ARTERITIS. EMBOLISM.
Internal and external arteritis. Thrombosis, from inflammation. Embolism. Bruising. Stretching. Ligature. Lesions. Extension of clot, color, consistency, adhesion, lamination. Composition of clot. Condition of vessel. Changes in muscles. Causes: muscular tension, embolism. Heart clots, venous clots. Infecting debris. Symptoms: paresis or paralysis on exertion. Local suffering, tenderness, firm swollen artery, derangement of nutrition and function, atrophy. Chronic arteritis: Atheroma. Changes in serosa. Fibrous thickening, atrophy, dilatation. Strongylus. Treatment: rest, anodynes, alkalies, massage.
Inflammation of arteries has been divided into external and internal arteritis, according as it affects the fibrous sheath of the artery or its inner lining membrane.
In external arteritis the exudation of lymph often forms a protecting layer around the vessel, while the inner coats continuing sound the current of blood remains unimpaired. Even when suppuration takes place in the vicinity of a large artery, that vessel may pass through the center of the abscess and convey the blood as freely as before. The nutrition of the vessel thus detached from the surrounding tissues is maintained by its accompanying nutrient artery, though if the abscess is large there is danger of a deficient supply. The frequent presence of such arteries traversing an abscess should make the surgeon careful how he breaks down the bright pink bands occasionally seen to stretch across such cavities.
Internal arteritis, or inflammation of the internal coat of an artery is incomparably more serious and mainly because it determines the coagulation of the contained blood and consequent plugging of the vessel. This is but one manifestation of the general law that in inflamed tissues the fibrine-forming elements are produced in excess, and when blood comes in contact with these it tends to coagulate (thrombosis). On the other hand the inflammation in the arterial coats may ensue from the pressure of a blood clot formed in the veins or heart and carried on with the current until it reaches an artery too small to admit it (embolism).
The inflammation may be confined to a limited space as when an artery is bruised, stretched so as to tear through its inner coats, or interrupted by a ligature. It may on the other hand be diffused over a greater extent of the vessel, and in some cases two inflamed portions are separated by intervals of sound artery.
Anatomical features of the inflamed artery. In active inflammation of the internal coats of an artery, it contains blood clots, and if the inflamed surface is not very limited in extent the vessel is completely plugged and the clot forms up to its nearest transverse branch on the cardiac side, precisely as if the artery had been tied. The resulting clot is sometimes tubular, so that an impaired circulation is still carried on. The clot varies in length according to the extent of vessel inflamed, or the distance from the inflamed spot to the nearest diverging branch. The clot is usually fusiform in outline and is firmly attached throughout more or less of its diameter, and occasionally so firmly that it is all but inseparable from the serous membrane. The narrowed ends of the clot mostly float free in the liquid blood and portions from the end most distant from the heart will sometimes get detached, and by blocking up smaller arteries give rise to new centres of disease. This is a true instance of embolism or plugging.
The clot has nearly always a grayish or yellowish white color in the larger vessels, such as the posterior aorta, and an uniform pink or red streaked with yellow in the small. It is possessed of great firmness and elasticity. That portion of the surface which was not attached to the arterial walls, during life, is clear, smooth and glistening, while the portion which adhered to these walls is rough, irregular, and broken into shreds. It is usually composed of concentric layers showing its mode of formation.
Clots of this kind analyzed by M. M. Lassaigne and Clement were composed of water 74 parts; fibrine and albumen 25 parts; and alkaline salts 1 part.
The vessels filled by these clots are very irregular in their outline being thick and bulging at one point and thin and constricted at another. The outer coat is rarely the seat of morbid change, though it sometimes shows branching redness and thickening from exuded lymph. The internal coat where the clot was attached is intensely and unnaturally red, and a rough granular surface has given place to the healthy, smooth glistening appearance. In old standing cases the clots can only be separated from such surfaces by dissection with the knife. Other portions of the surface than those to which the clot adheres are usually smooth and polished, though rough granular and injected patches are sometimes met with independently of clots.
The muscles formerly supplied with blood by the obstructed arteries are pale, discolored, unnaturally firm, and if some time has elapsed since the plugging their fibrillated structure is made out with difficulty.
