can arise during the formation and duration of heart-clot is the
production of an embolus of the pulmonary artery, completely filling up
its cavity, arresting respiration, and causing sudden death by
asphyxia. More frequently smaller portions of heart-clot become
detached and are transported farther along by the blood-current.
Finally, they become arrested in vessels of smaller calibre. In these
they may remain for a short time, and then become dissolved and
resorbed, leaving the calibre of the vessel free after their
disappearance, or else they form permanent plugs and give rise to
inflammation, coagulation, or hemorrhage. According to the
investigations of Lefeuvre,[55] which are both clinical and
experimental, it would appear that the obstruction of the arterial
distribution to any given part is almost immediately followed by
engorgement of tissue and hyperæmia of the capillaries of the affected
region. Feltz[56] has further shown that this condition is brought
about by reflux from the veins and paralysis of the capillaries. It is
not infrequent, moreover, to find hemorrhage into the tissues as a
direct sequela of this changed condition of circulation.
[Footnote 55: _Brit. and Foreign Med.-Chir. Review_, Oct., 1871.]
[Footnote 56: _Traité clinique et expérimentale des Embolies
capillaires_, Strasburg, 1870.]
These are, in fact, the conditions described under the name of
infarctions. Small detached particles may be detached from the cardiac
clot, if it be found in the left cavity, and transported after a
similar manner by the blood-current of the aorta and its divisions
until finally arrested in the different {734} viscera of the economy
(spleen, kidney, liver) or in the arteries of the extremities.[57] In
these different situations they give rise, when finally arrested, to
results which differ considerably according to the structure of the
organs or tissues where they become impacted. In certain instances,
carefully studied by Senhouse Kirkes, the disintegrated and puriform
contents of old fibrinous coagula are carried throughout the vascular
system and determine marked typhoid phenomena. The patient is attacked
with irregular paroxysms of fever of intermittent type, diarrhoea,
vomiting, and extreme feebleness. Kirkes explains these symptoms partly
by the obstructions occasioned by small emboli, partly by a sort of
poisoning due to the transformation of the fibrin. The accidents thus
occasioned at times very closely resemble those which characterize
pyæmia.[58] The fluid contained in the interior of the old clots, which
give rise to these accidents by reason of their transformation, is
thick, grumous, and puriform. It is surrounded by a sort of
pseudo-cyst, and is composed mainly of altered fibrin and red and white
blood-corpuscles.[59]
[Footnote 57: _Gazette hébdomadaire_, 1856. Legroux reports a case of
acute rheumatism accompanied by endocarditis and followed by
concretions in the left cavities of the heart, and obliterations of the
arteries of the limbs by emboli without gangrene ensuing.]
[Footnote 58: _Dict. Encycl. des Sci. méd._, _loc. cit._]
[Footnote 59: _Pathol. Soc. Transact._, vol. xiv. p. 65, cases by J. W.
Ogle.]
Pulmonary apoplexy and hæmoptysis often take place in connection with
the presence of a fibrinous clot of the right heart. This connection,
however, is not absolute, and many cases of right cardiac coagulum have
been observed in which neither of these complications became manifest.
When there has been pre-existent valvular disease, especially of the
mitral, these sequelæ more surely follow than when there has not been
this organic disease. The connection between the pulmonary apoplexy and
the valvular affection is even more intimate than that of the
hæmoptysis, and the same statement is also true of its relationship
with cardiac thrombosis.
Upon this subject Hayden[60] writes as follows: "Pulmonary apoplexy
seeming to require it as a necessary antecedent condition, while
hæmoptysis, though generally associated with thrombosis in the last
moments of life, frequently does occur independently of it."
[Footnote 60: _Dis. of the Heart_, vol. i. p. 529.]
The doctrine of Ludwig, as supported by Niemeyer,[61] that the
pulmonary apoplexy is directly due to stasis and deposit in the
capillaries of blood-corpuscles, does not appear possible if we accord
faith to the researches of Waters,[62] who has shown an
intercommunication between the bronchial vessels and pulmonary veins;
and reasoning upon this basis we have a strong confirmation of
Virchow's theory of hemorrhagic infarction (Hayden) consequent upon
embolism.
[Footnote 61: _A Textbook of Practical Medicine_, 1869, vol. i. p.
156.]
[Footnote 62: _The Human Lung_, 1860, p. 201.]
