Volume 3 — DISEASES OF THE BLOOD, AND OF THE HÆMATOPOIETIC SYSTEM. (continued 7)

There is much variation in different cases as regards the severity of the paroxysms, and the mildest offer a striking contrast to the severest, the essential symptomatic characters of the affection, however, being preserved. In mild paroxysms the pain is comparatively slight, the anguish or heart-pang is less, and the heart's action may be but little or not at all disturbed. Such paroxysms occasion annoyance without great suffering. Different cases, and the same case at different times, exemplify varying degrees of severity.

Recurrences of angina take place as a rule, to which there are but few exceptions. The intervals between the paroxysms vary in different cases, and often in the same case. Their recurrence is not governed by any law of periodicity. Generally, they are at first infrequent, and their frequency increases slowly. With increase in frequency their severity is apt to be increased. At first, and for a certain length of time, they are occasioned by some apparent exciting cause. A common cause is the exertion of walking, especially against a current of wind. Often for a considerable period patients are exempt whenever they are at rest. Sooner or later, in most cases, attacks are produced by other causes, such as a fit of anger or other mental emotion, and finally without any appreciable existing cause. I have known attacks to be caused by the act of swallowing solid food, so that eating became a source of terror to the patient. They occur in some cases during sleep. Occurring after intervals of a few moments, the affection in this respect resembling certain cases of tic douloureux, it doubtless would be difficult by any description to convey an adequate idea of the lamentable condition of the patient.

On account of the wide range of the gradations as regards the degree of severity or mildness, of the diversity of symptoms referable to the different forms of disease of the heart with which the affection may be associated, and of the varied disorders which may be accidentally connected, the clinical picture of angina is by no means uniform. There is, however, no practical advantage in making formal varieties of the affection. Eulenberg makes four different types, their differential characters being based on the different nerves supposed to be especially affected, as follows: 1st, excito-motor cardiac angina; 2d, regulator angina; 3d, excito-motor sympathetic angina; and 4th, vasomotor angina. Assuming that there is ground for these pathological distinctions (which, to say the least, admits of doubt), in a practical point of view they involve difficulties not compensated for by important bearings on diagnosis and treatment. One point of distinction, however, has important bearings—namely, the existence of angina with or without organic disease of the heart. It cannot be doubted that in the vast majority of cases angina is incident to some form of cardiac lesion. That it may exist without any appreciable lesion is admitted. The propriety of recognizing it as a functional disorder rests on the latter fact.⁵ Practically, the coexistence of organic disease of the heart or otherwise, and, if organic disease exist, its nature and extent, are points which it is important to take into account in the diagnosis with reference to prognosis and treatment.

⁵ Of 71 cases analyzed by Gauthier, in 3 only was the affection to be regarded as purely functional. Vide Eichhorst.

DIAGNOSIS.—The diagnostic points in cases of angina are the præcordial seat of the pain, its radiations thence into the shoulder and upper extremity, generally of the left side, the character of the pain, the accompanying anguish and sense of impending death, the coexisting disorder of the heart (which occurs as the rule), and the voluntary immobility of the body. These are positive criteria which, if marked, render the diagnosis easy and certain. The diagnosis is further substantiated by finding the signs of organic disease of the heart, especially if there be lesions at the aortic orifice or within the aorta. Well-marked angina is in itself strong presumptive evidence of organic disease of the heart. Not infrequently the existence of the latter is for the first time discovered by an examination suggested by the occurrence of an attack of angina. The cases in which the diagnosis involves difficulty are those in which certain of the above-mentioned diagnostic points are either wanting or not well marked.

The affections which may be mistaken for angina are gastralgia and intercostal neuralgia. In gastralgia the pain is seated below the præcordia. It may radiate in different directions, but does not extend to the upper extremities, and is not accompanied by irregularity of the heart's action. The patient writhes and changes the position of the body in the effort to obtain relief. There is not a sense of impending death. The paroxysms are of much longer duration than those of angina. These differential points should suffice for the discrimination.

An acute attack of intercostal neuralgia does not differ so widely from angina, but the differential points are generally distinctive enough for a positive diagnosis. The pain in intercostal neuralgia is not seated in the præcordia. It does not shoot into the upper extremities; it is increased by the act of inspiration; the peculiar anguish of angina is wanting; the action of the heart is likely to be regular; and the diagnosis is confirmed by finding tenderness over circumscribed areas in the intercostal spaces anteriorly, laterally, and posteriorly.

