Chapter III

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THE CLINICAL PATHOLOGY OF VENOUS INSUFFICIENCY OF THE LOWER LIMB

Clinical insufficiency is a dysfunction of the mechanism of venous return from the lower limb. It produces a wide range of clinical disorders but most commonly presents as varicosity of the superficial veins. However, it must be emphasized that some patients suffering from venous insufficiency, even to an advanced degree, do not have varicose veins. Unfortunately, in the past, superficial varicosities have been considered as a clinical entity in themselves, with the result that the underlying pathology has not been properly appreciated.

A large number of factors may be involved in the development of venous insufficiency. To understand how each has its separate effect, and how they may interact, the concept of 'pathological reserve' of the pump is useful, so long as it is carefully distinguished from 'physiological reserve' (see Chapter II).

The pathological reserve is the capacity of the pump to sustain damage without a clinically significant fall in efficiency. A clinically significant fall is one which produced signs or symptoms.) It will depend on the number and distribution of the valves in the deep and superficial veins, the number and size of the perforating veins, the biochemical and Histological structure of the vein wall, and the degree of development of the muscles and fascia.

The greater the number of valves present, the greater the number which must be damaged before retrograde flow can occur. The more numerous and wide the perforating veins, the more likely is a localized region of thrombophlebitis to involve one, and the more directly will pressure be transmitted to the superficial veins when the valve is rendered incompetent. Variations in the structure of the vein wall will determine whether or not a given abnormal pressure pattern will cause varicosis. The strength of the muscles and fascia will determine the pressure abnormalities produced by a given pattern of valvular incompetence.

The more important factors concerned in the development of venous insufficiency are shown diagrammatically in Fig.23 (diagram available from: E-mail: fegan@fegan.com).   The exact role of some of these is difficult to define at present and much research remains to be done on the effects of inborn differences in the biochemical structure of the vein wall and on the changes produced by cyclical alterations in the hormonal activity in women. However, in most cases, severe disorganization of the venous return mechanism is due to the presence of one or more of four principal lesions. They are:

1. Proximal obstruction of the deep veins.

2. Incompetence of valves in the deep veins.

3. Incompetence of valves in perforating veins.

4. Incompetence of valves in superficial veins.

Before discussing these lesions in detail it is necessary to clarify the concept of valvular incompetence. This may be primary or secondary.

Primary valvular incompetence. Primary valvular occurs when a venous valve has been irreparably damaged. Usually this is the result of a thrombotic episode in which the valve has become involved. Subsequent recanalization of the vein occurs, but the valve cusps which have been involved in fibrous adhesions persist only as remnants on the vein wall. The valve is not capable of function and can never be restored. A much rarer cause of primary valvular incompetence is rupture of the valve cusps, and congenital absence of valves produces an equivalent condition.

Secondary valvular incompetence. The difference between primary and secondary valvular incompetence is shown in Fig. 24 (diagram available, e-mail: fegan@fegan.com). Secondary valvular incompetence occurs in the superficial and perforating veins. The cusps of the valve are normal, but fail to meet, due to an increase in the diameter of the vein. As the dilatation of the vein progresses, a triangular gap appears at the lateral attachments of the valve cusps and allows leakage of blood into the segment of vein below the valve. It is likely that turbulent retrograde flow is established. This turbulence, once established, may interfere with the blood supply to the vein wall via the vasa vasorum, or subject the collagen fibres to an abnormal stress. Either of these changes may be the prelude to the atropic changes preceding varicose dilatation. However, two important facts must be appreciated in regard to secondary valvular incompetence. They are:

1. The initial dilatation of the vein is always from below. Only after the cusps become incompetent from this cause does regurgitation of blood occur.

2. Secondary valvular incompetence does not cause irreparable damage to the cusps, and hence in most cases is reversible if and when the vein returns to its normal diameter. Restoration of competence can be achieved if the abnormal pressures which are responsible for the venous dilatation are relieved. This fact is readily demonstrated in the case of pregnant patients, many of whom achieve a substantial degree of recovery following delivery.

It has been shown phlebographically that the application of an elastic stocking reduces the size of dilated veins and allows incompetent valves to return to function (Keane & Fegan, 1966).

Proximal obstruction of the iliac veins. Occasionally the large intra-abdominal veins may be significantly compressed by pelvic tumours. These conditions should be borne in mind, but they do not often give trouble in the diagnosis of venous insufficiency.

