A system of practical medicine. By American authors. Vol. 3

by Unknown

CARDIAC THROMBOSIS.

BY BEVERLEY ROBINSON, M.D.

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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 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 Kirkes¹ 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 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. Pasta⁴ (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.

¹ Med.-Chir. Trans., 1844, pp. 281–325.

² Dict. de Méd. pratique, vol. viii. p. 558.

³ Ziemssen's Cyclopædia, vol. vi. p. 292.

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 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.

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).

⁶ Med.-Chir. Trans., 1844, pp. 162–188.

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.

Coagulation of the blood is a very complex problem. Many theories seek to explain it. On the one hand, it has been said the fibrin pre-exists in the blood, and by the fact of the slowing of the circulation, the reduction of the temperature, etc. the fibrin separates from the blood and coagulates. Again, it is admitted that the fibrin does not exist formed in the blood, but that a fibrinogenous material is present which is acted upon by the hæmoglobin or globulin contained in the red globules, the leucocytes, and the corpuscles of connective tissue, and sometimes is, sometimes is not, caused to precipitate as fibrin (Virchow). The exact conditions which occasion the activity of the globulin are unknown. The reaction which takes place has been said to resemble that which takes place between amygdalin and emulsin when prussic acid is formed, or between myrosin and myronic acid when the volatile oil of mustard is produced. Further, it is stated, in accordance with accurate chemical investigations, that the plasma of the blood contains a substance called plasmin, which separates itself into fibrin which coagulates and into fibrin which remains dissolved in the blood (metalbumen, Robin). These fibrins are evidently of two kinds. The plasmin divides itself under the influence of slowing of the circulation, the action of acids, of foreign bodies, of oxygen in excess, etc.; it remains intact in a fluid condition when the vascular walls and globules are healthy, the blood circulating with normal rapidity, and in presence of alkaline principles.⁸ According to Foster,⁹ "Coagulation is the result of the interaction of two bodies, paraglobulin and fibrinogen, brought about by the agency of a third body, fibrin ferment." Schmidt concludes that when blood is shed a number of white and intermediate corpuscles fall to pieces, by which act a quantity of fibrin ferment and of paraglobulin is discharged into the plasma. These meeting there with the already present fibrogen give rise to fibrin, and coagulation results.

⁸ Dict. de Méd. et de Chirurgie pratique, vol. viii. p. 569.

⁹ A Textbook of Physiology, p. 22, New York, 1880.

As regards the formation of clots within the body, it is supposed that injured or diseased spots or foreign bodies first attract, and then, as it were, by irritation cause the death of, a certain number of corpuscles.¹⁰ The views of Schmidt of the fibrino-plastic function of paraglobulin are not accepted by all investigators; and some authors believe that the fibrinogen as well as the fibrin ferment arises from the white corpuscles.¹¹

¹⁰ Pflüger's Archiv, vi. (1872), p. 413; xi. (1875), pp. 291 and 515; xiii. (1876), pp. 93 and 146; quoted by Foster.

¹¹ Frédericq, L., Recherches sur la Coagulation du Sang, Bruxelles, 1877, quoted by Foster.

According to Bristowe,¹² the frequency of sanguineous concretions does not depend upon sex, but is in a certain relation with age. He has remarked, for example, that they are proportionately more often met with at the extremes of life than toward middle age. This might be explained satisfactorily, perhaps, on the supposition that at these periods the circulation is at times very feeble, owing either to congenital feebleness on the one hand or chronic organic affections on the other. At all events, when we seek for the causes which have most influence in determining the formation of cardiac concretions previous to death, we find—I. the mechanical, or those which act specially in slowing the current of blood through the heart. These causes may exist within the heart or may be removed from it. II. The vital or pathological. These causes are of somewhat difficult determination at times, and pertain usually to affections in which there is notable blood-change, in which the quantity of the fibrin has been augmented absolutely or relatively, or to those of infectious type—viz. diphtheria; or to those constitutional in nature—phthisis, cancer, etc. III. The inflammation of the endocardium or endocarditis. This is admitted by Andral, in a note upon the etiology of cardiac concretions in the work of Laennec, as having special importance. Bouillaud also attributed their formation in certain cases to the chemical action of pus which was present in the economy.

¹² Pathol. Society's Trans., vol. xiv. p. 71, quoted by Bartholow.

I. Amongst the mechanical causes we should mention all organic lesions of the heart, all obstacles in the pulmonary circulation, and possibly, by analogy, certain badly-defined lesions of the pneumogastric nerves. All the stenoses and dilatations of orifices, all irregularities of the valves or heart-walls, all depressions or roughened parts of the walls,¹³ may determine the beginning of a concretion. In the same way, a small mass of fibrin deposited on a calcareous valve after transport from one of the veins of the limbs may originate a voluminous heart-clot. Dilatation of the heart, pericarditis, every cardiac change which weakens the contractile power, is a predisposing cause of cardiac thrombosis. Every organic lesion of the heart tending toward that final stage of asystolism so often encountered, and which weakens so greatly cardiac contractility; pouching of different portions of the cardiac wall, or aneurism; pressure upon the right heart by a mediastinal tumor or a sacculated aneurism of the arch of the aorta,¹⁴—all these have great power in producing intra-cardiac thrombi. The mechanism of these different lesions was familiar to Kreyssig, Laennec, and Hope. At the same time it must be admitted that these changes in the heart are not of themselves always sufficient to give rise to fibrinous deposits. We encounter stenoses and regurgitations at orifices very frequently, and concretions, on the other hand, are relatively rare. Moreover, we find heart-clot at times when there is no cardiac alteration. We believe, therefore, that the heart lesion is an aiding factor—that in the last moments of life, when the force of the heart's contraction is weakened and the conditions of the blood favor coagulation, they will act with special power.

¹³ Pathol. Society's Trans., vol. xiv. p. 71, cases by J. W. Ogle.

¹⁴ Walshe, Dis. of the Heart, Lond., 1873.

