The veins of the lower limb must not be viewed as a series of inert venous conduits but rather as a complex pumping mechanism capable of returning venous blood to the heart against the force of gravity in the upright position. If active thrombosis is excluded, it is some form of failure in this mechanism that underlies nearly all venous disorders in the lower limb. The essentials of normal anatomy and physiology will be described first, especially those aspects that may undergo change and cause venous problems.

Unlike arteries, the veins are specifically designed to allow flow in one direction only, towards the heart, and this is achieved by the presence of numerous valves arranged along their length (Fig. 1) 423. Only in the common iliac veins, vena cava, the portal system, and in the cranial sinuses are these valves lacking. They form an essential part of the venous pumping mechanisms returning blood from the lower limbs against gravity and act to protect the peripheral tissues from back pressure set up by columns of blood when the patient is upright. Each valve is made up of two gossamer thin cusps which in spite of their delicate appearance are surprisingly strong (Fig. 2) 424. The cusps are supported by the vein walls and their integrity as functioning valves depends on this support having sufficient strength to resist forces dilating the veins and tending to separate the cusps. The vein walls are thin but capable of considerable distension or contraction and these qualities are provided by circumferential rings of elastic tissue and smooth muscle. When the patient is upright and standing still, the veins are maximally distended and the diameter may be several times greater than in the horizontal limb at rest. The veins are very flexible; if the limb is elevated so that all blood leaves the veins, not only do they contract down to minimal size, but also collapse into a thin ribbon-like shape. Such a highly flexible, thin walled structure which collapses easily does not allow suction to be transmitted along its length and siphonage plays virtually no part in the movement of venous blood. It is incorrect to think of blood ever being sucked from one part of the venous system to another in the limbs.

As with arteries the interior of the veins is lined with endothelium, providing a non-thrombogenic surface, but in the case of veins, where slow flow and long periods of stasis might encourage thrombosis more easily than arteries, there is an enhanced protective mechanism providing prostacyclins to prevent aggregation of platelets, and actively forming fibrinolysins (plasmin) capable of dissolving thrombus and clot.

The deep veins lie beneath the deep fascia but do not all serve the same function, merely varying in size. They may be divided into two major categories.

The major veins in the limbs and the numerous branches joining them serve as conduits, taking blood back from the tissues towards the heart. These are the veins depicted in most anatomical diagrams starting as plantar veins running to tibial veins, through popliteal and superficial femoral veins to common femoral and iliac veins, and so into the inferior vena cava (Fig. 3) 425. However, these veins make only a limited contribution to the active pumping of blood upwards against gravity which is so essential in the lower limbs and this function is largely dependent on the venous sinuses within muscle that act as highly efficient pumping chambers.

The lower limbs have powerful muscles capable of great effort. During activity these require a copious flow of blood. Distributed throughout these muscles are numerous venous sinuses (Fig. 4) 426. Their shape varies considerably in different muscles, some being long and thin (for example in the peroneal muscles) and others being broad and bulky, as found in the soleal and gastrocnemius muscles. The greater the effort required of the muscle, the larger the venous sinuses will be. Because the sinuses are surrounded by the muscle fibres they are strongly compressed when the muscle contracts and blood within them is driven out through connecting veins to join the main conduit veins (Fig. 5) 427; the connecting veins are valved and situated at the heartward end of each sinus. Blood that has crossed the capillary beds of muscle passes through numerous small vessels into each sinus which fills to capacity from this source or until it is emptied by the next muscle contraction. In addition, veins communicating with superficial veins perforate the deep fascia and enter many sinuses near their distal ends (Fig. 6) 428. The valves of these perforating veins allow flow inwards to the sinuses but prevent outward flow from them and, in this way, blood accumulated in superficial veins can enter the muscle sinuses when they are slack. Each sinus, together with the surrounding muscle fibres, forms an elegant and effective pumping chamber emptied at each contraction and propelling blood towards the heart. The valve arrangement in the conduit veins ensures that blood only moves in this direction and protects the sinus from unwanted reflux once contraction has ceased and the sinus is empty. Thus, the sinus can only fill from the intended sources, the muscular capillary beds, perforating veins, and interconnecting veins running between sinuses. All the muscles in the lower limbs, ranging from diminutive muscles, such as the plantar, to the massive muscles of the calf, contribute to this widespread pumping system which is often collectively termed the musculovenous pump. Sometimes this is referred to, for convenience, as the ‘calf muscle pump’: however, this implies that the muscles of the calf are the only ones that matter when, in fact, all muscle groups in the leg * 2 and foot play an important part and are also implicated in any disorders that may arise.

Because of their valves, all veins are capable of contributing to venous return against gravity, in response to pressure by surrounding muscles or by any form of external pressure.

Changing the position of the limb from dependency to elevation will cause blood trapped between valves to empty proximally so that a form of pumping can be provided by repeatedly changing the position of the limb.

The underside of the foot provides a substantial pumping mechanism, partly because of the muscles within it, but perhaps even more so by the bodyweight compressing the underside of the foot against the ground at each footstep. The pool of blood in the capacious venous plexus under the foot is emptied upwards and, in the normal state, prevented from returning by valves in superficial and deep veins of the lower leg. Loss of effective valves here plays a significant part in venous disease.

Proper venous return from the lower limb depends upon an intricate pumping mechanism requiring numerous effective valves. Failure of the valves for any reason will reduce the effectiveness of venous return in the upright posture and may lead to an undesirable state of unrelieved venous pressure, or venous hypertension.

In addition to the deep vein systems of conduits and pumping chambers described above, there is a system of superficial veins lying outside the deep fascia subcutaneously. This commences as a network of fine veins mainly from the skin itself, that merge into branch veins running into two principal superficial veins, the long and the short saphenous veins (synonyms—greater or internal, and lesser or external). These, together with their branches, form two clearly identifiable systems but there is free interconnection between them. Figure 7 429 shows a typical arrangement of the superficial veins, including those branches commonly involved in venous disorders. There is much individual variation in the details and some of these variants will be discussed later. The long saphenous vein runs subcutaneously up the inner leg and thigh to the groin where it passes through the fossa ovalis to join the common femoral vein (Fig. 8) 430. The short saphenous vein passes through the deep fascia somewhere between midcalf and knee and runs for a short distance beneath the fascia to end by joining the popliteal vein at a variable level but usually opposite the femoral condyles (Fig. 9) 431; here it commonly gives off an upward extension (sometimes called the Giacomini vein) which may run deeply in continuity with the profunda femoris vein, or superficially curving round to join the long saphenous vein by its posteromedial branch in the upper thigh. Both saphenous systems have valves at intervals along their length and these valves become more numerous in the lower part of the leg, in keeping with the progressive increase in pressure to be resisted down the length of the limb when upright (Fig. 10) 432.

The superficial veins, draining skin and subcutaneous tissues, play a major role in the regulation of body temperature. In hot conditions, greatly increased blood flow through the skin causes it to act as a radiator, aided by evaporation of sweat, very effectively losing body heat. The superficial veins dilate to remove the rapid flow of blood and, in warm conditions or during exercise, these veins are maximally dilated, but in cold and inactive circumstances are constricted and inconspicuous. In venous disorders, enlarged or varicose veins will reflect these changes and in the very conditions in which patients wish to uncover their limbs the venous defects are most obvious.

The saphenous veins empty blood at their terminations into popliteal and common femoral veins but they can also empty by numerous perforating veins running from the superficial veins through the deep fascia to join deep veins (Fig. 11) 433. It has been estimated that there are over 60 such perforating veins distributed over all aspects of a lower limb. These perforators are often paired and many run directly into the deep conduit veins but, as previously said, others communicate with the venous sinuses in muscles (Fig. 6) 428. Some perforators are more liable than others to be involved in venous disorders and have been given eponyms after the authority first drawing attention to them, but this is an oversimplification because other perforators, found extensively over the lower limbs, are, in fact, often implicated in venous disorders.

Most perforators are valved to allow only inward flow from superficial to deep veins but it is probable that the arrangement of fibres at the fascial apertures also plays a part in preventing outward flow when muscle contraction causes a sharp rise of pressure within the sinuses. Small perforators, less than 2 mm in diameter tend not to be valved and presumably are responsible for equalization of pressure by outflow from deep to superficial veins.

When the limb is horizontal, superficial drainage is partly through the saphenous terminations and partly by the perforators to the deep veins. However, when upright, there is normally very little pumping action sending blood up the saphenous veins and the perforators play a major role in venous return from the superficial veins. When one stands still, the saphenous veins tend to fill steadily, but after muscular contraction, the resulting fall in deep venous pressure attracts flow from superficial to deep veins, through the perforators in the direction allowed by valves. Thus, in an upright and actively moving person most superficial drainage is by multiple perforators up the length of the limb rather than following each saphenous vein to its termination. When upright but motionless, both superficial and deep pressures remain equal, rising slowly in parallel fashion to maximal, and there is a slow drift of passive flow up both sets of veins; in this state, even a single movement causing muscle contraction to empty the deep veins will be immediately followed by flow from superficial veins, via perforators, into the deep veins. Because the saphenous veins and their branches have numerous valves the continuous column of blood in these veins becomes segmented between the valves as each part empties inwardly through its own group of perforators (Fig. 12) 434. In this way, a continuous column of blood up a saphenous vein becomes a series of cascades between the valves.

Reversed flow through perforators in a leg, that is to say outwardly from the deep veins, can often be demonstrated in apparently normal limbs when the popliteal vein is compressed so that surface veins are artificially caused to take on the role of collaterals. This phenomenon becomes a permanent feature in post-thrombotic deep vein obstruction where the perforators and superficial veins become part of a regular collateral system allowing continuous outflow, up the superficial veins, and past the underlying obstructed deep veins (Fig. 13) 435. Such collateral veins may become greatly enlarged by forceful flow through them. In other circumstances, primary failure of the valve mechanism in a perforating vein may allow it to become the source of downflow in superficial veins with incompetent valves and this will be discussed presently. Occasionally, failure of perforator valves allows forceful ejection from intramuscular venous sinuses on contraction and causes enlarged, tortuous veins in the vicinity.

Only three forces create movement of venous blood in the limbs: arterial pressure across the capillary beds, the musculovenous pumps, and gravity.

1.In the arteries, pressure created at each heartbeat pumps the blood towards the peripheral capillary beds and is only slightly assisted or impeded by gravity, depending on the position of the limb. When standing upright and motionless, venous blood derived from peripheral capillary beds starts back towards the heart at a low pressure and slow delivery. This transcapillary flow leads to a slow build-up of pressure sufficient to give a drift of blood back to the heart. Eventually, this process causes a prolonged rise of capillary and venous pressure in foot and ankle region to 100 mmHg or more, which has undesirable consequences if maintained too long. This aspect will be discussed further.

2.By far the most powerful force creating venous return flow is the musculovenous pumping mechanism that can handle large volumes rapidly and generate a force well in excess of that required for venous return against gravity. Operation of the ‘pump’ (Fig. 14) 436 is followed by a sharp fall in venous pressure in the lower part of the limb and, as will be seen later, extensive damage to this pumping system by thrombosis can seriously impair the well-being of the limb.

3.The third force causing venous flow is gravity itself. If the limb is elevated above the horizontal, flow towards the heart occurs by simple gravitational downflow without any need for assistance by transcapillary pressure or the musculovenous pump. Elevating the limb to promote venous flow is an important principle in the treatment of conditions where venous return is impeded for any reason. When the limb is in a dependent position, a normal set of valves in deep and superficial veins will, of course, prevent reflux of blood against the normal direction of venous flow. A failure of competence in the valves will, however, lead to retrograde flow down the limb when the patient first stands, or after an exercise movement has created slack veins in the lower part of the leg. In the superficial veins, this is the basis of the most common venous disorder of all, simple varicose veins.

When a person with normal veins rises from horizontal to upright position and the veins steadily fill by arterial inflow, the venous pressure in superficial and deep veins in the foot and ankle gradually rise over the next 30 to 60 s to that exerted by the column of blood from foot to heart level, about 100 mmHg, dependent upon overall height. This assumes that the subject stands still without movement because as soon as this occurs blood is pumped upwards and the pressure within them drops. A series of movements, such as walking, will empty the veins in the lower leg very effectively (Fig. 14) 436 so that the pressure within them drops to around 20 mmHg and whilst movement continues it remains there (Fig. 15) 437. On ceasing to walk and standing still the venous pressure again climbs steadily over the next minute to its previous level but even a small single movement of the lower limb will cause a significant drop for many seconds. When capillary flow is greatly enhanced by muscular activity, each muscle contraction creates a corresponding increase in venous return and fall in the venous pressure. Without effective musculovenous pumping, removing the large flow of blood through contracting muscle, a most damaging rise in venous pressure occurs, giving severe venous hypertension. The characteristic changes and harmful effects caused by this will be discussed later but the causes for ineffective pumping are summarized in the next section.

Venous insufficiency, a state of inadequate venous return in the upright position and accompanied by venous hypertension, may occur in the following circumstances.

1.The overwhelming of the pumping mechanism by massive downflow in superficial veins with deficient or defective valves, as often occurs in simple varicose veins.

2.Widespread impairment of the musculovenous pumping mechanism during active venous thrombosis, for example, acute deep vein thrombosis.

3.Obstruction or deformity in the main venous conduits as a consequence of venous thrombosis (post-thrombotic syndrome).

4.Loss of deep vein valve competence, or replacement of the deep veins by enlarged, valveless, collateral veins, as occurs in post-thrombotic states.

5.Inborn deficiency of deep vein valves or inherent weakness in the vein walls with consequent valve failure (valveless and weak vein syndromes).

6.Prolonged inactivity of the muscles with the limbs in a dependent position, as in paralysis or disease states inhibiting use of muscles. However, the blood flow through muscles will be correspondingly reduced and venous hypertension may not be too severe.

It should be noted that arteriovenous fistula, by direct arterial inflow to the venous side, can cause venous hypertension and the characteristic venotensive changes resulting from this (see later).

There is much variation between individuals in the prominence of normal superficial veins when standing. Not only may the calibre of veins be very different between one person and another but the ease with which they are seen will differ greatly according to the depth of subcutaneous tissue and general skin texture. The superficial veins of a lean athletic person will appear large and easily seen but in the amply covered subject, perhaps with equally large veins, they will be far less obvious. Superficial veins may vary from one hour to the next in changing conditions of heat or cold. In women, the size of veins is greatly affected by the hormonal state; for example, there is obvious enlargement just before menstruation, and in pregnancy there is substantial prolonged enlargement which may be an important factor in the development of varicose veins. Other variations are related to vasomotor control; for instance, the tone of superficial veins in the lower part of the leg increases considerably on standing as part of a vasomotor reflex, adjusting veins to meet the increased pressure. For these reasons size alone is not a satisfactory indication of abnormality in a superficial vein unless the enlargement is gross. However, certain other changes may be present that allow immediate recognition of abnormality.

This change in the veins has been recognized since antiquity and is the most significant visible sign of abnormality. The Latin ‘varix’ (pleural ‘varices’), possibly derived from ‘varus’, meaning bent, specifically refers to tortuous dilatation of a vein. The word varicose is defined in medical dictionaries as describing veins that are tortuous, twisted, knotted, or lengthened. It may be seen in greatly varying forms, in small calibre veins running over a considerable distance, in a convoluted mass of enormously enlarged veins (Fig. 16) 438, or, at the other extreme, a single bulge. This change is almost always associated, intermittently or continuously, with substantial flow in reverse direction to that natural for the vein. By far the most common example is seen in superficial vein incompetence where strong gravitational downflow occurs repeatedly in varicose veins, with progressive enlargement and increasing tortuosity in the affected veins. Conversely, high flow in a normal direction, at increased pressure, intermittently or continuously, will cause enlargement but seldom accompanied by tortuosity.

A saphenous vein, as opposed to its branches, seldom becomes tortuous, perhaps because it is too robust, but often one or more saccules may be seen or palpated along its length (Fig. 17(a)) 439. The term ‘saphena varix’ is given to a saccule which commonly develops close to the long saphenous termination (Fig. 17(b)) 439. Usually a saccule is immediately below valve cusps (Fig. 17(c) and (d)) 439 which are leaking heavily and the gross turbulence this causes on coughing gives rise to a characteristic, palpable thrill, readily confirmed by Doppler flowmetry and functional phlebography. It is possible that this turbulent jet of blood beneath the cusps creates a phenomenon similar to the post-stenotic dilatation in arteries described by Holman; occasionally a saccule arises within a cusp, but again this can be attributed to turbulence in malaligned cusps. However, this assumes that the initiating defect is the leaking valve but, alternatively, the primary fault could be weakening of the vein wall causing separation of the cusps and a resulting valvular incompetence, with the saccule as obvious evidence of structural failure in the wall. Perhaps it is most likely that both processes combine, each aggravating the other. However derived, the presence of a saccule is clear indication of an incompetent valve and, therefore, reversed flow down the vein when upright and exercising. Saccules are occasionally seen separately from valves but usually this dichotomy will be part of a more extensive process, with a grossly enlarged and sacculated vein due to generalized weakening of its walls.

Varicose veins commonly become adherent to overlying skin and may so stretch it that the dark blue venous blood shows through very clearly. This fragile covering will be vulnerable to minor trauma which may cause heavy haemorrhage.

Extensive patterns of radiating venules are commonly seen around the ankle and on the foot (corona phlebectatica). These flares of veins (Fig. 18(a)) 440 indicate venous congestion with increased venous pressure. They occur more readily in the weakened tissues of the elderly and are not necessarily the precursors of ulceration. These veins must be distinguished from small clusters of intradermal venules (thread or spider veins) seen on the thigh or upper leg increasingly as middle age approaches; these may signify underlying venous disorder (Fig. 18(b)) 440 but often occur without any evidence of an abnormality.

Varicose veins commonly give a palpable impulse when the patient coughs. This is because there is no functioning valve between the abdomen and the vein, and it confirms incompetence in the valves of deep and superficial veins leading down to this point. A high proportion of patients with incompetence in the long saphenous system lack any valves in the deep veins above the saphenous termination so that abdominal pressure is easily transmitted to varicosities in the limb.

