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PATIENTS

W. G. FEGAN, M.Ch., F.R.C.S.I.

D. E. FITZGERALD, M.Sc., L.R.C.P.I. & S.I.

W. H. BEESLEY, M.B., B.Ch.

In reintroducing injection therapy as a treatment for varicose veins it is important to make quite clear that we are fully aware that injection therapy has been used before and has become widely and justifiably discredited. It is also important to point out that the old injection treatment gained popularity and support because of the early improvement enjoyed by patients after the initial thrombotic reaction in the vein had settled down. Follow-up of these patients has resulted in the discovery of a high rate of recurrence after six months, and in some the condition has been made a great deal worse than before treatment commenced. Nevertheless, investigation of the occasional successful case might well have revealed the secret of its success, knowledge of which would probably have altered the incidence of recurrence. The reasons for the discredit of the old injection therapy will be made clear later in this communication.

It is essential to explain as briefly and clearly as possible the complex mechanism by which blood is returned from the lower limbs to the heart, since this is a prerequisite to the understanding of the causes of varicose veins. The term varicose veins, like chronic mastitis, has been so widely used for so long that it is here to stay. It is an unfortunate terminology since it draws attention to one of the less important features of the disease. We are all aware that the patients with the greatest varicosities are not necessarily the most disabled, and that frequently in the very worst cases there are no varicosities. It would be wiser to introduce the term chronic venous insufficiency (CVI), which indicates that the primary abnormality is a defect in the mechanism of venous return from the leg.

There are, in each segment of the leg, one or more synchronized pumping systems: in the foot the plantar pump; in the leg the peroneal, soleal, anterior and posterior tibial pumps; and in the thigh the quadriceps and adductor pumping systems. In fact, every myofascial compartment is, in itself, a pump. If the valves of the pumps become injured, their reserve power is greatly reduced, but in this initial state there is no loss of clinical function, because the pumps, like all other organs in the body, are designed with a capacity much greater than is necessary for ordinary function.

The pumps register very low pressure in their diastolic phase. During this phase, blood is readily drawn in from the superficial veins. As soon as muscle contraction takes place, the valves in the perforating veins close, and filling from the superficial system ceases. The result of this is that, during walking, the pressure in the superficial veins drops to near zero twice with each step (Figs. 1 and 2). During this period of low pressure the walls of the superficial veins recover their tone. If low pressure is not rhythmically achieved during walking, pathologic changes will take place in the veins.

DIAGRAMS HERE 1, 2 AND 3 Captions to be typed

The essential abnormality in chronic venous insufficiency is the inability of the multiple pumping systems to reduce pressure in the superficial veins to near zero after the commencement of walking. This happens most commonly as a result of damage to the valves in the perforating veins, or to valves in the termination of the saphenous veins. (Fig. 3).

It is not widely appreciated that damage to the valves in the perforating veins is more important than damage to the valves at the termination of the long and short saphenous veins. The reason for this, in our opinion, lies in the method of diagnostic study commonly employed. Diagnosis of venous insufficiency is usually made upon the static limb, and the rate of retrograde filling from the saphenous opening can be demonstrated dramatically. However, if the valves associated with muscle pumps are intact, and functioning efficiently, then considerable retrograde filling from the saphenous opening can be adequately compensated for, with consequent maintenance of low pressure in the superficial veins. On the other hand, retrograde filling from the saphenous opening in a patient who has even a minor valvular defect in the perforating veins is a much more serious condition. The latter group of patients has a double defect in that (1) they have a reduced capacity to return blood to the heart, and (2) on walking, they actually pump blood at high pressure into the superficial venous grid (Figs. 4-7).

DIAGRAMS HERE 4 TO 7 Captions to be typed

It should be obvious therefore, that the study of the dynamic limb is more important than the study of the static limb, and in order to pick out the cases of serious incompetence it is necessary to measure the pressure in the affected superficial vein in the patient walking as well as standing.

This is, at present, impossible since there is no simple machine that is capable of recording the changes in pressure in the walking patient. We would like to stress once more that the assessment of the capacity of the pumps to reduce the pressure in the superficial system is the essential assessment of the abnormality. Retrograde filling from the termination of the long saphenous vein can be compared to a leaking ship that can remain afloat provided that the capacity of it's pumping system is in excess of the leak.

Failure to achieve low pressure on walking should be accepted as the essential pathologic feature of the disease. This failure is not directly proportional to the severity of the varicosity, but is reflected in the severity of the symptomatology.