PATHOLOGY AND MORBID ANATOMY.--In the great majority of cases clots
presenting different physical characters are found in one or more of
the cavities of the heart after death. According to the supposed time
of their formation, they have been very properly divided into--1,
cadaveric (post-mortem); 2, terminal (in actu mortis); 3, ancient
(ante-mortem). It is important at the very beginning of the
considerations which I shall make in regard to these formations to
determine, if possible, the physical characters of cadaveric and
terminal clots, so as to be able afterward to more clearly separate
from them the true cardiac concretions or those formed at a time more
or less removed from the period of death. Without much question, it is
owing to the indifference or neglect of later writers in making these
necessary distinctions that uncertainty has arisen in the minds of many
with respect of the age of many heart-clots. The cadaveric and terminal
clots would indeed have but slight pathological interest attached to
them were it not that occasionally during {735} life, in a spontaneous
manner, cardiac thrombosis suddenly takes place, and is always the
cause of symptoms of considerable gravity and which often occasion a
fatal termination.
I. Cadaveric Clots.--These present the characters of blood drawn from
the arm by venesection and which is allowed to coagulate in a vase. 1.
Sometimes they are large, soft, homogeneous, friable masses, distending
one or more of the cardiac cavities, and having an appearance very
similar to badly-cooked currant-jelly, and there is no apparent
separation of the fibrin and the globules. Such an aspect is found
particularly when the relative quantity of fibrin is below the normal
or the blood is deficient in plasticity. In alkaline poisoning and many
adynamic forms of disease this is notably the case.[63] It may likewise
occur in forms of death in which there has been considerable
obstruction to the circulation. 2. In a somewhat similar manner, when
the blood is removed from the influences which give it life and
stagnates, or is arrested within the heart, coagulation takes place and
the blood separates into two layers. The upper is fibrinous, and
resembles the buffy coat covering a clot after bloodletting; the under
layer is mainly cruoric, and encloses within its meshes by far the
larger proportion of the red globules. This latter mass always forms
the lowest stratum by relation with the position of the body after
death. Between these two layers, and from the fact of their smaller
density, we find more of the leucocytes. This formation of blood-clot
in distinct strata has been accomplished experimentally by Pasta,[64]
who poured some blood of an animal into the heart of an ox and allowed
it to deposit. The cruoric mass is always soft, and may be readily
washed from the fibrin by a stream of water. Frequently these clots
distend the cardiac cavities to such an extent that when they are
opened at the autopsy a portion will fall upon the table and the rest
is readily detached from them. The microscope shows the same condition
of globules and fibrin in these coagula as it does in those of a
venesection. According to Walshe, these cadaveric coagula are usually
voluminous, jelly-like masses of fibrin of a pale straw-color,
semi-transparent, and containing a quantity of serum in their meshes.
Never do they show the slightest signs of stratification, and are not
really adherent to the cardiac walls. Occasionally their prolongations
may be intertwined amongst the papillary muscles and fleshy columns.
According to Legroux, it appears difficult to understand how these
large masses of fibrin become separated from the blood and deposited in
the heart during life, and yet he is indisposed to regard them as a
strictly post-mortem production. They are for him simply the result of
the agony.[65] After death the serum is expelled from the clot in
larger or smaller quantity, and for a longer or shorter time according
to its own spontaneous retractility.
[Footnote 63: Magendie, "Lectures on the Blood," _Lancet_, 1839.]
[Footnote 64: _Dict. de Médecine_, t. viii. p. 560, Paris, 1868.]
[Footnote 65: _Gaz. hébdomadaire_, 1856.]
There are instances in which death has taken place very suddenly
(chloroform, lightning, blow on epigastrium), and the blood remains
liquid in the cardiac cavities and shows no tendency to coagulation
(Walshe). The intimate cause of this condition is difficult to state,
although the sudden shock to the nervous system is doubtless the main
explanation. Under these circumstances the lining membrane of the heart
is apt to become stained with the coloring matter of the blood.[66] At
times the ventricles of the heart contain no blood at the autopsy. This
is more frequently true of the left than of the right ventricle. Even
then the auricles are more or less full.
[Footnote 66: Bristowe, in _Reynolds's System of Medicine_, vol. v. p.
106.]