Normally a superficial vein does not feel warm to the touch when compared with the neighbouring skin. Veins carrying a strong reversed flow of blood that has just emerged from a deep vein at true body temperature, as in simple varicose veins, often show obvious warmth to the touch, in comparison with skin alongside. This is valuable confirmation of the vein's abnormal state. Similarly, enlarged veins caused by arteriovenous fistula will feel warm to the touch.

When the limb is elevated the veins will empty and the space occupied by large varicose veins becomes a hollow or a groove readily palpable or even visible. This is particularly marked when the surrounding tissues have become fibrotic in response to venous hypertension. Such hollows are often incorrectly diagnosed as fascial apertures enlarged by abnormal perforating veins. In fact, the hollow signifies no more than a large vein, but such a vein may have special significance, possibly related to surge from an underlying perforator.

Enlarged tortuous veins, that is to say, varicose veins, arise in three circumstances of unnatural flow.

1.Simple (or primary) varicose veins. These occur only in the superficial veins of the lower limbs and are by far the most common variety of varicose veins. Such veins have no competent valves and are subject to substantial gravitational downflow when the patient is upright and moving (see Fig. 30 459). This retrograde flow is in reverse to the natural direction allowed by valves and it is plausible to say that varicose veins are caused by the turbulent reversed flow beneath inadequate valves. Equally plausible, however, is to argue that veins with inherently weak walls expand in width and length so that valve cusps separate and allow reverse flow to occur. In this case, as with saphenous saccules discussed earlier, varicose veins could be the result of a vicious circle of weak walls and valve failure, causing turbulent, reversed flow expanding the walls still further. Certainly there are many studies by light and electron microscopy confirming degenerative changes in the wall structure in these circumstances but the question is whether this is a primary process or secondary to undue stress on the walls. This debate is unresolved and both circumstances may play a part, each aggravating the other. Whatever initiates the retrograde flow, it is a useful rule to regard tortuous veins as veins with intermittent or continuous reverse (retrograde) flow in them. Certainly this is true in commonplace, simple varicose veins, which are the expression of a dynamic phenomenon and not merely static distension.

2.Secondary varicose veins. Tortuosity is often seen in superficial veins carrying reversed flow as part of a collateral mechanism compensating for obstruction in a neighbouring deep vein. This is an acquired response and it seems that enforced reversed flow against the natural direction will cause enlargement and tortuosity in previously normal veins, for example, suprapubic veins acting as collaterals to iliac vein obstruction (see Fig. 58(d) 579), or in oesophageal varices in portal hypertension. By contrast, veins acting as collaterals but taking flow in their natural direction, enlarge but seldom show tortuosity, for example, in long saphenous branches overlying obstructed popliteal or femoral deep veins. The determining factor seems enforced reversed flow. (Note that clinical observation is often confused by the coexistence of deep vein obstruction and simple superficial vein incompetence in the same limb.)

3.Arteriovenous fistula. Tortuosity is often present in lesser veins in the vicinity of an arteriovenous fistula but the major veins leading from it enlarge without tortuosity.

Tortuosity (varicosity) in veins gives a strong indication of reversed flow in them and this may be due to either gravitational downflow in incompetent superficial veins (as in simple varicose veins) or enforced reversed flow. This occurs most commonly in collateral branch veins past deep vein obstruction but is also seen in veins near to arteriovenous fistula.

It is possible for both states to be present in the same limb.

As explained above, venous hypertension of varying severity is a common consequence of venous disorder. Raised venous pressure will cause a corresponding increase in capillary pressure and, if sustained over long periods with inadequate relief, will cause characteristic changes in the skin and subcutaneous tissues. These are mainly the result of excess capillary transudation carrying with it protein molecules (Fig. 19) 441 and leading to deposition of fibrin which forms a barrier to nutritional exchange between capillaries and the surrounding tissues. Other substances are also extravasated, including haemosiderin which eventually gives the characteristic brown skin pigmentation of venous hypertension. The venotensive changes listed below will take many months, or even years, to develop fully. They occur in varying combinations of severity and extent, and are to be found where the venous pressure is greatest. In this respect their position in the lower leg is gravitationally determined but an exception is seen with arteriovenous fistula where the high venous pressure is related to the arterial inflow in that vicinity. A number of conditions can cause venous hypertension, and the following changes may be seen in varying degree in any of them as a direct result of the raised venous pressure.

This is mainly due to oedema which may be localized or found extensively over the limb, according to the nature of the venous abnormality causing it. The volume of overdistended veins can also make a significant contribution to the bulk of a limb, especially in foot and leg, when the patient is standing. It must be remembered that there are a number of other causes for oedema in a limb and these are summarized in Table 1 214 and Fig. 19 441. Inadequate lymphatic drainage causing oedema (see Chapter 9 64) can be an added component to venous disorders, particularly in congenital states.

A characteristic diffuse fibrosis develops in the subcutaneous tissues. This may vary from a slight thickening at an early stage, through to extensive areas of hard tissue in which the veins form large hollows and grooves evident when the leg is elevated. These changes may be accentuated by fat necrosis and chronic inflammatory changes. The terms ‘lipodermatosclerosis’ or ‘liposclerosis’ are often used to describe induration due to venous disorder.

This is one of the most characteristic signs of venotension and is due to the accumulation of haemosiderin in the skin. It is often the earliest change to be seen and should immediately arouse suspicion of a venous disorder. If accompanied by the other changes given here, it is diagnostic of venous hypertension (see Fig. 46(a) (iii) 490).

If venous hypertension and the changes it causes remain untreated, progressive deterioration in skin nutrition leads to small areas of tissue death which coalesce to form an ulcer. A venous ulcer will always be surrounded by pigmented skin and at least some induration (see Fig. 47(a) 495, Fig. 56(a) 557, and Fig. 57(g) 572,573,574) but there is great variation in severity and extent of these accompanying features; in long-standing ulcers the neighbouring skin may also show a characteristic white scarring known as ‘atrophie blanche’. The changes given above are typical of venous ulceration and distinguish it from other forms of ulcer which often require completely different treatment. Correct diagnosis of the various ulcers that may be seen on the leg and foot is of considerable importance and is discussed later (see Ulcers of the leg).

In venous hypertension the skin is particularly prone to eczema and is excessively vulnerable to any sensitizing agents or allergens applied to it. Pigmented areas are most affected, but often small patches of eczema can be seen overlying varicosities and clearly related to their distribution (see Fig. 46(a)(ii) 490). In these circumstances, pruritus will be a prominent symptom and scratching will damage the skin further. Once eczema has become established, it may appear on distant parts of the body as a more general sensitization. The appearance of eczema in the vicinity of varicose veins should always be a warning that progressive skin changes are likely. All too often eczema is aggravated by sensitization to medical products applied to the skin, or materials in the fabric of elastic stockings. Antibiotic creams are particular offenders in causing skin reactions.

In women, discomfort associated with varicose veins is most marked over a few days before menstruation. This is often described as aching, stinging, or burning and the veins become more prominent;

Nocturnal cramps often appear related to varicose veins. This is particularly evident when the cramps occur only on the side affected by varicose veins. Moreover, attacks of cramp may cease following successful surgery to the veins. This association with varicosities is well established but ill understood; however, nocturnal cramp is a common condition in older people so that it is difficult to predict when elimination of varicosities will relieve it and no promise upon this should be given to patients before treatment. In the elderly, care must be taken to distinguish between simple cramp and ischaemic nocturnal rest pain; both are relieved by standing out of bed but in ischaemia the ankle pulses will be reduced or absent on palpation or Doppler flowmeter examination.

There is little relationship between the size of varicose veins and the discomforts complained of. Large, long-standing varicose veins may cause no admitted discomfort and, indeed, in these patients it may be difficult to persuade them to have treatment. Relatively small varicosities lying directly under the skin or intradermally, particularly if they have appeared recently, often seem to cause most discomfort, especially premenstrually in women.

If venous disorder is accompanied by venotensive changes then one or more of the following symptoms is also likely to be present.

Pruritus This is commonly an early sign of venotensive skin change and repeated scratching by the patient may break the skin, possibly initiating an ulcer.

Increased discomfort The sense of general discomfort and heaviness or actual pain is increased. If an ulcer is present, this certainly causes discomfort, and often real pain if the ulcer is infected with Staphyloccus aureus or Streptococcus viridans. An ulcer will produce discharge varying from watery fluid through to frank pus and may be accompanied by unpleasant odour. Such manifestations cause the patient distress and a feeling of social insecurity, accentuated by the bandages or strong stockings used in treatment. Within a society venous ulcers are a significant cause for disability, often under-rated, and absence from work.

Venous claudication Extensive post-thrombotic venous obstruction in popliteal and femoral veins may so impede venous return that a few minutes of exercise cause considerable increase in venous pressure, well above the normal maximum. This is accompanied by a bursting sensation in the calf which quickly becomes unbearable and forces the patient to stop walking. (The term claudication, derived from the name of the Emperor Claudius, means ‘limping’. It is most commonly used in connection with states of arterial insufficiency but is also used by neurologists for symptoms caused by compression of the cauda equina.) In venous claudication, the clinical features of venous obstruction will always be present and fully confirmed by the special investigations. Care must be taken to ensure that the claudication is not in fact due to arterial insufficiency coincidentally present with a venous disorder. In ischaemia, swelling of the foot can be due to the patient hanging the leg out of bed in order to relieve rest pain; this is not rare and, if the limb is elevated because it is misdiagnosed as a venous disorder, the severity of the condition is greatly aggravated and may lead to loss of the limb.

It is important to have a clear statement by the patient of their complaint and the reason for dissatisfaction with their veins. Visible varicose veins tend to be blamed for any discomfort in the limb but this may have a very different origin and the symptoms must match the venous abnormality.

Certain aspects of medical history are important, particularly the likelihood of a previous deep vein thrombosis, so often long forgotten but yet a potent cause of venous disorder. In this respect, any history of ‘white leg of pregnancy’, major fractures of lower limbs or pelvis, prolonged immobilization in traction or plaster of Paris, or of major illness, should be enquired for. A family history and the age of first appearance of varicose veins may have a bearing upon prognosis and policy of management. Knowledge of previous treatment is essential as this will have fragmented anatomy of the superficial veins.

Unless stated otherwise, examination is carried out with the patient upright, that is to say in the position in which venous problems arise and venous defects are most evident. This is best done by asking the patient to stand on a strengthened couch or platform with appropriate handrails on the wall nearby.

Careful inspection in good light is fundamental to observe the pattern of prominent veins and detect any skin changes of venous disorder (Fig. 20) 442. The feet must be included in this and, if there is any hint of previous deep vein thrombosis, the pubes and lower abdomen must also be inspected. There is much to be learnt from the scars of any previous operations. If tortuous veins are present these must be traced along their full length and for this an oblique light throwing the veins into relief is most helpful. The following questions should be borne in mind.

Do the veins fall within long or short saphenous distribution or is this uncertain; is another and unusual source possible?

Is visible evidence of venous hypertension present, particularly pigmentation, swelling, and ulceration?

Light touch, almost brushing the skin, is very helpful in detecting or locating veins. Consider the following questions.

If there is apparent swelling, is there any pitting oedema?

Are varicose veins ‘hot’ to touch, do they show a cough impulse?

If there is an isolated bulge on the inner thigh, is there a thrill on coughing indicating an underlying jet of blood through a leaking valve?

This is a most important step, defining clearly the overall pattern of enlarged veins, including those that are not visible. The ‘tap-wave’ test is an essential skill in this respect.

In the standing patient with fully distended veins, a tap or sharp compression of a vein will send a corresponding wave of movement along its length, easily detected by light touch. Thus, one examining hand ‘taps’ on the vein in its lower part (so that valves do not dampen the effect) whilst fingers of the other hand locate the signal in its upper part (Fig. 21) 443, moving progressively up the limb. In this way veins not detectable by any other clinical means are easily located and traced along their length. This procedure does not reveal much about function and is not reliable in assessing valve competence but it does swiftly map out the pattern of veins otherwise concealed from touch or sight, and this alone can turn speculative diagnosis to a probable one.

With the limb elevated to 45°, the veins will empty so that large subcutaneous veins become a gutter or a hollow. This can prove a valuable addition to ‘mapping out’, and in the detection of varicose veins concealed by subcutaneous fat the presence of a hollow helps in the recognition of early venous induration. It has already been pointed out that a hollow is seldom due to a fascial deficiency but is the site of a large varicosity and does not necessarily signify that an enlarged perforator underlies it.

The features so far described give the observable changes that may be present in venous disorders. These give indirect evidence of abnormal function in veins but few are diagnostic of a specific state. Of the clinical tests, relying solely on the examiner's senses, only two are capable of giving a specific diagnosis. In both the following tests the use of an encircling rubber band to occlude superficial veins is avoided, partly because it may cause artefacts by constricting the deep veins, and also because it does not localize the superficial veins at fault.

This test is based upon demonstration that temporary selective occlusion of one or more superficial veins by localized finger pressure will delay the filling of varicose veins when the patient first stands after the veins have been emptied by elevation of the limb (Fig. 22) 444,445. It shows that the varicose veins fill by downflow in the vein selected for occlusion and, therefore, its valves must be incompetent. This is of great diagnostic value and accurately identifies simple (primary) varicose veins. When positive it is virtual proof of this, but no great reliance can be placed on a negative result in the exclusion of superficial vein incompetence, for example, when the likely pathway of incompetence has been misidentified (say, long saphenous), and the real source of incompetence is elsewhere (say, short saphenous) and has been overlooked. Other aspects of this test are considered later in the section discussing superficial vein incompetence, the state it is pre-eminent in recognizing.

This type of test depends upon the change in the distended varicose veins of an upright patient exercising whilst a selected superficial vein is occluded to prevent downflow (Fig. 23) 446. In the first stage it is shown that exercise by rising on the toes does not deflate the veins. Then, the main pathway of incompetence previously identified by selective Trendelenburg test, often a saphenous vein, is occluded by localized finger pressure and the patient is exercised as before. If the varicose veins become less prominent and softer to touch, it is clear that, when downflow in the superficial vein is prevented, exercise succeeds in emptying the varicose veins. This confirms that the deep vein pumping mechanism is functioning satisfactorily and the fault lies in the superficial vein under test which is capable of filling the varicosities as fast as they are emptied by the deep veins. A positive response gives meaningful confirmation of this; an uncertain or failed response raises suspicion of deep vein insufficiency but does not give acceptable proof of this. This test is referred to again in the section on superficial vein incompetence.

With superficial vein incompetence these clinical tests can give a firm diagnosis, sufficient to act upon clinically. In other venous disorders reliance has to be placed on investigation with instruments measuring speed and direction of flow, pressure or volume change, or outlining of the veins and displaying their function by phlebography or ultrasonic imaging (ultrasonography).

The basic defects that characterize venous disorder become apparent when exercising in an upright position and are readily detected by instruments and imaging techniques.

Demonstration of flow by ultrasound. The directional Doppler flowmeter and ultrasonography

Flow in the direction that should be opposed by valves is abnormal and its presence indicates that the valves are incompetent or absent. A directional Doppler flowmeter (or more correctly, velocimeter) can detect this with great clarity. With this instrument a piezoelectric crystal in the probe emits a continuous ultrasound signal that is reflected back by red cells to a receiving crystal. According to the speed and direction of movement of the red cells, there is a Doppler shift in the phase of the signal which is recognized by the machine and made apparent audibly, by a needle gauge, by LED display, or by oscillograph; a permanent record is provided either by a chart recorder or by some form of computer printout. In order to facilitate the passage of ultrasound between probe and tissues a coupling gel is used on the skin. If a lightweight, flatheaded probe is used this can be held in the hand against skin without displacement when the patient moves (Fig. 24) 447,448 and allows rapid repositioning of the probe so that several different sites may be examined in quick succession. The signal generated represents the speed of flow but not the volume; thus a high speed jet of blood leaking through valve cusps may cause a strong signal which can be misleading if more representative flow a short distance away is not sampled. However, such sharply localized, high velocity flow in itself confirms the presence of a leaking valve although it does not necessarily indicate the overall severity of incompetence. In tortuous veins, confused directional signals may be obtained due to the close proximity of conflicting flows or from uncertainty about the orientation, upwards or downwards, of the segment of tortuous vein under the probe. These difficulties can be resolved by asking the patient to cough in order to create a spurt of downward flow, or, by deliberately pressing the vein below the probe to cause a small peak of upward flow. The Doppler flowmeter is at its best over superficial veins such as a saphenous vein or its varicose branches. Much useful information can also be obtained from the deep veins, but here there may be uncertainty in distinguishing which deep vein is being picked up or, indeed, whether the signal is coming from an intervening superficial vein, for example, a short saphenous vein overlying the popliteal vein. The characteristic superficial vein flow patterns found in the various venous disorders are described later in this section. It is sufficient to say here that the directional Doppler flowmeter used in this way can give immediate positive confirmation of incompetence in superficial veins or give warning that deep vein problems may be present.

Pulsed beam ultrasonography provides a much more sophisticated demonstration by giving an image of veins and their valves on a display screen. It will show movement of these structures and also the direction and speed of blood flow within them. This is particularly valuable for detailed study of short lengths of deep veins and will be described further under Imaging techniques. Similarly, phlebography may be used to visualize the pattern of flow within superficial and deep veins.

Increased flow in superficial veins in the normal direction can be highly significant and occurs in two circumstances. It may occur when superficial veins, including saphenous veins, are acting as collaterals past occlusion in the underlying deep veins (see Fig. 13 435 and Fig. 57(b) 566,567). It will also be found in the veins above an arteriovenous fistula but here an added feature will be strongly pulsatile return flow in time with the heartbeats. This must be distinguished from the weak pulsation often noticed in fully distended veins, congested by a short period of standing without movement and due to transmission of pulsation from neighbouring arteries. It is most evident in venous disorders where valve incompetence causes rapid congestion within the limb; pulsation may also be found, and is easily seen, in cardiac failure with tricuspid valve incompetence.

