted using this technique and build up a large number of
very satisfied patients and a good successful reputation.
On the chartered day of our hospital a lecture known as the Bartholomew Moss
in honor to our founder was delivered by a distinguished medic. This particular
year Sir George Godber, director of the British Medical Service, delivered it. In
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conversation after diner he asked the master was their anything new happening
in the hospital. The master of the hospital told him that they had an assistant in
the VV outpatient who thought he could have better results with injections then
with surgery. “That’s the sort of person I would like to meet,” said Sir George
Godber and I was invited to talk to the great man. He was very interested and
asked me did I come to London often and if so if I would call upon him, which I
did. He received me in his magnificent office in the Alexander Flemming
Buildings where he assembled his “think-tank” and asked me to repeat the story
I told him in Dublin. There were surgeons, pathologists, obstetricians and
representatives of a cross sections of the medical profession. He consulted each
of them and asked them if my story held water. They agreed at which point Sir
George asked me where I had published my work. I said that I hadn’t and that I
felt that if I had written it up and had sent it to a journal, it would have been sent
out to an assessor who would have turned it down and then published it in his
own name in some other journal. That was the explanation that I offered for the
fact that I had not published. But the real explanation was that I was dyslexic
and therefore handicapped. Sir George became a little bit annoyed; he rang up
the editor of the Lancet who agreed to read my paper without sending it out. Sir
George packed me off to produce a paper with one of his staff who was really
responsible for the article that appeared a few weeks later in The Lancet.
Treatment
In order to treat the derangement of the veins of the leg you must understand
normal arrangement. The venous blood from the skin is collected in the
superficial veins. The collected blood tends to run downwards under the
influence of gravity. When you walk the deep veins with their valves act as
powerful pumps and they are able to pump the blood back against gravity.
Between each step the pressure in the deep veins drops. During this lowpressure phase blood flows in from the collecting superficial veins to the deep
veins and is then pumped up to the heart. The valves in the perforating veins are
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set to allow blood only to pass from the superficial vein to the deep vein. We are
presented with patients who have two different abnormalities of their veins. One
is the varicose vein and the other one is a VARIX on the vein. They are
produced by totally different physical mechanisms and physiological changes.
The varicose vein is a hypertrophic vein starting in the lower leg related to an
incompetent connecting vein, which allows the pressure from the deep vein
pumping system to pass into the superficial vein. It is not necessarily associated
with the flow of blood. The essential defect or problem change is the inability of
the pumping system to reduce the pressure in the superficial veins. This failure
to produce low pressure in the superficial veins results in hypertrophy of the
muscle wall in the vein as well as a dilutation and elongation of the vein.
A varix is usually due to a retrograde turbulent jet, impinging on the wall of the
vein, causing a muscle to disappear and the vein to bulge, where it is being
bombarded by the jet.
A varicose vein has the ability to recover once the abnormal high pressure is
reduced by restoration of the efficient pumping of the deep vein pump. The
treatment of varicose veins should be focused on restoration not eradication
(stripping).
It should be widely understood that varicosity in the superficial veins is not a
relentlessly progressive degeneration. Advantage should be taken of the ability
to recover when the abnormal factor in their production, such as standing,
pregnancy and leakage from the pump are removed. The subsequent use of the
elastic stockings, following the removal of the abnormal factor.
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Fibrosis of veins
The fibroblast is the key cell in the restoration of the pump. The fibroblast does
not enter the lumen of the veins in ordinary circumstances. It is necessary to
remove the lining of the vein to allow the fibroblast entry. Ideally one should
have the minimum of altered blood in the vein and the maximum of fibroblast
to achieve rapid and complete fibrosis. If you are able to locate leaks and fibrose
a superficial vein with the minimum of clot formation you will achieve good
results.
Observation of clinical changes has been the greatest help in the treatment of my
patients, of course as well as knowledge of the basics of collecting and pumping.
Surgeons will naturally use surgery, where as surgery is impossible injecting the
upstanding patient without pressure makes the work of the fibroblast
impossible. The treatment of the standing patient in the Royal Northern
compared to the recumbent patient in the Rotunda Hospital combined use of the
empty vein followed by compression and walking were obviously necessary to
achieve the desired result of a fibrotic vein not a thrombose vein. I have been
very encouraged by the good results of people who followed my technique
accurately. I think it is necessary that surgeons should explain to people the fact
that there are at least two good ways of treating varicose veins and the choice
should be left to the patient.
Many surgeons did not agree with my technique and used it to clear up veins
after a subsequent visit following surgery. These bunches of veins which follow
surgery were due to incompetent perforators. If they had been treated with
injection first it would probably not have needed to strip out the long vein.
