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FUNCTIONAL AND SURGICAL ANATOMY
The venous return to the lower limb is by two systems, deep and superficial. The two systems are connected by the perforating veins which pass through the deep fascia. The most important perforating veins are in the medial part of the lower-third of the leg. Throughout the course of the deep, perforating and superficial veins are the venous valves. The valves permit flow of blood upwards in the superficial and deep veins. More important Is the fact that the valves in the perforators normally allow flow only from the superficial to the deep veins.
The normal lower limb has a physiological mechanism (the muscle pump) which effectively relieves the high venous pressure of the upright posture. The efficiency of the muscle pump depends on the competence of the lower limb venous valves. During exercise, the leg muscles squeeze the deep veins and empty them. During relaxation of the muscles, the superficial veins empty into the deep veins, so that superficial venous pressure decreases to below normal resting pressure. Superficial veins are not surrounded by skeletal muscles thus do not empty by muscular compression. The long and the short saphenous veins have a valve at their junction with the femoral and the popliteal vein.
Venous valves may be incompetent in the superficial, deep and the perforating veins. Valves may be damaged beyond repair usually as a result of deep vein thrombosis or there may be a congenital absence of the valves. At times, the valves are normal but the vein tends to dilate abnormally possibly due to hereditary connective tissue defect.
VARICOSE VEINS OF THE LOWER LIMB
Primary Varicose Veins
These are varicose veins without an obvious predisposing cause. There is no
evidence of deep vein thrombosis. There is often a positive family history of the disorder. The initiating cause is unknown. The valves, whose cusps are essentially normal, become incompetent as they cannot meet in the dilated vein. One theory suggests that the affected patients have a generalised abnormality of connective tissues, so that the weak vein wall tends to dilate abnormally in response to prolonged hydrostatic pressure. The main valves affected are those at the saphenofemoral (lying at the junction of the long saphenous and common femoral veins), saphenopopliteal and at the site of perforating veins. When the valves become incompetent alone or in conjunction, the dilatation of superficial veins takes place. The long saphenous and its tributaries are involved most frequently.
The aggravating factors associated with an increased Incidence of varicose veins are female sex, parity, constricting clothing, prolonged standing, marked obesity, and consumption of oestrogens (oral contraceptives).
Secondary Varicose Veins
After thrombophlebitis of the deep veins, there is an attempt at recanalisation but valves in the deeper system get destroyed. The muscle pump mechanism does not function well and the limb is chronically exposed to a high venous pressure when the individual is in an upright position. The high pressure in deep veins is transmitted through incompetent perforators to the superficial veins, particularly on the medial aspect of the leg. The high pressure interferes with local tissue nutrition and ulceration (varicose ulcer) may occur. The superficial veins also tend to become varicose. This condition is important to recognise clinically as the removal or ligation of the superficial veins is not advisable as this further impedes venous return from the lower limb.
Varicose veins in very young people (below the age of 20) may be due to congenital arteriovenous fistulae . Varicose veins associated with congenital or acquired arteriovenous fistulae may show arterial pulsation, thrill or bruit.
Symptoms and Signs
It is not difficult to diagnose varicose veins by little more than visual inspection. The condition may either be widespread in both legs, or restricted to a single varix. Due to varicosity, the vein wall is thickened but the thickening may not be uniform and through an area of relatively unsupported venous wall, an outpouching may result. Should this be at the saphenous opening it is called a 'saphena varix', and can be distinguished from a femoral hernia due to a palpable thrill when the patient coughs or the vein below is tapped with a finger. In general, л varicosity of the long saphenous system is seen on the medial side of the leg and thigh while that of the short saphenous system is seen on the posterolateral aspect of the leg. In a long standing case, however, because of liberal communication between the two systems, varicosity in one may spread to the other. On gross examination, the venous dilatation is irregular, causing outpouchings, rather than cylindrical.
