to show that neither of the two exclusive theories accounts for the
state of the blood and of the circulation in cyanosis. If the condition
of the cyanotic parts, due to acquired valvular heart disease or
various morbid states of the pulmonary tissue of an acute character be
compared with the same parts in cyanosis from malformation of the
heart, striking differences are discernible. If the simple condition of
cyanosis of the part due to localized pressure on the veins be
examined, the differences are even more perceptible. In the
malformation there is an admixture of blood; in the other condition
there is no opportunity for the intermingling of the currents. In the
latter the cyanotic area becomes swollen, and the intensity of the
color may become lessened through the oedematous condition; in the
former the skin of the cyanotic infant rarely if ever presents any
swelling; the veins of the part show little, {716} if any distension,
as is so frequent in the latter; cases of malformation in which
subsequent endocarditis with additional obstruction occurs may show
oedema and swelling similar to cases of acquired valvular disease. In
these cases of cyanosis the condition must be due to a want of aëration
of the blood, since it never appears until such alterations of the
pulmonary tissue and circulation are reached as to render it certain
that the blue coloration is due to a want of aëration of the blood.
Fulness of the veins and oedema may be present, but never general
cyanosis.
Another important consideration in the production of cyanosis does not
seem to have been fully appreciated. It is the fact that in all cases
of obstruction of the pulmonary artery the collateral circulation,
carried on by very varying channels, the bronchial arteries, the
oesophageals, the coronaries in some cases, the internal mammaries and
intercostal arteries in rare cases, or by the ductus arteriosus
Botalli, which alone must be always inadequate in marked narrowing of
the pulmonary trunk,--the collateral circulation must always remain
insufficient for carrying sufficient blood to the lungs for aëration.
Kussmaul was the first to call particular attention to this fact; and
it is to this condition of insufficient channels for the blood reaching
the lungs that certain cases of cyanosis must owe their causation.
Hence it must be that, in all the complex conditions found in cases of
cyanosis from defective development of the heart, a want of due
arterialization or aëration of the blood is at the foundation of the
state as seen in the cyanotic area. Whether it results in a given case
from excessive admixture of venous blood with the arterial when the
current reaches the capillaries, or from venous stasis due to central
obstruction, of which pulmonary-artery narrowing or closure is the
type, or whether from a failure of sufficient blood to reach the lung,
as where the collateral circulation remains imperfect, or as seen in
certain cases of defective development of the lungs, is most difficult
to ascertain. That sufficient consideration has not been given to the
third possible factor in the causation of cyanosis--viz. failure of the
blood to reach the lung, as distinguished from general venous
congestion alone--is evident. That intermingling of the blood from the
two sides of the heart must inevitably reduce the red color is
certain--that in very many cases the reduction in color does not cause
cyanosis can be readily understood from the consideration already
offered. The cases of free admixture in which cyanosis does occur may
coincide with a condition of very imperfect collateral circulation to
the lungs, and hence with a low aëration of blood of the left
ventricle, insufficient, therefore, to bring up the color of the blood
from the right side of the heart above the cyanotic point.
Whether non-aëration of the blood from failure to reach the lungs,
apart from general venous congestion, is a sufficient explanation of
the cyanosis in a large majority of cases or in the whole number, is
not apparent from the records of reported cases. Much more accurate
post-mortem accounts, made with a view to determine the question, than
at present exist will be required. In a number of well-reported cases
of defective pulmonary artery with a free admixture of blood the
pulmonary collateral circulation is found to be well developed, and no
cyanosis had appeared, or had been but trifling and inconstant. In
other cases of quite as marked pulmonary obstruction with but slight
commingling of the blood through abnormal apertures and but
slightly-developed collateral circulation, cyanosis has been found
intense and constant. In the two conditions the possibilities for
general venous congestion are about the same, though perhaps not equal,
while the striking difference, apart from the admixture of the
blood-current, consists in the conveniences for the aëration of the
blood.