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Physiology
In order to understand blood flow in veins one must accept the fact that blood
has got to be moved, it has no capacity to move itself. Blood vessels themselves
can become pumps and with their valves they can drive blood back to the heart
and overcomes gravity which is tending to bring blood in the downward
direction away from the heart. Blood in capillaries has the remains of the
capillary pressure which is sufficient to allow the blood to be collected. Once it
is collected in the small veins it is then acted upon by the absence of pressure in
the vein distally. Blood will go from high pressure to low pressure it can be
directed by valves. It can be affected by the compression of the vein by forces
from outside. It can be affected by gravity. In venous return of the blood from
the skin, blood is collected by a combination of capillary use and the gravity in
the downward direction. The blood is collected; it flows in the downward
direction until it meets a valve that it closes. It collects in the small veins until
`the pressure is sufficient to open the valve above. This pressure in the collecting
superficial veins goes on building as you stand. As soon as you start to walk the
pressure in the deep vein drops between each step. When the gradient is
favorable between the superficial and the deep system, this opens the valves in
the perforating veins and allows the deep vein to fill from the collecting
superficial veins. The blood is now forced by the pumping action by the deep
veins against the pull of gravity and is driven up towards the heart. When you
relax the muscle in your leg between steps, by virtue of gravity the blood flows
back in the reverse downward direction. The reverse flow is stopped by closure
of the valves. The pressure after the valve closes drops and the deep vein fills
again from the superficial vein.
No name
One must constantly remind oneself that blood does not move unless it is acted
upon either by gravity, muscle in the wall in the vein, or external compression.
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The blood tends to flow down the superficial veins and it is pumped up the deep
veins by muscular external compression on the deep vein.
The deep veins are pumps that overcome gravity the superficial veins are
collecting tubes that depend on gravity for the movement of blood in them.
Muscle in the wall of the superficial veins plays very little part in movement of
blood. When the vein relaxes it is to accommodate a larger volume of blood.
The blood is moved from the superficial vein to the deep vein by the
development of the favorable pressure gradient.
The deep veins, when they are compressed by walking, empty almost
completely and when the muscle in the leg is relaxed the pressure drops
considerably and the pressure drop is transmitted to the superficial veins. This
drop in pressure empties the superficial veins and allows the muscles in the
superficial vein to contract. The muscle in the wall of the superficial vein is
constantly contracting and relaxing to accommodate the volume rather than to
move the blood. The pressure in the superficial veins can de dropped
considerably without the movement of blood. Movement of blood and pressure
changes are not necessary consequential. If you have an incompetent valve in
the perforating vein, the pressure in the superficial vein can be altered from
pressure in the deep vein. The pressure can be transferred from the deep vein to
the superficial vein without the movement of blood. It is necessary to drop the
pressure in the superficial vein to allow the muscle to relax and recover tone. If
this is not done rhythmically by walking, the muscle in the superficial vein is
overworked. After a period of years the overworked muscle in the superficial
vein hypertrophy the vein also dilates and elongates. The division of the
perforating vein allows the pressure in the superficial vein to be dropped by
other competent perforators. After a period of walking with elastic stockings the
varicosity can disappear.
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Varicosity
Varicosity is hypertrophy. It is due to an increase in pressure and work. It would
be more correct to say that it is due to failure to decrease than to increase work.
The pressure in the superficial vein must be dropped to allow the muscle in the
vein wall to recover its tone.
Comparison of treatments
The treatment of varicose veins by surgery is frequently accompanied by
anesthetic, this procedure has recognised mortality. No work has been done to
compare the mortality difference between injection, compression and surgery.
We can say in the tens of thousands of cases treated that as far as we know there
have been no deaths from treatment by injection sclerotherapy. The cost of
injection compared with surgery is very different and the use of hospital beds
unnecessarily should be considered. It is necessary now that if possible the
double-blind trial of the treatments of varicose veins should be performed. This
is necessary for the forming of patients for hospital management. Unfortunately
this has not been planned or executed. Whose responsibility it is has not been
defined, but I would think it should be government lead with authority from the
College of Surgeons. It will be costly and time consuming but it might be
worthwhile.
The Fibroblast
Varicose veins are so obvious and impressive that we sometimes can be excused
for thinking that their cause lies in themselves apart from the fact that there is an
occupational effect and a hereditary factor, varicose veins are in most causes
secondary to a defective pumping system.
Blood is pumped out from the heart but the blood going in to the lower limb has
got to be collected and returned to the heart against the force of gravity. This
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requires regular pumping this is dependent upon walking. If your pumps are not
working the results will double defects:
a. You do not return the blood to the heart and
b. The escape of the pressure reduced in the pumps to the superficial veins
does not allow them to enjoy a low pressure which is essential to their
normal function.
The wall of the superficial vein has got a thick layer of muscle which is
contracting and relaxing all the time but its blood supply and its function are
advantaged when the pressure is low. Low pressure in superficial veins is
essential to allowing the muscle in them to regain tone and function properly. If
the pressure is not intermittently reduced it puts an extra workload on the muscle
which undergoes the expected hypertrophy.
