Manual of Surgery by Alexis Thomson (golden son ebook .TXT) 📕

To relieve the pain, warm fomentations or lead and opium lotion should be applied. Later, ichthyol-glycerin, or glycerin and belladonna, may be substituted.

When, at the end of three weeks, the danger of embolism is past, douching and gentle massage may be employed to disperse the œdema; and when the patient gets up he should wear a supporting elastic bandage.

The infective form usually begins as a peri-phlebitis arising in connection with some focus of infection in the adjacent tissues. The elements of the vessel wall are destroyed by suppuration, and the thrombus in its lumen becomes infected with pyogenic bacteria and undergoes softening.

Occlusion of the inferior vena cava as a result of infective thrombosis is a well-known condition, the thrombosis extending into the main trunk from some of its tributaries, either from the femoral or iliac veins below or from the hepatic veins above.

Portions of the softened thrombus are liable to become detached and to enter the circulating blood, in which they are carried as emboli. These may lodge in distant parts, and give rise to secondary foci of suppuration—pyæmic abscesses.

Clinical Features.—Infective phlebitis is most frequently met with in the transverse sinus as a sequel to chronic suppuration in the mastoid antrum and middle ear. It also occurs in relation to the peripheral veins, but in these it can seldom be recognised as a separate entity, being merged in the general infective process from which it takes origin. Its occurrence may be inferred, if in the course of a suppurative lesion there is a sudden rise of temperature, with pain, redness, and swelling along the line of a venous trunk, and a rapidly developed œdema of the limb, with pitting of the skin on pressure. In rare cases a localised abscess forms in the vein and points towards the surface.

Treatment.—Attention must be directed towards the condition with which the phlebitis is associated. Ligation of the vein on the cardiac side of the thrombus with a view to preventing embolism is seldom feasible in the peripheral veins, although, as will be pointed out later, the jugular vein is ligated with this object in cases of phlebitis of the transverse sinus.

The term varix is applied to a condition in which veins are so altered in structure that they remain permanently dilated, and are at the same time lengthened and tortuous. Two types are met with: one in which dilatation of a large superficial vein and its tributaries is the most obvious feature; the other, in which bunches of distended and tortuous vessels develop at one or more points in the course of a vein, a condition to which Virchow applied the term angioma racemosum venosum. The two types may occur in combination.

Any vein in the body may become varicose, but the condition is rare except in the veins of the lower extremity, in the veins of the spermatic cord (varicocele), and in the veins of the anal canal (hæmorrhoids).

We are here concerned with varix as it occurs in the veins of the lower extremity.

Etiology.—Considerable difference of opinion exists as to the essential cause of varix. The weight of evidence is in favour of the view that, when dilatation is the predominant element, it results from a congenital deficiency in the number, size, and strength of the valves of the affected veins, and in an inherent weakness in the vessel walls. The angioma racemosum venosum is probably also due to a congenital alteration in the structure of the vessels, and is allied to tumours of blood vessels. The view that varix is congenital in origin, as was first suggested by Virchow, is supported by the fact that in a large proportion of cases the condition is hereditary; not only may several members of the same family in succeeding generations suffer from varix, but it is often found that the same vein, or segment of a vein, is involved in all of them. The frequent occurrence of varix in youth is also an indication of its congenital origin.

In the majority of cases it is only when some exciting factor comes into operation that the clinical phenomena associated with varix appear. The most common exciting cause is increased pressure within the veins, and this may be produced in a variety of ways. In certain diseases of the heart, lungs, and liver, for example, the venous pressure may be so raised as to cause a localised dilatation of such veins as are congenitally weak. The direct pressure of a tumour, or of the gravid uterus on the large venous trunks in the pelvis, may so obstruct the flow as to distend the veins of the lower extremity. It is a common experience in women that the signs of varix date from an antecedent pregnancy. The importance of the wearing of tight garters as a factor in the production of varicose veins has been exaggerated, although it must be admitted that this practice is calculated to aggravate the condition when it is once established. It has been proved experimentally that the backward pressure in the veins may be greatly increased by straining, a fact which helps to explain the frequency with which varicosity occurs in the lower limbs of athletes and of those whose occupation involves repeated and violent muscular efforts. There is reason to believe, moreover, that a sudden strain may, by rupturing the valves and so rendering them incompetent, induce varicosity independently of any congenital defect. Prolonged standing or walking, by allowing gravity to act on the column of blood in the veins of the lower limbs, is also an important determining factor in the production of varix.

Thrombosis of the deep veins—in the leg, for example—may induce marked dilatation of the superficial veins, by throwing an increased amount of work upon them. This is to be looked upon rather as a compensatory hypertrophy of the superficial vessels than as a true varix.

Morbid Anatomy.—In the lower extremity the varicosity most commonly affects the vessels of the great saphena system; less frequently those of the small saphena system. Sometimes both systems are involved, and large communicating branches may develop between the two.

The essential lesion is the absence or deficiency of valves, so that they are incompetent and fail to support the column of blood which bears back upon them. Normally the valves in the femoral and iliac veins and in the inferior vena cava are imperfectly developed, so that in the erect posture the great saphena receives a large share of the backward pressure of the column of venous blood.

The whole length of the vein may be affected, but as a rule the disease is confined to one or more segments, which are not only dilated, but are also increased in length, so that they become convoluted. The adjacent loops of the convoluted vein are often bound together by fibrous tissue. All the coats are thickened, chiefly by an increased development of connective tissue, and in some cases changes similar to those of arterio-sclerosis occur. The walls of varicose veins are often exceedingly brittle. In some cases the thickening is uniform, and in others it is irregular, so that here and there thin-walled sacs or pouches project from the side of the vein. These pouches vary in size from a bean to a hen's egg, the larger forms being called venous cysts, and being most commonly met with in the region of the saphenous opening and of the opening in the popliteal fascia. Such pouches, being exposed to injury, are frequently the seat of thrombosis (Fig. 66).