The primary cause of arterio-sclerosis is not definitely known, but its almost constant occurrence, to a greater or less degree, in the aged suggests that it is of the nature of a senile degeneration. It is favoured by anything which throws excessive strain on the vessel walls, such as heavy muscular work; by chronic alcoholism and syphilis; or by such general diseases as tend to raise the blood-pressure—for example, chronic Bright's disease or gout. It occurs with greater frequency and with greater severity in men than in women.
Atheromatous degeneration is most common in the large arterial trunks, and the changes are most marked at the arch of the aorta, opposite the flexures of joints, at the mouths of large branches, and at parts where the vessel lies in contact with bone. The presence of diseased patches in the wall of an artery diminishes its elasticity and favours aneurysmal dilatation. Such a vessel also is liable to be ruptured by external violence and so give rise to traumatic aneurysm. Thrombosis is liable to occur when calcareous plates are exposed in the lumen of the vessel by destruction of the endothelium, and this predisposes to embolism. Arterio-sclerosis also interferes with the natural arrest of hæmorrhage, and by rendering the vessels brittle, makes it difficult to secure them by ligature. In advanced cases the accessible arteries—such as the radial, the temporal or the femoral—may be felt as firm, tortuous cords, which are sometimes so hard that they have been aptly compared to “pipe-stems.” The pulse is smaller and less compressible than normal, and the vessel moves bodily with each pulsation. It must be borne in mind, however, that the condition of the radial artery may fail to afford a clue to that of the larger arteries. Calcified arteries are readily identified in skiagrams ([Fig. 65]).
We have met with a chronic form of arterial degeneration in elderly women, affecting especially the great vessels at the root of the neck, in which the artery is remarkably attenuated and dilated, and so friable that the wall readily tears when seized with an artery-forceps, rendering ligation of the vessel in the ordinary way well-nigh impossible. Matas suggests infolding the wall of the vessel with interrupted sutures that do not pierce the intima, and wrapping it round with a strip of peritoneum or omentum.
The most serious form of arterial thrombosis is that met with in the abdominal aorta, which is attended with violent pains in the lower limbs, rapidly followed by paralysis and arrest of the circulation.
Thrombo-Phlebitis and Thrombosis in Veins
Thrombosis is more common in veins than in arteries, because slowing of the blood-stream and irritation of the endothelium of the vessel wall are, owing to the conditions of the venous circulation, more readily induced in veins.
Venous thrombosis may occur from purely mechanical causes—as, for example, when the wall of a vein is incised, or the vessel included in a ligature, or when it is bruised or crushed by a fragment of a broken bone or by a bandage too tightly applied. Under these conditions thrombosis is essentially a reparative process, and has already been considered in relation to the repair of blood vessels.
In other cases thrombosis is associated with certain constitutional diseases—gout, for example; the endothelium of the veins undergoing changes—possibly the result of irritation by abnormal constituents in the blood—which favour the formation of thrombi.
Under these various conditions the formation of a thrombus is not necessarily associated with the action of bacteria, although in any of them this additional factor may be present.
The most common cause of venous thrombosis, however, is inflammation of the wall of the vein—phlebitis.