traumatism, and marasmus; in all of which groups an abnormal condition
of the endothelium is to be met with.
Thrombi from compression are frequently formed in veins, in the
vicinity of growing tumors. Their presence is most constant when the
vein is compressed between a resistant surface, especially bone, and
the tumor. A compression of the smaller blood-vessels within an organ,
as the liver or kidney, may take place in consequence of chronic
interstitial inflammation, or the growth of cancerous or other
malignant tumors in such organs. The production of this form of
thrombus is sought for in the treatment of certain aneurisms by direct
pressure, the resulting stagnation of blood being followed by a
coagulation within the aneurismal sac.
Thrombi from dilatation are met with both in dilated arteries and
veins. In aneurism and varix a slowing of the blood-current is
present, and the intima of the diseased region is frequently in such
an abnormal condition that a clotting of the blood readily takes
place. The shape and situation of the dilatation are of importance in
promoting the formation of the thrombus; the more pedunculate and the
more voluminous the sac the more certain is the thrombosis.
Traumatic thrombi result from a direct injury to the vessel. This may
be mechanical, as in the application of ligatures for the obliteration
of vessels, the tearing of the veins during childbirth, and the
infliction of wounds of every variety. The injury may likewise be
chemical, from the action of caustics; somewhat analogous to which,
are the effects of heat and cold. Allied to the traumatic thrombi are
those which arise {59} from acute inflammation of the intima extending
from wounds or inflammatory processes in the vicinity of
blood-vessels.
Marantic thrombi are those whose origin is attributable to that
enfeebled condition of the body known as marasmus. This represents a
weakening of the several functions, especially the circulation,
respiration, and locomotion. Such may take place in disease or old
age; and it is important to bear in mind those diseases in which
marasmus is likely to arise, as thrombosis often proves a complication
of such affections. Protracted fevers, as typhus and typhoid,
puerperal diseases, the disturbances following surgical operations,
chronic wasting diseases, as the tuberculous and scrofulous
affections, are all likely to be accompanied by thrombosis. Stagnation
of the blood, as well as alterations of the intima, is an important
local condition in this variety of thrombosis, which is usually
valvular or parietal at the outset, and may be both arterial and
venous. Such thrombi are likely to become continued and to serve as a
frequent source of embolism.
Thrombi are also divided into primitive, or autochthonous, and
secondary varieties. The primitive thrombus is one which owes its
local origin to conditions existing at the place of its formation and
attachment. The secondary variety demands for its existence a
primitive thrombus, whose place of development is remote in time and
seat, and from which a part has been transferred to serve as the
nucleus for the secondary formation.
The continued thrombus is often confounded with the secondary variety.
Continuance is rather a quality of all thrombi, and is essentially
growth, whether by lamellation or agglomeration. Such continued
thrombi are extended in the course of the circulation, usually by a
conical end, which is pointed toward the heart in the case of venous
thrombi, but away from this organ when the thrombi are arterial.
Parietal and obstructing thrombi form another subdivision. The former
arise from a limited part of the wall of the heart or blood-vessel,
and project into its cavity. They are always in contact with flowing
blood, and are white or mixed in color and primitive. They may attain
a considerable size, and may eventually become obstructing thrombi.
The latter are so called when they are of sufficient size to cause a
considerable or total obstruction to the current of blood. In the last
case the vascular canal is wholly filled by the thrombus. The shape of
the older parietal forms is usually globular or pedunculate, owing to
the growth in all directions except at the place of attachment; the
obstructing thrombi are elongated.
Thrombi are also characterized by consistency and relative absence of
moisture. A thrombus is brittle and dry as compared with a clot. In
distinguishing between the two, difficulty arises only in the case of
a thrombus which may have formed within a few hours before death.
Post-mortem clots are moist, elastic, readily withdrawn from
blood-vessels, and have a smooth and lustrous surface. Their color is
either red, gray, grayish-yellow, or yellow, and is very often mixed.
The lighter colors are due to causes which favor the precipitation of
red blood-corpuscles before actual clotting takes place, or which
occasion an increase of the white blood-corpuscles in fibrin. The
thrombus becomes adherent to the vessel wall within a few hours, after
its formation, in the case of the red thrombus, and at once, in the
case of the white variety. A clot is never adherent, although it may
seem so from its entanglement between the trabeculæ and {60} tendons
of the heart and the cavernous framework of venous sinuses. Such
apparent adhesions are easily recognized by the smooth, shining,
intact intima which is disclosed after the removal of a clot.
The thrombus not only tends to become enlarged by further depositions
of material from the blood, but it also tends to become diminished in
size from the contractile properties of its fibrinous constituent.
Moisture is forced from the thrombus in consequence of this shrinkage,
and its dryness is increased by subsequent absorption through the wall
to which it adheres.
