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W. G. FEGAN

Diseases loosely grouped together under the heading varicose veins are fundamentally different and require different management. It is extremely important to make an effort to determine the nature and the location of the underlying pathology in every case before commencing treatment. The anatomy and physiology of the venous pumps of the lower limb have been investigated and described in detail [1, 8, 10, 10a], but it is important to remember that every segment of vein which contains a pair of competent valves and that can be compressed by surrounding tissues is an effective pump unit. There are many hundreds of such units in a normal leg. There is, therefore, a considerable reserved pumping capacity. This is the reason why localized derangement of venous pumps is frequently asymptomatic for many years.

Venous insufficiency is a common complication of pregnancy. It is a generalized disease involving both legs. Since the underlying pathology is different from that in non-pregnant patients I will discuss it now. An essential feature is an inhibition of the smooth muscle in the walls of the veins [5]. This leads to secondary valvular incompetence. The veins and valves usually return to normal after pregnancy is over. Many of these women, however, have additional pathology of their venous pumps, such as damaged and non-functional perforating vein valves which, before they became pregnant, was adequately compensated for. The additional stress of pregnancy in such patients may precipitate symptoms and in these cases return to a normal post-partum condition is less likely. The importance of avoiding standing and of walking as much as possible is stressed. Any localized incompetent perforating veins in the feet or calf are dealt with. These measures are usually sufficient and certainly reduce the incidence of superficial thrombophlebitis.

In non-pregnant patients the presence of varicose veins is not necessarily associated with symptomatic pump dysfunction. Conversely pump dysfunction does not necessarily result in prominent varicose veins. The essential changes in superficial varicose veins are dilatation and secondary valvular incompetence. The initiating lesion in most cases is an incompetent perforating vein in the calf. This probably is caused by thrombosis and recanalization of perforating vein following minor injury. Because of the reserve pumping capacity already mentioned symptoms are unusual at this stage, but the superficial veins in communication with the incompetent perforating vein are subjected to local changes in blood pressure and flow. High pressure generated in the deep veins during muscular contraction is transmitted to

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them and the minimum pressure achieved during muscular relaxation is higher than in normal superficial vein at the same level. There is a gradual ascending dilatation of the superficial vein so involved (Fig. 1). This is associated with secondary valvular incompetence. The changes also affect perforating veins that are situated proximally and which link the involved superficial vein with the deep veins. Eventually, in the case of the long saphenous vein the valves below the saphenofemoral junction are involved. When the perforating veins and/or the termination of the superficial vein become incompetent, reflux of blood from the deep veins is possible. It will be appreciated that unless the calf pumps are relatively unimpaired significant reflux of blood will not be achieved because obviously blood will not flow down a superficial vein unless the lower part of the vein is first cleared of blood. This retrograde flow of blood has one very important characteristic. Because it is partially obstructed by the cusps of incompetent valves it becomes turbulent, and an effect of this on the vein wall - the production of vibrations - can often be detected by palpation. We think that turbulent retrograde flow may be responsible for the remarkable dilatation that sometimes occurs and for the developments of sacculations that usually appear below the valve cusps. There is evidence to suggest that dilatation and incompetence of superficial veins may occur in a descending fashion [9]. But I feel that this is the situation in a minority of cases only. It is notable that many patients with saphenofemoral reflux volunteer that they first noticed dilatation of veins in the leg rather than the groin and it is extremely rare to see patients with dilatation and incompetence limited to the upper part of the long saphenous vein.

From the point of view of treatment we classify our patients into three groups.

Group I: These patients have gross varicose veins and minor symptoms. Treatment is not aimed at providing cosmetic relief because patients in this group do run a definite risk of developing uncontrolled or excessive superficial thrombophlebitis and although this is rarely complicated by pulmonary embolus, it is an extremely painful and temporarily incapacitating condition and if perforating veins are involved it may result in varying degrees of pump dysfunction. The patients are sometimes treated firstly by flush ligation [7] and subsequently by obliteration of the one or two incompetent perforating veins that were the likely initial cause of the condition. I, personally, prefer to look for and deal with incompetent perforating veins first, because in some cases following adequate treatment there is evidence that the secondary dilatation and incompetence of the proximal superficial veins may be reversed [11]. In cases in which this happens flush ligation, a procedure not entirely without risk, is unnecessary. This group of patients represents a small percentage, about 15% of those who attend our clinics. They are not problem cases and the recurrence rate, no matter what form of treatment is applied, is extremely low.