Cardiac lesions in cases of angina are to be excluded by finding no physical signs of their existence. But it is to be remembered that angina is not infrequently associated with lesions not readily recognized by signs—to wit, obstruction of the coronary arteries and fatty degeneration of the heart. Persistent feebleness of the heart's action and symptoms other than angina incidental thereto render it probable that one or the other or both of these lesions exist. It is probable that these lesions have been overlooked in examinations after death in some of the cases in which angina has been reported as not connected with any organic affection of the heart.

PATHOLOGY AND ETIOLOGY.—The paroxysms of angina have the distinctive traits of neuralgic affections as regards the character of the pain, its extension in the course of sensory nerves, the occurrence of intermissions, the absence of fever, the functions of digestion and assimilation remaining often unaffected, and the attacks not always being referable to any exciting cause. The association of the affection, as a rule, with organic disease of the heart is evidence of course of some pathological connection. What is this connection? A difficulty in answering this question arises from the fact that the affection is associated not with any one lesion, but with different lesions. It may be associated with obstruction (usually from calcification) of the coronary arteries, with insufficiency of the aortic valves, with rigidity from calcareous degeneration of the aorta, with aortic aneurism, and with fatty degeneration of the heart, these different morbid changes existing either singly or more or less of them in combination. The question then resolves itself into another—namely, What is the pathological condition common to these different lesions which stands in a special etiological relation to angina? It is a logical conclusion that the affection must depend upon some condition which is common to these lesions. The association with the lesions is too frequent to be explained by mere coincidence. The etiological relation involves evidently a condition which exists only in a small proportion of the cases of these lesions. This statement is a logical deduction from the great infrequency of angina and the frequency of these varieties of organic disease of the heart. I submit, as the most rational theory, that the pathological condition on which the angina depends is ischæmia of the heart. This theory is supported by the frequency of the instances in which in cases of angina the coronary arteries are obstructed; by the fact that not very infrequently this is the only lesion found after death (two instances having fallen under my own observation within the past year); by the association with aortic insufficiency and rigidity of the aorta, lesions which interfere materially with the supply of blood to the heart if it be admitted that the blood is driven into the coronary arteries, not during the ventricular systole, but by the recoil of the arterial coats in the ventricular diastole; and by the association with fatty degeneration of the heart when, owing to the weakness of the heart's action, the supply of blood to the muscular structure of the heart must be diminished. That the sudden withdrawal of a supply of blood to a part may occasion neuralgia is shown by the intense pain in the limb which directly follows embolism of the femoral artery. Moreover, general anæmia, as is well known, favors the recurrence of neuralgia in various situations.

The cardiac nerves in which the pain is seated are doubtless sensory fibres of the pneumogastrics. Their anatomical connections with the brachial plexus will explain the extension of pain to the left upper extremities. To account for the pain in parts which have no direct connection with the cardiac nerves, it may be assumed that in angina, as in other neuralgic affections, a centripetal influence conveyed to the nervous centres may occasion pain referable to different situations. This explains the shifting of pains which is one of the diagnostic traits of neuralgia. The explanation of the disturbed rhythm of the heart's action so often coexisting with the neuralgic pain is not more difficult than in cases of functional disorder disconnected from angina. For what is to be said of the rationale the reader is referred to that portion of this article which treats of Functional Disorders of the Heart.

Angina, as a purely functional affection—that is, not symptomatic of any organic lesion of the heart, and not due to any structural change in, nor mechanical pressure upon, nerves—is obscure as regards its pathology and etiology, but not more so than many other neuralgic affections. As already stated, cases in which it is thus purely functional are few in number—fewer even than has been supposed, because there is reason to believe that lesions have been overlooked. Moreover, cases which have been reported render it probable that in some instances in which the heart has been found free from appreciable lesions nerves entering into the cardiac plexuses may be the seat of structural changes or may be subject to pressure from a morbid growth. But there are cases in which no lesions are discernible during life, and in which the existence of lesions is disproved by complete recovery. The affection under these circumstances must be regarded as purely functional. There is no positive knowledge of the etiology in these cases. The affection has been attributed to gout, to hysteria, to the action of cold, to the use of tobacco, and to other causes. These causes may have a certain amount of agency, but there is an unknown intervening link in their etiological connection concerning which, in the present state of our knowledge, it is useless to speculate.

