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This is a report on the treatment by injection therapy, of 5,000 people suffering from varicose veins. They have all been treated by me, personally, in the last ten years. There has been no selection of cases. A large proportion were suffering from one or more of the complications of varicose veins, including eczema, oedema, ulceration, thrombophlebitis, etc., and over 100 has a history of deep vein thrombosis. One third of the cases were treated during pregnancy.

We recognize no contra-indication to treatment by injection therapy. Our five year recurrence rate is less than 20%. Our recent results lead us to believe that this will be considerably reduced in the next five years. There has been no mortality and no embolic phenomena following treatment.

This work began as a result of observations made while injecting varicose veins, during pregnancy, at the Rotunda Hospital, Dublin. There we noticed that a vein could behave in many different ways after the introduction of a sclerosing fluid. Sometimes the result was a rather terrifying, widespread, superficial thrombophlebitis. On other occasions there was no reaction whatsoever to the injection.

Again, we noticed that, in some patients, the vein went into spasm and remained a hard, stringy, cord-like structure without any reaction in the surrounding tissue.

This led us to question the possibility that one of these reactions could possibly be followed by re-opening of the vein, while the other reaction might be permanent and irreversible.

We also noticed that we could produce whichever of these effects we desired. If pressure was applied immediately after the injection and continued uninterruptedly, the inert, cord-like vein resulted, while, if pressure was not applied immediately and continuously, the red, tender, painful, swollen vein of traumatic, superficial thrombophlebitis resulted and, in cases where pressure was discontinued to early after the injection, the vein underwent a change from the stringy-cord-like vein to the large, red, tender, painful, swollen vein, immediately the bandage was prematurely removed.

It was important for us to find out exactly what was taking place in these veins. As we were unable to find any literature describing the exact step by step process by which a thrombosed vein re-opens, we decided to carry out histological investigations on some 50 cases of superficial thrombophlebitis.

From the histological appearance of the sections of these 50 cases, we came to the conclusion that the process of re-opening had nothing to do with capillary invasion bur was purely a mechanical one, resulting from the interplay of three factors:

1. The pressure of the blood in the adjacent unthrombosed portion of the vein.
2. The reaction of the clot.
3. The weakness of the vein wall.

Slide I shows small, slit-like channels developing between the vein wall and thrombus.

Slide II shows these channels developing between the vein wall and thrombus.

Slide III shows that the crescent shaped, slit-like, circumferential channel in slide II has now become circular and full of blood and the organized thrombus is displaced to one side of the channel.

We came to the conclusion, from examination of these sections, that if external pressure had been maintained until such time as fibrosis was complete, the chances of re-opening, even of a thrombosed vein, could be greatly reduced.

We next decided to section some 50 cases treated by the immediate uninterrupted compression technique which technique I will describe briefly at the end of this paper.

In these cases, the vein was emptied before the injection of the sclerosant. The sclerosant was maintained in a short, 2 inch segment of the vein, between two compressing fingers, for 30 seconds and pressure, by means of a soft rubber pad, bandage and elastic stocking was applied immediately and maintained without interruption, for six weeks.

Histological section of veins treated in this manner showed a very different picture – we saw from this that:

• One, there was no thrombus formation
• And two, that there was tremendous thickening of the endothelial lining.
• And three, that considerable fibrosis had taken place in the greatly thickened wall of the vein.

We have found this reaction to be maintained over a period of five years.

The sections shown here were taken some four years after injection by this technique and show clearly the endothelial proliferation and considerable fibrosis and thickening of the wall of the vein. This reaction is limited to the area between the compressing fingers 1-2 inches approximately, and is unlikely to injure a competent adjacent valve, thereby reducing the chances of rendering the patient a disservice. We have not encountered any reactions from spill over into the deep veins.

Our technique is as follows.

Step one is to select the site of injection.

We have found it of great help, when attempting to locate the sites of incompetence, to consider three factors:

• First, palpation of the fascia of the leg, which has proved most helpful.
• Secondly, our knowledge of the position of the communicating channels and,
• Finally, the pattern of the varicosities.

If one examines a dozen or so legs by running the tips of one’s fingers up and down them, one will suddenly become aware that there are weaknesses or depressions in the deep fascia.

It will be found that these depressions usually correspond with the localized blow-out in the vein and with the site of a communicating channel between the deep and superficial veins.

Digital pressure at one or more of these points will control the filling of the superficial veins. These depressions are the sites of election for ejection.

Having marked this point, a needle is introduced into the vein, the leg is elevated, and all the blood is emptied out of the superficial veins. Two fingers are placed on either side of the point of entry of the needle and the sclerosant, (1 cc of 3% Sodium Tetradecyl) is injected. It is maintained in the exact segment of the vein chosen for a period of 30 seconds and not allowed to mix with the blood, on either side of the compressing fingers.

Bandaging is then commenced, above and below the compressing fingers, a soft rubber pad is placed over the site of injection, and the bandaging completed. The distal portion of the leg is bandaged and an elastic stocking is drawn over the bandaged leg. The patient is advised to walk immediately and not to remove either the bandage or the elastic stocking until the next visit in one week's time.

At this visit, a second injection is given, if necessary. If not, the pressure bandages and stocking are re-applied and maintained in position until there is no tenderness in the vein.

We would like to point out here that the commonest site chosen by us for the first injection has been the Hunterian communicating vein, usually just above the medical condyle of the femur.

We have been gratified to observe, on six occasions, the disappearance of large sapheno-varices following the blockage of this abnormal Hunterian incompetent communicating channel.

This latter observation is of importance with regard to the evaluation of "so-called" Trendelenburg's operation.

The principle of our treatment has been to concentrate rather on the restoration of the efficiency of the peripheral pump than on the obliteration of the superficial varices; we recognize that high pressure in the superficial veins is only part of the disability and that, perhaps, in some cases the impaired venous return is a greater handicap.

From the recognition of this observation, we decided that it was worthwhile destroying the leaking communicating vein in a person who had had deep vein thrombosis.

We have treated more than 100 of these cases by the compression technique which I have just described and, although the leg has not returned to normal, improvement in all cases has been gratifying and long lasting.

There has been a disappearance of the dilated superficial veins, a great reduction in the swelling and, in nearly all cases, complete loss of the tiredness and bursting sensation.

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