adopted on account of the well-known contents, which have a grumous or
purulent appearance[79] and are of fluid consistence. They are limited
by a cyst-wall, and are firmly attached to the walls of the heart
either by a single pedicle or by a series of roots intertwined with the
columnæ carneæ or musculi pectinati. Usually they occupy situations in
the cardiac cavities somewhat removed from the direct current of the
blood. The favorite situations for them are at the apex of the left
ventricle or in the appendix of the right auricle. According to
Rokitansky,[80] they almost invariably occupy the left ventricle, but
the observations of later writers show conclusively that this is an
error (Bristowe). Thus, Hayden states that in his belief the right
chambers are much more frequently the seat of thrombosis than the left
chambers. This difference is explained by the greater tendency to
stasis in the right heart, where also there is less considerable
muscular development. Of 44 fatal cases of valvular lesion, he cites 24
instances of cardiac thrombosis on the right side of the heart, and 12
instances on the left side. No case is reported by him in which the
coagulum existed solely on the left side.[81] They have been found
inserting upon the cardiac valves, and in this situation, owing to
their pedunculated formation and varying position, have sometimes
occasioned curious physical phenomena. A rare instance of this kind is
cited by Walshe,[82] where, the mitral valve being perforated, the
concretion caused at one time a systolic, at another a diastolic,
murmur. They vary in size from a pullet's egg to that of a hazelnut,
and exist singly in a cardiac cavity or are in considerable {739}
numbers. When we attempt to detach them from the cardiac parietes, we
frequently tear through some of their roots and leave small masses
behind. When quite numerous they are also small in size, and may then
be wholly lodged in the interspaces between the fleshy columns. Under
these circumstances they are usually continuous with one another and
extend their processes underneath the muscular bands, which are only
attached by their extremities to the walls of the heart.[83] These
clots have been found in the heart free of all attachments. In one such
instance reported by Pitres[84] they were very numerous and were
contained in all the cavities of the heart. This was a rare example.
Their surface is usually smooth and the cyst-wall occasionally very
thin. The cyst itself may be unilocular or divided into a number of
smaller intercommunicating cavities. Occasionally, through rupture of
the sac-wall, the contents have been emptied into the cardiac cavity
outside. The color of these globular or ovoid concretions is buff or
brick-red, and corresponds very nearly with the fluid contained in
their interior. The different coloration of the contents is due mainly
to the larger or smaller proportion of the coloring matter of the blood
mingled with them. Sometimes these ancient concretions are covered by
coagula of later formation, and it is only after close inspection that
we can determine their real character. The endocardium is usually
intact at their level, and rarely shows signs even of irritative
inflammation. Hence we conclude that in an analogous manner with
preceding forms of coagula they owe their existence to a constitutional
alteration of the blood. Whilst the rule is that on section these
globular concretions offer an interior consistence which is more or
less softened, yet occasionally we encounter one in which the structure
is homogeneous throughout, and presents very closely the appearance
everywhere revealed by its external aspect. The elements, under these
circumstances, of the sac-wall and the interior part of the concretion
are almost identical. Under the microscope these are recognized as
being mainly compound granular bodies, oil-globules, some imperfect
cells, or altered blood-corpuscles surrounded by a network of fibrin.
After a brief period, and in consequence of disintegration, the
contents of these cysts may resemble pus and show certain differences
in their constituents according to their appearance. "When white or
buff-colored they consist almost solely, if not solely, of molecular
matter, oil, and broken-down corpuscles, with which are frequently
mixed compound granular cells and colorless acicular crystals. When
presenting a brick-red or chocolate hue they exhibit, in addition to
the elements just mentioned, numerous blood-corpuscles more or less
altered, and consequently more or less indistinct, and occasionally
also ruby-colored, rhomboidal, hæmatoid crystals."[85]
[Footnote 79: _Pathol. Society's Trans._, vol. xiv. p. 65 _et seq._]
[Footnote 80: _Path. Anat._ (Syd. Soc. trans.), vol. iv. p. 217.]
[Footnote 81: _Dis. of the Heart and Aorta_, Part ii. p. 1020.]
[Footnote 82: _Dis. of the Heart_, 4th ed., p. 106 _(b)_.]
[Footnote 83: Bristowe, in _Reynolds's System of Medicine_, vol. v. p.
107.]
[Footnote 84: _Bull. Soc. anatomique_, Feb. 5, 1875.]
[Footnote 85: Bristowe, on "Softening Clots in the Heart," _Path.
Society's Trans._, vol. xiv.]