Symptoms depend on the extent of the back pressure. The commonest is a tired and aching sensation in the lower limb. The symptoms of primary varicose veins are rarely severe and most patients seek advice for cosmetic reasons. Secondary varicose veins often cause more severe symptoms. Progression to varicose ulcers (on the Inner aspect of the leg) is relatively common whereas this complication is unusual with primary varicosity.
The patient is examined recumbent with the leg at rest and the empty veins are palpated to identify the circular gaps in the deep fascia through which the deep perforators pass. There is usually one such gap over the shin of the tibia, one below near the ankle and one few centimetres above the knee.
It is necessary to differentiate between primary and secondary varicose veins. The secondary veins are associated with an incompetent deep venous system and incompetent perforators. When ulceration, brawny Induration, and marked hyperpigmentation are present, one can be reasonably certain that deep venous insufficiency exists and that the varicose veins are secondary. Otherwise, they are usually primary.
In case of incompetence of a perforator, a localised varicosity may be seen.
The majority of cases belong to a combination of incompetency of the saphenofemoral valve and many perforators.
Several complications of varicose veins may arise. Minor trauma tends to cause severe venous haemorrhage. Dermatitis, skin pigmentation, etc. are associated with chronic venous stasis. The pigmentation is due to rupture of the cutaneous capillaries and deposition of haemosiderin from extra vasated red blood cells.
Tests for Competence of Venous Valves
The precise location of the incompetent or absent valves in primary varicose veins is important from the effective treatment point of view. Certain tests based on the intelligent use of the tourniquet have been described.
Brodle-Trendelenberg Test
With the patient lying, the limb is raised to empty the veins. A rubber tourniquet is applied at the saphenofemoral junction at the fossa ovalis (4 cm below and lateral to the pubic tubercle), tight enough to occlude the vein (pressure by the thumb over the fossa ovalis may be used Instead). The patient is made to stand. Normally, the gradual filling of superficial veins occurs from below after the patient stands. When the tourniquet is removed, filling continues to be gradual. If there is rapid filling from above, this means incompetence of the saphenofemoral valve. If the saphenous vein fills ,up before the tourniquet is released, incompetence of the perforating veins is also indicated.
A modification of this test is that after emptying the veins, three rubber tourniquets are placed around the leg and thigh at different levels and the patient is made to stand. Tourniquets are removed at different occasions, starting with the lowest one first. If the veins fill rapidly at a particular level, it indicates incompetence of the perforating channel at the level. If this does not occur and the veins fill up only slowly, the communicating veins are functioning normally (see also below).
Three Tourniquet Test
Here one tourniquet is tied, after emptying the veins as in Trendelenberg test, around the thigh below the saphenofemoral junction, another below the knee and the third just above the knee. These tourniquets prevent blood flow to each blow out from above as well as from below. The patient is now asked to stand up and the appearance of varicosity is looked for within 30 seconds in each segment with tourniquets in position. The legs are also observed for retrograde filling of the distal segment after removal of the tourniquets one by one from below upwards. The exact level of the perforator which is incompetent can thus be assessed.
Perthe's Test
A tourniquet is applied round the upper thigh, sufficiently tight to occlude the long saphenous vein. With the tourniquet in position, the patient is asked to walk for a few minutes. If the deep veins and the communicating veins (perforators) are functioning normally, the superficial veins shrink. If the superficial veins get dilated, either the deep system is blocked or the perforators below the level of the tourniquet are incompetent.
Mom'sse/'s Cough Impulse Test
The limb is elevated to empty the veins. The patient is asked to cough forcibly. If an expansile impulse is felt in the long saphenous vein, it may be presumed that the saphenofemoral valve is incompetent.
Schwartz Test
It is performed with the patient standing. The fingers of the left hand are placed just below the saphenous opening and the right middle finger is tapped over the most prominent part of the varicosity in the leg. A palpable impulse is indicative of incompetence of valves between the site of percussion and palpation due to absence of valvular barrier to the upward wave of blood.