The only variety of malformation of the heart in which intense and
constant cyanosis must inevitably be present is that very rare form of
{717} transposition of the great trunks, the aorta springing from the
right ventricle, the pulmonary artery from the left, with closure of
the septum ventriculorum; the pulmonary veins enter the left auricle
bearing red blood, and the venæ cavæ the right auricle with blue blood;
if the ventricular septum is closed, the aorta necessarily carries blue
blood to the systemic circulation, and the pulmonary artery is filled
with red, carrying it back to the lungs, whence the fluid has just
come. In such relation of the principal trunks, even if the ductus
arteriosus Botalli and the foramen ovale remain open, cyanosis is
necessarily present. The bulk of the blood in the aorta is blue: the
only points in which it comes in contact with red blood are, first, at
the foramen ovale: here the intermingling is not sufficient to bring it
above the cyanotic color; and, secondly, at the ductus arteriosus, and
here the tube is not favorably directed for a copious intermingling of
the two bloods, neither can it probably ever be sufficient in itself
for this purpose. Hence the aortic blood is almost wholly venous. If
these two foetal openings did not persist life could not continue
beyond a few hours, or even a few minutes, after birth. In such a case
the cyanosis does not depend on general venous congestion, and
specimens are reported of this sort in which the great vascular trunks
were without obstruction, life having been maintained for a few months;
adult existence is probably impossible. If, however, with such
transposition of the vessels to the improper ventricle, the septum
ventriculorum remains widely open, cyanosis may be absent or
inconstant, because, apparently, admixture of the blood and also
aëration are sufficiently free. But in cases of transposition of the
vessels, or even in the much more frequent specimens without
transposition, when the track to the lungs is defective either from
want of a collateral pulmonary circulation or directly from impervious
pulmonary artery, cyanosis becomes more intense and more constant or
comes in more frequent paroxysms, irrespective of the presence or
absence of evidences of general venous congestion.
It would seem to result from this grouping of facts, and looking at
them from a reverse bearing to Moreton Stillé's point of view, that
distal rather than proximal obstruction of the pulmonary artery, taken
as a type, was the cause of cyanosis. Admixture of arterial and venous
blood must reduce the redness of the arterial stream, just as certainly
as red paint mixed with black varnish will render the black less
intense: whether admixture alone ever produces a deep cyanotic hue of
the surfaces is probably more than doubtful; that admixture will
prevent constant cyanosis seems certain, when cases of complete
transposition of the vessels with open septum ventriculorum are
compared with those with closed septum, the other conditions remaining
the same. General venous congestion from pulmonary obstruction or other
causes outside the pulmonary tissue produces cyanosis, but of a sort
quite unlike the typical cyanotic condition of malformation of the
heart. It may therefore be doubted if the cyanosis seen in obstruction
of the pulmonary artery is due to general venous congestion; it may be
wholly produced by conditions on the other side of the
obstruction--viz. want of aëration of the blood, which must ever remain
the essential feature of cyanosis. This supposition allows of an easy
explanation of the difference between cases of apparently equal
obstruction of the artery, in some of which cyanosis is present and in
others absent; it also allows of the explanation of inconstant or
paroxysmal cyanosis where the obstruction, and consequently the venous
congestion, is uniform and permanent.
{718}
CARDIAC THROMBOSIS.
BY BEVERLEY ROBINSON, M.D.
DEFINITION.--In general, this name is given to every deposit of
coagulated blood or fibrin in one or more of the cardiac cavities. By
its derivation ([Greek: thrombôsis], coagulation, from [Greek:
thrombys], clot) it further implies the manner in which the coagulum is
formed and all the morbid alterations connected with it.
SYNONYMS.--Heart-clot. _Fr._ Thrombose cardiaque; _Ger._
Blutgerinnungen im herzen; _Lat._ Thrombosis cordis; _It._ Trombo;
_Sp._ Trumbo.