The changes eventually taking place in the thrombus are known as
organization, calcification, and softening.
Organization is the transformation of the thrombus into a mass of
fibrous tissue. This is accomplished, according to the researches of
Baumgarten,[21] by an outgrowth of endothelium from the intima of the
vessel, the thrombus being absorbed as the growth of tissue advances.
In the case of a thrombus due to the ligation of a vessel, a
granulation-tissue also makes its way into the thrombus between the
ruptured coats, and the new-formed fibrous tissue which replaces the
thrombus becomes vascularized through this granulation-tissue. The
vascularization of thrombi surrounded by unbroken walls is most likely
to result from the extension into the thickened intima of new-formed
branches of the vasa vasorum. Cohnheim claims that the organization of
the thrombus may take place solely through the entrance of migratory
cells, without any active participation of elements of the vascular
wall. The canal is thus obstructed or obliterated by a fibrous tissue,
which is pigmented or not, as the pre-existing thrombus contained red
blood-corpuscles or not. These, when present, become transformed into
granular or crystalline hæmatoidin, which may remain as a permanent
constituent of the new-formed tissue.
[Footnote 21: _Die sogenannte Organisation der Thrombus_, Leipzig,
1877.]
Even when the thrombus is completely obstructing at the outset, it is
not necessary that a total obliteration of the vessel should result
from its organization. It not rarely happens, either before or after
the thrombus has yielded to the fibrous growth, in consequence of the
shrinkage of the fibrin of the thrombus or of the contraction of the
fibrous tissue replacing it, that gaps arise which become
communicating canals. Through these the blood flows, and the vessel
thus becomes only obstructed, not obliterated. The sieve-like tissue
thus formed is spoken of as the result of a cavernous or sinus-like
transformation of the thrombus. The length of time necessary for the
removal of the thrombus and its replacement by fibrous tissue varies
considerably. A vascularized granulation-tissue may be present within
a week, and in the course of a month the thrombus may have been wholly
removed, or a period of months may elapse and the thrombus and
granulation-tissue still be present side by side.
The calcification of a thrombus takes place when the latter becomes
impregnated with salts of calcium and magnesium. The condition may be
present in thrombi which are exposed to a rapidly-flowing arterial
stream, as well as in those which lie in venous pockets outside the
course of the direct current of blood. The well-known phlebolites are
examples of the latter variety. A calcified thrombus may be intimately
united to the vascular wall, the results of calcification and
organization being associated. Calcification and, in particular,
organization represent favorable {61} events in the history of
thrombosis, as through their occurrence the process comes to an end,
and disturbances, either local or remote, are prevented.
The softening of the thrombus, on the contrary, is always a source of
danger. This is partly due to the nature of the products of the
softening, whether bland or septic, and partly to the mechanical
disturbances produced by the transfer of portions of the softened
thrombus to remote parts of the body. All thrombi may become softened.
When the process of organization advances normally, the softened parts
are absorbed as rapidly as the formation of vascularized fibrous
tissue progresses. If this formation is checked or stopped, the
process of disintegration still continues. White corpuscles undergo
fatty degeneration; red corpuscles give up their coloring matter and
become converted, like the fibrin, into granules, and there results a
granular detritus. This is present as a viscid, semi-fluid material,
either red, gray, or yellow, according to the color of the thrombus.
This simple softening is to be regarded as essentially chemical in
character, and begins at the oldest portion of the thrombus and
advances toward the periphery. Its products are capable of absorption
without the production of serious disturbances, and are usually
prevented from direct entrance into the blood-vessel containing the
thrombus by the continuation of the latter from new coagulation or
deposition upon its surface. The thrombus is thus extended as the
softening progresses.
When the thrombus is comparatively free from red blood-corpuscles, the
softened product, in consequence of its yellowish color, opacity, and
viscidity, resembles pus. The so-called encysted abscesses projecting
into the cavity of the heart, from its wall, are parietal and globular
thrombi, in the interior of which softening has occurred. This form of
softening is called simple or bland, as it is free from any evidence
of local suppuration, inflammation, or general constitutional
disturbance attributable to an absorption of poisonous material.
Septic softening is accompanied by general evidences of a
blood-poisoning, and by the local phenomena of purulent inflammation.
A suppurative thrombo-phlebitis or arteritis, occurs; that is, an
acute inflammation of the wall of the vessel, corresponding in its
origin to the seat of the thrombus, and characterized by the formation
of pus. In the earliest stage the softened thrombus need not present
products differing in appearance from those occurring in simple
softening, but their effect is manifested by a rapidly-advancing
inflammation of the vascular wall and by the evidence of septicæmia.
Inoculation with such material produces a group of symptoms classified
under the head of blood-poisoning.