Causes. The causes of arteritis are often obscure. Goubaux conceived that it was frequently determined by extreme muscular tension. In support of this view he adduced the facts that it has been mainly observed in the horse, in which such stretching of the muscles is greatest, and that its most common seats have been where the muscles and vessels are most liable to stretching. Thus it is frequent in the posterior aorta towards its termination or in other words where the adjacent muscles (psoæ) are very liable to laceration from slipping backward or from efforts to disengage the limbs when fixed in soft ground; the femoral and auxiliary arteries are likewise frequent seats of inflammation and are likely to be overstretched when the limbs slip outwards.
Embolism or Plugging of the arteries must be accepted as another cause. This is referred to under endocarditis, as an occasional consequence of the detachment of clots and fibrinous substances from the internal membrane of the heart. The detached mass in this case passes from the heart into the aorta and thence through its divisions until it reaches a vessel too small to receive it, when it is at once arrested and determines inflammatory action in the plugged vessel. When arrested in some soft organ such as the lungs, liver or brain the resulting inflammation often gives rise to extensive suppuration and abscess. In other situations its effects may be confined to inflammation, the shutting off, of blood from particular parts, the impairment or loss of their function and nutrition, and finally atrophy and degeneration.
But the heart is not always the primary source of such clots. Virchow and others have demonstrated by post mortem examinations in cases of plugging and by a number of experiments on the lower animals, not only that such clots may have their place of nativity in some distant and diseased part of the body and proceed in the veins to the heart, and thence through the arteries to other distant parts of the body where they plug the vessels and induce a train of morbid changes; but that such embolism arteritis and abscesses can be produced at will by the introduction into the circulation of solid and insoluble (infecting) bodies. Fragments of decaying and suppurating tissue and the elements of tubercle and cancer may be thus equally carried onward in the current of the circulation, and reproduce themselves at those points where their course is arrested. This is a mode in which secondary deposits of these morbid matters are determined. Embolism and arteritis in the body and limbs occurring in this way necessarily have their point of departure in pre-existing disease of the lungs. The clots loosened from the capillaries or veins of the lungs are carried through the left side of the heart into the arteries of the body at large to be arrested in some of the smaller vessels. I have seen plugging of the digital arteries of the hind limbs, to occur in this way in a horse that had been suffering from inflamed lungs.
Microbes and toxins may pass harmlessly through healthy parts, including the pulmonic circulation, to establish colonies and embolism beyond where the tissues have become debilitated. Thus Gamgee records a case of embolism of the anterior mesenteric, right external iliac and right femoral arteries, supervening on an attack of strangles.
Symptoms of acute arteritis. These consist largely in impaired muscular power in the part, indications of acute local suffering, such as trembling and tenderness to the touch, if the obstructed vessel lies within reach it can be felt as an exquisitely tender cord-like mass, and the limb on the distal side of the embolism and dependent on the diseased vessel for its blood supply is anæmic and cold. In the distal portion of the embolic artery and its branches pulsation has ceased. If the lesion is extensive there may be more or less fever, but a limited arteritis in a small vessel may escape this complication. If the disease is of long standing there is atrophy of the tissues formerly supplied by the embolic vessels. The secondary derangement of nutrition and function are as varied as the organs affected and will be noted below in the special article on thrombosis and embolism.
Chronic arteritis. Atheroma. This is an indolent inflammation supposed to result mainly from strain and overwork, and manifested by thickening and clouding of the serosa, with cell proliferation, softening and fatty degeneration. The diseased substance becomes soft, pultaceous, slightly greasy, and under molecular degeneration it breaks up and is even in part washed on in the blood stream. Other degenerations may occur in the inflamed walls of the artery. The exudate may become organized, constituting fibrous thickening. It may become the seat of calcareous degeneration. It may yield to the blood pressure, becoming slowly attenuated (atrophy), and even dilated (aneurism by dilatation). As a cause of chronic internal arteritis in the horse should be named the presence in the vessels of the larva of the strongylus armatus. The posterior aorta and anterior mesenteric artery which are the most commonly infested by these parasites are frequently attenuated, dilated and calcified in this connection.
Treatment. Acute arteritis should be treated like any other local inflammation, by rest, soothing applications (fomentations, astringents, icebags), and alkaline salts. It has been proposed to manipulate the affected artery and contained thrombus, but this can only tend to block the smaller arteries farther on, and perhaps with even more injurious results. The liberal use of alkalies on the other hand, if effective in dissolving any portion of the clot, returns this to the blood stream in a condition that will not endanger further embolism. The agents usually employed are carbonates of ammonia, potash or soda, and iodide of potassium.