It is to the rupture of cysts of similar characters with those just
detailed that may be properly ascribed pyæmic symptoms occasioned by
the diffusion of their contents in the circulation.[86]
[Footnote 86: Ogle, _loc. cit._]
Coloration.--The color of ancient coagula varies from a dull white to
that of a grayish, slightly yellowish, or slate tint. These extremes of
color and all intermediary shades depend upon the age of the clot, the
manner of its formation, the larger or smaller number of red corpuscles
shut up in its fibrinous texture, and the chemical transformations it
has undergone. In order that the opinion at first formed of the age of
a clot by its coloration may be of some value, it is essential that
this ocular examination may be further aided by the results of
microscopic investigation. Occasionally, as already stated, the ancient
coagula are covered by clots of late formation, but these may
ordinarily be distinguished by even slight inspection.
{740} Consistence.--Usually the ancient coagula are firm, friable, and
without elasticity. They are then readily detached from their
insertions by traction, and always come away in small masses. On other
occasions they offer considerable cohesion, and preserve their form
when we attempt to tear through or break them. The degree of friability
is in proportion with the regressive alteration of their substance.
Sometimes the clinical history apparently indicates that a heart-clot
has remained soft during several years (Walshe). Coagula, however,
which have evidently been formed for a considerable period are
frequently fibrinous or cartilaginous in their structure, and a deposit
of calcareous material in their interior or upon their surface is
occasionally found.
Organization.--The question as to whether the coagula formed within the
cavities of the heart can become organized has been variously
determined. Amongst those authors who speak of the progressive
evolution of the clot, some admit the possibility, others absolutely
deny it. That these cardiac clots are frequently coherent, firm,
fibrous, or lamellated is no proof that they may become organized,
since the same features prevail in the old coagula contained in an
aneurismal sac. These latter, as we are aware, are readily separated
from the membranous walls which surround them, and never take on a
similar structure to theirs or give evidence of a new vascular
formation in their interior (Legroux). Cruveilhier, Monneret, and Robin
consider these coagula to be dead structures incapable of organization.
Those who believe in the possibility of the clot becoming organized
support their convictions by referring to certain rude resemblances
with organized tissues; yet even these (Hunter, Laennec, Bouillaud)
have never established their statements by any unquestioned examples.
Moreover, we should remember that formerly investigations were made in
a very imperfect manner. The instruments employed were insufficient and
poorly adapted to accurate research of this kind. Whenever the
organization of a clot was admitted, it was in connection with a
preceding inflammation of the endocardium, which itself occasioned a
plastic exudation. This exudation, becoming organized, was the means,
according to them, of introducing a new vascular formation into the
clot. According to the later researches of Virchow, Billroth, Feltz,
etc., there can be no doubt as to the vascularization at times of
ancient coagula contained in the vessels. In regard to cardiac coagula,
we should urge the facts of their greater size and different situation
as rendering their organization very improbable. Moreover, hitherto no
experimenter has injected any vascular twigs in a cardiac thrombus. To
sum up: whilst it appears possible that a cardiac clot may become
organized in view of what has been shown to take place in vessels,
still the facts thus far closely observed do not corroborate strongly
this opinion, and we cannot pronounce ourselves in an absolute manner
(Raynaud). Amongst the coagula least likely to become organized are the
very large ones and those connected with the heart-walls by a narrow
pedicle.
DIAGNOSIS.--From the preceding signs and symptoms can an accurate
diagnosis be established of the presence within the cardiac cavities of
fibrinous coagula? Evidently not if these formations be of small size
and be situated where they do not interfere notably with the
circulation. This is eminently true of those which are formed slowly in
the auricular appendix or at the apex of the ventricle. In order that
even a probable diagnosis of cardiac thrombosis should be made, it is
essential that the coagulum should occupy a certain space, that it
should be fixed near or at one of the orifices, or interfere in a
perceptible degree with the valvular play. Due consideration is always
to be had for etiological conditions when these can be wholly or in
part known. If, for example, there be present an acute or chronic
affection of the heart, and in a sudden manner, without apparent or
sufficient {741} cause, the symptoms and physical signs pointing to
greater disturbance of the function of this organ become developed, we
naturally suspect the formation of a cardiac coagulum. And this is
true, although the signs of this production are not dissimilar to those
indicating structural heart disease. Thus, the rapid development of
præcordial dyspnoea, of rapid, tumultuous action of the heart, of
feeble, depressible, irregular pulse, and of extreme pallor or lividity
of surface, combined with coldness of the extremities and extreme
anxiety, gasping for breath, and jactitation, indicate under like
circumstances the formation of heart-clot. This diagnosis is further
confirmed when upon listening to the respiration we find that the air
enters and goes out of the lungs freely, and that there is no evidence
in the lungs of any sudden obstruction or inflammatory condition. Of
course it is very important for the physician to be familiar with the
patient's previous condition and antecedents. If the accidents just
referred to become developed without these facts being known, it would
be far more difficult to make a diagnosis of cardiac clot than when the
accidents take place whilst the patient is being constantly watched and
when the physical state never varies without being observed and noted.