With exercise, in the upright position, the venous pressure within the limb normally falls, and when exercise ceases (Fig. 15) 437 it takes at least 20 s before the original pressure is regained (restitution, refilling, or recovery time). In states of superficial or deep vein valvular incompetence the refilling time may be decisively shortened by reflux of venous blood down the limb and this is characteristic of conditions causing venous hypertension (Fig. 25) 449. Measurements of venous pressure changes in response to exercise may be obtained by the following means.

By direct insertion of a needle or plastic cannula into a foot or ankle vein. The pressure is best measured by a calibrated electronic transducer and the changes shown as a tracing on a chart recorder as they occur.

By indirect methods without the need to puncture a vein, and indicating the scale and rate of pressure changes rather than by giving accurate measurement. Photoplethysmography, described below, is a simple but effective way of doing this and in most circumstances can give a good estimation of valvular competence by gauging the recovery time.

The limb volume closely parallels the venous pressure so that when the patient is standing still it is maximal but after exercise, which has expelled blood from the limb, both venous pressure and limb volume will fall. The reduction in volume will indicate the amount of blood expelled by exercise; the time taken for the volume to return to its original value is a good indication of valve competence. With fully competent valves this will be at least 20 s, but when superficial or deep valve incompetence is present this will be shortened according to the severity of the condition. Various methods may be used for measuring and recording volume changes as they occur (plethysmography).

Fluid plethysmography The leg or foot is immersed in water within a fixed chamber and the amount of fluid displaced from this is measured. The weight of fluid may cause artefacts and the range of exercise possible for the patient is somewhat limited. Nevertheless, it is capable of giving reliable results.

Air plethysmography The leg is surrounded by an air-filled PVC chamber and the amount of air entering or leaving is measured to give changes in limb volume. It allows the patient more freedom of movement but must be carried out in conditions of stable temperature to prevent errors from thermal expansion or contraction of air within the container. In use, this proves to be a practical method, reliably indicating the speed and degree of volume change with exercise.

Electrical impedance plethysmography This method estimates the volume change within the limb by alteration in the electrical resistance which varies with the volume.

Strain gauge plethysmography The limb is encircled by a slender elastic tube containing mercury or similar electrically conducting fluid, the resistance of which will vary as the diameter of the elastic tube changes. Thus, when exercise reduces the volume, the elastic tube will shorten to give a broader diameter and the resistance will fall; as the volume is regained the tube is stretched and the resistance increases again. This method is simple to apply and gives a good indication of the volume changes occurring in the limb. However, it is only sampling the changes at one or two levels and cannot measure the expelled volume; its main value is in gauging the recovery time.

Photoplethysmography This method (Fig. 26) 450,451 photoelectrically estimates the number of red cells in the skin capillary bed underlying the transducer. A light emitting diode, which gives off no heat likely to cause artefacts, illuminates the capillary bed with infrared light. This is absorbed by haemoglobin in the red cells and the amount transmitted back to a photoelectric sensor will vary in accordance with the number of red cells underlying it. The signals are recorded as a line tracing on a chart recorder or computerized display. It has been shown that the degree of congestion of red cells in the skin capillaries bears a close relationship to the venous pressure in the limb and, thus, the signal from the photoplethysmograph closely parallels the venous pressure changes. It can certainly give a good estimation of the recovery time following exercise and this is its chief value. If two successive recordings are made, without changing the probe position or the instrument settings, comparison of the rate and extent of venous pressure change in different circumstances can be achieved, for example, in response to exercise with and without saphenous occlusion (see Fig. 34(c) 465). The method has certain vagaries but, with experience, can give a good portrayal of venous changes in the limb, taking only a few minutes and with no discomfort to the patient. It is a very practical method for assessing the effectiveness of musculovenous pumping, the overall competence of valves, and the likelihood of venous hypertension being present.

Maximum venous outflow (MVO) Plethysmography, usually by strain gauge, may be used to measure the maximal speed at which venous blood can leave a limb and from this estimate any restriction in venous outflow. With the patient horizontal and the lower limbs elevated, a pneumatic cuff is used to cause venous congestion. The cuff is then abruptly released and, from the tracing on a chart recorder, reduction in volume (limb circumference if a strain gauge is used) over the first few seconds is expressed as a percentage of the total fall in volume. For example, in a normal limb 90 per cent of the total fall in volume will occur in the first 3 s ( Fig. 27 452, left) but in ileofemoral obstruction with poor collaterals, perhaps only 45 per cent fall would occur in the same time ( Fig. 27 452, right).

Although useful, estimation of maximal venous outflow does not give specific information and adds little to that gained from the other tests with instruments described above. However, it can help in excluding a venous cause in an oedematous limb, so that unnecessary phlebography is avoided but, overall, the information gained is greatly inferior to that from techniques visualizing veins.

If the special tests with instruments have not satisfactorily explained the nature of the venous disorder then a technique visualizing the veins can be used. This will not only display abnormal outline to the veins, such as occlusion or deformity, but will show if valves are defective or absent. In addition, abnormal patterns of superficial or deep venous flow, in response to exercise, can be demonstrated. The two main techniques are functional phlebography and ultrasonography.

Phlebography has been transformed over recent years by several factors, particularly the use of a non-irritating osmolar opaque medium, such as Iohexol, which causes no discomfort and does not precipitate phlebitis, the introduction of the image intensifier which allows prolonged viewing without exposing the patient to excessive radiation, and the realization that the patient must be examined in the position that causes venous problems (Fig. 28(a)(i)) 453, that is to say, upright. With the exception of acute thrombosis in the deep veins, it is only when the patient is near upright and exercising intermittently that many features of venous disorder become apparent. The essence of functional phlebography is to study the functioning of the veins whilst they are working to return blood against gravity. This will allow valve function to be gauged and the causes for inadequate musculovenous pumping to be identified; occlusion or severe deformity in deep veins can be recognized, unnatural enlargement or tortuosity can be seen, and unusual flow patterns, for example collateral flow in superficial veins, are recognized. It is essential that the pattern of venous return should not be distorted by using such artefacts as constricting bands (Fig. 28(a) (ii)) 453. The opportunity to witness events is very brief and is limited by the fact that only part of the limb can be viewed at one moment, the need to keep the amount of opaque medium within safe limits, and the rapidity with which the changes come and go with exercise.

It is not really possible for a radiologist to give comprehensive functional examination of a limb without knowing the likely nature of the problem that he should concentrate upon. It is essential that he should be well briefed by the surgeon or, even better, that the surgeon should be present, guiding the radiologist through the features to be looked for. For these reasons, functional phlebography is a skilled and rather specialized examination. It is important to record the rapidly changing events in some fashion for subsequent study and much can be learnt from this. Depending on the sophistication of apparatus, either multiple static films can be taken or the whole procedure recorded videographically. One problem is to know the relationship in depth of veins one to another and misinterpretation is all too easy without some method of clarification. The simplest way is to take two views of the limb in different rotations so that the relative shift in the veins gives an immediate understanding of their relationship. Before starting, various manoeuvres are rehearsed with the patient, such as exercise by rising up on the toes or rotating the limb inwards and outwards. Any movement by the patient causes immediate changes within the veins, dispersing the opacified blood and quickly creating a confused picture, and for this reason requests to exercise or rotate the limb must be carefully timed. Throughout the examination it must be remembered that only streams of opacified blood are seen and it is quite possible for a large vein to remain invisible because the opacified stream has chosen other channels; failure of a known vein to appear does not necessarily mean that it is occluded and different ways may have to be found to persuade opacified blood to enter it. Functional phlebography is not an easy method but it is immensely rewarding to those who familiarize themselves with it. It is not possible here to describe functional phlebography in detail, but some of the main manoeuvres will be outlined and examples of the results that can be obtained are given in the sections upon the various disorders. The method preferred by the Oxford Vascular Service is described here (Fig. 28(a) (iii)) 454, but other centres have evolved their particular techniques for dynamic phlebography and obtain similar results.

If the patient is tilted foot down to 50° or more and contrast medium is introduced by needle into a superficial vein on the calf, it will be seen to drift down the superficial veins until checked by a valve and soon appear in the deep veins of the leg. This downward movement is because the specific gravity of the opaque medium is higher than that of blood. If injection is continued up to, say, 100 ml, the deep veins will fill steadily so that they are clearly outlined up to the iliac veins and beyond (Fig. 28(b) (i)) 455. Even a small exercise movement will cause rapid movement upwards in the deep veins with partial emptying of the superficial veins and segmentation of opacified blood between their valves. If movement continues the picture will quickly become confused and all opaque medium will soon leave the limb. During the phase of static filling, opacified blood enters tibial and peroneal veins by multiple perforators, but often it will similarly enter large venous sinuses, the pumping chambers, lying within muscles. This is a normal phenomenon but, for instance, if a single large gastrocnemius vein fills in this way it may be mistaken for a short saphenous vein. Static filling of the deep veins, as just described, is the first stage in functional phlebography and will test the ability of the deep veins to fill normally. Judicious exercise movements may be given during this stage and subsequently to study the patterns of flow. The valves of the deep veins can be shown by lowering the head of the table to near horizontal, so that the veins deflate slightly; the table is then rapidly returned to near vertical again (the swill test), which causes the valve cusps to fill and gives a clear impression of their number and, to some extent, their competence (see Fig. 1 423, Fig. 28(b)(ii) 455, and Fig. 48(e) 503).

The procedure is carried out as described above, with the needle introduced through any convenient enlarged vein on the calf; this has the advantage that the direction of movement of the blood from these veins with slight exercise gives an important indication of function. When about 5 ml of medium has been injected the patient is asked to give a small exercise movement and the effect of this is watched on the screen. In simple incompetence of superficial veins the medium will sweep downwards and appear in deep veins (Fig. 28(b) (iii)) 455; in occlusion or severe deformity of deep veins, the medium will be swept up the superficial vein as collateral flow (see Fig. 13 435). In other cases where perhaps both superficial and deep valves are incompetent heavy surge back and forth may be seen with exercise (Fig. 61(b)) 597.

Other sites for injection may be used, including varicosities on the thigh. If the deep veins fail to fill and the opacified blood streams up superficial veins, as may happen in post-thrombotic syndrome, it may be necessary to reposition the needle to a foot vein to give maximum opportunity for outlining deep veins in the leg.

Contrast medium injected moderately quickly, with the patient in only slightly head-up tilt, will tend to outline the vein in an ‘upward’ direction and, in effect, trace it to its ‘origin’. In superficial incompetence this method is of value in showing the source of incompetence, for example, a short saphenous termination ( Fig. 28(c) 456 (i)) or a recurrent set of varicose veins of uncertain origin (see Figs. 53(a)(iii) and (b), (c), (d) 551,552,553,554). This method gives little information on function but it can be combined with information gained from functional phlebography to give comprehensive views of the veins at fault (Fig. 28(c) (ii)) 457. However, the filling of veins by varicography is capricious and results can be misleading until experience is gained.

Pulsed beam ultrasound scanning creates an image of tissue interfaces and moving blood on a video display unit. This can be used to portray a section through arteries and veins in any plane, from horizontal to vertical. The plane is chosen to show the structure under study to best advantage. In this way a portion of vein over some inches may be shown with its walls and valves clearly outlined and any movements by them demonstrated. The direction and speed of blood flow within the vessel at any point can be individually picked out by a Doppler flow facility and recorded separately (duplex); colour flow scanning (triplex) has the additional feature of displaying flow in a colour representing its direction of movement and showing the velocity by the intensity of the colour (Fig. 29) 458. Thus, the vein walls and lumen can be outlined and flow studied, clot may be recognized by absence of flow and immobile vein walls, and the structure of valves and their competence can be scrutinized in detail. The anatomy of veins can be visualized preoperatively, for example, to demonstrate the level and manner of short saphenous termination; individual deep veins and their branches can be distinguished and flow patterns displayed, so that, for instance, incompetence in a gastrocnemius vein can be recognized (immediately apparent by colour flow) and the reflux within it estimated to assess its significance. This is possible because the diameter and speed of flow within any designated vessel can be measured and from this the volume of flow, either expelled upwards or refluxed downwards, can be calculated. In the popliteal vein this will indicate the effectiveness of the musculovenous pump below the knee or, conversely, the severity of reflux in the deep veins at that level.

The advantages of ultrasonography are that it is non-invasive and can be used for prolonged viewing with repeated cycles of exercise in a way not possible with phlebography and, moreover, the running costs are decidedly less. It is an excellent method for special study of localized areas of vein, both for research and in the practical management of some venous problems. It is already a practical alternative to phlebology for detecting acute thrombosis or in the display of specific structures, such as a short saphenous termination or a valve suspected of leaking. Its potential for future development is considerable and eventually it may displace phlebology for many purposes in the lower limb.

In the upright position, each contraction of the muscles in a normal limb pumps blood upwards and it is prevented from returning by effective valves. The immediate reduction in the venous pressure and slackening of the deep veins in lower leg and foot caused by this gives opportunity for superficial veins to empty into the deep veins, ready to be pumped up with the next movement. Normally the valves in the superficial veins limit this inward flow so that only a short segment between each valve can empty through the corresponding perforating veins and disorderly widespread transfer of blood from superficial to deep veins is prevented. However, if there is extensive incompetence in the superficial valves, it is possible for blood to spill over from deep veins at high level, down the superficial veins and, finally, to enter the deep veins at low level every time these veins fall slack after muscle contraction (Fig. 30) 459. This is the mechanism underlying the development of simple or primary varicose veins and is, by far, the most common venous disorder.

Such abnormal downflow is gravitationally determined. It only occurs when the patient is upright, or nearly so. In addition to muscular activity, it occurs as a single episode, when the patient rises from horizontal to vertical position, or when simple external pressure to calf or foot partially empties the deep veins. It will not occur with exercise unless there is a reasonably effective deep vein pumping mechanism. In this way, a retrograde circuit of flow is set up, spilling over from a deep vein somewhere above a musculovenous pumping mechanism, down incompetent superficial veins and through perforators to enter deep veins below the pumping mechanism. This may be any group of muscles in the leg or the foot itself, as described earlier. Endless repetition of this cycle of reversed flow causes the superficial veins to become enlarged and tortuous, that is to say, to become varicose veins. However, the main stem of the saphenous veins appears too robust to develop this change and it is the branch veins that do so. Varicose veins are the response to a dynamic process of strong reversed flow and not just by static distension.

A typical retrograde circuit (Fig. 31) 460 is based on a superficial vein, often a long or short saphenous vein with defective or absent valves. The circuit has four components.

In a retrograde circuit based on an incompetent long or short saphenous vein, its upper end provides the source, its main stem and incompetent branches form the pathway of incompetence, and one or more perforating veins are the re-entry points ( Fig. 32 461 and Fig. 33 462. The deep veins receiving this downflow may be principal conduits, such as the tibial veins, or the venous sinuses (pumping chambers) within any muscle group in the leg, or the veins of the foot (Fig. 33(b)) 462. Although the source is usually the upper end of a saphenous vein, any communication between deep and superficial veins at high level may take on this role; not infrequently pelvic veins provide a source, especially during pregnancy, giving varicosities in vulva and upper thigh, and these may persist after childbirth (see Fig. 39 475,476). Less usual sources are particularly likely to occur when superficial vein anatomy has been fragmented by previous surgery, for example, after high saphenous ligation, a midthigh perforator may become the source of recurrence ( Fig. 53(d) 554 (iii)). There are numerous variations on this theme but each has the same components, a higher level source, a pathway of incompetence, and re-entry point(s) provided by perforating veins at lower levels, including the foot. This state is usually curable by removal of the source and the pathway of incompetence, but enlarged re-entry points (one or more perforators) that allow backflow may also require closing off. An understanding of the retrograde circuit in superficial vein incompetence is essential in the good management of varicose veins and treatment will not be successful unless these components to the circuit are accurately recognized and effectively obliterated by sclerotherapy or removed by surgery. The more completely this is done, the more effective and permanent treatment will be. Several typical retrograde circuits of superficial vein incompetence are illustrated in Figs. 34, 35, 36, and 45 463,464,465,466,467,468,469,488,489.

These arise when there are two or more sources of incompetence causing the varicose veins, for example long and short saphenous vein incompetence both contributing to varicosities on the calf, or a pathway of incompetence that starts in long saphenous vein and then crosses over to join the short saphenous vein from which the varicose veins arise, or vice versa (Fig. 37) 470.

It has already been mentioned that there are many possible unexpected sources of incompetent downflow in superficial veins, such as the internal pudendal vein from the pelvic deep veins or when previous surgery has fragmented normal anatomy; moreover it is also possible for retrograde circuits of incompetence to arise in conjunction with other forms of venous disorder. Some examples of these less usual states are given below.

Varicosities from a long saphenous source may be visible in short saphenous territory or vice versa; one variant of this is a vein running upwards for a short distance before linking on to a branch of the other saphenous system and so giving rise to the apparent paradox of upward flow in a simple varicose vein (Fig. 38) 471,472,473,474. With pregnancy, vulval varicosities arising via pudendal veins from the pelvic veins may appear and persist to provide an obscure source of superficial vein incompetence down thigh and leg (Fig. 39) 475,476. In its most extreme form, this will be even more extensive, taking its source from massive incompetence in the ovarian veins and through the pelvic veins ( Fig. 40(a) 477,478 and (b)); it will be accompanied by severe premenstrual discomfort in the pelvis and in limb varicosities (pelvic congestion syndrome). This is exactly comparable with the equivalent state, in the male, of incompetence in a testicular vein leading to varicose veins at its lower end, but here outside the pelvis and showing as a varicocele in the scrotum; the venous return from this is to pelvic veins but it also has easy communication with veins in the upper thigh.

These patterns of incompetence follow an unexpected course, either by crossing over from one limb to the other or because flow passes from the source in an upward direction for an appreciable distance before cascading down the limb. An example of the former is long saphenous incompetence taking its origin via pubic varicosities crossing over from a surviving branches in a saphenous stump of the opposite side following inadequate surgery there (Fig. 41(a)) 479,480. An example of paradoxical flow may be seen in an extension from the short saphenous vein running upwards to emerge on the inner aspect of midthigh and acting as the source of downflow in a long saphenous vein incompetent below this level (Fig. 41(b)) 481; high ligation of the long saphenous vein will not cure this condition as the fault does not lie here.