Among the mechanical causes which are removed or distant should be mentioned all those which interfere with the pulmonary circulation. Such are the effects left behind by pneumonia, pleuro-pneumonia, or the compression of the blood-vessels by old congestion of the lungs. In these cases, when the vis a tergo is impaired somewhat, and an obstacle is placed in the pulmonary capillary circulation, even if cardiac thrombosis does not directly result at first, we may have thrombi form in the pulmonary veins. In the same way, the nervous affections which are accompanied with slowing of the circulation tend to produce coagulation of the blood. All lesions, as we have said, of the pneumogastrics act in the same direction. In proof of this we should cite the experiments of Meyer of Bonn, of Longet, and of Blondet, who produced fibrinous concretions in the hearts of animals by tying or cutting the pneumogastric nerves. At the same time, the heart-beats became more rapid, wavering, unequal, and less energetic than in ordinary physiological conditions. After all, however, all these mechanical causes are but predisposing causes, for they do not always produce cardiac concretions. Frequently, as we have said already, the obstruction to the circulation may be present, and yet at the autopsy no fibrinous deposit be found in the heart. In order that the mechanical causes act efficiently to produce coagula, it is essential that they be aided by the conditions of the blood which favor it.

All concretions do not form with the same rapidity nor are they of the same size. At times their production is sudden, and but a few hours elapse before the fatal termination is reached. Again, it is affirmed that weeks, and even months, may pass before the concretion has reached a volume sufficient to cause entire stoppage of the heart's contractions. In the former category are found, of course, the softer, least consistent coagula—usually, however, very voluminous; in the latter are the smaller, more elastic, and resistant concretions, at times even presenting a stratified structure¹⁵ and surrounded habitually by a clot formed during the latter moments of life, and having a large proportion of cruor in its composition. The heart affected with fatty degeneration should, if we consider its weakened power and deficient contractility, be a predisposing cause of stagnation first, and finally of the formation of intra-cardiac thrombi. As a matter of observation in the dead-house, however, such hearts are not frequently accompanied with fibrinous deposits in their cavities.

¹⁵ According to Legroux, roughening of the walls or valves gives rise to stratified coagula of moderate size, or else to those small clots which deposit on the surface or margin of the valves (Dict. Encycl. des Sci. méd., article "Concrétions sanguines," Paris, 1876).

All diseases which by their nature and duration produce great exhaustion of the vital powers tend strongly to produce fibrinous coagula in the heart. This is eminently true of those which at the same time do not occasion a diminished plasticity of the blood. It is often assumed that mere stasis in the blood-current through the heart is essential to the formation of clots in its cavities, and to lend support to this belief reference is made to the phenomena which take place in bleeding. It is not true, however, that stasis is necessary to coagulation, and the proof is afforded when we take a bundle of twigs and by beating the blood forcibly produce the separation of the fibrin. Besides a slowness of the circulation, there must be, once again, an obstacle in the heart itself, and even then polypoid concretions are not always formed.¹⁶

¹⁶ Gaz. hébdomadaire, Paris, 1856.

II. The Vital or Pathological Causes.—In this class of conditions leading to cardiac thrombosis are included all diseases in which certain special changes have taken place in the blood itself. Among these we should mention, first, certain sthenic inflammatory affections in which the proportion of the plasmin (fibrin and metalbumen) is notably elevated, and in which, on this account, there is a strong tendency to the separation of fibrin from the blood and to the formation of cardiac concretions. In fibrinous pneumonia and acute rheumatism this is particularly true, and amongst the numerous accidents we have to dread in the course of these diseases none strike us with more dread than the possible production of intra-cardiac thrombi. In fibrinous pneumonia this complication is so frequent that Bouillaud has enunciated the following pathological law: "Fibrinous concretions exist constantly in patients who succumb to a frank, acute pleuro-pneumonia, well characterized, which has reached the second stage."¹⁷ According to Raynaud, this is without question a great exaggeration, and results from the confusion this learned author evidently made between terminal clots and those formed some time previous to death. Nevertheless, there is here a proof of the great frequency of coagula occasioned by this disease, and of the strong tendency to their formation which the condition of the blood must afford. What we have said of fibrinous pneumonia and acute articular rheumatism is not true, singular to say, of lobular or broncho-pneumonia. The lesions of this form of pneumonia are those of a catarrhal inflammation of the lung, and the blood does not offer during its course the remarkable tendency to coagulation that is shown in fibrinous pneumonia. Usually, the heart-cavities and the vessels are filled after death with a liquid of a black or violet-brown color, very often sticky.¹⁸ The fibrin in the heart-cavities in pneumonia is fibrillar, and does not present those changes which indicate that it has been deposited for a long while. Moreover, these coagula do not present physical characters which show any considerable degree of age. They are usually terminal coagula, or at least formed within a few days of the fatal termination. Do globular vegetations occur in pneumonia? At times they do, but they are at least very rare as compared with the fibrinous conditions just referred to.

¹⁷ Gazette méd., 1843, vol. xi. p. 270, quoted by Armand, Thèse de Paris, 1857, p. 41.

¹⁸ Damaschino, Thèse de Paris.

There are other general conditions in which there is a marked tendency to the formation of cardiac coagula. In the puerperal state, according to Simpson, it is occasioned by the resorption of many new elements which vitiate its composition and thus occasion this result. In the poisoning following upon glanders or pyohæmia intra-cardiac thrombi are often found. Lancereaux has found in this latter disease fibrinous deposits in the right ventricle and pulmonary artery around small masses composed of pus-cells. In the different cachectic states, such as those caused by chronic Bright's disease,¹⁹ advanced phthisis, and cancer, although we have a diminution in the proportion of red globules, there is present at the same time a relative increase of fibrin; and the consequence is that concretions are often formed in the heart. In fact, it is in these cachexiæ that we often encounter those fibrinous cysts which will be described under the title of [Morbid Anatomy].

¹⁹ Here the retention of the excreta is an important factor in the formation of cardiac thrombosis (Bristowe).

Many well-known authors have declared that diphtheria was very powerful in producing fibrinous concretions in the right heart some time previous to death. Among those who have written specially on this subject we would mention Winkler,²⁰ Richardson,²¹ Meigs²² and Robinson.²³ According to the latter writer, elastic fibrinous clots twisted in the valves and adherent to the cardiac walls are developed frequently in children at a period quite removed from that of the agony, and at a time when they are not as yet in a condition of extreme weakness. Except in exceptional instances this influence of diphtheria to produce cardiac coagula is doubted by Parrot.²⁴ He admits its power, particularly when it is complicated with membranous croup, and in these examples he believes the precocious formation of coagula is determined probably by the asphyxic condition. Whilst denying the influence of diphtheria, Parrot freely acknowledges that measles, especially when complicated with broncho-pneumonia, tends to produce cardiac concretions. The same tendency is recognized by Harley in the early stage of scarlet fever where there is high pyrexia.²⁵

²⁰ Die Bluthlumpen dann der Häutiger Bräune, Wien, 1852.

