Part 51

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.

THROMBOSIS AND EMBOLISM.

Definition. Thrombosis—clotting in the vessel. Embolism, blocking of the vessel. Thrombus may form in any bloodvessel. Embolism occurs in arteries. Clot follows the blood current. Causes of clotting—fibrinogen, paraglobulin, fibrine ferment; foreign bodies; parasites; air; blood that has been exposed, transfusion; ærial germs; disease germs; chemical coagulants; high and low temperatures; breaches of endothelium; congestion or inflammation of the serosa; stasis of blood and extension of clot; ligature near a branch vessel: deoxidation and carbonization of blood, marasmus; neoplasms; traumas of the vascular coats. Infarction, causes of blocking; disintegration of clots, softening, liquefaction, ulceration, action of microbes; excess of white globules; air; fat; parasites. Pathogenesis; complete occlusion of vessel; infarction; sequestrum; collateral circulation; embolism of external iliac or femoral artery; effects on pulse; during rest; atrophy; lameness comes on with exertion; disappears under rest; circulation inadequate to sustain active function. Embolism of internal iliac artery; effect on pulse; on tail and pelvic organs. Embolism of axillary artery; effect on pulse, action, nutrition. Embolism of mesenteric artery; verminous; effects on innervation and circulation; spasms, congestions, paresis; involution. Treatment: expectant; alkalies; gentle exercise, time.

Definition. =Thrombosis= is the blocking of a blood vessel by a clot formed in its interior by the deposition of layer above layer on its inner coat.

=Embolism= is the blocking of a bloodvessel by a clot or other solid body formed at a distant point of the circulation floated on in the blood stream, and arrested when it reaches a vessel too small to transmit it.

A thrombus may be formed at any point of the circulatory apparatus (heart, arteries, veins) whenever the conditions are such as to determine coagulation of the blood. An embolism on the contrary is a disease of the arteries since in these the blood current, proceeding centrifugally from the greater to the lesser, inevitably carries the moving solid to a point too narrow to allow of its further progress. Thus clots originating in the systemic veins or right heart pass to the lungs and produce embolism of the pulmonary arteries whereas those formed in the pulmonary vein or left heart are arrested in some part of the systemic arteries. Clots formed in the portal vein however are arrested in the hepatic vessels into which that trunk breaks up.

Causes of Thrombus. The production of a thrombus may be due to the condition of the blood or of the vessels. The researches of Buchanan, Schmidt, Hammersten and others show that two albuminoid elements, fibrinogen and paraglobulin, present in the living blood, and a fibrine ferment mainly derived from the white corpuscles in process of change or destruction, determine powerfully the formation of fibrine and clot. Hewson, Brücke and Lister have shown that blood may be maintained fluid for many hours in an unimpaired vein, or turtle’s heart though it may have been removed from the body, the important condition being that the vein shall retain its vitality and suffer no derangement of its endothelium. Lister has even shown that blood may remain fluid for many hours in a sterilized glass tube which has been filled by passing the tube carefully into such a vein without disturbing its lining membrane, or imparting motion to the liquid. In such a case a thin film of coagulum only, forms on the interior of the glass tube. In healthy blood, without addition of any extraneous matter, and kept perfectly still, the plasma and globules retain their integrity, and the former its fluidity for a length of time. But if shed into a basin it coagulates at once.

a. Changes in the blood. Contact with foreign bodies generally determines this change and prompt coagulation. Transfixing the artery with a needle, even a silver one, the entrance of parasites (actinomycosis, strongyli, filaria), the presence of pus, and of certain infectious microbes and their products, the introduction of solid particles and even of air into the vessels, the transfusion of blood which has been exposed to receive ærial germs, or which contains microscopic clots, or the globules of which have become modified by contact with a basin or other vessel, even the transfusion of defibrinated blood may cause coagulation. The danger is always greater if the blood is drawn from a different genus and unfitted to live in the blood of the recipient. Disease germs are especially dangerous if adapted to colonize the serosa of the vessel and destroy its epithelium. A decrease of the density of the blood favors coagulation, a lowering of one thousandth rendering it syrupy, and various chemical agents induce or favor coagulation, thus acetic acid, valerianic acid, alcohol, the salts of iron, and above all the salts of lime act in this way. Very high and low temperatures throw down the fibrine as a grumous precipitate, but the clot remains soft.

b. Changes in the vessels. Any disturbance or alteration of the endothelium sets free the so-called fibrine ferment, and precipitates coagulation. Lister found that contact of ammonia with the interior of an otherwise living vein caused a thrombus. So in all endarteritis and phlebitis coagulation takes place on the serosa and quickly blocks the vessel. Even in the capillary vessels the same principle holds, and in inflammation minute coagula (thrombi) form in the capillary network throughout the whole inflamed area. This explains not only the capillary blood stasis but the thrombosis of inflamed arteries and veins. In these two latter the clot increases and extends in the direction of blood stasis:—in the artery toward the heart as far as the next colateral branch, and in the veins away from the heart as far as to the next colateral trunk. On the distal side of the arterial thrombus the blood flows off freely toward the capillaries, but on the proximal or cardiac side it is absolutely stagnant up to the next branch through which it can freely flow into the capillary plexus. Into this stagnant blood the fibrine ferment, produced by the altered white globules in the clot already formed, slowly extends until the whole has formed a firm coagulum. Beyond this the actively moving blood carries off and dilutes this ferment so rapidly that it can exert no appreciable effect on the fibrine-forming elements. The principle is an important one in surgery, as the clot formed entad of the ligature will be extensive in proportion to the distance from the first colateral trunk, and in inverse proportion to this clot will be the danger of secondary hæmorrhage. In veins the same rule holds, with this difference that as the blood is flowing toward the heart it empties the vessel on the cardiac side, and stagnates on the distal side up to the next colateral branch. Hence it is that a thrombus in a vein always extends away from the heart, while that of the artery extends toward it.

Another cause of coagulation is the deoxidation of the blood and the excess of carbon dioxide. This occurs in the stagnant blood in the vessels and above all in the capillaries. The normal trophic changes in the serosa, fail to take place in contact with blood in this state, and the resulting changes in the white and endothelial cells set free fibrine ferment and determine coagulation. Stasis of the blood from any cause (ligature, pressure, embolism), tends to this condition and the extension of the coagulum.

A thrombosis of marasmus has been observed in anæmic and debilitating diseases, and apart from the microbian invasions in a certain number of those affections, this may be looked on as due in part to the lessened density and other changes in the blood and to the debility of the serosa of the vessels.

The compression of the vascular walls or their penetration by neoplasms, tumors and ulcers, is another cause of coagulation and thrombus, also a varicose or aneurismal dilatation, with weakening of the vascular walls, or dilatation of the heart with structural changes in the endocardium as stated under that heading, or compression of the smaller vessels and capillaries by an exudate in process of organization, or a similar obliteration under the action of extreme cold. Injury to the serosa of the vessel by stretching, bruising, laceration or section determines a thrombus starting from the injured endothelium. In the smaller vessels the thrombus is usually deep red from the entangling of a large quantity of red globules, whilst in the larger arteries the greater part of the globules pass on and the coagulum is largely buff or straw colored.

Again in obstruction in the smaller arteries, the inactive capillary plexus and the tissue beyond are liable to become gorged with blood with excess of red globules, from the adjacent capillary network, constituting infarction, and ending in gangrene. In cases in which this is prevented by the action of intense cold the part may remain pale, as white infarction.