These occur when deep vein impairment and superficial vein incompetence coexist. Certainly, a saphenous vein acting as a collateral past deep vein occlusion is often oversized and incompetent but, as the predominant flow is continuous collateral upflow, confusion in diagnosis seldom arises. However, when the lower part of the limb has been spared thrombotic damage and is capable of effective pumping to produce an area of low venous pressure, it is possible for incompetent saphenous branches to spill down to the low pressure area and show the features of typical simple varicose veins. For example, if the femoral vein is occluded in midthigh, but there is no thrombotic damage to the deep veins below the knee, a saphenous vein acting as collateral may develop varicose side branches running down to the foot (Fig. 42(a) (i)) 482. These veins may have no collateral function but become varicose by allowing flow down to the low pressure areas created in foot or lower leg by exercise. Similarly, in iliac vein occlusion, a typical long saphenous vein incompetence, with varicose veins, may develop in the limb beneath this, taking its source from the collateral flow passing from common femoral vein to uppermost saphenous branches and across the pubic region (Fig. 42(a) (ii)) 482. A crossover variety of this sort occurs when an incompetent long saphenous vein of the opposite limb takes source from pubic collaterals that have crossed over to join its superficial epigastric and pudendal branches (Fig. 42(b) (i) and (ii)) 483,484. It is important to recognize this since otherwise surgery to treat apparently simple saphenous incompetence may damage valuable collateral vessels.

The central feature of superficial vein incompetence is lack of effective valves in these veins. This may arise because there is an inborn weakness in the valve cusps or the vein wall, or there is a deficiency in the number of valves. Many patients give a family history suggesting an inherited defect and the fact that simple varicose veins not infrequently first appear at the age of 14 or 15 supports the belief that some form of inborn weakness is responsible in at least some patients. Some authorities believe that the fault is in the vein walls which allow valve cusps to separate and leak. This may certainly be true, but examples are seen where virtually no valves are present, or only vestigial ones, in the superficial veins concerned. It is likely that there are several different

causes for valve failure, each leading to the same final result of incompetence and varicose veins. (See under Spectrum of valve deficiency.)

Many varicose veins first appear in pregnancy and although most will recede again, others will persist (Fig. 43) 485. A likely mechanism is the dilating effect of oestrogen upon the vein walls, affecting their role in retaining valve cusps in good apposition and any uncovering any imperfections here. Apart from this, women are more prone to superficial vein incompetence than men in a ratio of about 2 : 1, again probably due to hormonal influence; this is supported by the fact that women's varicose veins are always more troublesome and prominent just before menstruation. Jobs involving prolonged standing have been shown to increase the likelihood of varicose veins and the incidence increases with age.

Unsightly varicose veins are the most common expression of superficial vein incompetence and women are more likely to complain of this than men. Varying degrees of discomfort are attributed to the clearly visible defect and although this is usually correct, the possibility of another cause should not be overlooked. However, it is possible for the reverse to be true and for the patient to have heavy, uncomfortable legs, caused by substantial superficial vein incompetence but without any visible varicosities. This ‘concealed’ incompetence is not uncommon and is caused by a ‘straight through’ variety of saphenous incompetence which connects with perforators without any intervening varicosities (Fig. 44) 486,487. Conversely, obvious varicose veins may seem unrelated to symptoms elsewhere in the limb, for example, the misleading pattern of varicosities found in the thigh when a large, clearly visible varicosity arises from the saphenous termination and ‘bypasses’ a competent valve in the uppermost long saphenous vein but then joins this vein in its incompetent lower part (Fig. 45) 488,489.

The more severe forms of superficial vein incompetence, with or without varicosities, may overwhelm the pumping mechanism and give rise to venous hypertension. In mild cases this may cause an area of pigmentation, swelling, and slight induration near the ankle, perhaps with a tendency for eczema as shown in Fig. 46(a) 490,491,492,493; in more severe cases venotensive changes will be more extensive and often include ulceration ( Fig. 46(b) 494, Fig. 47 495,496,497,498, Fig. 52 549,550, and Fig. 63(a) 617), which is considered later in this Section. These changes are not specific to superficial vein incompetence (primary varicose veins) and it is important to remember that other venous conditions which create venous hypertension, such as deep vein impairment, can also be a potent cause but require different management.

The general aspects of this have been considered in some detail earlier and will only be summarized here in relation to superficial vein incompetence. The history must always include enquiry for possible previous deep vein thrombosis with pregnancy, serious illness, or limb fractures. This will give warning that deep vein impairment is possible; it is then essential to examine the lower abdomen and pubic region for varicosities acting as collaterals past occluded iliac veins. The following procedure is appropriate and is carried out with the patient standing, the position in which venous problems become evident.

1. Inspection The general pattern of prominent veins and varicosities on all aspects of the limbs and on the lower abdomen is noted, together with any suggestion of saccules on the saphenous veins. The lower leg and foot are scrutinized for signs of venotension. If there is any possibility of diabetes the underside of the foot should be inspected to exclude neuropathic ulceration. General medical considerations should not be overlooked at this stage; because varicose veins are an obvious defect, symptoms are often wrongly attributed to them.

2. Mapping out The importance of commencing examination with a careful mapping out of the abnormal veins and other veins connecting with them cannot be overstated. This is done by inspection, palpation, and use of the tap-wave technique (see Fig. 21 443); the foot must be included and, if there is any suspicion of previous deep vein thrombosis, the lower abdomen and pubes. It may be combined with other observations on the varicosities, such as cough impulse and increased warmth; if there is a palpable saccule on a saphenous vein check for a thrill on coughing in keeping with a leaking valve here.

3. Pathway of incompetence The likely pathway of incompetence from which the varicosities arise should be selected, based on the findings at mapping out.

4. Trendelenburg test A selective Trendelenburg test, using fingers, not any form of tourniquet, should be applied to the suspected pathway of incompetence (see Fig. 22 444,445). This is the key test upon which diagnosis and decision for treatment depends. Perthes' test, exercising by rising on the toes with the pathway of incompetence occluded, is carried out as useful confirmation of the diagnosis (see Fig. 23 446).

In many cases the examination so far will have given clear evidence of the diagnosis and will have accurately identified the pathway of incompetence. However, sometimes the tests are inconclusive and, in any case, it is always useful to have further confirmation. This is easily and quickly provided by use of the directional Doppler flowmeter.

5. Directional Doppler flowmetry The probe is usually placed over the saphenous vein in the lower thigh or upper calf and the response to coughing, squeezing the calf, and rising on the toes noted (see Fig. 24 447,448). If the pathway of incompetence has been correctly identified, a burst of downflow should follow each exercise movement (Fig. 34(b)) 464. If this does not occur, it is possible that the muscles so far exercised are not involved in the retrograde circuit and the effect of raising the foot clear of the ground, with knee straight, should be tried. If varicosities run to the foot this may produce a surprisingly vigorous response.

When downflow has been demonstrated, the test is repeated with the suspected pathway of incompetence occluded by finger pressure well above the probe to confirm that this eliminates the downflow (Fig. 34(b)) 464. The Doppler flowmeter is also a valuable tool in mapping out and demonstrating interconnection between veins, for example, between varicose vein and saphenous vein, or long and short saphenous systems. This is done by placing the probe on one vein and giving sharp compression with the fingers to the other vein; if there is any connection the brief movement of blood this causes is easily transmitted to the vein under the probe.

6. Photoplethysmography If obvious venotensive skin changes are present, and especially if there is ulceration, further evidence will be needed to give positive confirmation of the cause as superficial vein incompetence. This may be elegantly provided by some form of plethysmography and a simple, practical way of carrying this out is by photoplethysmography (see Fig. 26 450,451). It can be used to demonstrate that an abnormally brief recovery time after exercise is restored to near normal when the suspected pathway of incompetence is selectively occluded by finger pressure (not a constricting band) (Fig. 34(c)) 465. An unequivocal response can be accepted as sufficient evidence but if there are any remaining doubts, functional phlebography or ultrasonography may be advisable to exclude deep vein impairment.

7. Functional phlebography This should not be carried out as a routine in varicose vein cases but only when there are special features that require clarification. This method has already been discussed (Fig. 28) 453,454,455,456,457 but the indications and findings in superficial vein incompetence are summarized here.

It gives positive identification of simple incompetence and demonstrates its source if other means have failed to do this.

It gives reassurance that the deep veins are normal and well valved or, conversely, that some form of deep vein impairment is present.

It assists the surgeon by displaying variable anatomy such as the termination of the short saphenous vein.

It identifies an unusual source of incompetence, such as the pelvic veins.

On phlebography the features of superficial vein incompetence causing varicose veins will be:

A demonstration of enlarged and tortuous veins arising from a pathway of incompetence such as a saphenous vein;

Downward flow in varicosities immediately following an exercise movement and entering the deep veins by perforators lower in the limb (Fig. 48(a)) 499.

When the deep veins have been passively filled, not only will this confirm their normal outline but it also gives opportunity to demonstrate the source of incompetence. The patient is asked to make several exercise movements and the area of the suspected source is closely watched on the image intensifier. It is often possible to see spill-over from deep to superficial veins, with flow down the pathway of incompetence (Fig. 48(b), (c) and (d)) 500,501,502, but the radiologist must be given clear guidance by the surgeon upon the probable source.

The swill test will give an overall impression of valves in the deep veins and will often give additional information about the source and pathway of incompetence (Fig. 48(e)) 503.

In short saphenous and recurrent varicosities it may be easiest to locate the source by varicography, using the upward trace technique, as described earlier. The flow of medium will often follow the pathway of incompetence upwards and, via the source, into the deep veins (Fig. 48(f)) 504. This upward flow is capricious and may be diverted before it reaches the objective but usually succeeds. The fact that the patient is near horizontal means that the veins are semicollapsed and this makes it more difficult to evaluate the importance of veins displayed.

8. Ultrasonography Ultrasonography by B mode duplex scanning or by colour flow imaging, previously described (see Fig. 29 458), is particularly useful in short saphenous incompetence where it can give positive confirmation of downflow in an incompetent vein and display the level of short saphenous termination. Similarly it can be used to display details of incompetence in a gastrocnemius vein causing perforator outflow in the calf, or in a groin recurrence.

Treatment of superficial vein incompetence and its manifestations

Varicose veins without accompanying venotensive changes

Here three levels of treatment may be recognized, cosmetic, alleviation of symptoms, and elimination of the underlying incompetent veins to give a lasting cure.

Lesser varicose veins can be disguised by appropriate make-up or the use of elastic support hose. Some patients will settle for these options but most will want the unsightly varicosities banished so that in summer the uncovered limb is blemish free. Sclerotherapy can accomplish this, often with lasting benefit, but in more gross varicose veins the best cosmetic result, and the most lasting, will be given by appropriate surgery, eliminating the source of incompetence without obvious scars, a skill the surgeon should be able to offer.

Symptoms of heaviness and tiredness accompanying varicose veins can certainly be relieved by use of elastic support hose or elastic stockings (see Fig. 59(c) 593), combined with a policy of elevating the limb whenever possible (Fig. 49) 505. However, this is not a cure and elastic support is often tedious to wear, particularly in hot weather. The most effective method will be the elimination of superficial vein incompetence by sclerotherapy or by surgery.

Treatment here will aim at a cure, that is to say complete elimination of the superficial incompetence which causes the unsightly varicosities and symptoms from venous stress. The essentials are correct identification of the source and pathway of incompetence, and their obliteration by sclerotherapy or by surgery. Most failures in these aims are the result of inaccurate identification of the source or inadequate elimination of the pathway.

With this method a suitable chemical, such as 3 per cent sodium tetradecylsulphate, is injected into the varicose veins, or the pathway of incompetence leading to them; this will destroy the endothelium and create a reaction within the veins that eventually seals them into a fibrous cord. To achieve this goal an ‘empty vein–compression bandage’ technique is used. The veins to be treated are identified whilst the patient is standing (Fig. 50 (a) and (b)) 506,507 and likely sites of injection marked with a felt-tipped pen. Injection into an artery is a grave hazard likely to cause extensive gangrene; this is most likely to happen in the vicinity of the ankle and this area should be avoided as far as possible. Although rare, measures to combat anaphylaxis must be at hand (adrenaline, hydrocortisone, antihistamine, intubation).

The patient is then repositioned sitting up on a couch with lower limbs horizontal (Fig. 50(c)) 508, or with legs over the edge in moderate dependency to give slight distension of the veins. Needles, with syringes containing sclerosant attached, are inserted into selected veins and taped to the skin (Fig. 50 (d)–(i)) 509,510,511,512,513,514. The patient then lies flat, the limb is elevated to empty the veins, and the sclerosant is injected (Fig. 50 (j)–(n)) 515,516,517,518,519. In this way, a small quantity of sclerosant produces maximal effect without causing blood clot. While the limb is still in elevation, pressure pads are placed over the sites of injection and a firm bandage applied (Fig. 50 (o)–(v)) 520,521,522,523,524,525,526,527. This prevents blood from re-entering the veins when the patient stands and minimizes clot formation; it also presses the inner walls together to ensure that they will bond firmly with fibrous tissue. Provided that the veins are kept empty in this fashion little discomfort follows the procedure and obliteration of the vein is likely to be permanent (Fig. 50 (w) and (x)) 528,529. Compression is maintained for at least 3 weeks and the patient asked to exercise freely to discourage clotting spreading to the deep veins. Failure to apply effective compression will cause the injected veins to distend with clot so that they are painful (in fact, an induced superficial thrombophlebitis) and eventual recanalization of the vein is likely to occur; in a substantial vein, such as a saphenous vein, this will destroy any remaining valve function so that if the vein reopens it is a large conduit devoid of any restraint by valves and the recurrent state may be more severe than the original one. Although the method is very effective in small to medium calibre veins it does tend to give only temporary occlusion of the larger veins, particularly the saphenous vein itself, so that here recurrence not infrequently occurs after a year or two and further treatment is needed.

Sclerotherapy is seldom as complete as surgery in the obliteration of the incompetent veins and for this reason the patient will often be asked to attend at regular intervals so that further injections may be carried out to any returning varicosities. In this way, for a large set of veins, sclerotherapy tends to be a long-term policy of maintenance rather than the one-time cure intended with surgery. The use of compression bandaging, necessary with sclerotherapy, is undoubtedly tiresome and patients who have had treatment both by injection and by surgery often say that they preferred the surgical treatment. Sclerotherapy has its drawbacks, for example, a discoloration that may persist for many months afterwards, and although its exponents appear effortlessly to overcome these problems, it must not be regarded as an easy alternative to surgery with a requirement for little skill; quite the reverse is true. Injection into an artery, referred to above, is a potential disaster never to lose sight of; if, on sucking back, the needle produces any hint of arterial blood, by colour or pulsatile reflux, it should not be used but immediately repositioned elsewhere. Nevertheless, sclerotherapy is a most valuable method of treatment and in the case of lesser veins often can accomplish treatment scarcely possible for surgery. Perhaps the most reasonable view is to use surgery for the well defined patterns of saphenous incompetence, and use sclerotherapy to back this up when necessary or in the treatment of lesser varicosities. The combination of sclerotherapy with surgical treatment is discussed under Treatment of recurrent varicose veins.

The essential principle with surgery is that the source and the main pathway of incompetence are actually removed; in the case of a saphenous vein, this requires high ligation at its termination, flush with the deep vein, and stripping a substantial part of its length. If an incompetent saphenous vein is left in place, unstripped, it remains open as a valveless conduit running directly down to the low pressure areas beneath the musculovenous pumps, and is likely to form the basis of a new retrograde circuit of incompetence with renewed varicose veins (see under Recurrence below).

Surgical treatment should also remove the main varicosities through a series of small incisions otherwise these veins are liable to persist, much to the patient's disappointment, and will require final elimination by sclerotherapy. Moreover, these varicosities are the distal part of a pathway of incompetence and directly communicate with the low pressure areas so that they are constantly available to re-establish flow from higher levels; not only will they remain visible but they may progressively enlarge.

A further aspect that may require special attention is the site of inflow from incompetent superficial veins to the deep veins at low level, that is to say, the perforating veins. Usually, these are multiple points and it is not practical to identify and remove them surgically, nor is it necessary. However, in some cases one or two individual perforators have become enlarged and give heavy surge back and forth as the muscles contract and relax. When recognized, it is best to remove these veins, since otherwise they may form the source for a new pattern of varicosities running to the foot. However, the perforator must not be regarded as the main offender and its varying role in the venous disorders is considered later in this Section.

The best opportunity for surgical cure is at the first operation because recurrent veins based on a superficial vein anatomy fragmented by previous surgery are much more difficult to treat effectively. The first opportunity must not be wasted by inaccurate identification of the veins at fault or by inadequate surgery. Conscientious surgery for varicose veins is time consuming but very rewarding in terms of immediate comfort and lasting benefit to the patient.

When the characteristic skin changes of venous hypertension are evident and particularly when ulceration is present, care must be taken to be sure that the cause is simple incompetence in superficial veins and not a post-thrombotic deep vein impairment (Fig. 52) 549,550. Surgery to the veins appropriate for the former may well be wholly inappropriate for the latter. Once unequivocal evidence has been obtained that the cause is superficial incompetence and the pathway of this has been accurately defined, treatment may be carried out as described above. The presence of venotensive changes indicates a severe state of incompetence probably best treated by surgery because the large incompetent veins likely to be present may soon reopen after sclerotherapy and more lasting benefit will be given by surgical removal of the source and pathway of incompetence, including the varicose veins themselves.