Pratt's Test
This is to assess the Incompetence of perforators. With the patient in supine position, an elastic compression bandage is applied from the toes to upper-third of the thigh tp empty the varicose veins. A tourniquet is then tied just above the bandage. The patient is asked to stand up and the bandage is removed from above downwards. The appearance of blowouts indicates the site of incompetent perforators below or above the knee.
Doppler Test
It is a useful, simple and nonlnvasive aid in the diagnosis of deep vein thrombosis. The sensing probe, placed over the femoral vein in the groin, normally transmits a venous hum and pressure on the calf (or calf muscle contractions) changes the hum into a roar. If there is deep vein thrombosis between the calf and groin, the roar is absent.
Venography
A fine rubber tourniquet is applied just above the malleoli to occlude the superficial veins. An injection of 20 to 30 ml of Conray is given into a superficial vein of the foot in order to introduce the contrast medium into the deep veins. This is to detect the number and site of incompetent perforators and also for the site and the extent of deep vein thrombosis. Venography being an Invasive procedure, is not popular and moreover, it carries risk of venous gangrene, and should better be avoided.
Ambulatory Venous Pressure Study
To evaluate the functional status, venous pressure recording from a foot vein during exercise has been suggested but gives little information of diagnostic value.
Treatment of Varicose Veins
1. For minor varicosity, no treatment is prescribed.
2. Elastic stockings or crepe bandage may be used for early cases, for vari
cose veins that occur during pregnancy and for patients unwilling or unfit for surgery. Elastic- bandage provides support and prevents the condition from getting worse. It, however, does not cure the condition. Walking should be encouraged, and prolonged sitting or standing should be discouraged. The patient should be instructed to elevate the leg as frequently as possible to reduce the venous pressure.
3. Injection compression therapy (Fegan's method) With the patient standing, the needle attached to a syringe containing 1.0 ml of sodium tetradecyi sulphate is inserted into the filled vein. A little blood is withdrawn and 0.1 ml of the solution is injected to clear the needle. The patient now lies down and the limb is carefully elevated. The segment to be injected is isolated by firm digital pressure (Fig. 15.3) and injection is made in an empty vein. Immediately after injection, foam rubber pads are applied over the injection sites and covered by a layer of compression bandage. Continuous pressure on the veins is maintained for about 2 weeks. Multiple sites can be Injected at the initial visit and others subsequently.
This treatment is best reserved for small unsightly veins, lower leg perforators, and recurrent or persistent veins after operation. Sclerotherapy is best suited for varicositics below the knee.
Due care should be observed during injection, as extravasation of a sclerosant into the surrounding tissue can cause necrosis. Injection treatment Is contraindlcated if there is acute infective thrombophlebitis. It Is also not advisable for patients with deep vein thrombosis.
4. Surgery Gross varicosities are better treated by surgery unless there is some specific contraindication. The patient with deep vein abnormality Is not suitable for surgery.
Surgical Treatment
Surgery consists of flush Ugation, ligation with stripping or multiple ligatlons.
Ugation (1) For saphenofemoral Incompetence, a 'flush' ligature is applied at
the junction of the long saphenous vein with the femoral vein. Particular care is taken to see that between the ligature and the saphenofemoral junction there Is no Intervening tributary of the saphenous vein. For this purpose. the superficial epigastric, the superficial external pudendal, and the superficial circumflex Iliас veins must be ligated and divided
2) For saphenopopliteal incompetence, a ligature is applied at the junction of the short saphenous vein with the popliteal vein at the popliteal fossa and the short saphenous vein Is divided.
Ugation and stripping This involves ligation of the long saphenous vein and its tributaries at its junction with the common femoral vein in the groin. The entire saphenous may be removed by passing an intralumlnal stripper from the exposed saphenous vein at the ankle to the divided end in the groin and avulsing the entire vein. Once the main channel has been removed, most of the tributaries will also thrombose and add to the benefit.