Age and sex have an undoubted influence in the etiology. The affection very rarely occurs under middle life, and it occurs in men much oftener than in women.

PROGNOSIS.—As a very rare exception to the rule, a single paroxysm only may occur, the patient living for many years without any recurrence. Recurring paroxysms sometimes are separated by long intervals—weeks, months, and years. In the majority of cases, however, paroxysms recur with more and more frequency and with increasing severity. Under these circumstances death may take place after a long period of suffering.

The liability to sudden death is an important point in the prognosis. This may occur in the first paroxysm. An instance has fallen under my observation within a few months, there having been no signs previously indicative of disease of the heart. Calcareous obstruction of the coronary arteries was the lesion found after death. A person subject to paroxysms of angina must be considered as in more or less danger of sudden death with the recurrence of each paroxysm. The physician should be sufficiently impressed with the importance of this fact. While it is doubtful whether it be the physician's duty to apprise the patient of the fact, the danger should always be communicated to some discreet relative or friend. To do this is a duty which the physician owes to himself as well as to the patient. If he omit it, he exposes himself to censure should sudden death unexpectedly take place. The mildness of the paroxysms which have already occurred does not afford a positive security against the liability to a severe and fatal paroxysm. But it is a hopeful consideration that paroxysms may recur more or less frequently for an indefinite period without proving fatal. At this time I am cognizant of three cases in which paroxysms have recurred frequently for several years, the patients, with that exception, having had fair health. Let not the physician, therefore, predict with positiveness that a patient with angina will die sooner or later in a paroxysm. The uncertainty is a ground of encouragement as well as for apprehension.

The coexistence of organic disease of the heart and the nature of the cardiac lesions have a very important bearing on the prognosis. The danger is in proportion to the importance of these. Recovery is never to be expected when the affection is associated with well-marked cardiac lesions, and there is always great danger in the recurrence of paroxysms when the associated lesions are in themselves dangerous. Lesions which give rise to free aortic regurgitation and to fatty degeneration of the heart involve more or less danger of sudden death, irrespective of angina. It is evidence of greatly increased danger if paroxysm of angina be superadded.

During a paroxysm of angina the immediate danger is to be estimated by the symptoms denoting disturbance of the heart's action. The danger is great in proportion as the action of the heart is feeble, irregular, or intermitting. Per contra, the danger is less in proportion as the deviation from the normal force and rhythm is small. It may be said that there is no danger so long as the heart's action remains unaffected, but the disturbance may be slight or wanting at the outset of a paroxysm and afterward become fatally great.

A favorable prognosis may be entertained when there are no signs of cardiac lesion, and when there is little or no disturbance of the heart's action during the paroxysms. Let it be borne in mind that such cases are exceptional and extremely rare. Let it also be borne in mind that lesions especially apt to be associated with fatal paroxysms may be latent—namely, obstruction of the coronary arteries and fatty degeneration. The latter fact renders it proper that a favorable prognosis should always be formed with a reservation, while the fact that recovery takes place in a few well-marked cases of angina renders it improper to withhold encouragement whenever lesions are not discoverable and the paroxysms are not accompanied by alarming symptoms referable to the heart's action. The long tolerance of the affection in some cases is not to be lost sight of with reference to the encouragement which may be fairly derived therefrom.

The immediate cause of sudden death in a paroxysm is probably an arrest of the heart's action in diastole, or such a degree of diminution of the force of its action that the accumulation of blood within its cavities induces paralysis from distension.

TREATMENT.—It is important that a paroxysm of angina be treated as soon as possible, not alone with a view to the relief of pain, but to remove immediate danger. If the physician be present, an opiate in a form to act promptly should be given either by the mouth or hypodermically; the latter mode is to be preferred. Laudanum or a solution of a salt of morphia is the most eligible form if given by the mouth. If the heart's action be weak and irregular, a diffusible stimulant is indicated. If at once available, chloric ether, Hoffman's anodyne, and the compound tincture of lavender act efficiently. If these be not at hand, an alcoholic stimulant should be given, diluted but little, and the doses repeated at short intervals until the paroxysm ends and the disturbed action of the heart has ceased. The duration of paroxysms is generally so short that a physician is rarely present unless they recur after brief intervals. A patient, therefore, subject to angina should be provided with remedies and instructions as to their use at the instant a paroxysm occurs. The amyl nitrite, first recommended in this affection by Brunton, is a remedy of signal benefit in some cases. From two to five minims may be inhaled at the commencement of the paroxysm. It is especially indicated when the characters of the pulse denote arterial tension. Caution is to be exercised in its use if there be notable weakness of the heart's action. Sinapisms, stimulating embrocations, and fomentations applied to the chest have a certain measure of utility, but they should not take the place nor delay the use of remedies which are more efficient.