II. Terminal Clots.--These clots are found at a period more or less
removed from the time of death. It may be that they have been present
in the heart many days before the fatal termination is reached, or
indeed that the act of dying, when the whole organism is overcome by
the {736} numerous conditions which inevitably tend in this direction,
is mainly instrumental in their rapid production. Of course their
outward aspect as well as their intimate structure will vary greatly
with their age and with the disease which has been present. Never are
they formed entirely of cruor; frequently they are composed of a large
quantity of fibrin. Their coloration varies with the quantity of red
globules, leucocytes, and serum shut up in the meshes of the latter. In
the cruoric as well as the fibrinous clots time also works changes of
coloration. In the latter by the mere expression of the fibrin the
coagula become less shiny and take on a darker tint, and when deeply
colored by red globules they may go through many changes of tint from a
violet or red-brick color to a pink. Usually, however, these latter
changes require a much longer time to be effected than is properly
understood in the term terminal clot. The latter is white, with a
yellow or green tint, or again of a fleshy color with spots of deeper
hue upon their surface. These are nothing more than small masses of
blood, although to superficial inspection they may appear vascular. In
structure they may be homogeneous throughout, but this is extremely
rare, for in the same clot we habitually find different parts which are
evidently of different ages; and not only is this true, but what leads
more to confusion in regard to the precise age of a given clot is the
fact that a relatively old one is at times juxtaposed or intimately
annexed to a purely cadaveric one. To make the distinction of what
portion of clot has been formed some time, and what part in the agony,
is occasionally almost impossible. Owing to the manner of death or to
certain rapid chemical changes which may take place, the interior of
terminal clots is at times softened and filled with a puriform material
which is probably only softened fibrin.[67] These clots are more or
less firm and elastic. They adhere quite intimately by a number of
roots to the walls of the heart, and are twined around the chordæ
tendineæ, the musculi pectinati, and are closely attached after this
manner in the depressions between the columnæ carneæ. Sometimes they
send off long projections into the large vessels which proceed from the
base of the heart. These latter may be cylindrical in form and fill up
the vascular calibre, or appear like so many flattened and ribbon-like
strips. The elasticity of these clots is made especially evident when
we attempt to tear them away from the cavities in which they are
adherent. They come away in small pieces, and show a rough, irregular
surface where they have been torn asunder. Upon pressure the terminal
clots allow a smaller or larger amount of serum to exude from their
surface, according to their age and the site of their formation. If the
quantity be large, the clot is much reduced in size and changes
considerably its physical characters. It must be evident, therefore,
that if a clot be contained in the ventricle, and be submitted for any
notable length of time to active and forcible contractions, it cannot
contain any large amount of serum. In the auricles near the appendages
the clot does not bear any very strong outward pressure--not much more,
in fact, than it would in an aneurismal sac. Clots in this situation
may have existed, therefore, for quite a time before all or even a
great part of their serum has exuded (Legroux). Rarely, terminal clots
are somewhat stratified. The form of these clots is variable; usually
flat, they may also be globular, ovoid, or thick. As they pass through
the cardiac orifices they are narrowed. At a level with the sigmoid
valves the full margin of the cusps is marked upon their surface, and
discoid masses, formed usually almost exclusively of fibrin, fill the
cavities of the cusps and are moulded to their surface. To this
condition great importance has been attached as indicating the
formation of the coagula prior to death. In fact, Poullet[68] has
endeavored to prove irrecusably by experiments upon animals {737} that
in all cases where these masses were present the clot had been formed
quite a length of time during life. Raynaud,[69] although admitting the
ante-mortem foundation of these imprints, nevertheless holds that they
are produced in the act of dying. The author,[70] owing to the fact
that he has found more than once the amount of fibrin and globules
about equally proportioned in the deposits of the sigmoid sacs,
considers that they may be formed after death. In this opinion he is
upheld by Walshe, who goes even farther, and states that he has seen
coagula filling the right ventricle, the infundibulum, pulmonary
artery, and its branches, and tightly grasped by all these parts in
which this mark was apparent,[71] and yet the coagulum was certainly
formed post-mortem. This opinion was further sustained by more than one
case observed during life, and in which the final symptoms were not at
all those usually assigned to cardiac thrombosis. According to
Richardson,[72] the fact that the clot is grooved upon its surface or
contains a canicula through its interior is a positive proof of the
passage of the blood-current, and hence of its formation during life.
[Footnote 67: _Cycl. of Anatomy and Physiology_, p. 114, 1848.]
[Footnote 68: _Thèse de Montpellier_, 1866. In this sign Poullet also
endeavored to show a distinguishing feature between clots formed within
the heart and those transported from one of the large veins of the
extremities and arrested in the heart. Before Poullet, these sigmoid
prolongations had been mentioned by Gallard and studied by Chauveau of
Lyons and Gardner of Glasgow.]
[Footnote 69: _Dict. de Méd. et de Chirurgie_, vol. viii. pp. 562 and
565.]