If the skin is unbroken, or even when a substantial ‘clean’ ulcer is present, there is no reason why surgery should not be performed without any preliminary treatment. However, if infection, such as cellulitis or an ulcer discharging pus, is present, then the patient should have a short period of treatment in hospital with the limb elevated and systemic antibiotics given. This is maintained until the ulcer enters a healing phase, that is, its base is covered with ‘healthy’ granulation tissue, pus is no longer being formed, pathogenic organisms such as Staphylcoccus aureus or Streptococcus viridans have been eliminated, and the skin edges slope smoothly to a thin, grey line of regenerating epithelium extending on to the granulation tissue. At this stage, now that the ulcer is ‘clean’, there is no need to delay surgery by waiting for the ulcer to heal completely; healing can continue concurrently with the patient's postoperative mobilization once the cause for venous hypertension has been removed. This policy would not be appropriate where superficial vein incompetence is accompanied by the more fundamental problem of primary valve deficiency (valveless syndrome—see below) because here the benefits to be expected of surgery may be so marginal that the ulcer could fail to heal without continued elevation.

There is, undoubtedly, an appreciable recurrence rate for varicose veins and other expressions of superfical vein incompetence treated by sclerotherapy or surgery. The recurrences created by surgery can sometimes be more formidable than the original state. The causes of such failure in treatment may be summarized as follows.

Here it is soon apparent that the varicose veins have survived treatment. This may be due to one of the following factors.

Misdiagnosis of the original state where in fact the enlarged veins were, for example, not be due to simple varicose veins but deep vein impairment.

Two separate sources feeding the same varicose veins were present originally and too limited a procedure has been carried out.

Removal of the pathway of incompetence and/or the varicosities has been inadequate and the remaining veins fill easily from a secondary source or by reflux through an enlarged perforating vein. This may respond to sclerotherapy or require a further operation to complete the first procedure.

The varicose veins at first disappear but then reappear in the same distribution within a year or two. The following reasons may account for this problem.

Inadequate removal of the source This will usually be due to failure to ligate a saphenous termination flush with the deep vein. The branches that survive re-establish the source. This is most likely to happen when the original main pathway of incompetence, usually a saphenous vein, has not been removed.

Failure to remove or obliterate the main pathway of incompetence It has already been pointed out that if a grossly incompetent saphenous vein is left intact it will act as a conduit directly communicating with the low pressure areas below the venous pumping mechanisms (the original key failure). During exercise, such as walking, the upper end of this large vein will then be at low pressure in close proximity to the relatively high deep vein pressure in the saphenous stump. This is a strong inducement for a vascular connection to be established from the high pressure vein to the low pressure vein. Two types of venous connecting network may be formed:

1.Anatomical reconnection, based on surviving side branches of a saphenous stump ( Figs. 53(a) 551 and see Fig. 53(d) (i) 554). This can be avoided by flush ligation with the deep vein and stripping the saphenous vein down to knee level.

2.Non-anatomical reconnection (re- or neovascularization). In recent years it has been repeatedly shown that, even when the saphenous vein has been ligated and divided above any branches, a plexus of small veins may form between the stump and an unstripped, incompetent saphenous vein (Fig. 53(b) and (c)) 552,553. This process is not dependent on anatomical branches of the saphenous stump and can be avoided by removing the main pathway of incompetence, whether this is a saphenous vein or an enlarged branch, such as an anterolateral branch in the thigh. In the treatment of simple varicose veins it should be a fundamental principle that when the source of incompetence is surgically ligated the main pathway of incompetence should also be removed.

A latent second source has become active and surviving varicose veins have been taken over by this For example, if varicose veins are not removed at the time of long saphenous ligation and stripping, they form a ready-made, vacant pathway of incompetence which may be ‘acquired’ by a mildly incompetent short saphenous vein. This new source soon enlarges with the stimulus of unrestricted downflow (Fig. 53(d) (ii)) 554. Alternatively, some other source, such as a midthigh perforator, may take over in similar fashion ( Figs. 53(d) 554 (iii) and see Fig. 41(b) 481). The possibility of a second source opening up in this fashion is considerably reduced if the varicose veins are effectively removed surgically or obliterated by sclerotherapy at the first procedure since otherwise they are a constant and visible invitation for an incompetent vein at higher level to send an ever increasing flow down to them. A second operation can give a good result provided that every effort is made to ensure accurate location of the source and, if there are any doubts, to confirm this by functional phlebography and varicography, or by ultrasonography.

A minority of recurrent varicose veins will arise in the states, described presently, of either primary valve deficiency or weak vein syndrome In the latter, varicose veins may proliferate within a few months after a good initial result. The surgeon should not conclude too quickly that treatment cannot succeed, perhaps condemning the patient to a lifetime of strong elastic stockings, but should assess the case in detail, including phlebography. This may show there is an opportunity for carefully planned surgery, based on accurate information, which can be very successful.

Many varicose veins are labelled ‘recurrent’ when, in fact, they are due to a different set of veins, unrelated to the originals For example, several years after successful treatment of long saphenous varices a new set of varicose veins arising from the short saphenous vein may appear. This perhaps reflects widespread weakness in veins and valves, prone to incompetence and varicosis, but is not a contraindication to further treatment.

Hurried, inadequate treatment, insecurely based on an unproven source is a major factor in recurrent varicose veins. The source and pathway of incompetence must always be conclusively demonstrated by clinical tests and backed by Doppler flowmeter studies before surgery.

Residual varicose veins due to incomplete surgery or small veins that appear after an interval, are often best treated by compression sclerotherapy. There is a good prospect of response so that it is well worth a trial. This is no more than a completion of the original treatment, particularly when extensive varicosities have made complete elimination impractical at one operating session and survivors declare themselves later. Here, sclerotherapy is particularly valuable but in most cases adequate removal at surgery by multiple small incisions (Fig. 51(n)) 543,544,545,546 makes this additional treatment unnecessary. Some surgeons, in order to reduce time on the operating table, have a deliberate policy of doing no more than ‘high ligation and strip’, leaving the varicose veins for treatment by sclerotherapy later; however, this is tedious for the patient and misses an ideal opportunity to complete treatment by a single procedure.

Large recurrent varicose veins are often amongst the most difficult to treat. Previous surgery will have fragmented the anatomy of the superficial veins so that the new patterns are far less predictable. Some of the worst recurrences occur in the groin or behind the knee, over the site of saphenous ligation; there may be a history of several unsuccessful attempts to remove these but such attempts are always followed by early reappearance perhaps even larger and more uncomfortable than before. Such veins are unlikely to give more than a temporary response to sclerotherapy and surgery may be the only answer in spite of the previous failures. The problem is compounded by the fact that several sources of incompetence may be present and that the patient may suffer from a degree of weak vein syndrome. Nevertheless, with careful mapping out and study of flow patterns by Doppler flowmeter it is usually possible to understand the overall arrangement of the varicose veins, and the likely sources of flow down them from the deep veins. Guided by this information a combination of functional phlebography and varicography can give a good display of the key features, the sources, and pathways of incompetence upon which surgery can be based. No surgery should be considered without this detailed information and only a surgeon experienced in its interpretation and in carrying out such operations should embark on it; it is probable that exposure of the deep vein through dense scar tissue, traversed by large, fragile varicosities, will be needed in order to attain complete elimination of a leaking saphenous stump (Fig. 54) 555 and this may involve repair to the deep vein ( Figs. 51(d) 533 and 51(p) 548). Any lesser effort is likely to bring yet another failure when in fact a most satisfying result may be attainable. An example of the complex patterns that may be encountered is given in Fig. 41(a) 479,480. Such cases are not rare and require a special skill and perseverance. If weak vein syndrome is a factor, it may be wise to back up successful surgery with long-term use of elastic support up to the knee.

Having emphasized the difficulties of this aspect of venous surgery it must be stressed again that the best opportunity to carry out successful surgical treatment of varicose veins is at the first operation and the principles to be used in minimizing massive recurrence have been outlined in this section.

Two specific complications may arise in varicose veins as distinct from the changes caused by venous hypertension.

Varicose veins lying directly beneath the skin commonly become adherent to it and may so stretch it that it no longer provides adequate protective covering. Then, only the thinnest layer of skin and fragile, attenuated vein wall retain the blood, which shows inky blue through the membranous covering. This state is most likely to develop in varicose veins on the foot, ankle, and lower leg, particularly in elderly patients. The vein may burst with minor trauma or spontaneously when the patient is up and about. The ensuing haemorrhage can be copious but is easily stopped by finger pressure, or if the patient lies down with the foot elevated, and a firm pad and bandage applied. This can be an alarming experience for the patient and, although the aperture will be temporarily plugged with clot, it will soon bleed again (Fig. 55(a)) 556. There is little natural tendency for it to heal because the underlying vein remains open and the unsupported, devitalized skin lacks the vascular base necessary for repair processes. Treatment must be completed by elimination of the affected varicosity and in an elderly person often this can be most simply achieved by compression sclerotherapy. However, the problem is usually more than a local one and whenever possible it is better to treat the accompanying superficial vein incompetence surgically and at the same time to excise the point of haemorrhage and its underlying varicose vein.

Veins liable to this complication can often be recognized and treated before haemorrhage occurs. Patients with such varicosities should be given clear instructions how to control haemorrhage if it should occur before treatment.

The term ‘phlebitis’ used to have a different and sinister significance before the introduction of asepsis towards the end of the 19th century. In the early part of that century surgeons thought of it as an inflammatory process in veins, with two types; one, fibrinous phlebitis, usually with a favourable outcome; the other, suppurative phlebitis, likely to prove fatal. The fibrinous variety corresponds to present day superficial or deep vein thrombosis, but it was not realized that in the deep vein it was far from benign and could cause death by pulmonary embolism until Virchow described this in the mid 19th century. Even so the dominant fear of the pre-Listerian surgeons was of suppurative phlebitis, which as we now know was a bacterial, infective state filling a vein with purulent clot liable to enter the bloodstream, causing pyaemia, with high fever, rigors, widespread abscesses and, inevitably, death. It was a well recognized complication to surgery of that time, especially when veins were ligated (with unsterile material in a septic operating field), trapping clot that had suppurated and could only escape by entering the circulation. For this reason surgery to varicose veins was greatly feared. However, when the bacterial cause was understood, and with the development of aseptic surgery, it ceased to be a serious problem. For a long time the purely thrombotic form, whether in superficial or deep veins, was assumed also to be bacterial. With the realization that this was not so the terms ‘thrombophlebitis’, ‘phlebothrombosis’, or, simply, ‘vein thrombosis’ were introduced to emphasize their essentially thrombotic nature and to distinguish them from the very different infective, suppurative type. It is important to realize that the latter is still a potential danger if ever the high standards of modern surgery should fail or when an uncontrolled infective cellulitis surrounding a vein creates a septic thrombosis within it. Fortunately, this is treatable with antibiotics and elimination of the source of infection, but surgery and medicine sometimes have to be practised in primitive conditions and the efficacy of modern methods should not allow past lessons to be forgotten. The old dragon of suppurative phlebitis has been subdued but not slain and its retreat to the shadows uncovered another formidable dragon, venous thrombosis, damaging and dangerous, with which we continue to grapple (see Section 8.2) 65.

Thrombosis in varicose veins is quite common and may be accepted as a complication without any very serious implications. However, when thrombosis occurs spontaneously in previously normal veins, it may well signify a serious background condition hitherto unsuspected. This includes malignancy (for example, in the pancreas or bronchus), leukaemia or polycythaemia, vascular disease (especially thromboangiitis obliterans), and disorders of blood clotting. Whether it appears as single episode or recurring episodes in different parts of the body (phlebitis migrans), it is a clear indication for full medical screening to identify the cause. Varicose veins in the lower limb, however, can be regarded as sufficient explanation for local thrombosis without necessarily searching further for an underlying cause.

Thrombosis within a varicose vein, or any superficial vein, is accompanied by a tender swelling, often red and slightly warm to the touch, and until quite recently this was commonly regarded as an inflammation of the vein caused by infection. As explained

above, the old term of ‘phlebitis’ was retained until it was realized this was not so and that it must be distinguished from septic thrombosis in a vein secondary to a surrounding infection and which, by suppuration, is liable to cause a dangerous pyaemia. Now that it is recognized that the condition is a response to the thrombosis itself, the terms superficial thrombophlebitis or phlebothrombosis are used to denote this. Varicose veins are undoubtedly prone to thrombosis, partly because there are long periods of stasis in the unnaturally enlarged vein, for example when sitting, but also because production of fibrinolysin in the walls of a varicose vein is reduced. Even when quite a large thrombus has formed, blood continues to stream by it, continually depositing further thrombus so that the vein becomes progressively distended with clot. This does not, however, completely occlude the vein and studies by venography or by Doppler flowmeter show that, when the patient is upright and moving, blood continues to flow down the varicose vein, infiltrating its way round the clot and continually depositing further thrombus (Fig. 55(b)) 556. The vein becomes painfully over-distended and shows an inflammatory reaction. This gives the key to treatment, which is to apply external compression to prevent blood from continuing to flow through the affected vein. The process may limit itself to a few centimetres of vein or may go on extending progressively to involve a considerable area, perhaps the entire calf, when it may be mistaken for a deep vein thrombosis. It may extend into the saphenous vein and along its full length, and in these circumstances, occasionally, may release a pulmonary embolus. Apart from this, it is seldom life-threatening although very troublesome to the patient.

The tender red swelling on the leg, with an indurated cord of thrombosed vein is characteristic. The diagnosis can usually be safely made on clinical grounds alone but where deep vein thrombosis is seriously suspected, this should be checked by phlebography or ultrasonography rather than risk mistreating a life-threatening condition. Occasionally it is difficult to distinguish between superficial thrombosis in the long saphenous vein and a lymphangiitis but the latter condition will lack the firm cord of thrombosed vein and will be accompanied by high fever unlike the low pyrexia that may be present in superficial phlebitis.

Traditional conservative treatment is by applying a firm compression bandage (as in sclerotherapy). An anti-inflammatory agent such as indomethacin may be used to relieve pain but antibiotics are not necessary. If the condition is unusually extensive it may be advisable to put the leg in high elevation (but check for ankle pulses beforehand), with the patient encouraged in active movements and maintained like this until the condition starts to recede; at this stage mobilization is commenced in a firm support bandage. In most circumstances anticoagulants need not be used but in extreme cases the condition will resolve more rapidly with a few days of heparin followed by oral anticoagulation for some weeks.

However, active intervention is often greatly to be preferred because it will bring immediate relief from pain and ensure a rapid recovery. If a substantial set of varicose veins are present and the circumstances allow it, the most effective course is to carry out the appropriate operation for this without delay and at the same time to excise the thrombophlebitic vein; this will be curative for the phlebitis and the varicose state that caused it. When this course is not possible, the simple procedure of evacuating the clot from the thrombosed vein is very effective and may be carried out under local anaesthesia by a single 2-mm skin incision into it. The clot is then extruded by firm finger pressure and a pad and bandage applied without skin suture. This gives complete relief and, provided firm compression is maintained for several weeks afterwards, will cure the phlebitis so that the overall problem of widespread varicose veins can be tackled at a more convenient time.

The majority of patients with incompetence in the superficial veins, described in the preceding section, fall into a clearly defined group that responds well to treatment. However, there is a group, about 8 per cent of venous disorders, in which a more widespread defect is present and treatment far less satisfactory. There is no sharp demarcation between the two groups but, rather, a spectrum of defect with, at one end, well defined superficial vein incompetence and, at the other end, a widespread deficiency of functioning valves in both superficial and deep veins. This deficiency of valves in the deep veins must not be confused with the post-thrombotic state described presently because the patients give no history suggesting previous deep vein thrombosis and, on phlebography, the deep veins are widely open without any evidence of post-thrombotic deformity or occlusion.

In the spectrum of valve deficiency, the ‘well defined’ states at one end have a normal complement of valves in superficial veins but these are incompetent; moving along the spectrum, valves in both superficial and deep veins become increasingly deficient in number. The absence of valves without any evidence of preceding thrombosis, suggests an inborn error in the development of valves. This is supported by the not uncommon finding of incompetent superficial veins in early teenage boys and girls, and the occurrence of valveless deep and superficial veins in well recognized states of congenital venous abnormality, such as Klippel-Trenaunay syndrome. Deficiency of valves in the deep veins leads to ineffective venous pumping so that venous hypertension easily develops, particularly if the superficial veins also have gross incompetence. Patients with well valved deep veins have a robust pumping mechanism which is not easily overwhelmed even by substantial superficial vein incompetence and this may explain why many patients have large varicose veins without any evidence of venous hypertension. By contrast, other patients with similar varicosities show obvious venotensive changes and ulceration, possibly because they lie halfway along the spectrum of change, with poorly valved deep veins and a relatively weak pumping mechanism, easily overwhelmed by superficial incompetence; surgery to the superficial veins can restore a precarious balance with healing of the ulcer, but requiring some care to keep it so. At the far end, the predominant failure is in the deep veins and causes a pump insufficiency too severe to be remedied by removing incompetent superficial veins. These patients suffer from intractable ulceration, not amenable to any form of surgery to the superficial veins (Fig. 56(a) (i)) 557. For descriptive purposes this has been named here as the valveless syndrome but it is also known as primary valve deficiency and is, of course, one variety of chronic venous insufficiency. The main features of this state are summarized below.

Gross saphenous incompetence is often present, or incompetence may come from multiple sources; obvious varicose veins are not necessarily present.

Selective Trendelenburg test does not control enlarged superficial veins because of the incompetence in deep veins.

Severe venotensive changes, often with ulceration, are present.

Doppler flowmetry to enlarged veins shows surge back and forth with little purposeful movement in either direction (Fig. 56(a) (ii)) 558.

Photoplethysmography shows a short recovery time in keeping with an inadequate venous pump and incompetent valves; this is not improved by any manipulation of superficial veins.

Phlebography. The deep veins are widely open throughout with no evidence of previous deep vein thrombosis and few, if any, functioning valves can be demonstrated in them (Fig. 56(a) (iii)) 559.

Ultrasonography. This will confirm substantial reflux and lack of valves in the deep veins.

Clinical presentation of these cases is very similar to post-thrombotic syndrome and the diagnosis is usually made from phlebography or ultrasonography.

Provided that phlebography has shown the deep veins to be widely open but valveless, it is permissible to remove enlarged and valveless superficial veins. In borderline cases, this reduction in the load on the pumping mechanism may restore it to an adequate performance. In more severe examples it brings little or no benefit and treatment will have to rely upon the conservative measures of elevation whenever possible and the use of external support by elastic stockings.