²¹ Med. Times, vol. i. p. 23, 1860.

²² Am. Journ. Med. Sci., April, 1864.

²³ De la Thrombose cardiaque dans la Diphthérie, Paris, 1872.

²⁴ Dict. Encycl. des Sci. méd., vol. xviii. p. 484.

²⁵ Medico-Chirurg. Trans., vol. lv.

Notwithstanding the diminished proportion of fibrin in typhoid fever, and the impossibility of explaining, in many cases, any increase of the plasticity by local inflammatory disorders, cardiac concretions have been observed by Huss, Virchow, and Hardy.²⁶ Bucquoy also relates, after Huxham, an epidemic which reigned at Plymouth in 1742 amongst sailors who came from a long cruise, characterized by dyspnoea, cardiac palpitations, and intermittences of the pulse. Many of those attacked died, and at the autopsies made polypoid concretions of considerable elasticity and adherent to the walls of the heart were found. Another similar occurrence took place amongst the soldiers of the garrison of Rocroy in 1746. Quite a number succumbed after having shown symptoms similar to those of the sailors of Huxham. Cadaveric sections discovered in the left ventricle several hard, consistent cardiac thrombi.

²⁶ Quoted by Bucquoy, Des Concrétions sanguines, Paris, 1863, p. 36.

III. Endocarditis.—Whatever may be the opinion of different authors in regard to the frequency of endocarditis when intra-cardiac thrombi are present, it is certain that if it does exist the explanation of the presence of these deposits is clear and ample. In endocarditis we have both a local and mechanical cause and also a vital condition of fibrinous deposits in the heart. As a mechanical cause we know that often it is the cause of the stenoses of orifice which are present, and that further, by its effect in producing roughening or fissuring of surface, it offers a strongly predisposing cause of the deposit of fibrin. Ulcerative endocarditis acts still more efficiently in this direction, owing to the fact that it produces its effects as much on the surface of the valve, aortic and mitral, near the adherent portion and in the neighborhood of the cardiac orifice, as between its layers. The result is, that the surface is rough, unequal, presenting often cauliflower excrescences, and showing sometimes, in the midst of a mass of fibrin that has become deposited by degrees, portions of a softened, partially-detached valve which was the nucleus of the outer layers of fibrin. Further, endocarditis of both forms acts as a vital and efficient cause of cardiac thrombosis, in that it belongs to the class of inflammatory diseases which occasions an absolute increase in the proportion of fibrin of the blood (from ²⁵/1000, concrete fibrin 3, and metalbumen 22, to ⁵⁶/1000, concrete fibrin 17, metalbumen 36); and also, more especially in ulcerous endocarditis, by the transport of infectious materials into the blood, which still further tend to cause coagulation.²⁷

²⁷ At times there is complete deprivation of epithelium over a limited area, and in rare cases slight ulcerations of membrane. These two conditions are efficient factors of the exudation of plastic lymph.

SYMPTOMATOLOGY.—According to Laennec,²⁸ it is equally erroneous to attribute to cardiac thrombosis many symptoms which properly belong to an organic lesion of the heart (notably hypertrophy) as it is to believe that intra-cardiac thrombi never begin to form until the terminal period of life. According to him, Haller, Vinckler, Staneari, and Bonaroli²⁹ have observed obliterations of the internal jugular vein and carotid artery by very firm concrete fibrin, and he himself has seen a similar production in the inferior vena cava for the space of four fingers' breadth. Although these concretions were evidently formed during life, they occasioned no symptoms indicative of their presence, nor were there any obstructions in the course of the circulation which could explain their origin. Reasoning from these facts and from the phenomena which occur in aneurismal tumors, it seems highly probable that the blood should coagulate in the heart also during life. Later writers frankly admitted that coagulations in the veins caused partial dropsies, a usual instance of which is the white swelled leg, or phlegmasia alba dolens, from obliteration of the femoral vein.³⁰ This is not invariable, for I have seen, in patients who have succumbed to diphtheria, both venæ cavæ obstructed by coagula, without having observed during life either local or general oedema.³¹

²⁸ A Treatise on Diseases of the Chest, p. 183, Philada., 1823.

²⁹ Quoted by Morgagni, Epist. 64.

³⁰ Vide Bouillaud, Archiv. gén. de, Méd., t. ii. et v., quoted by Hope.

³¹ Thrombose cardiaque dans la Diphthérie, Paris, 1872, p. 43.

Scarcely any contemporary author doubts that cardiac thrombosis gives rise to more or less well-defined symptoms. What these are we shall now consider. Of course we are far less liable to-day, when the diagnosis of organic cardiac disease is so accurate, to attribute to intra-cardiac thrombi the signs, physical or rational, which properly belong to them, and which ancient observers could not differentiate. Nevertheless, there are complex cases in which one is at fault even in regard to this problem.

The symptoms of cardiac thrombosis vary naturally with their size, situation, and rapidity of formation. Certain authors have affirmed, for example, that the concretions formed in an auricle cause a greater amount of interference with the circulation than those elsewhere situated. This they do partly by reason of their size and the less contractile power possessed by the auricle, partly because from the auricle prolongations are sent off which occlude the cardiac orifices. When cardiac concretions form suddenly a few days previous to death, they always aggravate all the symptoms of an obstructed circulation.³² If the case be one of pre-existing disease of the heart, they soon obliterate the cardiac cavities and lead to a rapid fatal termination. According to Grisolle,³³ when the concretions are small and form an obstacle neither to the play of the valves nor to the cardiac circulation, they are not revealed by any appreciable functional trouble. The opinion of Grisolle in regard to small coagula is also shared by Legroux, especially when they are fixed at a distance from a cardiac orifice or concealed in a sinus. When, however, the thrombi are larger and interfere more or less with the course of the blood, they occasion very marked symptoms.

