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.