Varicosity is hypertrophy
In order to treat varicose veins you must locate the channels through which the
pressure in the deep veins is transmitted to the superficial veins. In practice this
boils down to locating incompetent perforators. If you can locate an incompetent
perforator and seal the leak you have started the process of curing varicose
veins.
Sealing the leak can be affected by a plug of thrombus or a fibrotic stricture. The
thrombus will recanalise but the fibrotic stricture is a permanent repair of the
leaking of the perforator.
The Fibroblast is the cell concerned with repair. Most of us are familiar with its
activity in wound repair. It is well known that a hematoma in a wound will delay
repair indefinitely. To get quick and firm repair you must have plenty of
fibroblasts and the minimum of thrombus. Essentially what you are doing in the
treatment of varicose veins is repairing the pump, by fibrosis, not plugging the
leaks with thrombus. The technique that I have advised is aimed at once
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destroying the intima. Destruction of the intima is the first step; the fibroblast
does not normally penetrate the intima, but once the intima is destroyed the
fibroblast can escape. The fibroblast are not seen at the area of the stripped
intima for 5 to 7 days and they do not lay down mature fibre tissue until their 6 th
week. Therefore the technique of finding and fibrosing the leaking perforator
requires the protection of compression for up to 6 weeks. It is also accelerated
by walking. This is why immediate and adequate compression, as well as
walking, are essential to facilitating firm fibrose repair. The fibroblast is
activated by the destruction of the intima under presence of thrombose. The time
frame of fibroblast maturation is similar to the osteoblast behavior at the site of a
fracture. They can be delayed or hurried by similar factors. To get a good result
in the treatment of varicose veins you must be able to produce good fibroblast
closure of the incompetent perforator. If you combine the injection of an empty
vein and immediate compression with the use of elastic stockings and walking
after injection, you will obtain good results. One might think this is exaggerated
but I have seen a sapheno varix measuring 4 inches disappear following the firm
fibrosis of a leaking perforator above the medial condyle of the femur. It is
essential to be able to locate incompetent perforators to fibrose them completely
and to advise your patient to avoid standing and to walk regularly after
treatment. The fibroblast is the cell of repair. It does not penetrate intact intima
and it cannot cope with a large amount of thrombus. The object of our treatment
is to return the hemo dynamics of the collecting and pumping of venous blood to
normal.
Varicose veins are perhaps the most common, obvious and misunderstood
condition afflicting the human being. They are treated by surgeons, who do not
understand the underlying cause, by stripping. This is equivalent to being sent
out to pick a bunch of flowers and only topping the blossoms. The primary
cause does not lie in the varicosity but in the pressure transmitted from the deep
pump to the superficial collecting system by an incompetent perforator.
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Superficial veins are essentially collecting channels and if they are subjected to
high pressure without intermittent low pressure they hypertrophy. The deep
veins have got relatively less muscle than the superficial vein and depends on
the muscle within the deep facia for its pumping compression. The superficial
vein expands and contracts to accommodate the volume of collected blood.
There is relatively much more muscle in the wall of the superficial vein.
Superficial veins can either develop varixes or varicosity. Varix are due to
turbulent retrograde flowing blood. Varicosity is hypertrophy due to failure to
produce intermittent low pressure. If you restore the competence of the two
systems and use the deep system to generate pressure and the superficial to
collect and then with the help of elastic stocking, walk regularly in a period of
weeks and months, you will improve the hemodynamics on returning venous
blood and improve the picture considerably. One must start by appreciating the
speed and complexities of pressure generated and flow developed. These are
sometimes so rapid that they defeat the ones ability to visualise.
To simplify such a complexed situation, it is wise to think of the superficial
veins as collecting veins depending on hydrostatic pressure for flow which is in
a downward direction and the deep veins depending on pumps for flow which is
in a upward direction (towards the heart). The perforating veins will normally
transmit blood from superficial veins to deep veins and when the valves and
valvular mechanism are defective pressure is transmitted (with or without blood)
from the deep to the superficial system.
The osmotic pressure of the plasma proteins must be respected. The lymphatics
will compensate for the spill of plasma proteins but the tissue fluid will not be
regularly be reabsorbed unless the pressure in the veins is kept low as well as the
blood being transported back to the heart. You are dealing with a complex
mixture of hydrostatic, osmotic and pump pressures. All inter dependent and the
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difference between the blood flow in a vein of a walking leg and the blood flow
in the recumbent patient with the legs raised stretches the imagination.
Veins are collecting cylinders, transmitting ducts and pumps all at the same
time. The blood in them is constantly changing its direction its philosophy its
volume and order of flow. One requires time to think on the complexity of
venous blood flow before one has a change to understand it.
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