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_.
_Causes of Embolism._ As already stated embolism results from a detached
portion of a thrombus passing to a smaller vessel and obstructing it.
Such detachment is favored by molecular softening, liquefaction or
suppuration in the clot or beneath it, by the destructive action of
microbes, or by friction or manipulation of the obstructed vessel.
Excess of white globules (leukæmia) favors the formation of minute
coagula and embolism. Bubbles of air, globules of fat, or cholesterine
crystals block the fine pulmonary capillaries, and the debris from
atheromatous patches, ulcers, and tumors opening on the inner wall of
the artery form emboli in various parts. Finally parasites, especially
the larval strongyli in solipedes and filaria and spiroptera in dogs,
themselves obstruct the vessels and determine coagulation.
_Pathogenesis._ In the larger arteries (aorta, radical stump of the
mesenteric artery) clots (as from strangles) rarely produce dangerous
obstruction. In the smaller vessels stenosis is complete and anæmia and
gangrene are liable to occur unless the blood supply is partially
maintained by anastomotic vessels. When the embolism affects a number of
smaller arteries or capillaries in a vascular organ like the lungs, the
blood filters in from the adjacent capillaries, in which circulation is
still carried on, and this passes through the softened and ruptured
capillary walls so that the tissue is charged with globules and
constitutes a _black infarction_. In the lung this usually affects one
or several lobulettes, forming a pear shaped mass corresponding to the
distribution of the obstructed vessel. The cut surface is black, compact
and granular. The lymph thrown out around it forms an organized fibrous
sac, and the unclosed sequestrum undergoes a slow necrobiosis, blanching
and liquefaction into a pus-like fluid which is removed by absorption.
Such results are met with in the parenchymatous organs (lungs, liver,
spleen, kidneys, etc.) and less frequently in the limbs. The symptoms
will correspond to the particular organ invaded.
In the fore or hind limbs the result is usually less radical. The
vessels below the obstructed trunk are connected more or less freely by
anastomosing branches, so that the circulation in the tissues below,
though somewhat restricted, remains active enough to sustain a fair
measure of nutrition. Apart from the suffering, attendant on the
preliminary inflammation, the morbid phenomena are largely confined to
the absence of pulsation in the lower part of the limb and the inability
of the muscles to sustain active contraction.
=Chronic Embolism of the External Iliac or Femoral Artery.= In this
condition the pulsations in the digital arteries are imperceptible, if
it has been of long standing there may be obvious atrophy of the muscles
of the thigh, but when standing quietly or walking there is usually no
lameness. In continuous rapid walking and above all in the trot,
however, he soon begins to halt on the affected limb, and this rapidly
increases, the joints bending under his weight, the toe dragging and the
animal threatening to drop altogether. If stopped and allowed to rest
for ten or fifteen minutes he gradually recovers and may be led quietly
back to his stable without a sign of lameness. But if again trotted
fifty or one hundred paces the lameness develops anew and disappears in
the same way when left at rest. The circulation in the muscles is enough
for a moderate nutrition but altogether inadequate to sustain active
work.
=Chronic Embolism of the Internal Iliac Artery.= In this case the
control of the muscles of the limb may be perfect but there is some
indication of paresis of tail, bladder, rectum and anus. Impaction of
the rectum is liable to occur. By examination through the rectum the
pulsations are felt to be strong in the aorta and external iliac, but
imperceptible in the internal iliac blocked by the embolus.
=Chronic Embolism of the Axillary Artery.= Here there are the same
general symptoms, the absence of the radial and digital pulsations, the
wasting of the muscles of the forearm, and the intermittent lameness,
developed rapidly by exercise and recovering promptly under rest.
=Acute Embolism of the Mesenteric Arteries.= This will be fully treated
under the title of verminous colic in solipedes. The blocking of the
branches, usually of the anterior mesenteric artery, leads to
derangement of the innervation, congestions, spasms, involutions and
other disorders. The presence of the strongyli in the fæces, the general
symptoms of intestinal worms, and the recurrence of the indigestions and
spasms would serve to indicate the nature of the complaint.
_Treatment of Chronic Embolism._ As affecting the arteries of the limbs
the repair must be largely left to nature, and we must place the patient
in condition, favorable to such repair. Except in the early stages
absolute rest is not necessary. Gentle exercise stimulating to a freer
circulation solicits a slow enlargement of the anastomosing vessels
(arterial or capillary), and when this has reached a given stage, weak
pulsations may again be felt in the vessels beyond and the muscles will
once more stand moderate work without lameness. Alkalies and iodide of
potassium may be given to solicit solution of the clot, but this can
rarely be counted on to the extent of rendering the vessel once more
pervious. A small paddock in which the patient can move around quietly
is desirable, and in a few months a tolerable recovery may have taken
place.
Embolism in other organs must be treated on the same general expectant
method, and a considerable time is usually necessary to secure a fair
recovery.