A still more important object of treatment than relief in the paroxysms is their prevention. During the intervals this object claims assiduous attention. First in importance is the avoidance of all exciting causes. Bodily exercise is to be kept within the limits required in order to incur no risk of a paroxysm being produced. The same precaution applies to mental excitement. Unhappily, this is not as easy as the avoidance of muscular exertion. John Hunter's saying, that his life was at the mercy of any scoundrel who chose to insult him, proved a prediction. He fell dead on receiving an insult from one of his colleagues at St. George's Hospital. Sexual intercourse I have known to prove an exciting cause. Excesses in eating and drinking are in this category. The diet, however, is not to be reduced below the full requirements for nutrition, and wine or spirits, as conducive to digestion, are in some cases serviceable. The use of tobacco is to be interdicted.

Coexisting affections which have no special pathological connection with the angina may act as auxiliary causes, and therefore claim attention. Gout is to receive appropriate treatment. Anæmia especially is to be removed. This condition strongly conduces to the development and the continuance of neuralgic affections. Chalybeate remedies and the dietetic treatment are called for if this condition coexist. It is a rational indication to supply the heart with good blood if it be true that angina depends on an ischæmic condition of this organ.

Associated cardiac lesions are to be treated according to symptomatic indications, as in cases in which angina does not occur. Digitalis may be used under the proper restrictions. I have known this remedy to prove highly useful in preventing the recurrence of paroxysms. Nux vomica is sometimes useful as a cardiac tonic.

Various drugs have had repute as empirical remedies. Of these may be mentioned the preparations of zinc, arsenic, the nitrate of silver, phosphorus, the bromine salts, the iodide of potassium, and quinine. There is no proof that these remedies have any special therapeutical effect in this affection, but that they are sometimes useful there is abundant testimony. Trial should be made of them, with proper care in their administration. Electricity in the form of the induced and of the constant current has been advocated as not only serviceable, but as effecting in some instances a permanent cure.⁶ Beard and Rockwell have found general faradization useful in a few cases.⁷

⁶ Vide Eulenburg in Ziemssen's Cyclopædia, vol. xlv. p. 54.

⁷ Vide Medical and Surgical Electricity.

Exophthalmic Goitre (Graves' Disease; Basedow's Disease).

This affection is characterized by three striking symptomatic events—namely, persistent increase of the frequency of the heart's action, enlargement of the thyroid body, and protuberance of the eyeballs. The name exophthalmic goitre relates to the last two of these three events. It is defective, inasmuch as it does not include the increased frequency of the heart's action, which is the primary one of the three events, and the only one which is never wanting. As an individual affection it was first described by Graves in 1835, although cases in which these events were associated had been previously reported. Parry collected 7 cases in which the affection of the heart was associated with thyroid enlargement, and in 1 of these cases exophthalmia existed. An account of these cases was published in 1825. The name Graves' disease, proposed by Trousseau, has been adopted by French, English, and American writers. Basedow's disease is the name given to the affection by German writers. The affection was described by Basedow in 1840 under the name Glotz augenkrankheit.

There are cases in which one of the events in this symptomatic triad is wanting, the cases in other respects corresponding to the affection. The exophthalmia is the event oftenest wanting, the goitre, the functional disorder of the heart, and the associated phenomena being the same as if protuberance of the eyeballs coexisted. In some instances the goitre alone is wanting. The name exophthalmic goitre is not strictly applicable to these cases, but that the affection is essentially the same as when the three events are present cannot be doubted. It is a chronic affection, being in the great majority of cases of long duration. Exceptionally, it is developed suddenly and disappears after a few days. In these cases the affection has been distinguished as acute, but its claim to be so called rests exclusively on the shortness of its duration.