As incompetence in deep veins is the main problem, it may be possible to improve this by one of the following methods:

Transposition of a deep vein into a neighbouring vein that is well valved, for example, implanting the upper end of a superficial femoral into the side of a valved profunda femoris vein nearby (Fig. 56(b)) 560. This may be useful in congenital states of valve deficiency including Klippel-Trenaunay syndrome.

Transplantation of a suitable venous valve taken from elsewhere in the body and inserted as an autograft into an incompetent deep vein, for example, using a valve from the brachial vein, or a saphenous vein of the opposite side, to transplant into the upper popliteal vein (Taheri's operation) (Fig. 56(c)) 561. Again, this may be of help in inborn states of valve deficiency.

Repair of prolapsing valve cusps by valvuloplasty (Kistner's operation). This procedure tightens up selected valve cusps when incompetence is caused by excessive length with one cusp prolapsing beneath the other (Fig. 56(d)) 562. A small number of patients with severe venous insufficiency have this form of incompetence in the femoropopliteal deep veins and may be suitable for the procedure. The operation has yet to gain general acceptance although successful cases are reported.

Use of a tendon or silastic sling around the popliteal vein to act as a substitute external valve (Psathakis). This procedure has yet to be evaluated independently, and there is some indication that deep vein thrombosis and pulmonary embolism may be a problem.

This is a different state from that just described, although both may coexist. The patients often have a strong family history of varicose veins and develop unusually large, incompetent superficial veins leading down to equally large varicosities (Fig. 56(e)) 563. With surgical treatment there is a strong tendency for further large, recurrent varicosities to appear within a year or two. Gross examples are seen following inadequate surgery, for instance, when the long saphenous vein has been ligated at too low a level or has not been stripped and the source of the recurrent varicosities is from surviving branches in a saphenous stump, perforators in the thigh, or interconnections between the saphenous systems. It is possible that extrinsic factors play a part; for example, some of the most severe cases are seen in people whose work involves prolonged standing and high consumption of alcohol, as in publicans and hoteliers. Clinical examination and phlebography gives a strong impression that the veins lack inherent strength and easily over-expand. This, indeed, may be the primary problem because weak vein walls will allow valve cusps to separate and become incompetent; deficiency of valves does not seem to be a cause because an adequate number may be present but grossly incompetent. Histological studies commonly find some degenerative changes in the vein walls of patients with varicose veins and in the state just described the primary defect may be an extreme form of this.

If there has been no previous treatment all the usual features of simple incompetence will be found, including good control with a Trendelenburg test, although the veins are unusually large. This does not contraindicate surgery but is rather an encouragement for conscientious surgery; saphenous ligation must not leave any branches at the upper end, stripping of the long saphenous vein must be at least to upper calf, and all major varicosities must be removed.

If the patient presents with recurrent varicose veins, the massive size of these and their unusual pattern may be daunting. However, with careful mapping out and use of the Doppler flowmeter, the source and pathway of incompetence may be identified. Further surgery must be carefully planned and this will require detailed phlebography to guide the surgeon. A good long-term result may be obtained but in the very nature of the condition further recurrence is possible and, as a last resort, strong elastic stockings will be required to control the varicose veins as a long-term policy.

The two states just described, the valveless syndrome and the weak vein syndrome, are ill defined and ill understood. However, it would be unrealistic in describing the venous disorders to give the impression that all categories are clear-cut and separate from each other. Certainly, most patients can be fitted into a well-defined category and rational treatment based upon this. In others, one of the ill-defined varieties just described may baffle the surgeon, or, it is possible for two separate categories of venous disorder both to be present in the same limb and give a very confusing picture. In these circumstances clinical expertise alone is not sufficient and the extra information provided by ultrasonic imaging and phlebography must be called upon to make sure that the best decision is made for the patient. Care must be taken to exclude the next category, the post-thrombotic syndrome.

Thrombosis in the deep veins of the lower limbs is a common complication in serious illness, pregnancy, following surgical operations, and after severe injury, especially in fractures of lower limbs or pelvis. It may be localized to a small area or extend massively through both lower limbs; in its lesser forms it may pass almost unnoticed but in its major form causes severe illness and a threat to life through pulmonary embolism. In the affected limb(s) the severity of the resulting venous obstruction gradually subsides, partly due to absorption of thrombus and recanalization of the veins but also due to the progressive enlargement of collateral veins, both superficial and deep, providing an alternative pathway of venous return. However, neither of these changes reflects a return to true normality and venous flow in the limb is all too often permanently impaired with corresponding disability (Fig. 57(a)) 564,565. The deep veins involved in this process will show the following changes in structure and function.

1.The vein may remain permanently obstructed, causing a persistently raised venous pressure beneath it and forcing other veins to act as collaterals.

2.The vein may recanalize but in this process it becomes severely deformed and the valves are rendered functionless. Not only does this channel offer resistance to venous return it lacks one of the essential characteristics of a vein, properly functioning valves (Fig. 57(c)) 568. Thus, the ability to pump is lost and heavy reflux occurs down the vein. It cannot make any contribution to venous return against gravity and by reflux it will actively invalidate any return achieved by neighbouring veins.

3.Collateral vessels formed from vasa vasorum, lesser deep veins, perforators, and superficial veins will undergo great expansion with separation of the valve cusps so that the valves become disabled; eventually large channels without effective valves are formed which compensate for obstruction in the deep veins but are unable to prevent heavy reflux of blood down their length when the patient is standing (Fig. 57(d)) 569. If only a small area is involved the effect may be insignificant but when major veins are extensively involved, venous return, which is adequate when the patient is horizontal, will suffer from the compounded difficulties of defective pumping units, resistance to venous outflow from exercising muscles, and heavy reflux in recanalized deep veins and collateral vessels when standing; this reflux rapidly reverses any benefit of venous return against gravity achieved by neighbouring undamaged parts of the venous system. The net result is a sustained high venous pressure in the limb, unrelieved by exercise, when the patient is up and about. This causes venous congestion and oedema, with the familiar changes of venous hypertension, pigmentation, induration of superficial tissues (dermatoliposclerosis), and, eventually, ulceration near the ankle. These long-term consequences of deep vein thrombosis are known as the post-thrombotic or postphlebitic syndrome and can give rise to severe disability in the limb. This is the commonest cause for chronic venous insufficiency but it is important to realize that similar venotensive changes can be caused by gross incompetence in the superficial veins, a state usually curable by surgery, in contrast with the post-thrombotic state which can be ameliorated but seldom cured (Fig. 57(e)) 570.

There is great variation in the extent of changes such a limb will show and this will depend upon location, extent, and importance of the veins involved. Several patterns can be recognized but one or more of these may be present in the same limb (Fig. 57(f)) 571.

1. Tibiopopliteal Here the deep veins below the knee are mainly affected. Small areas of thrombotic damage may give rise to perforating veins forcibly ejecting blood outwards, but more diffuse patterns can disorganize the massive pumping mechanisms in the muscles below the knee sufficiently to create severe venous hypertension and all its complications (see Fig. 57(g) 572,573,574). The deep veins in this region are so numerous and complex that it is often difficult to define the defect precisely or to demonstrate it satisfactorily on phlebography or ultrasonography. Moreover, it may be difficult to say whether the state found is due to episodes of deep vein thrombosis, possibly multiple and silent, or whether there is a diffuse valveless state due to an inborn weakness or deficiency in the valves which has become progressively more severe as the years pass. As with all forms of deep vein impairment, the superficial and deep veins in the foot may respond to the excessive venous pressure by becoming greatly enlarged to form a venous pool in which blood is sequestered as the foot is raised from the ground but forcibly ejected upwards when it is put down again. This shift back and forth to the foot can only be an added burden to the already damaged pumping mechanism.

2. Femoropopliteal This is a common and more easily recognized form of post-thrombotic state (Fig. 57(b) (ii)) 567. There is likely to be significant venous obstruction, with permanent swelling below the knee and all the undesirable effects of venous hypertension because the superficial veins, forced to act as collaterals, will ensure that venous hypertension is shared by the surface tissues. Added to this are all the undesirable effects of reflux in deep and collateral superficial veins.

3. Iliac The left common iliac vein is particularly vulnerable to thrombosis because it may be narrowed by the right common iliac artery passing over it. Thrombosis in this vein often fails to recanalize so that the venous outlet to the limb remains permanently obstructed. If the limb below this is otherwise virtually undamaged, it may cause little more than slight swelling and the development of tortuous collateral veins crossing from the left to the right side of the pelvis, usually visible as varicosities in the pubic region (Fig. 58(a)–(h)) 575,576,577,578,579,580,581,582,583,584,585,586,587,588,589,590. Beneath this it is possible for a typical long saphenous incompetence to develop, taking source from the pubic collateral veins, as described under the complex patterns referred to below. If this is not recognized, surgery to the saphenous system may damage important collateral veins in the groin.

4. Ileofemoral Iliac thrombosis is often accompanied by simultaneous thrombosis in the femoral and popliteal veins to give an ileofemoral post-thrombotic syndrome with a particularly severe pattern of venous hypertension combining the worst features of obstruction to the venous outlet, impaired pumping mechanism, and heavy reflux in recanalized deep veins and over-distended collateral veins (Fig. 58 (d)–(h)) 579,580,581,582,583,584,585,586,587,588,589,590.

These can occur if the great pumping units in the muscles of the leg are substantially undamaged and able successfully to reduce venous pressure in the ankle and foot. In these circumstances it is possible to find the long saphenous vein acting as a collateral but giving off branches which set up a simple pattern of incompetence by allowing downflow to the low pressure areas in the lower leg and foot or, indeed, pubic collaterals may act as a source for incompetent downflow in the limb on the opposite side. This has been described earlier and is illustrated in Fig. 42 482,483,484. Such contradictory flow and counterflow is not uncommon and all too easily confuses the diagnosis.

Plethysmography will show a poor response and shortened refilling time with exercise ( Fig. 58(f) (iv) 583 and Fig. 58 (g)(iii) 587); volumetric methods measuring expelled volume will find this substantially reduced. These findings cannot be restored to normal by any manipulation of superficial veins. Functional phlebography or ultrasonography will confirm and define the state of the deep vein and valves. This is essential evidence before deciding that no cure is available, and only conservative management can be employed.

Needless to say, with such a formidable catalogue of disability as the long-term effects of deep vein thrombosis, every effort must be made to avoid this complication occurring to patients under medical care. Much can be done to minimize its occurrence.

Treatment by surgery can, at best, give only limited benefit to a post-thrombotic syndrome and the mainstay of treatment will be by conservative means. The worst manifestations of post-thrombotic syndrome are essentially due to venous hypertension and even partial reduction of this brings great benefit. This can be achieved in two ways.

The requirements of conservative treatment in venous ulceration are in direct conflict with those of ischaemic manifestations. The treatment described below involves elevation or compression bandaging of the limb. In an ischaemic limb such treatment will severely aggravate its state and even cause its loss. Great care must be taken to ensure that such treatment is not carried out in these circumstances. If there is any doubt, the limb should not be raised above the horizontal and no form of compression bandage used until it has been proved that an adequate arterial supply is present.

1. Elevation of the limb above the horizontal

In this position venus return occurs by gravity without requiring any pumping mechanism. During elevation, with the feet above heart level, venous pressure in the extremity falls away and the higher the elevation the more complete this will be (Fig. 59(a)) 591. Maintained in this position ( Fig. 49(g) 505,(h)) all the adverse changes will steadily recede. However, it is clearly not practical to keep a patient indefinitely immobilized in this fashion, so, as a compromise, there will be an initial period of continuous elevation in order to get the worst lesions, such as ulceration, healed. This is then followed by increasing mobility alternating with spells of elevation. Eventually the proportion of the day to be spent in elevation, necessary to keep the limb healthy, will be learnt and the patient will have to try to arrange his or her life within this limitation. Usually it is possible and this measure alone may be sufficient to maintain the limb in a reasonable state. If the patient becomes careless about spending sufficient time in elevation, deterioration of the limb soon gives a sharp reminder. Each patient will have to learn his or her own requirements in this respect. A programme of this sort, particularly during the time of continuous elevation, will bring the serious disadvantages of prolonged immobility, unless this is counteracted by a firm policy of exercise. The time of continuous elevation to heal an ulcer must never be referred to as ‘bed rest’ but, instead, the patient must be urged to exercise their limbs and body repeatedly during the day, in fact, ‘activity elevation’. In addition, getting up for a few minutes active walking each hour will not harm the ulcer provided that exercise time is strictly limited, but will prevent the patient developing weak muscles and stiff joints. An initial period of instruction is necessary so that these principles are fully understood. The patient will then know how to control the health of the limb. This regimen is by far the most effective aspect of conservative treatment and although it puts quite severe restrictions on the patient's way of life this is a price most are prepared to pay to avoid the discomforts of uncontrolled venotensive changes. Clearly, in some patients the necessity to earn a living will prevent their following the programme they know to be necessary but even here ways of managing may be found. An example is that of a chef who worked every summer at a high salary in a top hotel, enduring steady deterioration in his limb as the season passed but then spent the winter in Mediterranean sunshine giving the limb proper care. He knew exactly how to heal the ulcer when opportunity allowed.

2. Improving efficiency of the damaged pumping mechanism by use of external support

The ability to pump blood upwards against gravity is impaired in a post-thrombotic limb by the following factors which may be influenced, harmfully or beneficially, by external compression.

Occlusion or severe deformity in major veins causes obstruction to venous return. Numerous lesser veins will dilate to provide a compensatory collateral mechanism but little can be done to assist this process which is a response to the venous changes in the limb. However, the superficial veins play a large part and any form of external compression, especially elastic compression, can impair this important mechanism. In superficial incompetence, firm compression of the superficial veins brings great benefit by preventing heavy downflow in them but in post-thrombotic syndrome similar pressure in the upper calf or thigh can cause increased discomfort and deterioration in the limb by impeding collateral return. For this reason elastic support used in post-thrombotic syndrome must be carefully graduated to avoid compression where the main collaterals lie.

There is valvular incompetence because of widespread loss of effective valves, both in recanalized deep veins and in over-expanded lesser deep veins and superficial veins now acting as collaterals. No conservative measure can adequately restore valvular competence in these limbs. Any external compression designed to reduce reflux in these valveless veins may also impair their vital function of venous return and the advantages gained in controlling reflux will be lost by the disadvantages of restricting collateral return. Again, notice how this contrasts with superficial incompetence where elastic compression to the incompetent superficial veins brings no disadvantage because these veins are not acting as avenues of venous return. The elastic stocking so successful in superficial incompetence may be completely inappropriate to the post-thrombotic syndrome and this is a fundamental distinction between the two conditions.

Widespread over-expansion of the superficial and deep veins in the leg and foot is created by the sustained high venous pressure and, in effect, forms a large venous pool which constantly handicaps the venous pumping units that have survived undamaged. On muscle relaxation these healthy pumping chambers will be immediately flooded by blood from the unwanted venous pool and much of their effort is wasted on reducing a pool which has inexhaustible replenishment from above. In the case of the foot, when it is raised, blood which should be available to the pumping units cascades down to the underside at the very moment it should be entering the venous pumping chambers; on return of the foot to the ground the blood is forced up again, giving a surge of high venous pressure in the lower leg. Reducing the venous pool by external support to the foot and lower leg, strong enough to resist the venous pressures, can take away this undesirable element and bring some relief to the overburdened pumping mechanism. Here external support can be of real benefit but if inexpertly applied can impede collateral return as explained above. It is quite wrong to think that crude compression is a virtue in the post-thrombotic limb—it must be used with discernment and then may bring benefit. There are two main forms of external support that can be used: inelastic containment and elastic compression by stocking or bandage.

This is the principle used in the paste bandage. This form of external support is often more successful than any other type in the ambulatory treatment and healing of a venous ulcer, and this is especially true in post-thrombotic syndrome. Although these bandages are combined with various medical ingredients, it is the mechanical properties of the bandage when it is properly applied, rather than the ingredients, that make it so successful. In its basic form it is a 7.5-cm cotton bandage impregnated with zinc oxide paste. This is applied from the toes up to the knee whilst the limb is well elevated so that the veins are completely empty (Fig. 59(b)) 592. Care is taken to lay it on in a series of overlapping loops so that at no point is it tight or exerting a constricting effect. In this way it will set to form a strong, inelastic shell encasing the elevated limb. When the patient stands, overfilling of enlarged veins will be immediately resisted by the shell, but venous pressure at any point will not rise above the hydrostatic pressure between that level and the heart. The tension exerted by this external support is determined by the fluid, the venous blood, contained within it and gives a perfect graduation of pressure, decreasing up the limb. The large venous pool in foot and lower leg is held to a minimum and the efforts of functioning pumping units are not wasted on a large venous pool immediately replenished from above; the veins and capillary beds are prevented from excessive distension by the external support but at no point is the external pressure greater than that in the superficial veins so that collateral upflow will not be impeded. When the patient walks venous pressure around the ankle will be reduced to the lowest levels attainable in that limb; when the patient is at rest, with the leg horizontal or elevated, there is no residual pressure from the external support to impede arterial inflow. By contrast an elastic support will give sustained compression between 20 and 40 mmHg or more of residual pressure, a significant handicap to arterial perfusion.

Although it provides the most effective form of external support, the paste bandage has the disadvantage that it cannot be taken off and put on again at will. Once applied it will usually be left in place for up to 3 weeks and its replacement cannot be satisfactorily done by the patient. This requires some skill, notalways easy for others in the family. For this reason it tends to be used only during the time necessary to heal an ulcer and has the great advantage that it allows this to occur while the patient is up and about. Once the ulcer has healed the external support can be changed to a more convenient elastic stocking, which may be sufficient to prevent recurrence.