There is a disturbing Incidence of saphenous neuropathy when the entire long saphenous (from ankle to groin) has been avulsed. Now most workers have abandoned full length stripping in favour of knee-to-groin stripping.
Multiple Ligatlons of Incompetent Distal Perforating Veins The distribution of perforators is not constant. The common sites, however, are (Fig. 15.5) the following.
1. In the lower -third of the thigh
2. One just below the knee
3. The ankle perforators (three to four in number).
The Incompetent perforators are explored via separate small incisions, dissected down to and through the fascial orifice and ligated deep to the fascia with 3-0 silk.
Postoperatively. the legs are supported with elastic bandages for approximately 6 weeks. Elevation of the legs in bed minimises postoperative swelling.
Walking is encouraged, but standing and sitting are forbidden.
Results of Surgery for Long Saphenous Primary Varicose Veins
Unless the ligature is placed flush with the femoral vein. poor results are to be anticipated. A meticulous dissection with visualisation of all the tributaries is the only reliable way to avoid an inadequate operation. If Ugation is not high enough.the short proximal stump becomes markedly dilated and insufficiency is then transmitted by way of the missed branches remaining in the stump.
At times, failure to Identify and treat other sources of reflux such as saphenopopliteal or midthigh perforator may produce recurrence.
Complications of Varicose Veins
1. Thrombophlebitis Superficial thrombophlebitis may be spontaneous in onset or results from minor bruises or trauma. A tender, red Indurated cord is typically present along the course of the varicose tributary. The patient may be febrile and has leucocytosis. Treatment is symptomatic and Includes analgesics for pain, local heat, compression bandages and the patient should be up and about. Bed rest and anticoagulation is not necessary. High doses of antibiotics should be given and the long saphenous vein should be ligated and divided to safeguard against embolism.
2. Eczema Dermatitis and skin irritation can cause itching and severe excoriation from scratching. It may also be an allergic response to local application of ointment. The eczema will respond to local application of zinc oxide ointment or to steroid cream.
3. Venous ulcer (Discussed later.)
4. Haemorrhage Haemorrhage from a ruptured varicose vein is usually profuse. Elevation of the leg and a firm bandage will control bleeding.
5. Periostitis The venous ulcer of long standing situated over the tibia may produce periostitis of the underlying bone.
VENOUS ULCERATION
Ulcers typically occur on the lower medial aspect of the leg just above the medial malleolus. Most patients have varicose veins (therefore .also known as varicose ulcers) and they occur much more frequently as sequelae of deep vein thrombosis.
Pathology
Incompetence of valves in the deep communicating veins and less frequently in the superficial system produces stasis of blood, and a rise in the local venous pressure. The high venous pressure causes leakage of fluid of large molecules from capillaries into tissue spaces. This results in fibrinogen escaping into tissues which is converted to fibrin. A pericapillary cuff of fibrin forms and acts as a diffusion barrier. This thickening in the wall of the capillaries affects the transport of oxygen and nutrient substances required for cellular survival. There is thus local cellular necrosis and ulceration.
There is further evidence to suggest that local venous hypertension opens up the normally closed arteriovenous shunts, and arterial blood reaches the venous channels by bypassing the capillary Circulation. The shunting of arterial blood produces local tissues anoxia, necrosis and ulceration.
These changes are confined to the skin and subcutaneous tissues in the lower inner half of the leg, and are limited by the deep fascia in the earlier stages. In more advanced ulcers, the process Involves the deeper structures as well. When the ulcer heals the subcutaneous fat is never replaced and there is formation of scar tissue. In advanced stages, the skin, subcutaneous tissues and deep fascia become welded together into a firm solid mass.
Clinical Features
The ulcers are large and shallow, with an irregular sloping margin, and the base is often formed by unhealthy granulation tissue. Ulceration is mainly confined to the lower half of the leg. They are usually associated with oedema of the leg.