In recent years interest has been stimulated in those cases of deep vein thrombosis which subsequently show the presence of a permanent occlusion of the left common iliac vein at the point at which the vein is compressed by the right common iliac artery passing over it. It may take the form of an intraluminal occlusion of the vein, due to failure of recanalization of a thrombus in this region, or it may consist of a perivenous fibrosis. A natural by-pass is formed by enlargement of the lumbar, sacral and superficial abdominal veins. Whether or not this collateral circulation is adequate in all cases remains to be determined. A variety of surgical procedures designed to relieve the obstruction directly have been advocated (Cockett & Thomas, 1965).These include disobliteration of the vein with patch angioplasty, and by-passing the obstruction by a saphenous vein transfer. The necessity for this has been questioned (Doporto & Fegan, 1966), as it is believed that failure of the distal parts of the venous pump play a more significant role in the production of symptoms.

Presently, venographic and manometric investigation of these patients is being carried out prior to, and following, correction of the distal pump leaks by compression sclerotherapy in an effort to resolve this question. Preliminary results (Doporto & Fegan, 1966) suggest that in most instances the collateral circulation develops spontaneously to a degree which is adequate for the free return of venous blood, and that the clinical features of the 'post-thrombotic limb' can be cured by sclerosis of the incompetent perforating veins alone. However, it must be made clear that neither correction of perforator leaks nor removal of proximal obstructions correct the damage to the valves in the deep veins.

Incompetence of valves in deep veins. This occurs following deep vein thrombosis. These patients form a definite clinical group, and suffer from oedema. Frequently they complain of a bursting sensation in the leg and we feel that this is most probably due to stretching of the deep fascia.

At present there is no acceptable method for the repair of damaged valves in the deep veins, although McLachlin et al. (1965) have described a method of venous valve replacement which they have used successfully in dogs. Bauer (1955) has advocated ligation of the popliteal vein in such cases, but so far we have little experience of this approach.

Incompetence of valves in perforating veins. This may be due, in rare instances, to congenital absence of malformation. In many other cases the exact origin of the incompetence is unknown. The most common sites of perforator incompetence are in the lower part of the leg. This is a region particularly liable to minor traumatic incidents. Thus it appears likely that perforator incompetence in this area frequently results from localized thrombosis in the vein following a blow. The thrombosis is either silent or the symptoms of it are masked by the local irritation of the injury. The valve cusps become involved by the thrombus and, following recanalization of the thrombus, the valve remains functionless. Thus the high pressures which occur in the deep veins during exercise are transmitted directly to the poorly supported superficial veins. The phasic reductions in pressure which normally occur in the superficial veins during diastole of the pump are no longer present, and the superficial vein dilates. Before dilatation occurs, however, the wall of the superficial vein undergoes a considerable degree of hypertrophy and the muscular layer thickens significantly. Svejcar et al. (1964) have demonstrated an increase in the muscle content of 15% in varicose veins and 12% in potential varicose veins. Eventually the hypertrophy gives way to atrophy, and stretching of the venous wall occurs.

Incompetence of valves in superficial veins. Secondary incompetence has been referred to already. It occurs due to the dilatation of the vein wall and proceeds in an upward direction. The sequence of event in the development of superficial varicosities is represented diagrammatically in Fig.26. Finally, reflux in downward direction completes the clinical picture.

OTHER  AETIOLOGICAL  FACTORS

Alterations in the thrombotic and lytic properties of blood and blood vessels. These may be responsible for the occurrence of deep and superficial vein thrombosis. Certainly in both of these conditions changes occur which can be confirmed by platelet adhesion tests and the partial thromboplastin time (Hume, 1966). Whether or not they are of significance in the genesis of the condition is not clear, however, and a detailed appraisal of these factors is beyond the scope of this monograph.

Arterio-venous shunts. Large arterio-venous shunts produce dilatation of the superficial veins. In most instances these patients have been readily diagnosed by the presence of unilateral limb hypertrophy.

Hormones and varicose veins. The earliest published report suggesting a possible endocrine involvement in varicose veins is probably attributable to Sicard and Gaugier (1927), who inferred, as a result of clinical observation, that there was 'an absence of an endocrine secretion from thyroid or ovary associated with this physiological condition'. Since then many investigators have suggested that the painful symptoms often associated with varices in women may be caused by some imbalance in the circulating steroid hormones. The clinical evidence relating hormones to venous disorders in women may be summarized as follows:

1. Three to four times as many women as men have varicose veins (Foote, 1949; present study).

2. Painful symptoms in varicose veins are confined almost exclusively to women (present          study).

3. Both the appearance of varicose veins and the onset of pain are often cyclical in occurrence and seem to be related to changes in the circulating hormone levels, e.g.