The definition offered is not wholly satisfactory, because, although it
is accurate as far as it goes, it is not complete. It does not
distinguish between concretions of different origin, etiology, mode of
formation, and age. No separation is made between fibrinous deposits
which increase from the beginning and layer by layer in the cavities of
the heart, and those transported there from a distance and forming a
nucleus for fresh deposits. To make the definition anything like
exhaustive would require many references to the general history of
THROMBOSIS AND EMBOLISM; we therefore direct our readers to that
article for what relates to the common facts of these morbid processes,
retaining for the present only those matters which relate specially to
the heart.
Heart-clots may be formed--1, during life, when the patient enjoys,
apparently, good health and strength; 2, toward the termination of
life, when the general forces are evidently depressed, or at the final
stage, when life ebbs low and the agony has appeared; 3, after death.
These clots have therefore been divided into cadaveric clots, those of
the agony, and ancient clots. To the clots of the agony exception is
properly taken, for the reason that agony is a term employed with a
somewhat badly-defined signification. At what period does it begin? Is
it not frequently of different length? Does it always exist? The
answers to these different questions render our objection proper, and
show that we had better employ the word terminal for coagula of the
second division.
Manifestly, the separate varieties of coagula have not an equal
importance. The clots which are post-mortem productions are only
interesting for their physical characters, which, fortunately, are well
marked, and enable us at once to distinguish them from the two other
varieties. The coagula in the first two divisions have an interest both
clinical and pathological.
The ancient clots are invariably accompanied with signs and symptoms
which should reveal their presence. As much might be affirmed for the
terminal clots in the majority of instances and when the patient is not
already in extremis. The pathological study of these varieties has
great value, and especially in so far as it will the better enable us
to distinguish the clots formed some time previous to death--be it of
shorter or longer duration--from those which are but the result of the
gradual stagnation of the blood-current in a weakened and wellnigh
powerless organ. Amongst the clots which are formed in the venous
system, some are transported, and pass {719} immediately through the
heart, to be arrested finally in some of the larger or smaller arterial
trunks, whilst others remain in situ in the heart, and are constantly
increased by successive additions or layers of new fibrin or cruor.
The nomenclature to be desired is one which would assign different
distinguishing names to each variety of coagulum, so that at once its
origin, mode of formation, and perhaps too its age, should be exactly
determined. The ancients employed the term polyp for deposits of every
description in the heart, but such use of the word was, generally
speaking, erroneous, since the true polyp is a very rare disease of the
cardiac cavities. Bartholetti and Pissini first made use of it, and
considered without doubt that the false polyps or fibrinous deposits in
the heart were of analogous nature with the true polypi which are found
so frequently in the uterus and nasal cavities. No doubt (as has been
inferred) the term polyp in regard to these formations came into
habitual use owing to lack of familiarity on the part of the older
writers with the varied aspects of clots, as well as their ignorance of
the distinct appearance offered by sections from them under lenses of
great power. This mistake, therefore, is to-day not to be wondered at,
if we duly consider how imperfect and unusual in olden times were
pathological researches. Heart-clot was, as will be seen in the
historical sketch which follows, the subject of numerous prolonged and
animated discussions. As a result of these latter, it was ultimately
believed that the great differences of appearance and formation which
exist between coagula depend in great measure upon their relative age,
and it is for this reason that the basis of distinction between their
varieties rests mainly upon the period of time previous to a death at
which they are formed. When we speak, however, of polypiform concretion
or deposit, we approximate nearer the truth and indicate in a measure
the local origin of a coagulum. Many others have employed the terms
post-mortem and ante-mortem as being the only suitable terms with which
to make a distinction between the coagula formed during active
existence and those which are revealed only with the scalpel in the
dead-house. In the consideration of this subject the symptoms shall be
fully described which indicate the presence of heart-clot found during
life, whilst in regard to clots formed in extremis or after death it is
desirable particularly to show the pathological characters which shall
definitely place them. For all that pertains to embolism of the heart
we shall refer the reader, except when it is essential to mention
certain details, to other articles in this work. Certain authors have
erroneously, it is believed, regarded this subject of heart-clot as one
of mere pathological interest, stating that the dead-house is the only
place to study its origin and many of its organic effects. This opinion
should be combated with vigor. Such a view is far too restricted, and
it is here believed that the clinical aspects of cardiac thrombosis are
worthy of attentive study, and that something better and further should
be attained than merely to watch the downward course of a patient thus
affected, and to bear in mind the pathological sequelæ of this disease.