Before the appearance of frank ulceration, the skin in the affected area often shows eczematous changes. The skin becomes pigmented due to deposition of haemosiderin derived from the breakdown of extravasted blood in the subcutaneous tissues. In the early stages, venous ulcers are painful and this is made worse by infection.
Differential Diagnosis
A venous ulcer will heal by local measures, elastic support and elevation. The ulcer is cleaned with normal saline or cetrimide. The local application of strong cleansing agents is avoided as their irritation may delay healing and precipitate a severe eczematous reaction. Simple nonadherent dressings are recommended as these can be easily changed. When the ulcer is grossly infected, systemic antibiotics (according to specific sensitivity of the organism) are used.
The patient is confined to bed with the foot-end of the bed raised. When combined with active calf exercises, the local venous pressure is decreased. Those with uncomplicated ulcers and minimal oedema are treated by the ambulant method. The use of firm elastic compression bandages reduces effectively the local venous hypertension. The bandages are worn during the day only and at night, the patient is instructed to sleep with the foot of the bed elevated. The bandages are reapplied in the morning before getting out of bed.
If the ulcer cannot be controlled by conservative measures, surgery is indicated. The ulcer base is excised down to healthy tissue and split skin grafts are applied to the raw area. Permanent elastic support is recommended to all those who have had a venous ulcer and patients should be warned to take care of their legs as there is always the possibility of reulceratlon, especially after minor trauma.
DEEP VEIN THROMBOSIS
Deep vein thrombosis (DVT) Is more common in Northern Europe and the USA than In Asia and Africa. The difference has been attributed to differences in diet, fibrinolytic activity, ethnic origin and climate.
The thrombosis may commence in a venous tributary to later extend into the main deep vein. The pelvic and calf veins are more commonly affected than others.
RIfk Factors In Deep Vein Thrombosis
1. The incidence increases with advancing age and is more common in women than men.
2. In case of previous deep vein thrombosis, there is a higher risk of a further thrombotic episode.
3. The risk of deep vein thrombosis is increased in patients with cancer.
4. Trauma to the lower limb and pelvis significantly Increases the risk of thromboembolism.
5. Deep vein thrombosis is seen in 30 to 40 per cent of non coagulated patients with acute myocardial infarction. This may be due to venous stasis.
6. The risk is increased manifold during pregnancy and the postpartum period.
7. Oral contraceptives (oestrogen) increase the risk of venous thrombosis. This risk is similarly increased when they are administered for suppression of prostatic cancer.
8. Prolonged immobilisation with no calf muscle activity increases the risk.
9. Patients with blood group A have an Increased risk compared with those who are of the group 0.
10. Patients with a deficiency of antithrombin III may have a family history of deep vein thrombosis and thromboemboUsm.
Pathogenesis
Virchow, in the mid 1800s, recognised three general causes of vascular thrombosis — injury to the vessel wall, stasis and increased coagulability of the blood.
1. Injury to the vein wall Damage to the endo-thelium exposes subendothellal collagen with the result that tissue thromboplastin is released and thrombosis occurs.
2. Venous stasis The aggregates of blood cells and fibrin, which formally wash away in the stream of blood, tend to accumulate due to stasis and lead to subsequent thrombus formation.
3. Changes (n the coagulability of blood Blood may be in a hypercoagulable state in conditions which predispose to deep venous thrombosis (DVT) including malignancy, pregnancy and surgery although the exact mechanism of the hypercoagulabillty is unknown.
Platelets play an important role in the early phase of thrombus formation. As the platelet aggregate grows, procoagulants are released and the local stasis and hypercoagulability further help to increase this aggregation. Once initiated, the coagulation process produces retrograde thrombosis.