Certain types of elastic stocking, skilfully fitted can come near to giving the same effect as a paste bandage. A strong one-way-stretch elastic stocking up to the knee, fitted accurately to give a snug fit but no compression when the limb is elevated, will immediately resist any expansion of the veins when the patient stands; this comes quite near to the principle of inelastic containment whilst having the advantage of being easily removable. Its elasticity is used to give accurate conformity with the limb and to allow it to be pulled on and off over the prominence of the heel, but, being one-way-stretch, it does not suffer from down-pull. Skilled fitting of this sort is not always available and the tendency is for the patient to be directed towards the convenience of easy fitting using a two-way-stretch stocking. Because of the need for the latter to grip the calf in order to resist down-pull, it is not suitable to provide inelastic containment. Strong elastic webbing bandage laid lightly around the elevated limb, without any compression, can also be used to give a form of inelastic containment, but this form of bandage is so often misused (see below) that it is best avoided unless the circumstances ensure proper use.

A great variety of elastic stockings of various strengths are available. These may or may not envelop the toes, and extend from the foot up to the knee or to the thigh; depending on the strength required they may be fashioned as stockings or tights (Fig. 59(c)) 593. The compression they give is graded so that light support gives 14–17 mmHg pressure (Class I in the United Kingdom), medium support gives 18–24 mmHg (Class II), and strong support gives 25–35 mmHg (Class III) compression at foot and ankle level. Above this level the stocking is so designed that the compression tapers off in parallel with the lessening venous pressure up the length of the limb when the patient is standing. In this way heavy compression in, say, the thigh, and constriction of venous outflow, is avoided. In most countries clear standards are laid down and in the United Kingdom the Drug Tariff of the National Health Service gives strict specifications for the various classes of graduated compression hosiery together with indications related to the severity of venous disorder and other conditions for which they are suitable. The manufacturers keep within these specifications and have succeeded in evolving knits that give compression with relatively little downwards pull but, nevertheless, the majority available are two-way stretch and will require support either by gripping the calf or, at higher levels, by suspender or as tights. In post-thrombotic syndrome the high venous pressures quickly generated when the patient is standing will require controlling with a relatively strong stocking giving 25- to 35-mmHg compression in foot and ankle. This has been found to be optimal but is really insufficient to resist full venous pressure; however, the stronger the stocking the higher the residual elastic compression when the limb is elevated and no longer needs compression. When a limb is raised above horizontal or when the patient is lying flat there is no significant venous pressure in the limb and any form of external support, inelastic or elastic, serves no useful purpose. An elastic support will, however, continue giving residual compression and this can be most undesirable by reducing arterial flow in the impoverished tissues near the ankle in post-thrombotic syndrome.

The importance of avoiding an elastic stocking which may impede collateral return through superficial veins has already been emphasized above. Many patients with post-thrombotic syndrome try various forms of elastic support but find they actually increase their discomforts and abandon their use. A stocking that brings comfort to the patient is likely to be beneficial but one causing discomfort may actually be doing harm. The patient must not be coerced into wearing stockings if the benefits are not apparent. With an active ulcer which is extremely tender and discharging purulent fluid, an elastic stocking is not in any way suitable; it will cause too much pain and within a short time will be saturated with exudate. An ulcer at this stage requires a spell of elevation to bring it to a healing phase, followed by ambulatory treatment in a paste bandage and, finally, healing maintained by a skilfully fitted elastic support. In the post-thrombotic limb it is often a matter of trial and error to see if the patient can be suited. In simple incompetence of the superficial veins (primary varicose veins) where all that is required is firm compression to stop the downflow in the incompetent veins, the fitting of elastic stockings is far less critical and often an ulcer will heal with their use. However, this is the very variety of venous disorder where surgery or sclerotherapy is highly successful and it should not be necessary to condemn these patients to the undoubted nuisance of permanent elastic support.

In post-thrombotic syndrome, a skilfully applied paste bandage is invaluable in healing a venous ulcer whilst the patient is ambulatory. An elastic stocking for the same purpose is less effective and often not tolerated by the patient. The principle of inelastic containment is far more desirable than elastic compression. However, external support of any sort is insufficient on its own and a policy of elevation whenever possible is essential.

In this condition enlarged surface veins are usually acting as collaterals to underlying occluded deep veins. In these circumstances, not infrequently, a saphenous vein may have several competent valves along its length and is, therefore, a most valuable valved pathway of venous return that must be preserved. However, more often phlebography will have shown that it has no competent valves and it is tempting to consider its surgical removal in order to eliminate at least one cause for rapid build up of venous hypertension by reflux along its length. But this will also be destroying an important compensatory collateral mechanism and the disadvantages of this may outweigh the advantages of eliminating the component of incompetence. Moreover, Doppler flowmetry may show continuous upflow, accentuated by exercise, without reflux except briefly when the patient first stands. This implies that it is an important collateral which must not be removed without good evidence of alternative pathways of venous return. Phlebography may have supplied this, but useful confirmatory evidence may be obtained by phlethysmography during exercise with and without selective occlusion of the saphenous vein in question; occlusion may cause deterioration in the ability of the limb to reduce venous pressure by exercise and gives clear warning that the vein should not be removed. In true post-thrombotic syndrome there are few circumstances in which removal of the superficial veins will bring benefit. One such circumstance may be when there is an intractable ulcer directly overlying an enlarged perforator carrying collateral outflow, demonstrated by phlebography or ultrasonography. Elimination of this may redistribute collateral outflow and reduce the intensity of venous hypertension overlying the perforator and so enable the ulcer to heal. The use of phlethysmography with selective occlusion of the veins concerned, as just described, may support this procedure but without some such evidence it is not justifiable to remove enlarged superficial veins or perforators indiscriminately.

In post-thrombotic syndrome the real requirement is the replacement of occluded veins and valveless channels with good, well-valved veins. However, our ability in this respect is extremely limited but the following procedures may occasionally prove helpful.

1. Palma's operation

This is appropriate for the relief of oedema in post-thrombotic occlusion of an iliac vein, usually the left side, when the deep veins below the inguinal ligament are relatively undamaged. The long saphenous vein of the opposite limb is divided in the lower thigh and mobilized to swing it across to the affected side for anastomosis with common femoral or profunda femoris vein (Fig. 60(a) (i), (ii), and (iii)) 594. If successful, this acts as an additional collateral vein providing a substantial venous outlet for the limb. Swelling may be considerably reduced but severe venotensive changes such as ulceration near the ankle are unlikely to be improved because these are the result of thrombotic damage at lower levels in the limb. A corresponding procedure using a PTFE vascular graft with external supporting rings, running extraperitoneally between the femoral vein on the affected side and the lower external iliac vein of the opposite side, and supported by a temporary arteriovenous fistula, has given a number of reported successes ( Fig. 60(a) 594 (iv)).

2. Popliteal to upper femoral vein bypassing (May-Husni operation)

This is designed to relieve the effects of deep vein obstruction in lower or midthigh. The long saphenous vein of the same limb is anastomosed to the lower popliteal or posterior tibial vein in order to provide a more effective outflow from the deep veins below the knee and taking it upwards to re-enter deep veins in the groin above the obstruction (Fig. 60(b)) 595. This will be particularly effective if the saphenous vein is well valved and a number of successes have been reported. However, so often this vein is already acting as an effective collateral so that the rearrangement brings little improvement and, of course, it does not eliminate the heavy reflux in naturally occurring deep and superficial collateral veins throughout the limb which are so often grossly incompetent. This operation may be supported by a temporary arteriovenous fistula to ensure the new venous channel is well distended with continuous flow and does not thrombose in the early postoperative healing period.

3. Restoration of valve function

Transposition of a deep vein into a neighbouring vein that is well valved, for example, implanting the superficial femoral into a valved profunda femoris vein alongside, as described earlier. This is seldom applicable in post-thrombotic syndrome.

Transplantation of a suitable venous valve taken from elsewhere in the body. This is most unlikely to be appropriate in thickened, deformed post-thrombotic veins or in the multitude of collateral veins.

Repair of prolapsing valve cusps (Kistner's operation) is not in any way appropriate in post-thrombotic syndrome where the valve cusps are thickened, deformed, and adherent to neighbouring vein wall.

Various procedures with synthetic vein grafts, often supported by temporary arteriovenous fistulae, are under trial in the lower limb but these suffer from the serious defect that they are not valved ( Fig. 60(a) 594 (iv)). Attempts to evolve synthetic vein grafts for use in the lower limb are severely limited at present by inability to provide any satisfactory valve mechanism.

External valves. A sling may be used around a vein to act as a substitute valve. Psathakis has reported favourable results in over 200 patients using a tendon or silastic sling attached to flexor tendons of the knee and placed around the popliteal vein in patients with venotensive changes, including many with post-thrombotic syndrome, thought to be due to reflux in this vein. The theory is that when the flexor muscles contract whilst walking the sling tightens around the vein and prevents reflux in it. Its efficacy and the possible incidence of thromboembolism await independent evaluation.

Operations reconstructing the veins in post-thrombotic syndrome are very limited, with few suitable cases, and are best left to the experts specializing in this field.

The diagnosis of ‘incompetent perforator’ is frequently made but often incorrectly so. The following summary may help to put this into better perspective.

Inward flow from the superficial to deep veins is normal but it is greatly enhanced in superficial vein incompetence as part of the retrograde circuit of gravitational downflow (see Fig. 30 459). This is an essential feature of the most common venous disorder, superficial vein incompetence, but the perforator is not at fault—it is performing its normal function in exaggerated fashion (see Fig. 61(a) 596). However, in many patients, there may also be a brief outward surge as the muscles contract or the foot is placed to the ground, alternating with the predominant downward and inward flow (Fig. 61(b)) 597. This represents a degree of incompetence in one or more perforators, probably because they have been over-enlarged by heavy inflow from the varicose veins, but is not the primary fault. However, it can certainly be an aggravating factor if venotensive changes are present, and, after surgery to the varicose veins, may become the source of downflow to the foot. For these reasons an enlarged perforating vein showing surge is best eliminated at surgery when it is detected.

The upper termination of long and short saphenous vein (Figs. 48(b) and (c)) 500,501, midthigh perforating veins ( Fig. 53(d) (iii) 554, and Fig. 61 (c) (i) 598), and veins connecting between the pelvis and upper thigh (Fig. 39) 475,476 are all examples of perforatoring veins which commonly become incompetent and act as the high level source for a pathway of simple incompetence. In similar fashion a perforator on the leg below the knee may act as a source of downflow to the foot (Fig. 61(c) (ii)) 598. All the above are certainly ‘incompetent perforators’ and it is unfortunate that this term is also used to refer to heavy outward pumping through perforating veins below the knee and especially near the ankle.

Outward pumping may occur as part of a surge back and forth accompanying simple varicose veins as described above. Of far greater importance is its occurrence in the post-thrombotic syndrome as part of a collateral mechanism in venous return past occluded deep veins ( Fig. 13 435, Fig. 57(b) 566,567, and Fig. 61(d) 599). Here the perforator is playing a compensatory role and this must be recognized because it may be an important channel of venous return although inadvertently bringing high venous pressure to the vulnerable surface layers. There must not be an automatic response to remove an outward pumping perforator in the leg but instead the cause must be understood and its importance in collateral function assessed. Surgery removing this vein may sometimes be justifiable; for example, in post-thrombotic syndrome heavy collateral flow may be concentrated through one perforator and so increase local venous pressure that ulceration occurs over it. It is possible that removing this perforator will cause redistribution of collateral flow and dissipate the raised venous pressure over a wider area elsewhere in the leg. In this way the high venous pressure is no longer concentrated in one small area and the ulcer heals. The decision to do this rests on adequacy of alternative collateral pathways shown by radiography and the demonstration that recovery times at plethysmography are improved or, at least, not made worse by temporary occlusion of the perforator by finger pressure.

Incompetent gastrocnemius and soleal veins are perhaps the best examples of localized incompetent perforators capable of allowing passive reflux but on muscle contraction forcibly ejecting blood to the surface (Fig. 61(e)) 600. This is being increasingly recognized and diagnosed by phlebography or ultrasonography. Suspicion of their presence is usually aroused by unusual discomfort, venotensive changes, and a pattern of radiating varicosities on the calf. Surgery ligating such veins in popliteal fossa, carefully selected by phlebography or ultrasonography, may prove very successful but does require experience.

Certain arrangements of veins may be mistaken for direct leakage from the deep veins. In the midthigh, an upward extension of the short saphenous vein (Giacomini vein) may join the posteromedial branch of the long saphenous vein. In this way incompetence with its source in the short saphenous vein can give rise to long saphenous varicosities and may only be recognized when surgery ligating the long saphenous vein fails; even then it may be regarded as a midthigh perforator ( Fig. 41(b) 481 and Fig. 61(f) 601). In the upper calf a branch from an incompetent short saphenous vein may run across to the inner aspect and appear to be a true deep vein perforator (Fig. 61(g)) 602. An incompetent long saphenous vein, or its posterior arcuate branch, may run down to the lower leg in concealed fashion and give off a large branch running to the surface near the ankle where it is interpreted as coming from a perforator.

The venous system is subject to many minor aberrations such as duplicated deep veins, differing levels of short saphenous termination, or the presence of unusually large interconnecting branches between long and short saphenous systems in the thigh. All these variants originate in embryo during development of the venous system and, if the valves are inadequate, may account for unusual sources of incompetence but most are harmless and need not be detailed here. However, one particular abnormality deserves special mention. This is the persistence of the lateral vein of the lower limb to form a massive, valveless channel running superficially up the outer side of the leg and thigh, and terminating either in the profunda femoris or by running with the sciatic nerve into the pelvis to join the internal iliac vein (Figs. 62(a) and (b)) 603,604,605.

The importance of this is that there may be a concurrent failure in the development of the normal deep vein system so that the large, superficial channel forms the main venous return of the limb and inept surgery removing it may cause considerable embarrassment to venous return. Gross anatomical aberrations of superficial veins should always bring to mind the possibility of a corresponding failure in the deep veins which should be checked by phlebography before attempting any treatment.

These take the form of angiomata of capillary or cavernous varieties. The former are made up of multiple enlarged capillaries and venules to give a dark red blemish (strawberry naevus), often present at birth and disappearing within a year or two. The cavernous angioma forms a protuberant swelling composed of large irregular blood-filled spaces. It usually proves persistent and may show apparent enlargement in childhood. Often it affects no more than skin and subcutaneous tissues but may extend deeply, lying in and amongst muscle (Fig. 62(c)) 606,607. The boundaries of these lesions are not clearly defined but may be sufficiently limited to allow surgical removal. Surgery may require considerable skill as these angiomata cross anatomical boundaries and involve important structures which will require separating from the main mass by sharp dissection; the fringe of angioma that has to be left behind is usually unimportant. A small angioma may be treated by sclerotherapy or by laser.

Cavernous angiomatosis may occur as a congenital defect extensively over a lower limb or elsewhere in the body (Fig. 62(d)) 608. It is most obvious when the skin is involved, as a dark purple, irregular, compressible swelling but it often pervades the underlying layers extending into muscle and bone beneath. In the worst examples, this grossly abnormal venous state may be accompanied by severely defective deep veins which are either absent or lacking valves. A massive persistent lateral vein, referred to above, may be present. In such limbs venous return against gravity is likely to be severely defective and by the time adult life is reached venous hypertension causes a strong tendency to ulceration.

The extensive venous abnormality just described is often, but not always, accompanied by overgrowth in the bones to give increased length in the limb and this special variety is known as the Klippel-Trenaunay syndrome (Figs. 62 (e), (f), and (g)) 609,610,611. Because of the close association of severe venous malformation with overgrowth of the bones, any patient showing venous abnormality or angiomatosis should be examined for a change in the bone length. This change is usually made obvious by careful clinical examination comparing measurements between the bony points on the two limbs or simply by inspecting the patient in a standing position and looking for inequality in the levels of the corresponding bony prominences. Measurement by radiography is only necessary if study of progressive change over the years is required.

Over-lengthening of a limb may arise without any other abnormality and will then usually be seen in an orthopaedic clinic (Fig. 62(h)) 612, but it is often found as a previously unnoticed accompaniment of gross vascular abnormality, as in Klippel-Trenaunay syndrome. Even if obvious vascular changes are not present the possibility of deep vein abnormality, perhaps with large, valveless channels causing venous hypertension and eventually ulceration in the limb must be borne in mind. The association with a large superficial lateral venous channel and defective or absent deep veins has already been mentioned above. Another cause for over-lengthening of bones is the presence of multiple arteriovenous fistulae (Parkes-Weber syndrome) but this condition should be regarded as separate from the venous states just described (see below). When bony overgrowth is found by a venous clinic it is important to place the young patient under orthopaedic care. Inequality in the length of the lower limbs with tilting of the pelvis should be compensated for by raising the shoe on the normal side since otherwise it may cause arthritis of the spine at an early age. Surgical correction of the bone length, either by epiphysiodesis whilst the bone is still growing or, better, by bone shortening as a young adult, may be necessary, if the vascular state allows this.

It is well recognized that extensive congenital arteriovenous fistulae will cause overgrowth of bone in the vicinity. This leads to speculation that occult arteriovenous fistulae may account for bony overgrowth in Klippel-Trenaunay syndrome. This has not been demonstrated reliably and, although there are cases where both states undoubtedly coexist, the current view is that the two conditions have no direct relationship.

Congenital arteriovenous fistulae may be localized to, for example, part of the foot or leg. There is a corresponding overgrowth of neighbouring bone, with enlargement of the bony structure of the foot if localized there, or, if the entire limb is involved, 5 cm or more increase in its length.

The communications between artery and vein are through sponge-like vascular formations, each supplied by a single large artery which breaks into multiple branches connecting with a leash of enlarged veins running from it. An obvious pulsatile swelling may be present with discoloration of the overlying skin and large veins radiating from it; with a stethoscope, a machinery pumping bruit can be heard extensively over the limb. Massive arteriovenous shunting may cause an increased pulse rate which drops back to normal when the main artery to the limb is temporarily occluded (Branham's sign). The constant struggle to maintain blood pressure and the premature return of a large volume of blood may cause considerable cardiac enlargement with eventual heart failure. Brown pigmentation and ulceration of the skin in the distal limb is often present, due to the sustained venous hypertension characteristic of this condition.