(a) Many women get varicosities only during pregnancy and these return to normal soon after delivery (Fried et al., 1956).

(b) Many pregnant women with varicose veins get severe pain in their veins very early in pregnancy (McCausland, 1939; Fried et al., 1956).

(c) The condition of varicose veins in pregnancy deteriorates as the pregnancy progresses (Fried et al., 1956; present study).

(d) A considerable proportion of patients experience pain, often severe, localized in the veins of the leg, just before menstruation (Foote, 1947; McCausland et al., 1963; present study).

(e) There is an increase in venous distensibility during the second half of the menstrual cycle (McCausland et al., 1963).

4. There is an abnormally low incidence of abortion among women who develop varicose veins during pregnancy (McCausland, 1939; Marazita, 1946).

5. Painful symptoms in veins may be alleviated by administration of hormones (McCausland, 1939; Marazita, 1946; McPheeters, 1949; Aguero, 1946; Fried et al., 1956; present study).

6. A small number of women experience painful veins after sexual intercourse (present study).

It is evident, from a survey of the literature, that although most investigators are agreed that steroid hormones are involved to some extent in the aetiology of varicose veins, there is nevertheless considerable confusion as to the exact role played by these hormones in the genesis of venous disorders, and to the precise mechanisms involved. A comprehensive biochemical investigation is being carried out in this department in an effort to elucidate these problems.

Heredity and congenital factors. There is no doubt that certain inherited characteristics predispose to the development of venous insufficiency. The exact nature of these and their point of action is not clear. Many patients have a marked family history of varicose veins. Recent work has shown biochemical differences between normal and varicose veins (Prerovsky et al., 1962; Svejcar et al., 1963) and it is possible that these are inherited.

Anatomical studies (Kosinski, 1926; Cotton, 1961) demonstrated wide variations in the number of valves in the veins of the lower limb. The long saphenous vein may contain from three to eighteen valves. This variation in the number of valves is reflected in an increased or decreased pathological reserve of the muscle pump as a whole. Similarly, imperfect development of valves results in reduced efficiency of the system.

Standing. Chronic venous insufficiency is commoner among people whose occupations involve prolonged standing. We do not believe that standing is an initiating factor, since, if a history is carefully taken, most patients give a history of thrombophlebitis. However, standing is probably an aggravating and accelerating factor.

Pathological changes in the veins of the leg are usually caused by one of the following conditions:

1. A fully compensated leak from an incompetent perforating vein, which may result in the appearance of localized, symptomless, non-progressive varicose superficial veins.

2. A leak from a perforating vein which is not adequately compensated, and will ultimately result in the appearance of the signs and symptoms of venous insufficiency.

3. The post-phlebitic syndrome:

(a) without proximal obstruction,

(b) with proximal obstruction and adequate collateral vessels,

(c) with proximal obstruction and without adequate collaterals.

4. The venous insufficiency which occurs during pregnancy, the clinical appearance of which suggests general loss of tone in the vein walls with diffuse valvular dysfunction. These factors may well be aggravated by increased blood volume and increase in the work to be done by the pumping mechanism.

The post-phlebitic syndrome is uncommon. The changes in the veins which occur during pregnancy are probably just one manifestation of a generalized change in physiology and may well be related to an altered hormone pattern. Localized, symptomless, non-progressive superficial varicose veins require treatment for cosmetic reasons only.

It is proposed here to discuss more fully my ideas of the aetiology of the common type of venous insufficiency, No. 2 mentioned above.

A vast number of factors are concerned in the chain of events which lead to an advanced case of chronic venous insufficiency. The disease is insidious in onset and the early changes in the venous system of the leg may have occurred unnoticed years before a patient comes to the doctor for treatment. The following description is in my opinion the commonest sequence of events in the development of a case of venous insufficiency.

Many people sustain minor thrombotic episodes in their veins following slight trauma, and are completely unaware of these occurrences. Some people are more prone to thrombosis than others and those who take part in certain occupations and sports may be particularly liable to injury. For example, hurley players in Ireland wear no protective guards on their legs. The game involves striking a leather ball with heavy sticks and consequently the lower legs are very frequently injured.