Cohnheim lays special stress upon the presence of micrococci in the
softened material, and it is generally agreed that the virulence of
septic softening is connected with, if not due to, the presence of
microbia. A septic softening may be induced by besmearing, with septic
material, the outside of a blood-vessel containing a thrombus, and
this form of softening is usually associated with those conditions
favoring this relation. Such are the gangrenous wounds following
surgical operations, the putrid inflammatory processes affecting the
uterine wall after childbirth, the offensive inflammations of the
middle ear, and the like. It is possible for a septic softening to
occur independently of such contiguous or continuous relations with
the surfaces of the body. It is considered, {62} however, that the
micrococci present in a softened thrombus must have obtained admission
from without through one of the surfaces of the body, mucous or
cutaneous, or through undiscovered abrasions of even intact surfaces
of peculiar structure, as the alveolar wall or the intestinal mucous
membrane. The thrombus is regarded as affording a favorable soil for
the growth and activity of the organism.
The mechanical effect of a thrombus varies according to the venous or
arterial seat of the same. Venous thrombi, as they are continued
toward the heart, tend to become completely obstructing thrombi. In
most parts of the body the venous anastomoses are so numerous that the
obstruction of a vein is readily compensated for through the
collateral venous circulation. When such a compensation is prevented
by an extension of the thrombus from branch to branch, and finally to
the trunk, an accumulation of blood in the peripheral veins must
result. The remote parts become swollen, from the distension of the
vessels with blood and the transudation of liquid, and eventually
solid material from the blood. Venous thrombosis thus leads to oedema,
and even hemorrhage. The more rapidly the obstructing thrombus
extends, the earlier and more extreme is the oedema likely to become,
while the slower the advance of the thrombus, the more favorable is
the opportunity for an enlargement of the collateral vessels through
which a sufficient flow of blood is permitted to check oedema and
preserve nutrition.
Local mechanical disturbances from arterial thrombi are scarcely
perceptible till obstruction is produced, and the results of arterial
obstruction will be mentioned in detail in connection with the
phenomena of embolism. Cardiac thrombi may occasion local disturbances
from interfering with the action of the valves of the heart. Those
thrombi which are attached to the valves, especially when calcified,
may produce inflammation and aneurism of the opposed wall of the
heart, by friction. The most frequent mechanical disturbance from the
non-obstructing parietal thrombi of the heart and arteries results
from the detachment of fragments and their transfer as emboli to
remote parts of the body.
An embolus is a foreign body in a blood-vessel, usually too large to
pass through the smallest capillaries, and the disturbances resulting
from its presence are included under the term embolism. Although most
emboli are detached portions of thrombi, any foreign body of suitable
size may become an embolus. Such are tissues, as the pulmonary elastic
fibres, fragments of diseased valves of the heart and of the intima of
arteries, or portions of tumors growing into vascular canals. Others
are globules of oil entering the torn veins when fat-tissue becomes
crushed, or air-bubbles admitted through veins either wounded by
instruments or opened after parturition by the dislodgment of their
obstructing thrombi. Still others are granules of pigment derived from
the coloring-matter of the blood, as in melanæmia, or introduced from
without, as india-ink and cinnabar. The echinococcus has been found as
an embolus, and it is highly probable that the cysticercus, the
trichina, and other animal parasites may be disseminated as emboli
over the body.
Vegetable parasites, like the bacterium and aspergillus, have also
been included in the list, although the disturbances resulting from
their presence are less due to mechanical obstruction than to
colonization and growth. The experimenter uses the most various
objects as emboli--bits {63} of wood, rubber, and glass, globules of
mercury, fragments of tissue, etc. Emboli are to be regarded as of
arterial or venous origin. The arterial emboli are carried toward the
capillaries, while venous emboli are carried toward the heart. The
effect of both is partly or wholly mechanical, and partly due to the
specific properties of the constituents.
The mechanical effect of an embolus is manifested by the obstruction
it offers to the circulation, and the degree of the obstruction
depends upon the size, shape, and density of the embolus and the
nature and size of the vessel obstructed. An embolus may be so large
as to be unable to pass through the valvular orifices of the heart. A
long and narrow embolus might pass through a vessel which would not
admit one which was short and thick. A jagged and dense embolus, by
repeated blows or prolonged and forcible contact, might cause a
weakening or rupture of the wall of a vessel, and thus produce an
aneurism. Certain vessels (the terminal arteries of Cohnheim) furnish
the sole supply of arterial blood to a district, and when they are
obstructed, the results, to be mentioned later, differ widely from
those taking place where free vascular anastomoses exist. When a trunk
bifurcates, the larger branch usually receives the embolus.
Venous emboli are those which approach the heart by the peripheral
veins of the body or the pulmonary veins, and the liver by the
radicles of the portal vein. Emboli from the veins of the body are
carried through the right side of the heart, if not so large as to be
stopped at the tricuspid or pulmonary opening. As they enter the
latter, they are carried along its course under the influence of
gravity and the direction and force of the current, which are
determined by the direction and relative size of the bifurcations of
the artery, the right primary branch being larger than the left.