We consider that treatment should be directed toward the restoration of the efficiency of the pumps by permanently destroying the leaking points rather than to the eradication of superficial tortuous veins which may, in themselves, not be a very great embarrassment and are, in many cases, capable of reverting to normal appearance and function after the restoration of the normal pattern of pressure.

Tortuous varicosities are due mainly to continuously raised intravenous pressure rather than to intermittent high pressure. Veins are capable of withstanding high intermittent pressure, provided that it is followed by a period of reduced pressure during which they can recover their tone.

The cusps of the valves in tortuous veins are often normal and are only incompetent because the diameter of the lumen of the vein has been increased to such an extent that the valve flaps are unable to meet (see Fig. 6). When the leaks in the damaged perforating veins are remedied, the vicious cycle is broken. The tortuous superficial veins, relieved of their high pressure, return to their normal size, and the valves regain their competency. It is unnecessary and illogical to strip out veins simply because they are varicose. Most of these veins are potentially normal, and once the raised pressure in them is relieved, they may revert to their normal state.

DIAGRAM HERE Fig. 6

The functions of valves are threefold: (1) They constitute an essential element of the complex pumping grid. (2) They retain the high pressure within the deep system and prevent it's transmission to the superficial system. (3) They direct the flow of blood from the superficial to the deep veins.

Valvular incompetence may be of two kinds, which we have chosen to call primary and secondary. In primary valvular incompetence, valves become involved in fibrous adhesions and can never again function efficiently, whereas in secondary incompetence the valves is normal and the incompetence is due to dilatation of the vein. It is this secondary type of incompetence that is reversible after the pressure in the superficial veins is returned to a normal pattern after the restoration of the efficiency of the pumping system.

Our attention was first drawn to this by observing that saphenous varices disappeared spontaneously after the sclerosis of an incompetent Hunterian perforating vein. (Fig 7). We have observed this on numerous occasions in the last five years. Of the 14,000 patients treated by us, not one has required the high flush ligation treatment for the relief of symptoms, and in the vast majority of cases the dilated tortuous vein, above the highest Hunterian perforator, has returned to normal.

One cannot stress too often the importance of exact diagnosis as a prerequisite to any form of treatment. We consider it to be absolutely essential to locate accurately the incompetent perforating veins. This is most easily done by following a diagnostic ritual which we have laid down in our clinic.

The old form of injection treatment produced a painful and uncontrolled thrombus, which nine times out of ten recanalized. The end result in many cases left the patient worse than before treatment because normal valves became involved in the thrombus, and after reopening of the veins these valves were incompetent because of the resulting adhesions.

We must now attempt to make clear that our treatment is essentially different from the thrombus produced by the old injection technique. The object is to produce a short fibrous cord replacing the superficial vein and involving the perforating vein. In order to do this it is necessary to introduce a small amount of sclerosant into the superficial vein, that has been emptied by elevation of the leg, and to hold it isolated and unmixed with blood for a given period of time at the site of injection. This allows chemical necrosis of the intima to take place. If this vein is now compressed and maintained in a contracted state for approximately six weeks, a series of important changes take place. An analogy might be made to the revascularization of the head of a femur after avascular necrosis: the thrombus and intima are analogous to the head of a femur which has to be revascularized; the revascularization extends across the intima and involves the small amount of thrombus which invariably forms the vein (Fig. 8). At the same time, fibrous tissue is laid down in the wall of the contracted vein, producing an irreversible fixation.

DIAGRAMS AND CAPTIONS

The changes that have been observed in sections taken from treated veins at varying intervals after injection are as follows: Changes take place in the vasa vasorum, adventitia, media, subintimal layer, intima, and in the small amount of thrombus in the lumen. There is a marked contrast between the histologic changes in the vein treated by our technique and those in the thrombosed vein which resulted from the old injection technique.

The first comparison is the relative difference in thickness between the wall of the vein and the thrombus within it. In phlebitis, the diameter of the thrombus is many times greater than the thickness of the wall of the vein, whereas this proportion may well be reversed when compression is applied immediately after injection. In this case the wall is many times thicker than the thrombus (Fig. 9).

In the cases in which treatment is applied successfully a rich hyperemia from the vasa vasorum is observed. The new blood vessels are seen to grow into the media and can be observed to disrupt the internal elastic lamina at many points, passing through the intima and invading the thrombus.

The intima would appear to allow: (1) plasmatic substance from the small thrombus in the vein lumen to pass out into the media separating the muscle fibres, and (2) new blood vessels from the vasa vasorum to invade the thrombus. Large cells arising in the subintima pass freely in two directions - into the thrombus, and in the opposite direction into the media.