³² Hope, On the Heart, p. 486, Philada., 1846.

³³ Pathologie interne, p. 467, Paris, 1865.

Even before the days of auscultation there were certain rational signs which were dwelt upon with much force as showing the presence of cardiac concretions. Thus, Senac³⁴ writes that the patients thus afflicted feel a weight or oppression in the præcordial region which sometimes becomes extremely painful. Palpitations and irregularities of the pulse were also noted as symptomatic of these productions. Laennec believes that coagula of any size may be recognized; "when, in a patient who till then had presented regular pulsations of the heart, these suddenly became so anomalous, confused, and obscure that they can no longer be analyzed, we may suspect the formation of a polypous concretion."³⁵ He further adds that if the trouble takes place on one side alone of the heart, the fact is almost certain. When the coagula occupy the cavities of the right heart, the sounds of the left heart may remain normal whilst those of the right side are more or less distant and muffled (Legroux). Several authors, amongst whom we should mention Legroux, Bouillaud, Barth, and Roger, have mentioned amongst the physical characters which show the existence of intra-cardiac thrombi the sudden development of a blowing murmur limited to the præcordial region or propagated into the aorta. Sometimes this bruit was soft, sometimes harsh and rough. These writers have also noticed, in conjunction with grave general symptoms, the doubling of the first sound of the heart, making occasionally a sort of galloping murmur. As regards the recognition of concretions on one side alone, I acknowledge that after auscultating carefully several cases in which the autopsy showed coagula formed during life, I have been unable to note signs sufficient to justify a differential diagnosis.

³⁴ Traité de la Structure du Coeur, de son Action et de ses Maladies, t. ii. p. 470 et suix, quoted by Bucquoy.

³⁵ De l'Auscult., t. ii. p. 597, quoted by Hope.

The distinction appears to me difficult in like cases, for how explain that a trouble so considerable, even though it exists on one side only, should not influence the entire cardiac circulation? Moreover, it should be emphasized that the phenomena dwelt upon do not always manifest themselves when the cardiac contractions are perfectly normal. The heart-beats may be increased in frequency and the rhythm be changed. The passage, therefore, from a state of relative calm merely to that of extreme agitation is appreciated less readily. This is particularly true of the symptoms usually described as pertaining to the presence of terminal coagula. For here, at a period approximating the fatal termination, it is wellnigh impossible to determine accurately special symptoms. For this reason it is not surprising how authors have varied in their descriptions, and at best none of them are completely full and satisfactory. I have myself many times sought to recognize the blowing murmur given by Bouillaud as a physical sign of cardiac concretions, but in not a single instance have I been able to satisfy myself as to its existence. True it is that the cases I have watched with greatest care were those of children affected with toxic diphtheria, and it is possible, on account of the infrequency of valvular diseases during childhood, that more than once there may have been confusion between the signs afforded by newly-formed thrombi and those which belonged exclusively to a pre-existing disease of the endocardium.

Moreover, these murmurs have been heard and described by too many good observers (Walshe, Flint, Richardson) for any small negative evidence to weigh against that which is very positive. Sometimes they have been but the exaggeration of a bruit previously heard and which characterized an organic affection of the heart. Sometimes the presence of the thrombus has caused the diminution or complete disappearance of the pre-existing structural murmur. Again, these murmurs are discovered for the first time when the other signs indicate the existence of intra-cardiac thrombi. When they are heard under these circumstances they prove positively that the coagula have sent prolongations between the cavities of the heart or into the great vessels, so as to prevent the accurate coaptation of the valves or to obstruct the onward current of the blood. In the first case a regurgitant murmur is occasioned, tricuspid or mitral, which is heard at the apex; in the second case a basic murmur is detected, which is pulmonary or aortic. Usually these murmurs are systolic, although they may in rare conditions be diastolic. The murmurs have been heard more frequently on the right side of the heart, and have pointed by their location of greatest intensity to the obstruction of the infundibulum and pulmonary orifice. They are then basic or suprabasic, and carried upward toward the infra-clavicular region on the left side. These murmurs are heard very rarely on the left side—so infrequently, indeed, that Walshe cannot affirm that he has ever observed clinically one in this region. Theoretically, of course, such murmurs may be heard at any spot in the præcordial region, and with the first or second sounds provided their size and position in relation to orifices or valves could sufficiently account for them. Whilst there can be little question that murmurs do take place in the præcordial region wholly due to the presence of heart-clot, it is probable that their frequency and diagnostic importance is less than superficial consideration would cause one to believe. Thus, Flint³⁶ states that "the presence of coagula may occasion an endocardial murmur, but as a rule it is wanting, probably in consequence of the enfeebled action of the heart." Richardson³⁷ holds an analogous opinion, and writes: "There are sometimes abnormal sounds, but it is difficult to distinguish these from murmurs the results of valvular lesions." Walshe³⁸ is at variance with this view, especially in regard to the thrombal de novo murmur, and has "heard such a murmur when the examination post-mortem showed the fibrinous coagulum as the only probable cause of it."

³⁶ Disease of the Heart, Philada., 1870, p. 280.

³⁷ The Coagulation of the Blood, Lond., 1858, p. 428.

³⁸ Op. cit. (foot-note).

Auscultation.—In the heart the single, constant sign that has been observed consists in the modified tonality of the normal sounds. These are rapid, irregular, muffled, obscured, and distant. There is notable inequality also in the strength of successive beats, which is obviously explained by the great difficulty the blood encounters in traversing the heart. Now, as I have seen in frequent autopsies that the valvular mechanism of the left heart is ordinarily free from any fibrinous deposit, it is readily understood that it can produce the two sounds normal as regards situation and time, but greatly modified in transmission.

Percussion.—Percussion, except in particular cases which are rare, and in which the cavities are much distended by their contents, will only furnish us with negative signs. When the ventricles are swollen by large coagula, the percussion dulness will be extended laterally. As the right cavity is usually the seat of the deposit, it will be particularly marked toward the right of the sternum. In those instances where the area of præcordial dulness had been determined before the formation of the fibrinous concretion this extension becomes a physical sign of great value. It is to Piorry and the use of the plessimeter that we owe whatever of exactness belongs in like cases to this method of examination.