Eventually, a point of the artery is reached whose diameter is less
than that of the embolus, and the latter is stopped. This point
usually corresponds with a place of bifurcation, and the embolus
frequently rides the wall separating the branches.
Emboli from the radicles of the portal vein owe their most frequent
origin to thrombi associated with inflammatory processes in the
intestine, especially of the cæcum and vermiform appendage, to
inflammatory processes in the spleen and obstruction to the flow of
blood through the splenic artery, or to inflammatory changes
proceeding from the kidneys. Such venous emboli are carried toward the
heart, but are stopped on the way by the intrahepatic branches of the
portal vein.
Arterial emboli are those which enter the left side of the heart from
the lungs, which arise in the left ventricle or auricle, which may
pass through an open foramen ovale from the right auricle, or which
arise from the arterial wall. They are carried along the course of the
arterial circulation, and are distributed over the different regions
and organs of the body. Usually following the more direct course of
the circulation, they are more likely to enter the abdominal aorta
than to be carried toward the brain or upper extremities. Embolism of
the carotids, especially of the left carotid, is more likely to ensue
than embolism of the subclavians. Embolism of the coronary arteries is
rare, while embolism of the splenic artery, the left renal and left
iliac arteries, is comparatively common, and in the order mentioned.
When an embolus is found, or embolism suspected, the source is always
{64} to be searched for in those regions from which the affected part
receives its blood. The source of arterial and portal emboli is
usually found with ease, while the pulmonary embolus may come from so
wide a region, the body-veins, that much time may be spent before its
place of origin is discovered. An appreciation of the laws of the
transfer of emboli renders such a discovery almost certain.
When the embolus reaches a point beyond which it cannot pass, the
resulting disturbance depends essentially, as shown by Cohnheim, upon
the presence or absence of arterial anastomoses beyond the place of
obstruction. He gives the name terminal arteries to those which have
no anastomosing arterial branches. These are met with in the spleen,
kidneys, lungs, brain, and retina. If the obstructed artery is not
terminal, the embolus may produce no further disturbance, the
collateral supply of blood through the anastomoses sufficing for the
nutrition and function of the part. If, however, the vessel is a
terminal artery, and the embolus is completely obstructing, the supply
of arterial blood must be wholly cut off from the region beyond the
seat of obstruction.
If the embolus does not completely obstruct at once, it soon becomes
sufficiently large for this result to ensue in consequence of a
secondary coagulation. The rider assumes legs extending into the
arterial branches beyond the place of obstruction, and a body which
extends backward in the course of the circulation to the nearest
branch. The result of the total obstruction of the vessel is to cut
off the admission of arterial blood, producing a local anæmia. The
contraction of the elastic tissues of the part propels toward the
capillaries a certain quantity of the blood in the vessels beyond the
point of obstruction, till this force becomes neutralized by the
blood-pressure in the vessels surrounding the obstructed region. The
anæmic part may subsequently become engorged with blood; it may die, a
region of anæmic necrosis resulting, or the dead portion may become
softened.
The engorgement of the obstructed territory has received the name of
hemorrhagic infarction. A solid, wedge-shaped mass of a reddish-brown
color is present, whose shape is due to the arborescent branching of
the terminal arteries. According to Cohnheim, the engorgement of the
region with blood takes place from venous regurgitation into the
obstructed part, till the intravenous pressure is overcome by the
resistance of the tissues in the region affected. The capillaries and
larger vessels thus become distended, and an escape of liquid and
solid constituents of the blood takes place. If the veins are provided
with valves, or the venous regurgitant current is opposed by gravity,
the hemorrhagic infarction is prevented or greatly impeded.
Litten,[22] on the contrary, who has furnished a recent contribution
to this subject, claims that the hemorrhagic results of embolism are
not accomplished through venous regurgitation, unless increased venous
tension is produced by coughing, vomiting, and like efforts. His
experiments lead him to maintain that arterial blood from surrounding
tissues is supplied to the obstructed region through the anastomosing
capillaries. The force is not sufficient to drive the blood through
the capillaries into the veins beyond, but an accumulation takes place
in the capillaries, which become dilated and distended. The escape of
blood-corpuscles and {65} serum then takes place, the more freely, as
Weigert[23] suggests, the larger and more numerous are the
pre-existing spaces in the organ. Hence the infarction becomes the
most characteristically developed in such organs as the lungs and
spleen. Causes which obstruct the venous flow, as well as those which
increase the arterial tension, promote the hemorrhagic infarction.
[Footnote 22: _Untersuchungen über den hemorrhagischen Infarct.,
etc._, Berlin, 1879.]
[Footnote 23: _Virchow's Archiv_, 1878, lxxii. 250.]