The diagnosis is usually evident on clinical grounds and by finding that Doppler flowmetry shows strong pulsation within the superficial veins. Arteriography with serial pictures will confirm the diagnosis and often outline individual areas of fistulous communication and the arteries feeding them.

Small lesions may be treated by laser therapy but others, if not too extensive, may be treated by sclerotherapy or by appropriate plastic surgery. It should be noted that the skin involved in angiomatous change may easily necrose if it is raised or undermined.

Repeated sclerotherapy may bring considerable improvement in the cutaneous lesions. In some cases surgical excision and provision of skin coverage by a vascularized flap from the opposite limb may prove possible in order to give good skin coverage over, for example, the knee joint. However, the difficulties in doing this must not be under-rated; it is seldom possible to get beyond the angiomatosis and numerous vascular apertures may bleed copiously from the fringe that remains. Raising flaps of heavily involved skin may result in extensive necrosis and problems in skin coverage. Tissues involved in angiomatosis do not respond in a normal fashion if surgery is required and such problems are best left to surgeons with a special skill in this field.

If phlebography has shown that extensive valveless deep veins are present and causing venous ulceration, it is sometimes possible to reroute these veins by implanting them into a neighbouring major vein that is valved, for example, transposing a superficial femoral vein into a well-valved profunda femoris vein (Fig. 56(b)) 560. Transplanting valves from brachial vein or the long saphenous vein of the opposite limb is a theoretical possibility but in practice is seldom a convincing form of treatment (Fig. 56(c)) 561.

Usually a policy of conservative management will have to be followed. This will be by strong elastic support to compress the angiomatous lesions and to prevent progressive enlargement; special fitting of a full thigh length stocking with waist attachment may be required. In addition it is essential that a policy of elevation at every spare moment is followed in order to reduce venous hypertension and keep ulceration at bay.

Usually the limb is good in other respects and serves the patient well so that amputation must not be an option. With good conservative management a useful limb can be maintained indefinitely in a satisfactory state.

Very localized lesions can be surgically excised after careful evaluation by arteriography. But even comparatively small lesions may be better treated by transluminal embolization described below. Amputation of a limb must not be resorted to except in extremis; it may not solve the problem which can continue in the stump.

This requires expert planning and should be performed by an experienced vascular radiologist. A special indication for this is in cardiac failure when it is considered essential to reduce the arteriovenous shunting. The basis is occlusion of the feeding artery by transluminal introduction of an occlusive device, such as the Gianturco coil, under radiological control (Fig. 62(l)) 616. This is far better than attempted surgical ligation. However, it is possible to cut off too much arterial supply and abruptly reduce arterial pressure below that of the abnormally high venous pressure so that capillary flow ceases, resulting in extensive ischaemic changes.

In most patients conservative treatment will be the mainstay of treatment. Very strong elastic containment and elevation of the limb at every spare moment will be essential. If ulceration or haemorrhage occur, inelastic containment, by paste bandage, maintained for many weeks, can be most valuable.

Many young patients reach adult life without mishap and continue successfully, even through pregnancy (Fig. 62(k)) 615, using the methods outlined above. It is wrong to counsel anxious parents at an early age that the limb should be amputated either at that time or later, but rather to emphasize that every effort will be made to extend the useful state of the limb indefinitely.

Chronic ulceration of the leg, often causing considerable disability, is a common problem with significant economic consequences for the individual and for society. In European countries nearly 90 per cent of these ulcers arise from one or other of the venous disorders described above but in the remainder there are many other causes; in these, treatment suitable for venous ulceration may be in direct conflict with that actually required and in the case of ischaemic ulceration may jeopardize the limb. Because of the prevalence of venous ulcer, it is all too easy to assume that this is the diagnosis and to give wholly inappropriate treatment. It is important to identify accurately the underlying cause in each case so that treatment may be correctly based on this. The diagnosis of ‘leg ulcer’ is totally inadequate and must always be qualified by a statement of the cause, backed by full evidence for this diagnosis. This requires an understanding of the range of leg ulcers that occur and the disease processes underlying them. The description that follows is appropriate for European countries but it must be remembered that the prevalence of leg ulcers has considerable variation geographically and within ethnic groups. Fortunately, venous ulceration has distinctive features that usually allow positive identification; the recognition and treatment of venous ulcers will be considered first.

For the reasons described earlier, venous disorders are liable, in varying degree, to develop venous hypertension. If this is sufficiently severe it causes excess capillary exudation and formation of a fibrin barrier around capillaries, with diminished nutritional exchange between capillary blood and the subcutaneous tissues and skin. An important phenomenon involved in this, recently recognized, is the deposition of leucocytes in capillaries affected by venous hypertension (white cell trapping). Endothelial cells, activated by hypoxia, cause leucocytes to become adherent and release injurious products which damage the endothelium with consequent migration of leucocytes into surrounding tissue to cause further harm there. It is as if the leucocytes with their defensive and scavenging properties, so valuable in an inflammatory reaction, are mistakenly attacking impaired capillary walls and neighbouring tissue. The destructive effect is enhanced by obstruction to capillary flow by the adherent layer of leucocytes and by thrombus resulting from activation of platelets. The precise sequence has yet to be established but ‘leucocyte trapping’ seems to play an essential part in the changes leading to venous ulceration. Oedema, induration, and fibrosis, accompanied by pigmentation of the skin develop progressively and, without treatment, culminate in tissue death and ulceration. The same characteristic changes also develop distal to arteriovenous fistula due to the common denominator in all these conditions, venous hypertension. A summary of the main features of typical venous ulcer is given below.

The ulcer occurs where venous pressure is sustained at a high level and upon which unnaturally high peaks of pressure may be superimposed. Usually this is in the lower leg, occasionally on the upper aspect of the foot but never on its underside. Although the most common site is just above the medial malleolus it may occur almost anywhere on the leg according to the pattern of venous failure.

No age of adult life is immune but the occurrence of venous ulcer increases with age probably due to progressive deterioration in the musculovenous pumping mechanisms with advancing years. Up to 1 per cent of the adult population may be affected by venous ulceration at some stage in their lives, with women affected slightly more frequently than men.

Ulceration is preceded by venotensive changes of local oedema, induration (liposclerosis), and brown pigmentation of the skin caused by extravasated haemosiderin. These changes are always found in the vicinity of a venous ulcer and if surrounding skin pigmentation is not present in a white skin the diagnosis is in doubt. However, haemosiderin is of a similar colour to the melanin in a black skin which may be increased locally around any long-standing skin lesion and, since the two pigments cannot be easily distinguished, increased pigmentation is not a reliable guide to venotension in black patients; moreover, melanin may be reduced in various circumstances, such as use of steroid cream, so that lack of surrounding pigmentation cannot be used to exclude a venous ulcer; nevertheless all the other evidence of venous insufficiency will be present and recognition of the cause should not be difficult.

Other forms of ulceration do not show these changes although they may be mimicked to some extent by a surrounding cellulitis. Fluid exudate is usual but, depending on prevailing bacteria and presence of necrotic tissue, may become purulent, possibly with an offensive odour. The ulcer causes variable discomfort and usually only harmless commensual organisms are found on bacterial culture; however, if it is infected by pathogens, such as Staphylococcus aureus, &bgr;-haemolytic streptococci, or anaerobic organisms, invasion of surrounding tissues may cause considerable pain. Pain is also characteristic of an ischaemic ulcer and the importance of distinguishing this from a venous ulcer is discussed below.

Diagnosis is confirmed by the presence of substantial to severe accompanying venous disorder which is readily demonstrated by the usual clinical tests and by the special tests, including Doppler flowmetry, plethysmography, phlebography, or ultrasonography showing the characteristic abnormalities found in chronic venous insufficiency. Skin in the vicinity will show capillary stasis with laser Doppler rheography and a diminished oxygen tension.

This will depend on the type of venous disorder causing ulceration. In superficial vein incompetence, surgery will have a major role by removing the pathway of incompetence but in most other cases conservative treatment by elevation and external support will have to be relied on, as discussed earlier. In the healing of a venous ulcer, counteracting venous hypertension is the most important measure and the most effective way of achieving this is elevation of the limb ( Fig. 49(g)(h) 505, Fig. 59(a) 591 and Fig. 63(c) 619). Local applications to the ulcer itself are probably far less important. Strong antiseptics may actually be damaging and the ulcer is best cleansed by normal saline, and covered with an inert, non-adherent, moisture-preserving material such as a hydrocolloid gel. Steroid applications should be avoided since they may actually delay epithelialization and cause deterioration in the ulcer. Antibiotic preparations should not be used unless there is good reason, for fear of setting up a sensitization reaction in the surrounding skin which is particularly vulnerable to antibiotics (Fig. 63(e)) 621 and to other materials commonly used in ointments and dressings. If pathogenic organisms have been demonstrated, any necrotic tissue should be excised, and an appropriate antibiotic given systemically for a few days. It must be emphasized that local treatment to the ulcer will not be effective unless venous hypertension is controlled by elevation for a good proportion of the day and all through the night. A sophisticated alternative to high elevation, particularly if oedema is troublesome, is the use of a pneumatic compression device acting sequentially upwards by multiple chambers enclosing the limb. These machines, often used in the control of lymphoedema, are widely marketed and can prove very successful in the healing and subsequent prevention of recurrence of ulceration in chronic venous insufficiency.

Most venous ulcers will heal with the regimen just outlined and often it may be combined with limited ambulation if external support with a paste bandage is used. If the ulcer is particularly large the process may be speeded up surgically by removing excess granulation tissue and applying some form of split skin graft. This should only be done when the ulcer has clearly reached a healing phase with sloping edges and a thin grey line of epithelial ingrowth. In cases where surgical control of venous hypertension is not possible, the ulcer will soon recur unless the patient has been instructed in an appropriate way of life which will include elevation of the limb whenever possible and the use of external support ( Fig. 49 and 505 Fig. 59(a) 591,592,593, (b), and (c)). If a large ulcer proves intractable or it recurs repeatedly, a plastic procedure excising the ulcer and providing skin cover by a pedicle graft, or by a myocutaneous free graft vascularized by microvascular surgery, may give a fresh start but will require prolonged care to prevent eventual recurrence. In these circumstances it is imperative to make sure beforehand that ischaemia or malignancy is not the real cause for the ulcer's unsatisfactory response to treatment. The possible role of ligation of perforating veins is discussed earlier.

This state is comparatively common and its management conflicts directly with that of venous ulcer so that distinguishing one from the other is of crucial importance. The ischaemia is usually due to atherosclerosis so that the older patient is most commonly affected but it can be encountered in young adults.

The ulcer is usually painful and situated on toes, foot, or leg; it is especially likely to occur over bony prominences, such as toe joints, the malleoli, or the shin, where the impoverished skin is easily damaged by external pressure against the unyielding bone. The ulcer is ‘dry’, lacking exudate or pus because the circulation is insufficient to support inflammatory reaction (Figs. 63 (f) and (g)(iii)) 622,623,624. There will usually be a story of intermittent claudication, numbness of the toes and forefoot on walking, and a typical nocturnal ischaemic rest pain, relieved by sitting in knee-up position or hanging the foot out of bed (Fig. 63(g)) 624, and made worse by elevation. The ankle pulses will be greatly reduced or missing and this is confirmed by Doppler flowmetry. Sensation may be reduced, and the toes and forefoot show pallor on elevation (Fig. 63(f) (iii)) 623 with considerable delay in return of colour when the leg is placed horizontally again. Brown pigmentation of the surrounding skin, typical of venous ulceration, will not be present.

It is quite possible for venous ulceration to be accompanied by ischaemia, each condition aggravating the ill effects of the other (Fig. 63(h)) 625. Treatment of ischaemic ulceration is considered elsewhere but it must be emphasized that elevation of an ischaemic limb can only reduce further its depleted arterial supply which has scarcely sufficient pressure to mount the gradient to the forefoot. To treat an ischaemic ulcer as a venous ulcer is a serious error. Pain in a leg ulcer, especially if it is made worse by elevation, should always suggest that ischaemia is present and the adequacy of arterial supply assessed. If there is any doubt the limb should not be raised above the horizontal.

The most common cause for neuropathic ulceration is diabetes but other neurological conditions, including spina bifida, tabes dorsalis, syringomyelia, spinal cord or nerve injury, and even leprosy, should not be overlooked. The cause for ulceration here is loss of protective reflexes due to neuropathy. This leads to skin in the foot being given prolonged compression by body weight against bony prominences, such as the underside of a metatarsal head (Fig. 63(i)) 626, the calcaneum, or the malleoli, without the patient being aware that damage is occurring. The arterial supply may be good and ischaemia is not usually a factor.

The ulcer is characteristically punched out and situated over a bony prominence. Evidence of the accompanying neuropathy may be provided by absent ankle jerks and diminished sensation in the toes and foot. In diabetes the diagnosis is easily confirmed by raised fasting levels of blood glucose.

These ulcers eventually allow entry of infection to surrounding tissues and set up a smouldering cellulitis that painlessly destroys the interior of the foot by necrosis of ligaments, tendons, and muscles (Figs. 63 (j) and (k)) 627,628. A diabetic ulcer is an unstable state which may eventually cause loss of a foot in this fashion and should not be allowed to continue unhealed. Healing is achieved by control of the diabetes and protection of the ulcer from external pressure, or by surgery to remove the underlying bony prominence, or, if need be, by forefoot amputation.

Diabetes may, of course, coexist with true venous ulceration and should always be excluded as a factor in leg ulcers.

A primary neoplastic ulcer of the skin, such as malignant melanoma, or epithelioma is always possible. Basal cell carcinoma (rodent ulcer) is uncommon on the lower limb but the author has seen one case occurring in an area of venotensive change. Malignant change in a long-standing venous ulcer is a well known possibility (Marjolin's ulcer) but even so there may be a long delay before this change is recognized. The foot and toes are a relatively common site for malignant melanoma which may ulcerate.

Tropical ulcers, including cutaneous leishmaniasis and fungus infections, may be brought into temperate countries by travellers abroad.

Ulceration including tuberculosis and syphilis may be caused either as part of a systemic illness or as a localized infection. The possibility of lesions due to acquired immune deficiency syndrome (AIDS) should not be overlooked.

Any severe anaemia, sickle-cell anaemia, thalassaemia, hereditary spherocytosis, or leukaemia can provide obscure forms of chronic leg ulceration. It is wise to carry out routine blood examination at an early stage in the management of chronic leg ulcer.

Vitamin and nutritional deficiencies, uraemia, and other metabolic disorders may cause or aggravate chronic ulceration.

Skin sensitivity or allergy to materials at work, applied medicinally or for cosmetic reasons can either cause or aggravate ulceration. It is commonplace for leg ulcers to be exacerbated by inappropriate ointments, particularly antibiotics, cortisone, and antiseptics. A wide range of drugs taken internally may cause skin reactions and eventually ulceration but these lesions are likely to be widespread and not confined to a limb.

Trauma as a single episode commonly sets off an ulcer in the presence of venous stasis, ischaemia, and in many of the generalized states referred to in this section. The skin of patients on corticosteroids becomes fragile and especially vulnerable to minor trauma.

Misplaced injections during sclerotherapy may cause skin necrosis and prolonged ulceration. Many chemicals used medically or industrially can have the same effect. Particularly dangerous is inadvertent intra-arterial injection and many pharmaceuticals, including sclerosants and barbiturates, can cause extensive gangrene in the extremity; this may occur in medical procedures or by self-injection in drug addiction (Fig. 63(m)) 630. High pressure injection of grease, used in servicing automobiles, can cause widespread destruction of subcutaneous tissue and skin. Insect bites may inject necrotoxins followed by unpleasant, prolonged ulceration. Insect bites may also implant parasitic or protozoal organisms which cause chronic lesions but these are uncommon in temperate climates.

Recurring trauma, either caused at work or self-inflicted in psychiatric disorders or malingering (dermatitis artefacta), can be an occasional cause for ulceration. Injury to the skin may occur from radiation or chemicals possibly without the patient realizing it.

Patients with rheumatoid arthritis may develop intractable ulceration on the legs or feet caused by vasculitis and this is sometimes mistaken for venous ulceration.

Disorders such as systemic lupus erythematosus and polyarteritis can form lesions on the legs; these resemble the eczematous changes seen in venous disorder and eventually ulcerate. See Figs. 63n-o 631,632

The list of causes for leg ulceration given above is by no means complete but serves to illustrate the need to be constantly aware that one chronic leg ulcer in ten will not be venous in origin and will call for a special skill in diagnosis.

The following authoritative works give detailed accounts of the venous disorders and their treatment, together with comprehensive references to the most significant publications upon this subject.

Bergan JJ, Yao JST. Surgery of the veins. New York: Grune and Stratton, 1985.

Bergan JJ, Yao JST. Venous disorders. Philadelphia: W.B. Saunders, 1991.

Bradbury AW, Murie JA, Ruckley CV. Role of the leucocyte in the pathogenesis of vascular disease. Br J Surg, 1993; 80: 1503–12.

Browse NL, Burnand KG, Lea Thomas M. Diseases of the veins: Pathology, diagnosis and treatment. London: Arnold, 1988.

Dodd H, Cockett FB. The pathology and surgery of the veins of the lower limbs. Edinburgh: Churchill Livingstone, 1976.

Gardner AMN, Fox RH. The return of blood to the heart: venous pumps in health and disease. London: John Libbey, 1989.

Lea Thomas M. Phlebography of the lower limb. Edinburgh: Churchill Livingstone, 1982.

May R. Surgery of the veins and the pelvis. Philadelphia: W.B. Saunders and Co. Stuttgart: Georg Thieme, 1979.

Negus D. Leg ulcers. Oxford: Butterworth-Heinemann Ltd, 1991.

Nicolaides A, Christopoulos D, Vasdekis S. Progress in the investigation of chronic venous insufficiency. Ann Vasc Surg, 1989; 3: 278–92.

Nicolaides AN, Sumner DS. Investigation of patients with deep vein thrombosis and chronic venous insufficiency. London: Med-Orion Publishing Co, 1991.

Tibbs DJ. Varicose veins and related disorders. Oxford: Butterworth-Heinemann Ltd, 1992.