If there be a venous obstruction in one of the large veins of the
limbs, either at the time or prior to the formation of the cardiac
thrombus, the symptoms occasioned by it will give even more
significance to those which show heart trouble. The same information is
also afforded by sudden obstructions in different portions of the
arterial channels; and whenever these embolic transports take place
they show, with tolerable certainty, the pre-existence of an
intra-cardiac thrombus. As we can readily understand, it is far less
practicable to make the diagnosis of a clot which develops slowly, and
therefore gives rise to symptoms gradually, than of one which has
manifested itself more or less suddenly.
The physical signs of cardiac thrombosis as a complication of cardiac
disease are not necessarily very significative. This is true, first,
because there may not be an abnormal murmur owing to the weakness of
the cardiac contractions; second, because (even if it be present) the
murmur may be readily confounded with one already existing which is
occasioned by organic heart disease. Theoretically, the first sound of
the heart should be muffled by the presence of a coagulum of any
notable size which interferes with the play of the valves, but this
might be also occasioned by the presence of chronic cardiac valvulitis.
Still, if an abnormal murmur, harsh or soft in character, become
suddenly developed over the pulmonary or aortic orifice, where it was
known not to have previously existed, it is a physical sign which
points with much certainty to the presence of a heart-clot. Whenever
the signs and symptoms given above which show disturbance in the
heart's action occur in a similar sudden manner in the course of an
inflammatory or cachectic disease, such as pneumonia, cancer, or
phthisis, we should properly suspect the formation of an autochthonous
or embolic clot in the heart. These formations arise also, not
infrequently, as an instantaneous complication in the duration of acute
articular rheumatism, certain of the eruptive or acute
fevers[87]--_i.e._ measles, scarlatina, etc.--and the puerperal state,
as we have already pointed out in another portion of this article. In
pneumonia, as in the other affections just mentioned, if no fresh
inflammatory area either in the lungs or in another viscus can be
discovered which is sufficient to explain the occurrence of new
alarming symptoms of obstructed circulation, the difficulties of a
correct diagnosis are much less than if organic heart disease be
present. And this is particularly true because another solution of the
cause of the patient's condition is less available (Flint). Besides, if
it be sure that suddenly an endocardial murmur is developed where none
existed previously, this sign, {742} taken with the striking rational
and other symptoms referable to the heart, is one of great
corroborative value as regards diagnosis. Not only does cardiac
thrombosis occur under the circumstances mentioned already when we have
a certain right to expect it by reason of its relative frequency, but
occasionally it will become evident by its symptoms under conditions
where we have no right to look for its development. In these instances
it is only by a diagnosis of exclusion that we can discover the correct
interpretation of the phenomena presented. In the obstruction caused by
a heart-clot developed in the right cardiac cavities there is of course
stasis in the systemic venous circulation in consequence of the small
quantity of blood which can pass through the heart on its way to the
lungs. This condition, moreover, develops a peculiar dyspnoea which has
been very striking at times, and which has been particularly considered
by Richardson,[88] so as to differentiate it with an analogous but
dissimilar state which prevails when the obstruction exists in the
lungs or other portions of the respiratory tract. In the former case if
we listen carefully to the breathing the vesicular murmur is normal in
quality and pitch, although of exaggerated intensity, and the dyspnoea
is evidently due to the fact that the air lacks, so to speak, a
sufficient quantity of blood to arterialize it. Consequently, the
surface of the body is pale rather than cyanosed, and the heart-sounds
and pulse are feeble, tumultuous, or notably irregular. In the latter
case the lungs are congested or there is some other evident obstruction
of the larynx, trachea, or bronchial tubes which prevents the entrance
into the alveoli of a sufficient quantity of blood for the purposes of
hæmatosis. Hence a rapidly generalized cyanosis becomes developed, the
superficial veins are generally turgescent over the surface of the
body, and what with the irregular, feeble action of the heart, although
its normal sounds are distinctly defined, the violent convulsive
movements of the voluntary muscles, the abolition of the intelligence
of the patient toward the fatal termination, we have a sufficient
number of signs which point distinctly to an asphyxic state. Finally,
at the end of life in the former case it is the heart which first comes
to a stop, whereas in the latter the lungs are the organs which are
primarily arrested in their movements. These differential signs have
great practical importance. Unfortunately, there are instances in which
it is extremely difficult to assign in proper degree the symptoms
occasioned by the heart-clot on the one hand or obstructed respiration
on the other.