SYMPTOMATOLOGY.—Of the three cardinal events, the increased frequency of the heart's action is the first in the order of time. This precedes the other events usually for several weeks or even months. The frequency varies in different cases within wide limits—namely, from 90 or 100 to 150 beats, and even more, per minute. There is notable variation at different times in the same case. Generally, the frequency is greatly increased by exercise and mental emotions. In other words, irritability of the heart is in most cases a marked feature. As a rule, there are none of the disturbances of action, in other respects than frequency, which are found in cases of functional disorder not associated with exophthalmic goitre. The action may be intermittent or in other respects irregular, but in most cases the rhythm is not disturbed. The patient is conscious of the heart's action, and is annoyed by it, especially under any excitement; but there is not that distressing sense of the disorder which is felt in the paroxysms of palpitation with irregularity of action considered in the first division of this article. At the outset and for a considerable period there are no signs of any organic disease of the heart, or if the latter be present the association is accidental; the disordered action, as far as it relates to the affection under consideration, is purely functional. At a later period there may be enlargement of the heart as a result of long-continued increased activity of function. From the first cardiac murmurs are generally present at the base and over the body of the heart. These are blood-murmurs due to coexisting anæmia.

Following the increased frequency of the heart's action, after a variable period enlargement of the thyroid body occurs. The enlargement may be rapid, but in most cases it takes place slowly, and ceases when it has reached a moderate degree. Cases are exceptional in which the degree of enlargement is such as to occasion any obstruction to respiration. Almost invariably both lobes of the thyroid body are enlarged, but the enlargement is generally not equal on the two sides, and, as a rule, it is greater on the right side. The enlarged lobes are soft at first, afterward becoming hard. The subcutaneous veins over them are often distended. Pulsation of their arteries is apparent to the hand and to the eye. A systolic arterial blowing murmur and a continuous hum are heard when the thyroid region is auscultated. In some instances the murmur is like that of an aneurismal varix. As a rule, murmurs are heard over the carotid artery and the jugular vein. A thrill or fremitus is often felt by the hand placed upon the thyroid body. The thyroid enlargement is due at first chiefly to dilatation of the arteries and veins. Hyperplasia of the fibroid tissue occurs afterward, and then the enlarged gland becomes hard to the touch. The size of the enlarged thyroid body is often found to vary considerably at different times—a fact attributable to varying degrees of the dilatation of the vessels and of the consequent hyperæmia.

A notable protuberance of the eyeballs has sometimes been observed to take place suddenly, but, as a rule, it is at first slight and increases slowly. The degree of protuberance varies considerably in different cases. When marked, the patient has a remarkable staring expression. Both eyeballs are alike protuberant with very rare exceptions.⁸ The pupils are unaffected and vision is not impaired. The protuberance is sometimes so great that the globes cannot be covered by the eyelids. Under these circumstances inflammation of the conjunctiva ensues, and perforation of the cornea has been known to occur. The eyeballs can be pressed backward into the sockets without a degree of force which occasions pain, but the protuberance returns directly the pressure is discontinued. In most, but not in all, cases the consensual movements of the upper eyelid and the globe, when the latter is moved upward or downward, are impaired; that is, the movements of the lids do not follow those of the globes. That this symptom is not to be accounted for by the exophthalmia is shown by the fact that it is not a symptom when the protuberance of the eyeball is caused by an intra-orbital tumor. The symptom therefore has diagnostic significance. The ophthalmoscope shows the veins of the retina to be dilated and tortuous, with, in some instances, visible pulsation of the retinal arteries. Anatomical conditions to which the exophthalmia is, in a measure at least, referable, are enlargement of the intra-orbital vessels by hyperæmia and an increased amount of post-ocular fat. Paresis of the straight muscles, induced by stretching, is probably an important factor when the protuberance is great. These muscles have in some instances been found to have undergone fatty degeneration.

⁸ Allan McLane Hamilton, in his work on Nervous Diseases, cites a case reported by Yeo, in which the exophthalmia effected only the left eye, and the goitre was limited to the right thyroid body. Cases of unilateral goitre with bilateral exophthalmia have been observed.