Inspection and Palpation.—The cardiac impulse may be unaffected by the presence of the thrombus, and if it has been regular in rhythm previous to its formation it may still remain so. This condition is infrequent, however, and usually the pulsations become irregular, tumultuous, and rapid. The force of successive beats will also be different. These signs can be determined by the sight and touch.

Pulse.—The characters of the pulse are variable. Sometimes it presents manifest inequalities, occasional intermittences, and is extremely frequent. It may be quite feeble in the beginning, and afterward gain in strength. Sometimes, in spite of its weakness and depressibility, it retains its regularity and its rhythm is unchanged. The coagulum existing in the cardiac cavities, especially on the right side, explains the variations of the pulse. Effectively, at each contraction of the ventricle this chamber, containing a less quantity of liquid blood, projects a smaller amount of venous blood to the lungs. Besides, this quantity is insufficient to replace the volume of revivified blood which leaves the lung with each inspiration. Soon the left cardiac cavities contract with but small power upon an amount of blood below the normal, and yet it is with this supply that the left heart must satisfy the needs of all the organs. The arteries during life become nearly empty, and it is to this condition, as well as to the lack of synchronism between the action of the two sides of the heart, should be attributed the signs we recognize in the characters of the pulse.³⁹

³⁹ Robinson, loc. cit.

In some instances of cardiac concretions the sonority of the chest remains normal. In others it is obviously augmented, and even by percussion very lightly performed a sound of raised pitch is produced. According to Richardson, this acute emphysema is the direct result of an insufficient blood-supply in the capillaries which surround the pulmonary alveoli. Whilst such a condition may often be observed amongst children, it is not unknown with adults. The affirmation, therefore, of Walshe, that it can only be observed in young people, and that in adults its place is supplied by considerable pulmonary congestion, is not exact. Since Richardson first called attention to the exaggerated sonority of the lungs in cases of heart-clot, other observers have also referred to it. Lavirotte (1864) particularly has insisted on it as a proof of fibrinous deposition in the right heart, and has demonstrated with pathological specimens that it was occasioned by the exsanguinated state of the lungs and their hyperdistension with air.⁴⁰ On the other hand, Raynaud⁴¹ states that when the left cavities are the seat of the concretion there is considerable stagnation in the lungs, and they show signs of great congestion. Thoracic percussion becomes less resonant, and subcrepitant râles are heard in an extended area. Sometimes, even, a moderate hæmoptysis takes place. These signs of emphysema on one hand, of congestion on the other, are not spoken of by the majority of writers on this subject; yet when they are present they will serve to fix our diagnosis and render it more certain. With respect to emphysema, especially amongst children, we should mention its great frequency, and on this account perhaps proper value has not been given to it when found at the autopsy of a child whose death has been occasioned by cardiac thrombosis. When the cardiac thrombus is present in the right side of the heart, Legroux⁴² has shown that there will be a more or less turgid condition of the veins of the neck, and perhaps also of the right upper limb. With this distension of the veins we shall remark, according to him, a partial or general infiltration of the subcutaneous tissues. Sometimes the oedematous condition is limited to the face and neck; occasionally it extends below the diaphragm, especially on the right side of the body. The extent of the oedema will depend upon the number and size of the prolongations which are given out by the main coagulum. Occasionally these prolongations have been found not only blocking up the pulmonary artery, but also filling one or both venæ cavæ and branching out as far as the jugular and subclavian veins.

⁴⁰ Congrès Medico-Chirurgical, Lyon, 1864.

⁴¹ Dict. de Méd. et de Chirurgie, vol. viii. p. 573.

⁴² Gazette hébdomadaire, 1856.

In my own observations I have always found the veins of the neck manifest, without in a single instance reaching any great size, and never have I noticed the prominence of the eyes noted by Walshe. In these cases cyanosis was limited, and was notable in a marked degree only upon the lips, the cheeks, and in the upper extremities. The general or local infiltration of tissue I have never remarked, although closely looked for on several occasions. Some authors, indeed, have described a bluish appearance of the entire surface of the body, together with signs of general infiltration. The explanation given of these phenomena is that there is a general obstruction of the capillary circulation, and that the return of the venous blood to the cavities of the heart is rendered almost impossible. In other words, we have here a well-marked asphyxic condition. If this be true, it is only partially so, and there must be great variation in different instances of fibrinous deposition in the right heart. The rational symptom which was for me one of great value in the diagnosis of these cases was that of excessive pallor, not only of the face, but of the limbs and the entire trunk. This pallor appeared constantly to increase until the last moments of life.

Richardson indeed says the symptoms are those of syncope, not of asphyxia. The different processes of life are arrested on account of a simple absence of arterial blood, not owing to the presence of blood unfitted to reconstitute the tissues. The tendency to fainting is probably due, therefore, to the fact that the right ventricle being more or less completely filled by a fibrinous coagulum, the blood is prevented from passing through its cavity and entering the lungs. As a result, there will be but a relatively small portion of blood which becomes oxygenized after each right cardiac systole. When the clot occupies the left ventricle and auricle, there will be a reflux of blood into the pulmonary tissue, thus causing great congestion of this structure. So intense will this congestion become that occasionally hæmoptysis results and pulmonary apoplexy may be developed, due, doubtless, to rupture of the capillary vessels. This condition occurs before the right heart is much or at all obstructed by coagula. We can appreciate that the physical signs must, if properly noted, show manifestly in which cavity the clot is located. If it be in the right heart, anæmia and emphysema of the lung should follow; hence breathlessness and increased pulmonary resonance. If it be in the left cardiac cavity, the lungs become engorged very rapidly, and we should find dulness on percussion, moist râles, and perhaps an equal or even greater amount of dyspnoea.