[Footnote 87: Keating, _Am. Journ. Med. Science_, Jan., 1885, p. 122,
v.--an able article, entitled "Heart-Clot as a Fatal Complication in
the Acute Fevers of Childhood."]
[Footnote 88: _Medical Times_, vol. i. p. 330, 1856.]
We have in another place pointed out this fact where at the same time
there was present a membranous deposit of diphtheritic membrane
blocking up the calibre of the larynx and a cardiac coagulum distending
the right cardiac cavities.[89] In like manner, there may be an
inflammatory complication in the lungs themselves--_i.e._
broncho-pneumonia--which by its sudden beginning and the rapid rise in
the number of the respirations and the pulse should awaken a suspicion
as to the cause of these symptoms. An error in regard to the modifying
influence of this accident would be possible were it not that
broncho-pneumonia, even of limited extent, reveals itself by
stethoscopic signs, and, moreover, would not explain all the phenomena
which arise. These are: the excessive pallor, the special kind of
anxiety, the weakness and inequality of the pulse, the muffled
heart-sounds, and the very rapid death. In exceptional instances, when
the lungs are merely affected with hyperæmia, the characteristic signs
of cardiac thrombosis are more readily recognized.
[Footnote 89: Robinson, _loc. cit._, p. 48.]
That form of uræmia known as the dyspnoeic or respiratory, which has
been well described by Fournier, is sometimes confounded with
heart-clot. Its commencement is often sudden. Soon labored respiratory
action is very marked, and approximates true orthopnoea, although there
is absence of {743} pulmonary lesion. From the cardiac disturbance it
can be differentiated by the pulse, the cardiac rhythm, bodily pallor,
and the usual evidences of kidney disease.
The distinguishing features between pulmonary embolism or thrombosis
and the deposit of fibrinous coagula in the heart are extremely
difficult to delineate. At times the cardiac coagula manifest their
existence quite as suddenly as does pulmonary embolism. Nothing,
moreover, prevents the formation[90] at a simultaneous moment of a
coagula in the veins as well as in the heart. The puerperal condition,
which is a predisposing cause of an excessive relative amount of
fibrin, is likewise an efficient cause of both these formations.
Besides, we should add, there is no reason why the fibrinous coagulum
of the heart in changing position should not throw off a plug which
will block up the pulmonary artery completely. To separate these
conditions or to make a diagnosis between them other than one based
upon probabilities is not possible.[91]
[Footnote 90: Ball, _Des Embolies pulmonaires_, Paris, 1862.]
[Footnote 91: Vernay, _Gaz. médicale de Lyon_, Nos. des 13 Mars et 22
Mars, 1868.]
We do not consider it essential in this place to go farther and make
known the signs by which we shall be able to distinguish cardiac
thrombosis from certain affections of the larynx, such as laryngitis
stridulosa, oedema glottidis, and membranous laryngitis, or indeed from
asthma or functional disturbance of the heart. It is easy, indeed, to
confound this affection with organic cardiac disease, but what we have
already said should enable us to make the distinction with facility. In
certain infectious diseases, and more particularly diphtheria, death by
cardiac paralysis has been described. In these instances there would
seem to be a real impairment, functional or organic, of the structure
of the pneumogastric nerves, which is accompanied by an irregular
action of the pharyngeal muscles, by vomiting,[92] extreme slowness of
the pulse,[93] a remittent form of syncopal attacks, and powerless
action of the heart. No such combined symptoms appear in our
description of cardiac thrombosis, and they are therefore sufficient,
in our opinion, to substantiate the opinion of a morbid entity which
can be satisfactorily explained by recognizing solely a lesion of
nerve.
[Footnote 92: Jenner, _Diphtheria, its Symptoms and Treatment_, London,
1861, p. 42 _et seq._]
[Footnote 93: Maingault, _Actes de la Société méd. des Hôpitaux_,
5^{ème} Fascicule, 1861, Obs. 40.]
In many examples of death by heart-clot the aspect of the patient is
very much that of one who dies in the period of a collapse from cholera
(Flint), the great difference between the two states consisting in the
fact that in the latter there is no notable degree of dyspnoea.
