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.