I believe that following such an injury local thrombosis in the veins of the leg frequently occur, but, in most cases, the thrombus is rapidly lysed by the circulating blood and the vessel wall, and little permanent damage is done. In some instances, however, the thrombus becomes established and organization follows. When this occurs an irreversible pathological change in the vein has taken place.

If thrombosis and organization occur in a perforating vein in which there is a valve, I believe the first important step in the development of venous insufficiency has occurred.

In a matter of months a new channel develops in the thrombosed section of vein. The development of this channel is followed by the appearance of two pathological changes in the dynamics of venous return.

(a) The pumping capacity of the deep system of the veins, in a central direction, is reduced. Most of the blood still pumps towards the heart, but now some of the blood is pumped out into the superficial veins through the valveless perforating veins.

(b) The normal fall in pressure which occurs in superficial veins during walking no longer takes place. There is some reduction in pressure. This is not as marked as that found when perforating veins are competent.

This failure of ambulatory hypertension gives rise to two disabilities:

(a) The recovery period for the constituents of the vein wall (collagen, muscle and vasa vasorum) is not as good as before and therefore there is an increase in the tension to which the vein wall is subjected. The vein wall hypertrophies, then dilates and finally atrophies.

(b) The hypotensive phase in each step is inadequate for the creation of a favourable gradient for tissue fluid absorption and therefore for the removal of metabolites from the surrounding tissues.

The abnormal pattern of venous blood flow spreads to the adjacent segments. The spread takes place in the direction permitted by the valve. An ascending uniform gradual dilatation of the superficial veins occurs. The degree of dilatation is influenced by the strength of the overlying fascia and the reserve capacity of the pumping unit. The presence of strong fascia and of pumping units with a high pathological reserve proximal to the primary lesion will limit dilatation to the superficial veins. Thus, in some cases varicose dilatation is limited to the ankle. We believe that its extension is prevented by the presence in the calf of a strong layer of fascia (Sherman's fascia) and a powerful pump. Similar factors are involved when the dilatation is limited to the knee or the mid-thigh regions.

This type of valvular incompetence is quite different from the valvular incompetence due to the primary lesion. In primary incompetence the valve is destroyed and the lesion is irreversible. In secondary incompetence the valve is not destroyed and the incompetence is reversible. Temporary reversibility of incompetence may be achieved by (1) wearing an elastic stocking, (2) resting in bed for a few days. Permanent reversibility of incompetence may be achieved by (3) closure of lower incompetent perforating veins; this is followed by involution of the dilated veins. (4) Theoretically, by transposing the superficial veins beneath the deep fascia. (5) Following delivery of the pregnant woman.

A secondary incompetence of the superficial veins also involves some of the perforating veins and the termination of the long saphenous vein. Ultimately, incompetence of either a more proximal perforating vein or of the termination of the long saphenous vein develops. This results in the regurgitation of blood from the deep venous system into the superficial veins. 

The projection of incompetent valve cusps into the lumen of the vein over which there is retrograde flow of blood results in the development of turbulence. In our opinion it is not until this turbulence is established and the vein wall subjected to a new and abnormal stress that tortuousity and varix formation occurs. We believe that in the presence of turbulence the nutrition of the vein walls from the vasa vasorum in the adventia becomes more difficult and that irregular, patchy, atrophic changes in the vein wall result. Turbulence in veins, as in arteries, results in dilatation, the best-known example in arteries being post-stenotic dilatation of the aorta.

Symptomatology. The symptoms and physical signs commonly associated with venous insufficiency include excessive tiredness of the legs, oedema, pain, superficial varicosities and nutritional skin changes such as itching, eczema, pigmentation and ulceration. The exact mechanism by which each of these is produced is not clearly established except for superficial varicosities which have been dealt with in the earlier part of the chapter. However, some discussion of the different features is justified.

Several distinct types of pain occur in venous insufficiency. They are:

(i) Hot throbbing pain over angiectids.

(ii) Night cramps.

(iii) Venous claudication.

(iv) Linear pain along the veins.

(v) Generalized pain in the leg.

An investigation of the mechanism of pain production in venous disorders is currently being pursued in this department. Distension of the superficial veins by a balloon catheter causes pain accurately localized to the site of the balloon, but this is not an invariable finding.