[Footnote 70: _De la Thrombose cardiaque dans la Diphthérie_, Paris,
1872.]
[Footnote 71: V. (after Walshe) such a specimen, No. 3636 Univ. College
Museum, London.]
[Footnote 72: _On Fibrinous Deposits of the Heart_, 1860.]
Whilst attaching a certain amount of importance to the signs just
mentioned as indicating the age of a clot, Parrot[73] is disposed to
consider the color, consistence, intimate attachments, and histological
structure of far greater importance in determining their formation some
time prior to death. Usually speaking, the terminal coagula have gone
through no retrogressive changes as regards their primary elements. The
red globules are perhaps paler than normal, but the fibrillæ of fibrin
are still distinct and the leucocytes show well-defined nuclei and do
not contain any fat-granules. These coagula, both terminal and
cadaveric, are found more frequently in the right than the left side of
the heart (Bouillaud). For the terminal especially the right auricle is
a frequent location (Parrot). This does not coincide with the following
table, taken from Legroux, and which shows the relative frequency of
the products in the different cardiac cavities: In 48 cases concretions
were found "in all the cavities at the same time, 8 times; the right
cavities and the left ventricle, 2; the left cavities and the right
ventricle, 2; the two ventricles, 4; the two right cavities, 5; the two
left cavities, 3; the right auricle, 1; the right ventricle, 7; the
left auricle 8; the left ventricle, 8 = 48 times."
[Footnote 73: _Dict. Encyc. des Sci. méd._, Paris, 1876.]
III. Ancient Clots.--There are several varieties which differ
considerably in their outward conformation and appearances, and are
formed at a period more or less removed from the time of death: _(a)_
Stratified coagula, which are attached intimately to the cardiac walls,
and present frequently an aspect which has been confounded with that of
true vascularization. So intimate is their adherence at times that to
effect their separation the scalpel has to be used, and in the attempt
the endocardium is detached. This membrane is frequently affected at
the level of their attachments with an alteration of atheromatous
nature. The volume of these coagula differs considerably. According to
the old writers, they may have become large enough to fill the cavities
entirely of one side of the heart and weigh at least a pound.[74] This
is evidently an exaggeration, and coagula of this size could only be
formed after death. Still, very large clots, formed some time previous
to death, have been carefully described by Bouillaud.[75] These should
be considered very {738} exceptional cases, and according to
Raynaud[76] such masses would inevitably cause immediate death.
Notwithstanding this affirmation, an ancient clot so voluminous as to
fill an entire cavity has occasionally been found. Such an instance is
the one referred to by Parrot,[77] where the left auricle was found
distended by a stratified coagulum, whilst the other cavities were
relatively empty. Generally, the volume of these clots varies from that
of a walnut to that of a grain of millet. Sometimes they are flattened
out, cover a large surface, and extend from one cavity into another. It
is extremely infrequent to encounter a coagulum which fills more than
the one-third or one-half of the cavity which contains it. These
coagula have different shapes. They are ovoid, globular, sessile,
pedunculated. Their number is usually in inverse proportion with their
volume. When they have a certain mass and occupy the cardiac cavities
they are often unique.
[Footnote 74: Cited by Bucquoy, _Des Concrétions sanguines_, Paris,
1863, p. 62.]
[Footnote 75: _Traité des Maladies du Coeur_.]
[Footnote 76: _Dict. de Médecine et de Chirurgie_, vol. viii. p. 565.]
[Footnote 77: _Dict. Encyc. des Sci. méd._, 1 Série, vol. xviii. p.
481.]
_(b)_ Warty excrescences, which deposit generally upon the surfaces or
margins of the aortic or mitral valves, although they may be found
adherent to other portions of the endocardium. These warty growths or
vegetations are only so in appearance, for their real structure is
mainly that of fibrin. Rarely do we find them in the right heart. They
have a jagged mulberry or cauliflower aspect, and adhere to an
otherwise healthy endocardial lining or to points where an alteration
or fissure already exists. Sometimes they are in the form of rounded
pedunculated masses, as described by Laennec,[78] and have given rise
to no obvious symptoms during life. These deposits of fibrin should be
distinguished from morbid growths and exuded lymph. The latter may be
augmented in size by layers of fibrin, and may require close inspection
to clearly differentiate them. The two preceding varieties of clot are
often apparently due to some constitutional dyscrasia.
[Footnote 78: "Végétations globuleuses," _Traité d'Auscultation
médiate_, t. ii. p. 630.]