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Letter to the Editor, THE LANCET, 29 February 1964, pp. 491-492

 

VALVULAR  DEFECT  IN  PRIMARY  VARICOSE  VEINS

Sir,

We have been following the correspondence arising from Mr. Ludbrook's article on valvular defect in primary varicose veins.1

"Varicose veins" is an unfortunate description, since it calls attention to one of the least important aspects of this disease. Often patients with the most severe symptoms and signs have in fact no dilated, elongated, tortuous veins. A more appropriate name is chronic venous insufficiency. Mr Ludbrook, in our opinion, is correct in stating that valvular incompetence is due to injury to the valves, a defect in the vein wall, hormone imbalance, an increased blood-volume, or some other disorder. He is, we think, incorrect instating that this incompetence is primarily at the saphenofemoral junction. In over 15,000 patients treated by us in the past twelve years, many of whom had large saphenovarices, not one has required flush ligation of the saphenofemoral junction.2 3

The disappearance of saphenovarices after blockage of an incompetent hunterian perforator lead us to believe that the emphasis on the saphenofemoral junction in the treatment of varicose veins is misplaced. It is gratifying to learn that Mr. Hobbs (Feb. 15), too, has found that saphenovarices and vulval varices, disappear after blockage of an incompetent hunterian perforator.

We believe that the primary lesion in patients with chronic venous insufficiency is incompetence of a valve in one or more perforating veins. In this way the superficial veins are subjected to abnormal pressure, and consequently the portion of the vein above the incompetent perforator will, in time, dilate. The dilitation spreads upwards, causing secondary incompetence of the valves in the superficial veins. Only when the dilitation reaches the saphenofemoral junction do the valves at this site become incompetent. And when the perforator(s), transmitting blood at high pressure, are blocked, the superficial veins recover their tone; and their valves, including those at the saphenofemoral junction, regain their competence.

It is in these cases of secondary saphenofemoral incompetence that the Trendelenburg test or mid-thigh tourniquet test is misleading. Ludbrook states that a near-normal fall in pressure (45 mm. Hg) occurs in patients with varicose veins who exercise the leg after a mid-thigh tourniquet has been applied. Certainly there is some drop in pressure, but if there is an incompetent valve in a perforating vein below the tourniquet, then the fall will be slight. The pressure exerted by a mid-thigh tourniquet (really a modification of the Trendelenberg test) is sufficient to occlude both the deep and superficial veins. The test is an inadequate diagnostic procedure, and is responsible for many misdiagnoses and consequent failures of treatment. The pressure needed to block an incompetent saphenofemoral junction must of necessity also block the common femoral vein, since the presure in the deep veins here is the same as in the superficial veins. But if the test is performed with a finger exerting just sufficient pressure to occlude the long saphenous vein in the upper thigh, the superficial veins will nearly always be seen to fill from incompetent perforating veins. This resembles our diagnostic test previously described.2

In our opinion, Ludbrook's investigations of the intravenous pressures are inadequate and consequently misleading. He recorded pressure in the superficial veins only and then refers to "mean" pressure values. The results give a false picture of the functions and faults of the complex pumping mechanisms responsible for returning blood from the lower limbs. Pressures in the superficial and deep veins must be recorded simultaneously by an electronic manometer which gives a permanent record of the very rapid pressure changes in the leg movement.

We have so far made 83 intravenous pressure recordings, and have many tracings obtained simultaneously in deep and superficial veins. From these it can, in fact, be compared to that of the P.Q.R.S. complex on the cardiograph. Plainly, to take a "mean" pressure in a vein is as inaccurate as taking a mean potential for the P.Q.R.S. complex.

The pressure in the long saphenous vein, as Ludbrook says, does fall with exercise in the erect posture in patients with chronic venous insufficiency, and often it falls in a normal pattern. In this way many patients, because they have many normally functioning pump units, can compensate for a faulty valve in one or their perforating veins, and hence have no serious symptoms.

The fallacy of obtaining mean records of the intravenous pressure is shown by Ludbrook's statement that on exercise the superficial pressure at the ankle dropped in control patients from 95 to 45 mm. Hg. In fact, our tracings show that a healthy person can reduce the pressure in the superficial vein at the ankle to within 5mm. of zero during exercise. only by recording both deep and superficial pressures can one understand the mechanisms whereby the normally high-pressure system (deep) can receive blood from the low-pressure system (superficial). It is during the fraction of a second (when the muscle-pumps are in their early diastolic phase) that the pressure in the superficial veins exceeds that in the deep veins and creates a favourable gradient.

Ludbrook states that in what he calls primary varicose veins the calf-pump is functioning normally. This may or may not be the case, depending upon the condition of the valves in the perforating veins connected to this pump; but even if the calf-pump does function normally, the plantar, anterior and posterior tibial, peroneal, quadriceps, adductor and hamstring pumps must also be taken into consideration, since an incompetent valve in a perforating vein connected to any of these may lead to chronic venous insufficiency. In similar cases we have always found a leaking perforator in one or more of the remaining pumps, commonly the adductor or quadriceps pumps. The success of his mid-thigh tourniquet test may lie in his occlusion of an incompetent upper hunterian perforating vein, together with a secondarily incompetent saphenofemoral junction, and compression of the deep veins.

Ludbrook describes primary varicose veins as occurring in patients who have not had deep-vein thrombosis. Varicose veins are seldom primary, but usually follow some other condition, whether it be hormonal, lacerations, polycythaemia, trauma, &c. Perforating veins can thrombose without manifesting as deep-vein thrombosis; and probably quite small injuries often cause subclinical thrombosis confined to a perforating vein and a short segment of the superficial veins. After recanalization, the valve in the perforating vein will be incompetent.

In reply to Mr. Ludbrook's suggestion that our technique must of course be successful if most of the varices are sclerosed (Feb. 1), nothing could be further from our object. We aim to produce, as we have shown,2 a short segment of sclerosis in the superficial vein overlying the incompetent perforating vein, and including it. We have established that the perforator is, in fact, blocked by many biopsies at varying intervals after injection, at which time the perforating vein is cut across with a knife and no bleeding has taken place. Microscopic examination proves that these veins are totally occluded.

The good results using our injection technique do, in fact, remain constant with time. In a survey conducted recently on 1172 patients treated between 1956 and 1960, the results were satisfactory in 81%, and in the patients who carried out our instructions conscientiously, the results were satisfactory in 86%. The best results were in patients who were treated in 1956; this means they have stood the test of time for eight years. T average number of attendances per patient at our clinic is 5, and in 15,000 cases treated there has been no mortality. Had these all been treated by surgery there would, according to published figures, have been upwards of 40 deaths.

We shall be pleased to hear Mr. Ludbrook's views, and would like to know to what operation he refers when he talks about "before operation" and "after operation"? Was it solely saphenofemoral ligation or some more elaborate procedure?

GEORGE FEGAN          DERMOT FITZGERALD           BILL BEESLEY

Research Department, Sir Patrick Dun's Hospital, Dublin 2

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  1. Ludbrook, J. Lancet, 1963, ii, 1289.
  2. Fegan, W. G.. ibid. p. 109
  3. Fegan, W. G. Minerva Cardioangiol. Europ. 1961, p 481.

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