Difficulty of breathing appears to belong as well to the symptoms which indicate cardiac thrombus on one side of the heart as to those which characterize its presence upon the other. This symptom was first accurately described by Hope, since his day by Richardson and Meigs.⁴³ It has something special in its features which strikes one particularly, but may deceive unless closely observed. It takes place not because the movements of the thorax are interfered with, not because the entrance of air into the lungs is prevented, for the vesicular respiratory murmur is easily distinguished, but because the amount of blood furnished by the pulmonary artery is diminished. The anguish of the patient is sometimes terrible. The nares dilate, the chest expands spasmodically with each inspiration, and the patient is agitated, moans, and shows that extreme craving for air described by Van Swieten in the summæ anxietates. Under these circumstances, Hayden⁴⁴ states, the surface is cold, and often humid with perspiration. Pain and great oppression in the præcordial region have occasionally been referred to, as in the patient of Beau, who said, in placing his hand to his chest, "I have there a weight which has suddenly formed and which stifles me." Often the anxiety is extreme, and the painful sensations continue to increase steadily until death occurs. In rare instances the suffering, when it has reached a certain degree of intensity, may remain stationary, or even become considerably less. If such a respite occur, it is only temporary, however, and the anguish soon recommences. In milder cases sometimes, and apparently after dissolution or disintegration of the clot, the severe symptoms may by degrees disappear, and from this period the patient makes a steady, uninterrupted march toward recovery. I have only lately witnessed a similar example in a youth attacked with typhoid fever, which had reached the third week. There are constant and intense effort to breathe, extreme restlessness, and the patient will throw himself from one side of the bed to the other, and scarcely remain quiet for a few moments. These symptoms are usually more developed when there is concomitant cardiac disease of organic nature, and unless this be present may not be so pronounced as to concentrate attention upon them.

⁴³ Am. Journ. Med. Sciences, April, 1864.

⁴⁴ Cases 106, 107, and 111.

The brain scarcely shows the effect of congestion when the patient dozes for a few moments even in the midst of his great distress. These times of repose are frequent, but very temporary. In a little while the patient goes off in delirium or has a convulsion. Again, he relapses into coma, in which state death may take place. In some instances there has been obstinate vomiting during several days preceding a fatal termination. It is possible that this symptom favored the rapid development of the thrombus.

The preceding signs and symptoms will sometimes declare themselves suddenly in the midst of an inflammatory or cachectic affection, and will then point directly to the presence of a cardiac thrombus of considerable size which has rapidly formed, and which obstructs an orifice or interferes with the normal play of the valves. Again, there are all the physical evidences of an old organic affection of the heart, or those of acute endocarditis or pericarditis, and rapidly all the symptoms referable to the heart become greatly increased, whilst orthopnoea, pallor, and coldness of the extremities take place. If a careful examination of the chest reveals no intercurrent and pulmonary nor superadded cardiac affection, we may then fairly assume the existence of an intra-cardiac concretion. Nevertheless, we should remember that in many of these cases there is a close resemblance of the symptoms with those occasioned by a sudden rupture of one of the chordæ tendineæ in the course of acute endocarditis (Walshe).

We should not lose sight of the fact that at times a clot will form in the heart without giving rise to manifest symptoms unless the attention be specially directed to its formation. This will be true in instances where the coagulum forms slowly, is small, or occupies a place removed from orifices or valves. In a cardiac sinus, for example, a coagulum of inconsiderable size may remain fixed and latent for a long period. Such is not the case, as we already have shown, when the coagulum fills in part one or more of the cardiac cavities, is situated near an orifice, is attached to the walls by a pedicle which allows it to float freely in the ventricle, or is intertwined with the valves or chordæ tendineæ. Under all these circumstances, they give rise to the signs and symptoms we have dwelt upon above, and which ordinarily make known their presence. Occasionally, however, there is such a combination of symptomatic morbid phenomena relating to different organs that we are at a loss to separate them accurately and to determine how this or that symptom is occasioned. This statement is particularly true in regard to the distinguishing symptoms which indicate the presence of terminal coagula. At a period when the fatal termination is not far removed, and when it is extremely difficult both to recognize and interpret special symptoms, it is readily understood why those pertaining directly to cardiac thrombosis have not hitherto been fully and accurately described.

COURSE, DURATION, AND TERMINATIONS.—Cardiac concretions may form more or less rapidly, and in certain situations occasion death instantaneously and surely. This is eminently true of large coagula which fill up the infundibulum and pulmonary artery. Cases of this sort have been mentioned by various authors. Amongst others, we would specially direct attention to those instances in which sudden death has taken place during the puerperal state after severe post-partum hemorrhage. The patient has at times, in assuming an erect sitting posture, been attacked with a syncopal attack resulting in a few instances fatally.⁴⁵ In the same category we should include those examples in which sudden death has followed severe surgical operations.⁴⁶ Two cases of this termination, due to coagula in the right heart, are reported by Robert Lawson.⁴⁷

⁴⁵ Philada. Medical Examiner, March, 1849, paper by Charles D. Meigs; vide also Spiegelberg, Lerbuch der Geburtshülfe, and Lusk, The Science and Art of Midwifery, p. 597.

⁴⁶ Med. Times and Gazette, vol. i., 1873, p. 58; also Pathol. Soc. Trans., vol. xxvii. p. 70.

⁴⁷ Med. Times and Gazette, Feb. 8, 1873.

In cardiac dilatation this mode of death is not infrequently seen. It here seems to depend mainly upon stasis of blood caused by weakened power of contractility in the right heart and "by impairment of respiratory and nutritive attraction arising from feeble respiration and arrested tissue-change" (Hayden). The post-mortem revelation has afterward shown cardiac thrombosis to be the efficient cause of death. In diphtheria⁴⁸ and pneumonia such examples are not infrequently encountered. As Austin Flint⁴⁹ remarks, however, these coagula present almost identical physical characters with those formed after death, and consequently to fix precisely the moment of their production will at best be but a matter for conjecture. According to Walshe, it would be difficult to determine whether or not some of these almost instantaneous deaths occurred as a coincidence or as an effect. Besides, it is frequently impossible to determine the length of time they have existed before completely obstructing the circulation through the pulmonary artery into the lungs, and hence causing fatal syncopal or asphyxic phenomena. Bristowe⁵⁰ goes so far even as to affirm in the great majority of cases that cardiac concretions are unaccompanied with appreciable symptoms. In this statement he includes coagula of large size entirely filling one or more of the cardiac cavities, and doubtless formed within a few hours of the final termination. To quote his own words, "We ought to require very strong testimony indeed to convince us in any case that concretions found in the heart at the time of death have caused death, still more to convince us that those clots which resemble in every point the clots which are the mere result of dying have had this effect." How different does this sound from the opinions of B. W. Richardson,⁵¹ who attributes so many well-marked symptoms to the formation of voluminous moulded clots in the heart! And, indeed, is it not at variance with the views of a host of the best medical observers? We believe Bristowe goes too far, and that cardiac concretions are not infrequently the cause of very sudden death both in acute and chronic diseases.