Anæmia is usually associated with the foregoing cardinal symptoms. It is sometimes wanting. This was true of a case recently under my observation. If anæmia does not exist, the blood-murmurs referable to the heart and vascular system may be absent. If anæmia exist in a marked degree, there are present certain symptomatic phenomena referable thereto—namely, neuralgic pains in different situations, want of physical and mental endurance, hysterical manifestations, depression of spirits, etc. Mental irritability is apt to be a prominent trait of the affection. This may in a great measure be referred to sensitiveness occasioned by the exophthalmia. Owing to this, patients often avoid observation as much as possible. They naturally, women especially, are led to brood over the calamity of such a singular and conspicuous deformity. Breathlessness on exercise is a symptom more or less marked according to the increase in the frequency of the heart's action and the impoverishment of the blood. The appetite and digestion may or may not be impaired, and hence there may or may not be emaciation. It cannot be said that the affection is accompanied by fever, although in a certain proportion of cases the temperature of the body is half a degree or a degree above the normal range. Reports of cases embrace a considerable number of concurrent symptoms which are occasionally present, such as cephalalgia, insomnia, vertigo, amenorrhoea, neuralgia, unilateral sweating, etc. These have no special connection with the affection, but are incident to associated pathological conditions.

DIAGNOSIS.—The three phenomena which distinguish this affection are so obvious as well as characteristic that a diagnosis cannot well be avoided, after a description derived from books or lectures, when the first case presents itself in practice. The wonder is that the affection had not been clearly pointed out prior to the writings of Graves and Parry. Any difficulty in diagnosis relates to cases in which either the exophthalmia or the enlargement of the thyroid body is wanting, or to the incipiency of the affection when its characteristics are not fully developed. The bilateral protuberance of the eyeballs, the absence of local symptoms other than those caused by the exposure of the conjunctiva when the eyelids fail to cover the globes, the mobility and normal size of the pupils, the want of the normal consensus in the movements of the eyelids and the globes, and the replacement of the latter by moderate pressure, are the diagnostic points which distinguish the exophthalmia in this affection from that incident to intra-orbital tumor. The moderate increase of the thyroid body, its softness to the touch, its notable variations in volume at different times, its pulsation and the auscultatory murmurs which it generally furnishes, are diagnostic points distinguishing the enlargement in this affection from that of bronchocele. The persistent frequency of the heart's action is not less marked when either of the two phenomena just referred to is wanting than when both are present. The degree of frequency varies, but more or less increase is a constant symptom; and it is a symptom not likely to be present in either exophthalmia or in goitre unassociated with Graves' disease.

Aside from the symptomatic triad, the clinical history offers in different cases considerable diversity. The diverse inconstant symptoms as they occur in other pathological conditions are without diagnostic significance. A large proportion are incident to the anæmia so often associated with the affection under consideration.

PATHOLOGY AND ETIOLOGY.—Inasmuch as the persistent frequency of the heart's action is the first event in the order of time, the thyroid enlargement and the protuberance of the eyeballs being epiphenomena, it seemed a rational supposition that the latter events were dependent on the cardiac disorder. This view was held by Graves and his colleague, Stokes. A supposition much more rational is that the three events are united by a common causation. Anæmia has been supposed to be the causative condition. This supposition is disproved by the fact that anæmia does not exist in all cases. Moreover, anæmia is a pathological condition of frequent occurrence, whereas the affection under consideration is extremely rare. It is, however, very probable that anæmia may play an important auxiliary part in the causation, as it does in all the neuroses. With the knowledge of the sympathetic and vaso-motor nerves which has been acquired since the date of Graves' discovery, the pathology seems clearly to involve these components of the nervous system. This pathological view is perhaps generally held at the present time. But to interpret all the phenomena satisfactorily by reference to the known functions of these nerves is not easy. Vaso-motor paresis will account for the dilatation of the vessels, which is an important anatomical element in the enlargement of the thyroid body and the exophthalmia. On the other hand, acceleration of the heart's action is not an effect of paresis, but of excitation. To account for this incongruity there have been different hypotheses, which it does not fall within the scope of this article to discuss. Some autopsies have shown anatomical changes in the cervical sympathetic and its ganglia, but in others no morbid appearances have been found. Whether the pathology involves peripheral nerves alone or a central morbid condition in the spinal cord or the medulla oblongata is an undecided question. For facts and arguments bearing on the different points of inquiry relating to the pathological seat and character of the affection the reader is referred to other works.⁹ I will only add that in view of the fact of the exophthalmia and the goitre being, in the vast majority of cases, bilateral, it seems rational to suppose the pathological nervous condition to be central rather than peripheral. This is assuming that the three cardinal events involve a common causative condition, and not that the exophthalmia and goitre are dependent on the cardiac disorder. The termination in a certain proportion of cases in recovery goes to show that the affection does not necessarily involve structural lesions, and hence that it is properly included among the neuroses. The constancy and prominence of the disordered action of the heart render it proper to consider the affection in connection with the neuroses of that organ.

