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.