⁴⁸ Robinson, loc. cit.

⁴⁹ Diseases of the Heart, p. 276, Philada., 1870.

⁵⁰ Reynolds's System of Medicine, vol. v. p. 113.

⁵¹ "Lectures" in the British Medical Journal, 1860.

There are numerous instances in which the coagulum formed in the heart is of smaller size, does not form so rapidly, and besides occupies a position in which, as it does not interfere greatly with the function of the heart, death does not of necessity immediately take place. Little by little, however, the clot is added to, and before many days have elapsed symptoms of gravest import are pronounced. So usual is it for the phenomena connected with the formation of a large cardiac concretion to be accompanied by those which properly belong to another serious affection which may likewise occasion rapid death (pneumonia, endocarditis, typhoid fever, diphtheria, etc.) that we with the greatest difficulty separate the symptoms, and can assign to the intra-cardiac condition those doubtless occasioned by it.

The cases referred to above are not the only ones. Occasionally we meet with cardiac concretions after death which have evidently existed for a number of years, and sometimes without having ever revealed their presence by notable interference with the circulation or in any way affecting the habitual good health of the individual (Laennec⁵²). This is perhaps not to be wondered at when the coagulum is small and situated near the apex of the heart, in one of the auricular appendages, or in such a position as not to alter the play of the cardiac valves or obstruct the orifices. But when we see a whole cavity, as an auricle, forcibly distended by an old concretion which fills its entire cavity, the absence of all symptoms during life pointing to its existence occasions much surprise. Some of these large coagula have nevertheless, by a sudden change in their position, caused instantaneous death; others again, after giving rise to obscure symptoms affecting both the pulmonary and cardiac circulation, have likewise brought about a rapidly fatal termination.⁵³ Sometimes, in consequence of the condensation or atrophy of the clot, the phenomena which took place suddenly with great intensity and indicated its presence became gradually modified, and we have known one remarkable instance in a youth during the third week of an attack of typhoid fever where the accidents thus occasioned completely disappeared, and the patient left the hospital apparently cured.⁵⁴

⁵² Dict. Encycl. des Sci. méd., article "Concrétions sanguines."

⁵³ Edin. Med. Journal, April, 1868, v.—case by H. Douglas.

⁵⁴ What occurred in this case I am of course unable to state in a positive manner. All I know is, that the heart became suddenly obstructed, followed by weak, irregular pulse and dusky countenance, and that in twenty-four hours, under treatment with frequently-repeated doses of digitalis and carbonate of ammonia, the accidents subsided. Was there a solution and disintegration of an incompletely formed heart-clot? It seems to me probable.

COMPLICATIONS AND SEQUELÆ.—One, if not the gravest, complication which 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. Feltz⁵⁶ 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.

⁵⁵ Brit. and Foreign Med.-Chir. Review, Oct., 1871.

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 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

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.

⁵⁸ Dict. Encycl. des Sci. méd., loc. cit.

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 Hayden⁶⁰ 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."

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.

⁶¹ A Textbook of Practical Medicine, 1869, vol. i. p. 156.

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 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.

⁶³ Magendie, "Lectures on the Blood," Lancet, 1839.

⁶⁴ Dict. de Médecine, t. viii. p. 560, Paris, 1868.

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.

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 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, Poullet⁶⁸ has endeavored to prove irrecusably by experiments upon animals 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.

⁶⁷ Cycl. of Anatomy and Physiology, p. 114, 1848.

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.

⁶⁹ Dict. de Méd. et de Chirurgie, vol. viii. pp. 562 and 565.

⁷⁰ De la Thrombose cardiaque dans la Diphthérie, Paris, 1872.

⁷¹ V. (after Walshe) such a specimen, No. 3636 Univ. College Museum, London.

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, Parrot⁷³ 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."

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 exceptional cases, and according to Raynaud⁷⁶ 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.

⁷⁴ Cited by Bucquoy, Des Concrétions sanguines, Paris, 1863, p. 62.

⁷⁵ Traité des Maladies du Coeur.

⁷⁶ Dict. de Médecine et de Chirurgie, vol. viii. p. 565.

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.

⁷⁸ "Végétations globuleuses," Traité d'Auscultation médiate, t. ii. p. 630.

(c) Globular concretions or fibrinous cysts, the latter term being adopted on account of the well-known contents, which have a grumous or purulent appearance⁷⁹ 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 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 Pitres⁸⁴ 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

⁷⁹ Pathol. Society's Trans., vol. xiv. p. 65 et seq.

⁸⁰ Path. Anat. (Syd. Soc. trans.), vol. iv. p. 217.

⁸¹ Dis. of the Heart and Aorta, Part ii. p. 1020.

⁸² Dis. of the Heart, 4th ed., p. 106 (b).

⁸³ Bristowe, in Reynolds's System of Medicine, vol. v. p. 107.

⁸⁴ Bull. Soc. anatomique, Feb. 5, 1875.

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

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.

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 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 fevers⁸⁷—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, 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.

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."

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.

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 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 formation⁹⁰ 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

⁹⁰ Ball, Des Embolies pulmonaires, Paris, 1862.

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.

⁹² Jenner, Diphtheria, its Symptoms and Treatment, London, 1861, p. 42 et seq.

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 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 Hammer⁹⁴ 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!

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

⁹⁵ Armand, Des Concrétions fibrineuses polypiformes du Coeur, Paris, 1857, p. 49.

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 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.

⁹⁷ Gazette hébdomadaire, 1856.

