We saw that some .weakening of the wall is always necessary to the occurrence of aneurysm, but no such condition is required in the production of varicose veins, although a certain looseness of texture, in some cases hereditary, undoubtedly predisposes. The walls of veins are already thin, and the blood-pressure within them is low. In the case of the veins of the skin we are familiar with the fact that, as a rule, the blood pressure is not sufficient to overcome the atmospheric pressure to any considerable extent and the veins are flattened or partially collapsed, a slow and weak current passing through them. The circulation must be considerably excited, or the veins must be obstructed in order to make them stand out as cylinders under the skin. Such being the case it may be conceived that the thin-walled veins, accustomed to a slight blood-pressure, will readily dilate when exposed to an increased blood-pressure. Varix is always jIuc to some cause which is calculated to increase the blood-pressure within the veins, such as obstruction of the veins by thrombi, tumours, the gravid uterus, passive hypersemia from heart disease, and so on.
In the early stages of varix, as we have frequently an opportunity of seeing it in the legs, there is simply an exaggeration of this natural dilatation above the valves. When we stand erect the column of blood in the veins of the legs is, as it were, supported at each valve, and the downward pressure tells on the valve and the portion of the vessel forming the valvular sinus. Hence this part of the vessel is the first to dilate when the blood-pressure is increased, and the first sign of varix is an exaggeration of the knotted state of the veins. At the outset each valve forms a kind of fixed point, the dilatation occurring at its level, and diminishing as the valve next above is approached. As the dilatation increases and extends up from the valve, the vein increases in length as well as in calibre, and in order to be accommodated it begins to form Curves or Convolutions. Thus begin those sinuosities which are so characteristic of varicose veins, and which tend to increase as time goes on. The dilatation of the vein has a tendency to render the valves incompetent, and this occurs all the .sooner as the region of the valves is, as we have seen, the part where the pressure is most exercised. When the valves become incompetent the pressure tells much more on the walls of the veins, as the column of blood is now arrested at longer intervals. The pressure acts most on the dependent parts of the sinuosities, and will increase the projection of these. In this way we may have wide sinuses with their convexity downwards, and in some cases even diverticula or pouches projecting from the veins (see Fig. 258). In these exaggerated dilatations the blood stagnates greatly, and it is not uncommon for Thrombosis to occur. The vein is obstructed more or less completely by the thrombus, which may organize. On the other hand, the latter often dries in and becomes impregnated with lime salts. In this way varicose veins frequently become the seat of vein-stones or Phleboliths.
Chronic inflammation is common in the tissues around varicose veins wherever they may be, and so in the skin we often have very persistent eczema with a brown coloration of the skin, which may be referred to haemorrhage by diapedesis from the hyperaemic vessels. The skin is indurated and thickened, and this along with the swelling of the veins may be so great as to produce an appearance like that in elephantiasis. Ulceration is often induced, and the ulcer is sometimes deep and sluggish, and may persist for years. There is sometimes great thickening of the walls of the swollen veins at the base of varicose ulcers. This isr apparently, a compensatory thickening to resist the excessive pressure (see Fig. 259).
Fig. 258. - Varicose veins of leg which were removed by operation.
A varicose vein may burst. It may be opened by the ulcerative process, or it may come to the surface and by its increasing dilatation at last rupture. In the case of the leg the results are sometimes exceedingly serious. As one effect of the dilatation is to render the valves incompetent, the veins of the entire leg may come to be virtually devoid of valves. But the veins inside the abdomen are normally devoid of valves, and so it may happen that from the lower leg up to the heart there may be a single column of blood without an arresting valve. If now a vein rupture in the leg, the whole system up to the heart may be, as it were, tapped, and if the person is in the erect posture a fatal haemorrhage may result. The haemorrhage will cease if the person lies down, but cases have been known in which an immense amount of blood has been shed into the boots without warning.
Fig. 259. - Vein with hypertrophy of its wall from base of varicose ulcer, x 18.
Haemorrhoids are varicose veins of the lower rectum. At the lower part of the rectum a network of small veins surrounds the bowel, lying immediately under the mucous membrane. These veins communicate with the inferior mesenteric vein, which is a tributary of the portal, and with the internal iliac, which is a tributary of the vena cava. Any obstruction in the portal circulation, or abnormal pressure within the abdomen is apt to induce dilatation of this haemorrhoidal plexus. The dilated veins push the mucous membrane before them, and protrude as bluish flat nodules either immediately within or without the anus. They may assume considerable dimensions. The knots are composed originally of a congeries of small convoluted veins (Fig. 260, B), which may communicate so as to form a kind of cavernous tissue, but sometimes there are large ones (Fig. 260, A). Through time the mucous membrane undergoes alterations. The piles at each movement of the bowels are exposed to mechanical irritation, and so the mucous membrane is almost constantly in a state of catarrh. Then at intervals, when the blood-pressure is unusually great by reason of an attack of inflammation or otherwise, the veins rupture, and so there is bleeding both in the substance of the mucous membrane and on to the surface. The haemorrhoids thus get greatly altered. They become condensed from inflammatory new-formation of connective tissue. They sometimes become the seat of collections of blood, which may form blood cysts. Phleboliths may also form in the veins. More severe inflammations sometimes occur, resulting in abscesses, fissures, fistulas, ulcers.
Fig. 260. - Hemorrhoids of rectum, in section, natural size, r is internal surface of rectum, and m the mucous membrane continued over the hemorrhoid. At m1 is represented the muscular coat, the dilated veins being in the submucous tissue. At A, the veins are few but much dilated, one especially so, just beneath the mucous membrane. At B, the dilated veins are more numerous, but smaller. Both occurred in the same case. (Virchow).
Varicocele is a dilatation of the veins of the spermatic cord and the external scrotal veins. It affects in a greatly preponderating proportion the left side, the explanation of this being apparently that the left-spermatic vein has a circuitous course, and enters the renal vein at a right angle, while the right opens into the lower vena cava. The varicosity generally begins at the external inguinal ring, and extends downwards as far as the testicle. There is not infrequently atrophy of the testicle, and sometimes hydrocele or hsematocele.
Varix may occur in other veins, such as those of the Neck of the bladder and Prostate. It is also met with in the female in the Vesical plexus and veins of the Vagina, and this may be combined with varix of the Broad ligament. Varicosity also occurs in the veins of the Dura mater.