Night cramps are a frequent symptom of venous insufficiency, and often are a source of distress to pregnant women. They are relieved by exercise. It appears likely that they are due to stasis of venous blood in the intra-muscular venous sinusoids and metabolite accumulation.

Venous claudication occurs in patients with a history of previous deep vein thrombosis, and is a characteristic feature of the 'post-phlebitic limb'. It consists of a severe bursting sensation which occurs in the affected leg when the patient walks for a reasonable distance. Unlike arterial claudication it is not relieved by standing, although elevation of the leg is rapidly effective. Venous claudication is commonly associated with swelling of the leg.

The hot throbbing pain which occurs, usually over the sites of 'star bursts' or angiectids, is often aggravated during the immediate pre-menstrual period.

Much work remains to be carried out on the phenomenon of pain of venous origin. Evidence of the nerve connections to veins is scant (Ludbrook, 1966), but it is important to realize that these distinct types of pain exist, and that they are definitely associated with disorders of the venous return mechanism.

Nutritional skin changes. The nutrition of the skin, particularly in the 'gaiter' area immediately above the ankle, is frequently impaired as the result of sustained hypertension in the underlying superficial veins. The absence of a diastolic phase in these veins interferes with the normal tissue fluid exchanges and the regional venules dilate, giving rise to the 'ankle flare'. The latter may be extremely troublesome and there may be eczematous charges elsewhere, on the thighs, face and arms. Ultimately ulceration occurs, usually as the result of a small abrasion.

Oedema. Oedema of some degree occurs in 51% of patients with venous insufficiency (Beesley, 1964). The cause of this is similar to that mentioned above in the section on nutritional skin changes. The failure to achieve rhythmic reduction in pressure in the superficial veins results in an unfavourable diffusion gradient across the capillary wall. In many cases severe oedema obscures the presence of dilated superficial vein, and this may lead to diagnostic errors.

Congested leg of pregnancy. Changes may occur in the veins of the lower limb within two weeks of conception. The change most characteristic of pregnancy is called intradermal venular dilatation.  This often affects the foot and ankle first and to a greater degree, and, with the development of varicosis of the superficial veins, gives rise to the term 'congested leg of pregnancy'.

Another frequent lesion is the angiectid or 'star-burst', in which fine vessels in a radial pattern appear anywhere on the limb, but typically on the medial side of the upper leg and lower thigh.

Aguerro, O. (1946), Rev. Obstet. Gynec. 6, 155.

Bauer, G. (1955), Angiology, 6, 169.

Beesley, W. H. (1964), M. D. Thesis, Univ. Dublin.

Cockett, F. B. & Thomas, M. L (1965), Brit. J. Surg. 52, 816.

Cotton, L. T. (1961), Brit. J. Surg. 48, 589.

Doporto, J. M. & Fegan, W. G. (1966), to be published.

Foote, R. R. (1947), Lancet, 1, 83.

Foote, R. R. (1949), Varicose Veins. London: Butterworth.

Fried, P. H., Perilstein, P. K. & Wagner, F. B., (1955), Arch. Surg. 72, 253.

Hume, M. (1966), Arch. Surg. 92, 934.

Keane, T. F. L. & Fegan, W. G. (1966), to be published.

Kosinski, C. (1926), J. Anat. 60, 131.

Ludbrook, J. (1966), Aspects of Venous Function in the Lower Limbs. Springfield: Thomas.

Marazita, A. J. D. (1946). Med. Rev. 156, 422.

McCausland, A. M. (1939). Calif. & West. Med. 50, 258.

McCausland, A. M., Holmes, F. & Trotter, A. D. (1963). Am. J. Obstet. & Gynec. 86, 640.

McLaughlin, A. D., Carroll, S. E., Keads, G. E. & Amacher, A. L. (1965), Ann. Surg. 162, 446.

McPheeters, H. O. (1949), Lancet, 2, 69.

Prerovsky, I., Linhart, J., Dejder, R., Svejcar, J., Kruml, J. & Vaurejn, B. (1962), Rev. Czech. Med. 8, 171.

Sicard, J. A. & Gaugier, L. (1926). Pr. Méd. 34, 689.

Svejcar, J., Prerovsky, I., Linhart, J. & Kruml, J. (1963), Clin. Sci. 24, 325.

Svejcar, J., Prerovsky, I., Linhart, J. & Kruml, J. (1964), Amer. Heart J. 67, 572.

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