TREATMENT.—According to certain well-known authors, all curative treatment of heart-clot is useless (Bucquoy). Others, more sanguine, repose confidence in the internal use of alkalies, even when a fibrinous deposit in the cavities of the heart has commenced to form. A third class of observers, whilst they doubt the efficacy of any treatment under these circumstances in causing the disaggregation or absorption of an intra-cardiac coagulum, nevertheless believe we can limit the rapidity and size of its formation, and also retard the fatal termination, by giving time sufficient for adhesions to form with the cardiac walls. Richardson has proposed the administration of minim x doses of liquor ammoniæ at short intervals in an ounce of water, in order to dissolve existing coagula, and reports favorably upon its use. Gerhardt⁹⁸ counts upon better results from the use of a saline spray of bicarbonate of sodium of the strength of ½° to 1½°. This spray should be frequently inhaled, and in this manner, he believes, the heart is reached more directly and effectually. Successes are claimed by the use of this method of treatment. According to Flint,⁹⁹ the idea of giving any remedies with a view to dissolve solidified fibrin is absurd, whereas as a preventive treatment it is legitimate in circumstances where this state is likely to occur, and may even become an important therapeutic object.

⁹⁸ Deutsches Archiv für klinische Medicin, vol. v. p. 207, summarized in the Dublin Quarterly Journal of Medical Sciences, May, 1869, p. 421, quoted by Walshe.

⁹⁹ Diseases of the Heart, p. 285.

Alkaline remedies are said to have the power of holding the fibrin of the blood in solution. If this be true, they are certainly indicated to prevent coagulation. Moreover, if the fibrin in normal blood be held in solution owing to the presence of ammonia, it must be evident that this remedy is specially indicated in carrying out a secondary object of the prophylactic treatment. Bartholow¹⁰⁰ still maintains, however, that frequent small doses of ammonium carbonate afford the best chances of relief even when the coagulum is already formed. The latter distinguished author advises in cases which are most imminent intravenous injections of ammonia. The proportions should be one part of ammonia to three of water. The vein selected must be the jugular, and special precautions taken to avoid the entrance of air or a foreign body into the circulation. With attention to this formal indication there is little or no danger from these injections, as has been many times proven experimentally. Walshe¹⁰¹ regards the use of carbonate of ammonium, combined with bicarbonate of potassium, in five-grain doses, repeated three times daily, as a mere prophylactic, but as the best, after all, we possess, and recognizes from its use the only practical outcome from the enormous sacrifices of canine life made by Magendie in his experiments to illustrate his lectures on the blood. In spite of the numerous attempts to fluidify the blood, these efforts have always remained unsuccessful (Raynaud), and Legroux, who first proposed it, in his later writings abandoned the alkaline treatment as useless. The most he affirms that can be done is to combat with energy cardiac inflammations.

¹⁰⁰ Practice of Medicine, New York, 1880, p. 285.

¹⁰¹ Diseases of the Heart, 4th ed., London, 1873.

There is, however, a palliative medication which is indicated by the presence of the obstacles to the circulation within the heart. The general condition must be kept in view in carrying out treatment rather than the local signs. A properly combined therapeutic method in which the derivatives and counter-irritants play an important rôle offers, in Legroux's estimation, the best solacing means to oppose to the developed accidents. We must, however, maintain the patient in a quiet attitude and administer drugs which shall tranquillize pain and diminish anxiety. The counsel to keep the patient absolutely at rest is of primary importance in view of the sudden fatal accidents which have frequently occurred either in getting into bed after descending from it, or in sitting up and reaching for something the patient needs. The patient should be placed in bed in a semi-recumbent position, properly supported, and arrangements must be made so that all fatigue of eating and drinking or attending to his excrementitial functions are provided against. Of course we should treat a case of cardiac thrombosis complicating a frank inflammatory condition, such as acute endocarditis, certain forms of pleurisy or pneumonia, very differently from a case in which the state is one of relative feebleness or adynamia, as in the advanced stages of diphtheria, or after profuse uterine hemorrhage during or after confinement. In the first category of cases it may be in a few rare instances that local depletion of the blood by means of leeches or venesection is still indicated, especially if the patient be one of more than usual vigorous frame. In any example of this sort it is obvious that the internal use of the alkalies, the employment of revulsives (i.e. dry cups), and counter-irritants over the chest (as previously mentioned), adjoined, perhaps, to the action on the emunctories by diluent drinks, are the means which offer us the best guarantee of success. But how shall we act with our second class of cases? Certainly, we ought not for one moment, with our actual physiological knowledge, to consider the propriety of taking blood from a patient thus affected. May we use the alkaline treatment with reasonable hopes of benefit in a curative way? Yes, if we employ certain of the stimulating salts, like carbonate of ammonium, or even this salt combined with moderate doses of bicarbonate of potassium. We should remember, however, that these drugs are intended particularly to combat the pathological condition of the blood which apparently underlies the formation of fibrinous concretions in the heart.

Against the possible fatty degeneration of the cardiac muscular fibre, or the functional or organic affection of the pneumogastrics, which predispose to or accompany the production of cardiac coagula, we must make use of digitalis in small, repeated doses, and nux vomica or some other preparation containing strychnine. I have on more than one occasion seen these agents do evident good,¹⁰² and on this account am encouraged to urge their exhibition. With Hertz, we are not disposed to believe that digitalis, when given with a little precaution, and especially in urgent cases, is contraindicated by the danger feared by Gerhardt and Penzoldt, that it favors thrombosis of the right side of the heart and gives rise to new emboli.¹⁰³

¹⁰² Loc. cit., p. 68.

¹⁰³ Ziemssen's Cyclopædia, vol. v. p. 326.

It is almost needless to add that under like circumstances we should insist upon the frequent use of stimulants, like alcohol, chloroform, and ether, in the form of brandy, whiskey, spiritus chloroformi, or spiritus ætheris, or repeated doses of strong black coffee with one of the preceding preparations added to it. In regard to the prophylactic use of alkaline treatment continued during several days and in large or frequently-repeated doses, we advise against it for the reasons, first, that we do not know, in advance, the precise conditions in which fibrinous intra-cardiac coagula will form; and second, because though the alkalies have a well-known antiplastic action, they act as depressants to the general economy when employed in the manner mentioned, which is the sole method in which their internal use would be of some practical advantage.

Whenever we have in diphtheria a case in which there is at the same time obstruction of the glottis by a false membrane and clogging of the heart by a fibrinous coagulum, we should abstain from performing tracheotomy on account of its evident uselessness.¹⁰⁴

¹⁰⁴ Medical Times, vol. ii. p. 617.