The large subintimal cells appear to be totipotent. They can be observed to act as macrocytes, fibroblasts, or as a lining for venous sinuses, according to necessity. Otto Vos, in a personal communication, has told us that he has found that the concentration of aminoacids surrounding macrocyte cells can influence their behaviour. His work was done in vitro and helps to explain our findings in vivo.

Fibrous tissue is progressively laid down in the media and in the thrombus. The capillaries from the vasa vasorum regress, and the vein is now replaced by a hard fibrous cord which constitutes a permanent obstruction.

Sections taken after thrombosis show a very different picture. Many large venous sinuses appear through the thrombus. These dilate as the thrombus shrinks, and new venous channels are established through the substance of the thrombus. This does not happen when the amount of thrombus is minimal and the wall of the vein is thick, as after compression. There is an inverse relationship between vascularization of the thrombus from the vasa vasorum and the development of venous sinuses within the thrombus. The more prolific the vascularization, the less likelihood is there of venous sinuses developing and, therefore, of a new channel forming within the vein. The capillaries and venules which develop from the vasa vasorum never establish communication with the venous sinuses but regress after the organization of the thrombus.

When advocating the treatment of varicose veins in pregnancy it is often said that we are meddling, insomuch as we are treating a condition which four times out of five resolves in the puerperium.

This indictment of meddling is refuted on the following grounds: (1) If 20 per cent of the patients suffering from varicose veins during pregnancy do not recover in the puerperium, then this represents a large number of patients with varicose veins. One must make sure that 100 per cent recover. In order to do this, one must treat ALL pregnant women who have varicose veins. (2) If patients with varicose veins are not treated during pregnancy, it is very likely that the condition will continue to deteriorate past the critical point beyond which recovery in the puerperium is not possible. (3) Why should women suffer for months with a condition which is readily amenable to a safe and simple form of treatment. (4) The greatest reason for treating varicose veins during pregnancy is the absence of superficial and deep vein thrombosis and pulmonary embolism in the puerperium of patients so treated.

In 1952, we took over the responsibility of treating varicose veins in the Rotunda Hospital. At that time there was a special clinic which was concerned solely with the treatment of varicose ulcers. At the present time there is no patient with varicose ulceration attending the hospital, and there has not been for over four years. In the past five years there have been five cases of superficial phlebitis during the puerperium in patients treated in our clinic. These five cases were patients who did not complete their treatment. There has been no case of deep vein thrombosis or pulmonary embolism. All patients attending the Rotunda Hospital who have varicose veins are referred to this clinic. Because of the beneficial effect of prenatal treatment on the puerperal thrombotic complications, it is considered that a special clinic, such as the one in the Rotunda Hospital, should be attached to all large maternity hospitals.

Perhaps it appears that this simple technique is easy to perform and that all that is required is to inject a vein and then bandage it, but this is incorrect.

If 20 house surgeons are invited to perform 20 appendectomies, the likelihood will be 100 per cent success, but if the same 20 young doctors are invited to apply a bandage that has to stay in position without moving for six weeks, it would be surprising if the rate of success was moor than 50 per cent. In these hands the results of our technique would be extremely poor, since it is absolutely dependent on the uninterrupted maintenance of adequate compression applied immediately after injection. This is difficult to achieve for many reasons: (1) the shape of the patient's legs - sometimes tubular and sometimes conical; (2) excess adiposity; (3) the alteration in the size of the patient's legs due to either swelling or shrinkage; (4) the natural tendency of a bandage to come off the leg of a patient in bed at night.

It is essential therefore, to become adept at bandaging before commencing this treatment, and not to delegate this apparently trivial and unimportant part of the treatment to a subordinate. After a short time, most young doctors working in our clinic become expert and their results are indistinguishable from our own. They must, however, have the capacity to take infinite care with the simplest details.

DIAGRAMS AND CAPTIONS Last is Fig. 9

We should make it clear that we are in no way opposed to the surgical treatment of varicose veins when this implies accurate location of the perforators with their interruption and ligation followed by repair of the fascial orifice transmitting the perforators.

We are completely opposed to the old injection therapy which resulted in uncontrolled thrombosis.

The inherent advantages of our technique are as follows: (1) immediate relief of symptoms, (2) absence of mortality and morbidity, (3) simplicity of application, (4) an outpatient treatment, (5) inexpensive, (6) avoidance of phlebitis and pulmonary embolism in the puerperium.

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