The initial occluding thrombus is firmly adherent to the vein wall and is pale in colour. The propagated thrombus is red, loosely attached and may break off to form an embolus. If the thrombus remains in situ it becomes organised by an ingrowth of capillaries and fibroblasts. Recanalisatlon occurs and the lumen is restored. Radioactive fibrinogen (1-125) is preferentially taken up by the developing thrombus, and its Incidence in the UK was found to be as high as 30 per cent following surgery amongst those over 40 years.
Clinical Features and Diagnosis
The clinical spectrum varies greatly from no symptoms to severe pain and systemic signs of inflammation. In most, thrombosis causes an inflammatory reaction in the walls of the vein and this gives rise to the clinical features of pain, tenderness and low grade pyrexia. The location of the thrombus determines the location of the physical findings. The most frequent site is the calf, especially the venous sinuses of the soleus muscle and the posterior tibial and peroneal veins. Tenderness may be elicited along the course of the posterior tibial and peroneal veins. Roman's sign-pain
in the calf on dorsiflexion of the foot may be present.
At times even with extensive deep vein thrombosis, the patient may not experience any symptoms and a pulmonary embolism or the subsequent development of a post-thrombotic limb may be the only indication of a previous vein thrombosis.
Occasionally patients with severe illofemoral thrombosis present with a very swollen white oedematous limb (phlegmasia alba dolens). More commonly a massive proximal thrombosis causes a blue leg (phlegmasia cerulea dolens) and this may eventually progress to true venous gangrene in a few patients.
Only half of the patients with deep vein thrombosis present with clinical signs and 30% of those patients with physical signs have normal deep veins on venography. A ruptured Baker's cyst, cellulltis, lymphodema, torn calf muscles and calf haematomas can all mimic the signs of deep vein thrombosis.
Investigations of a Case of Deep Vein Thrombosis
About half of patients with this condition have no physical signs and the following investigations have, therefore, been suggested.
1. Venography It is impractical to use this investigation to screen large numbers of at-risk patients. In a suspected case (where local clinical features are not obvious and the pulmonary emobolic episode has taken place), however, it is a useful investigation. With the patient standing but not bearing weight on extremity being examined, radio-opaque contrast medium is injected into a vein on the dorsum of the foot. Serial X-rays can show calf, popliteal, femoral and iliac veins and determine the site, extent and nature of the thrombus.
2. Radioactive Jibrinogen uptake test Fibrinogen labelled with iodine 125 (1-125) is taken up preferentially by a developing thrombus; the labelled fibrinogen is given intravenously and the legs are scanned at several points with an external scintillation counter.
3. Doppler ultrasound detects changes in the velocity of venous blood flow. The sensing probe is placed over the femoral vein in the groin and in a case of DVT,
the venous hum does not .change into a roar on pressing the calf muscles.
ProphylaxI»
1. Early postoperative ambulation should be encouraged. It lessens stasis and lowers the incidence of venous thrombosis.
2. Physiotherapy and elastic stockings may reduce the occurrence of thrombosis.
3. The adhesion of platelets to subendothelial connective tissue at the site of damaged venous endothelium may lead to platelet aggregation and Initiate thrombus formation. Drugs like aspirin, dextran and chloroquin which interfere with different aspects of platelet function have been tried though with variable result.
4. Low dose heparin, 5000 units subcutaneously 2 hours before surgery, and subsequently at 12 hourly intervals for 7 days is most promising for preventing DVT. This does not significantly prolong the coagulation time as measured by the standard laboratory tests. The beneficial effect is thought to be through enhancement of a natural inhibitor of activated factor X. Heparin prophylaxis is, however, contraindicated in operations where even minimal bleeding could be disastrous (brain or eye surgery).
Treatment of Established Deep Vein Thrombosis
General Measures
These include the following.
1. Bandaging the whole limb with crepe bandage or stocking to Increase the deep venous flow
2. Bed rest with foot end of bed kept raised until the elevated temperature and the local signs (swelling, pain and tenderness) abate
3. After discomfort has settled and if the general condition permits, the patient Is encouraged to get out of bed.