Group II: This is the larger group with a degree of pump decompression associated with the presence of varicose veins. I think that there is general agreement that in this group multiple incompetent perforating veins should be dealt with at an early stage. The pump dysfunction is caused by multiple perforating and secondary superficial venous valvular incompetence. Oedema, pigmentation and ulceration are common. Because of oedema, multiple incompetent perforating veins may be difficult to detect clinically when the patient is first seen, and we often recommend a period of compression before commencing injection particularly if this is the case. Our results [6] in dealing with these patients compare favourably with surgery. Complications are rare and the expense of hospitalization is avoided. Others [3, 12] using this technique have also had acceptable results.

Group III: These are the patients with severe chronic venous insufficiency associated with varying degrees of obstruction and valvular incompetence of the deep veins in the leg and sometimes with proximal venous obstruction. It is necessary to explain to these patients that although treatment can produce, in most cases, very considerable improvement they will never be restored to normal. It is often quite impossible to detect incompetent perforating veins clinically because of oedema and in order to reduce the swelling of the limb one may have to resort to powerful elastic compression bandages. We always show the patients how to put the bandage on themselves and we tell them to remove the bandages at night and to sleep with the foot of the bed raised. Using this regimen it is usually possible to reduce the swelling sufficiently to be able to detect incompetent perforating veins and to commence treatment. When the first course of treatment is completed and ulcers - if they have been present - healed, we frequently advise the patients to continue wearing a firm elastic stocking. We follow them up at six-monthly intervals in our clinic and advise them to return immediately if they develop recurrent symptoms or signs.

The object of the technique is to produce a permanent fibrous occlusion at the junction between an incompetent perforating vein and the superficial vein. A meticulous search is made for the defects in the fascia through which the incompetent perforating veins pass while the limb is elevated and the superficial veins collapsed. Many such apparent defects are not, in fact, due to incompetent perforating veins but rather to dilated superficial veins. These can be excluded if all the defects are occluded by the examining doctor's fingers while the patient is recumbent and if, when the patient then assumes the erect position, filling of superficial veins does not occur while the doctor's fingers are removed from the fascial defects one at a time from below upwards. About 50% of the sites selected in this way are over incompetent perforating vein [2]. When the sites for treatment have been selected, injections are given, starting at the lowest site and working upwards. A 2 ml. syringe containing sclerosant and a fine (25 gauge) needle are used. The needle is introduced into the vein while the patient sits on an examination couch. A little blood is aspirated to confirm that the needle is in fact in the lumen of the vein. The patient then lies flat while the leg is elevated and the superficial veins collapse. The segment of vein to be injected is then isolated by firm digital compression above and below the point of entry of the needle. The sclerosant, 0.5-1 ml, is then introduced slowly over a period of about 30 sec. and a crepe bandage is applied above and below the compressing fingers to maintain isolation of the injected segment of vein. A layer of bandage is now applied over the injection site and a rubber pad is bandaged into position over this. A pad applied directly to the skin often causes irritation. As many of the selected sites as possible are treated at the first sitting. The bandage is then completed from the webs of the toes to above the level of the highest injection. Elastoplast is applied over the bandage to hold it in position and an elastic stocking is then applied. If the patient walks soon after injection and if the compression is satisfactory the amount of red thrombus in the vein is reduced to a minimum. The patients are usually reviewed every two to three weeks. Bandages are not removed until the doctor is ready to inspect the limb. The patients are not permitted to walk without bandages. Further incompetent perforators are sought and treated as at the first visit. We find it necessary to maintain compression for at least six weeks after the final injection. If this is not done recanalization is possible. Following successful treatment palpation of injection sites reveals painless, fibrous cords 3-4 cm. in length. The low incidence of extensive superficial phlebitis and the extreme rarity of deep vein thrombosis and pulmonary embolism is, in our opinion, attributable to the use of the empty vein technique, adequate compression and immediate ambulation after each series of injection. The latter requires considerable organization.

Patients are given an explanatory leaflet in the waiting room before entering the clinic and asked whether they have read it and understood it before treatment commences. If they are not prepared to carry out instructions, treatment is not given.