HISTORICAL SKETCH.--The questions which have a present interest in
regard to heart-clot are very different from those which formerly
engaged medical attention. No longer are we uncertain as to the
formation of these coagula during life, nor doubtful as to the various
and important effects produced by their transport in different organs
through the arterial and venous vessels. Thanks especially to the
inaugural thesis of Legroux (1827), to those of Le Marchand and Ball
(1862), to that of Bucquoy (1863), but particularly to the experimental
researches of Virchow (1846-56) and to the observations of Senhouse
Kirkes[1] in regard to the formation and transport of emboli into the
cerebral vessels, these facts are all matters of ordinary information.
There is little doubt that Galen had noted the formation of {720}
intra-cardiac thrombi during life, and attributed to them interference
with circulation and respiration, and, at times, sudden death. With the
exception of Salius, mentioned by Morgagni as having remarked oedema
due to this cause, we reach the sixteenth century before again meeting
with any detailed mention of a similar pathological condition. Helidé
of Padua, according to some,[2] Benivenius, according to others,[3]
were the first authors to give full descriptions of cardiac polyps.
This, indeed, was the term affixed for a long period to fibrinous
concretions in the heart, beginning with Sebastian Pissini (Milan,
1654), who first employed it. The name took origin, without doubt, on
account of their resemblance to polyps of the nasal fossæ, and perhaps
to the animal thus named. It was particularly at this period that they
acquired their significance, and became the subject of animated
discussions between distinguished physicians of the last two centuries.
Some, exaggerating their importance, attributed to them the gravest and
most important symptoms, although a chronic affection of the heart or
lungs present at the time was frequently sufficient to explain them;
others, like Kerkring (1670) and Jos. Pasta[4] (1737), who contested
the possibility of the blood coagulating during life, and believed they
were invariably cadaveric formations, took from them even a
pathological interest. This latter extreme opposition to reality
originated very soon a mixed conviction, which was that held by Senac
and Morgagni. These distinguished observers recognized that
intra-cardiac thrombi formed both during life and after death, the
former being rarely encountered. The later, or anatomical school,
confirmed these views, but also added testimony to show that ancient
and terminal concretions were not phenomena of such unusual occurrence
as had been previously held. Testa (1810) and Kreyssig (1824) connected
fibrinous deposits with inflammation of the heart, and the last-named
writer described a disease which he named carditis polyposa. This view
and that of Laennec, which attributed globular vegetations to an
inflammatory cause, are in our day disproved. Amongst those authors who
rendered certain the formation of cardiac clots during life, we should
mention a few others whose names have a special importance in this
connection as having made a special study of diseases of the central
organ of circulation. These are Corvisart, Burns, Andral, and
Bouillaud. Since this period the field of research has become far less
limited, and investigations have been made in regard to similar
coagulations in the large vessels of the body.
[Footnote 1: _Med.-Chir. Trans._, 1844, pp. 281-325.]
[Footnote 2: _Dict. de Méd. pratique_, vol. viii. p. 558.]
[Footnote 3: _Ziemssen's Cyclopædia_, vol. vi. p. 292.]
[Footnote 4: Quoted by Grisolle, _Pathologie interne_, Paris, 1865, p.
464.]
In 1856 a new era was established in regard to these formations, and
especially with reference to their transport. Virchow at this period
showed conclusively, after long-continued and accurate clinical
observations and experimental researches, that a clot formed on the one
hand in one of the large veins might be carried to the pulmonary artery
and block up more or less completely the supply of blood to the lungs;
on the other, that a portion of a thrombus formed in the left
heart-cavity might become detached and plug completely one of the
arteries of some far-removed organ, as the spleen or kidney, and thus
give rise to those ultimate effects which we now understand under the
name of infarction. Thus was first established the new pathological
ideas which have become familiar with the words embolus and embolism.