The diagnosis between coagulum of the right and left side of the heart
can be determined with some accuracy if strict attention be paid to the
effect of the presence of the clot on the normal cardiac murmurs. If,
for example, the clot is situated in the right ventricle, it is
probable that by interference with the tricuspid play it will render
the valvular sound occasioned by closure less distinct, and for this
reason the first sound of the heart will not be heard as well to the
right as to the left of the sternum. In a similar way, the diminution
of sound at the pulmonary orifice in the left second intercostal space
may be explained, for the extension of the concretion into the origin
of the pulmonary artery will almost certainly prevent the perfect
closure of its cusps (Richardson). In deposits of fibrin in the left
cavities of the heart we naturally distinguish less well the cardiac
sounds along the left border of the sternum than toward its right
margin. We also have congestion of the lungs, owing to the fact that a
smaller quantity of blood is able to pass through the partially-filled
left heart. To this is added a tumultuous, irregular action of the
heart and a feeble pulse. It is proper to add, however, that excepting
cases of chronic organic heart disease with dilatation or {744}
degeneration of the walls deposits of fibrin in the left heart are
relatively very infrequent.
In cases of acute endocarditis we have no means usually to distinguish
between the general symptoms of nervous shock and the physical signs
occasioned by cardiac thrombosis on the one hand, and rupture of a
valve or tendinous cord on the other. According to Walshe, this could
scarcely be otherwise, as clotting to a greater or less extent must
necessarily deposit around the spot where the tear takes place. In view
of a case reported by Hammer[94] of sudden cardiac failure in which the
symptoms prior to death pointed to possible intra-cardiac thrombosis,
and where at the autopsy thrombotic occlusion of one of the coronary
arteries was found, it is well to bear in mind the possibility of this
rare occurrence. The principal features of this case were the
suddenness of the collapse, pallor, slight dyspnoea, and extremely slow
pulse, ranging from 23 to 8 to the minute!
[Footnote 94: _Abstract of Med. Science_, 1878, p. 208; _Lond. Med.
Rec._, March 15th.]
PROGNOSIS.--The prognosis of fibrinous coagula in the cavities of the
heart is always extremely serious. The gravity of the situation is,
however, in some degree proportionate to their size, their situation,
and the rapidity of their formation. Thus, for example, those which are
spread out like a membrane over the interior surface of the heart, as
has been noted after endocarditis, are of less serious a nature than
those which are polypiform. As regards the polypiform concretions which
we encounter singly, which are small and formed slowly, they will be so
much more dangerous as the lobe held by the pedicle can become engaged
in the orifices of the heart or the vessels which take origin from
it.[95] Certain well-known observers, it is true, such as Bouillaud,
Barth, Roger, Racle, Meigs, and Armand, have stated their belief that
in rare instances these coagula may become dissolved and disappear.
Indeed, we ourselves have become convinced in more than one exceptional
case that the morbid phenomena manifested, both local and general, were
but the evident proofs of the beginning of fibrinous deposit in the
right ventricle of the heart, and yet we have seen these evidences
change their characters and finally disappear under proper treatment,
leaving the patients ultimately in as good health as they were previous
to their formation.[96]
[Footnote 95: Armand, _Des Concrétions fibrineuses polypiformes du
Coeur_, Paris, 1857, p. 49.]
[Footnote 96: We are more assured in regard to this possibility than we
were ten years ago (v. Thesis).]
Legroux does not believe cardiac concretions can be reabsorbed, and
with Cruveilhier he admits them to be dead formations. Nevertheless, he
admits that fibrinous cysts may entirely disappear by a process of
progressive liquefaction. Moreover, a case reported in his exhaustive
article which he observed makes him acknowledge that a fibrinous
coagulum may diminish, retract, atrophy, form adhesions with the
cardiac walls, and thus not interfere notably with the cardiac
functions.[97] The fact, however, that there may be no present
suffering does not shield such a patient surely from future accidents
of a serious nature brought on by his intra-cardiac condition. About
the diagnosis, however, of intra-cardiac thrombi, especially when a
perfect cure has been established, there always will remain an element
of justifiable doubt, and particularly in those conditions where an
underlying constitutional dyscrasia of grave import was present. This
latter state of itself often becomes either rapidly or eventually
mortal. Apart from the gravity of cardiac thrombosis in view of its
evidently pernicious influence upon the heart, it is likewise a very
serious affection on account of the possibility of its giving rise to
embolic transports into different viscera (brain, lungs, etc.), which
themselves may bring about a direct and speedy fatal termination. Even
when the embolic plugs do not occasion such considerable obstructions
{745} of important vascular channels as to cause rapid death, they may
fill up numerous capillaries of the economy with material of a kind
which shall be followed, sooner or later, by septic symptoms or those
of pyæmic poisoning.
[Footnote 97: _Gazette hébdomadaire_, 1856.]