These are local and general, they are usually due to faulty technique or faulty selection of patients [4].

Pain at the site of injection is occasionally troublesome. It is not necessarily associated with phlebitis or injection ulcers, in fact, no obvious cause may be found. It is important to make sure that the bandage is not too tight. Walking usually relives this pain, and a mild analgesic may be prescribed.

Superficial thrombophlebitis is usually due to failure to use the empty vein technique, the use of exercise amounts of sclerosant or inadequate compression. The condition is more likely in obese patients because of difficulty of maintaining compression. It is also more common in patients who do not take required exercise.

Injection ulcer is due to faulty technique. The incidence varies inversely with the experience of the doctor. The ulcers are usually painless but take several weeks to heal. They should be treated by dry dressings and compression.

Pigmentation of the skin occasionally occurs over the sites of injection. This is probably due to deposits of haemosiderin and usually fades after about a year.

Local paraesthesia and anaesthesia may occur if a cutaneous nerve is damaged during treatment. It recovers completely after a few months.

Clinically proven deep vein thrombosis and pulmonary embolism are extremely rare. The incidence of these complications is certainly considerably less than if the patients treated by injection sclerotherapy had been treated by surgery.

Intra-arterial injection of the sclerosant is extremely rare but obviously a very serious complication. The posterior tibial artery has been involved in most cases. It is obviously of the greatest importance to palpate this artery before giving injections in the area of the medial malleolous. If the complication occurs, local cooling, systemic heparinization and infusion with low molecular weight dextran are sometimes effective.

A small minority of patients develop allergic reactions during treatment. The usual manifestation of such reaction is a rash either localized to the treated limb or generalized. This may appear rapidly after the first injection or it may not appear until after the patient has been undergoing treatment for a considerable period of time. Patients who develop allergic reactions are obviously unsuitable to this form of treatment.

Anaphylactic shock occurs extremely rarely but because of its seriousness every clinic in which the treatment is carried out should have facilities for dealing with the situation. We must emphasize that in experienced hands complications are infrequent.

The contra-indications to compression sclerotherapy are as follows:

1. Obesity: As already mentioned compression is often difficult to maintain in obese patients; such patients should always be encouraged to lose weight. Although it is often possible to give injections in the lower part of the leg and provide considerable relief from varicose ulcers, it is usually foolhardy to attempt to inject these patients in the thigh because the bandages almost invariably become loose and ascending thrombophlebitis is a frequent complication if this.
2. Inability to walk: This again is a relative contra-indication. I would advise compression sclerotherapy for a bed-ridden patient, but I would not be adamant in refusing limited treatment for a patient with moderate arthritis and a painful varicose ulcer who could walk for a limited distance. Again, in such a patient injections might safely be given in the lower part of the leg but it might be wise to withhold treatment in the thigh because of the greater difficulty of maintaining compression in this region.
3. Allergy: An allergic response to the sclerosant is a definite contra-indication for further treatment by this method.
4. Oral contraceptives: Although there is no evidence to suggest that patients on oral contraceptives have a greater risk of developing deep vein thrombosis and pulmonary embolism if they are treated by compression sclerotherapy, we are nevertheless, reluctant to treat such patients. The rule in our clinic is that such patients must have stopped taking oral contraceptives for at least six weeks before commencing treatment.

The term "varicose veins" is used to describe several different pathological conditions affecting venous return from the lower limb. An attempt should be made to discover the underlying pathology in every case before commencing treatment. Varicose veins in pregnancy differ in aetiology and prognosis from varicose veins in non-pregnant patients. Prominent superficial varicose veins are not necessarily an indication of significant impairment of peripheral venous pumps. In severe chronic venous insufficiency there may be very few superficial varicose veins. Compression sclerotherapy is a satisfactory form of treatment for these considerations. Results compare favourably with those of surgery and complications are infrequent. The use of empty vein technique, small amounts of sclerosant and adequate compression are essential if good results are to be obtained and complications avoided. It is essential that patients walk immediately after treatment and as much as possible each day during treatment. Complications are usually due to faulty technique or faulty selection of patients. Contra-indications are limited, but treatment should be withheld if patients are not prepared to follow instructions. Excessively obese patients and patients who have difficulty in walking the required amount are also frequently unsuitable for treatment.

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