True it is that Virchow was not the first writer who had described the
facts relating to the translation of portions of coagulum from one
region to another of the circulatory system, and its fixation in a
particular arterial branch. Already this subject had been clearly and
succinctly narrated by Van Swieten. A passage in which the causes and
mechanism of apoplexy are referred to gives lucid explanation of this
doctrine: "Whatever causes change the blood, lymph, and the matter
which supplies the spirits, so as they cannot pass freely through the
arteries of the brain, but are there impacted. Such are {721}
frequently--polypous concretions in the carotid and vertebral arteries,
whether first formed about the heart or within the cranium itself."[5]
These ideas of Van Swieten had not, however, produced any very
permanent impression, and were almost forgotten, when Legroux (1827)
promulgated his view in regard to the possibility of portions of
coagulum being carried from the heart into different portions of the
arterial system. He published, in fact, two most interesting cases of
gangrene of the hand and forearm in which the efficient cause of the
disease was found in an obliterating embolus of the brachial artery,
which was evidently similar in its nature to the thrombus found in the
heart of his patient. It is interesting to remark that Legroux's
inaugural thesis, in which these facts were brought to light, was only
the forerunner of some very complete articles on the subject of cardiac
and vascular concretions, in which he goes over much of the ground
which was covered in Germany by the work of Virchow. Legroux published
his ulterior researches in the _Gazette hébdomadaire_, Paris, 1856, pp.
716 _et seq._ In fact, under the head of correspondence we find in No.
20 of the journal of this year (pp. 349 and 350) an interesting letter
from Legroux to the editor, in which he claims for himself the priority
of publication (Van Swieten excepted) of the facts pertaining to
intra-cardiac thrombi and their effects due to transport of detached
fragments into a region more or less removed from their place of
development (p. 34). As this claim, according to my researches, appears
justified, a part at least of the credit awarded to Kirkes, Virchow,
and Schützenberger as discoverers and disseminators properly belongs to
Legroux.
[Footnote 5: G. Van Swieten, _Commentaries upon the Aphorisms of
Boerhaave_, Aph. mx., vol. iii. p. 159, ed. London, 1774.]
In spite, however, of these investigations, and those of Allibert
(1828), Louis (1837), Baron (1838), and Paget,[6] who showed how the
blood could coagulate in the heart and by transport block up the
pulmonary capillaries, we cannot dispute the glory to Virchow of having
in some sort created this study. Owing to his great sagacity, he was
able to seal his studies and experiments with the stamp of a
master-mind. The new words embolus and embolism introduced by him refer
to a process which was previously but badly understood, and which now
fix, as it were, a domain in modern pathology. The theory of Virchow
found many advocates--many who were opposed to it in the beginning. In
consequence of this it was the origin of numerous works undertaken in
this new direction. Amongst the most important are the communication of
Schützenberger,[7] the thesis of Lancereaux (1862), the great work of
Cohn (Berlin, 1862), the article of Weber in the treatise of Pitta and
Billroth--which contains recent theories about coagulation of the blood
and the transformation of clots--and the memoir of Polaillon upon
cardiac embolism (Paris, 1879).
[Footnote 6: _Med.-Chir. Trans._, 1844, pp. 162-188.]
[Footnote 7: _Gazette médicale de Strasbourg_, 1857.]
ETIOLOGY.--So soon as the blood is withdrawn from the influence of life
it no longer remains fluid, but rapidly coagulates. Thus it is we find
frequently after death coagula filling the cavities of the heart and
extending in long ribbon-like bands into the larger vessels, more
particularly in the veins. What occurs here is very similar to what we
notice in a bowl which receives the blood of a venesection. Here the
blood thickens rapidly, the clot forms, leaves the sides of the bowl,
assumes the appearance of jelly more or less colored owing to the
corpuscles enclosed in the meshes of fibrin, and is bathed in a
quantity of ambient serum. A similar change takes place in the heart:
the serum is imbibed by the tissues and the clot remains in its
cavities.