⁹ For a résumé, vide article by Eulenburg in Ziemssen's Cyclopædia, vol. xiv.

In the etiology of Graves' disease sex and age have a decided influence. In very much the larger proportion of cases the patients are women. The proportion of 2 to 1, which is stated by some writers, is not sufficiently large. Out of 20 or more cases which have fallen under my observation, in 1 only was the patient of the male sex. The disease is extremely rare under puberty and after middle age. Between these extremes of age there is no special predilection of the disease for any particular period of life.

Of causes which are independent of sex and age we have no positive knowledge. In particular cases the disease has been attributed to traumatic causes, to fright or other kinds of mental excitement, to sexual excess, etc. The evidence of a causative relation in these cases is simply a post-hoc connection which obtains in but a single instance or at most in a few instances. Etiological speculations, in the absence of ascertained facts, are, to say the least, useless, and it is the most politic as well as the fairest statement to say that in the present state of our knowledge we have no adequate data for determining the causation of the affection.

PROGNOSIS.—Graves' disease has no direct fatal tendency. It may not interfere with fair health for a long period. It diminishes the ability to tolerate other diseases, and in this way indirectly it threatens life. If it supervene upon organic disease of the heart, the gravity of the latter is thereby increased and its progress hastened. It induces, as a result of long-persistent increased activity of the action of the heart, enlargement of this organ. Sooner or later, if the disease continue, dilatation predominates over hypertrophy of the heart, and then occur the evils incidental to the inability of this organ to carry on the circulation adequately. Want of breath on exercise, and at length constant dyspnoea, become sources of suffering. Generally, dropsy finally ensues, and thus, indirectly, the affection leads to a fatal result. In most cases, however, death is caused by some intercurrent malady before the effect upon the heart is sufficient to occasion grave symptoms. Aside from the effect upon the heart, the affection does not seem to involve an intrinsic tendency to any particular complication.

The affection tends to long continuance. I have not met with an instance of its rapid development and its disappearance after a brief duration. Instances of complete recovery are rare; that is, the exophthalmia and the goitre do not disappear entirely, and the action of the heart does not become perfectly normal. A close approximation to complete recovery is not very infrequent, and in some instances all traces of the affection disappear.

The cases offering most in the way of a favorable prognosis are those in which there is not great acceleration of the action of the heart, this organ being free from organic disease, and those in which, exclusive of the affection under consideration, there are no marked unhealthful conditions. Impaired appetite, lack of digestive power, defective nutrition, and persistent anæmia are unfavorable prognostics. Any important antecedent disease affects of course the prognosis unfavorably.

TREATMENT.—From what has been stated in relation to the etiology of Graves' disease, it follows that there are no known special causative indications in the treatment. It is, however, a rational consideration that anything in the habits and surroundings of patients which is prejudicial to health has perhaps some agency either in causing or in maintaining the affection. It is therefore an important part of the treatment to remove all causes of ill-health which can be ascertained. The treatment, in this point of view, will embrace injunctions respecting mental occupations and excitement, a proper proportion of time devoted to out-of-door life, an adequate diet, avoidance of dietetic excesses, moderation in the use of alcohol, the disuse of tobacco, the regulation of sexual indulgence, etc. Without going farther into details, the object, in general terms, is to place the patient under the best attainable hygienic conditions.

Any disorders which coexist may possibly be involved, if not in the causation, in the persistence of the affection. They claim, therefore, appropriate treatment. Diminution of appetite and difficulties relating to digestion are to be treated by measures which must vary according to the circumstances in each case, and which need not be here considered. Uterine troubles are to be removed. These have been supposed to stand in a special causative relation to the affection. The anæmic condition which is so frequently associated (in addition to the removal of its causes, if these be ascertained and if they be removable) calls for the long-continued use of chalybeate preparations in conjunction with dietetic and regiminal treatment. In a case under my observation in which recovery took place the patient took two grains of reduced iron three times daily for three years. It is generally advisable to change from time to time the preparation of iron, partly for the moral effect of giving a new remedy in order to secure perseverance on the part of the patient, and in part because, irrespective of this effect, changes seem to be of use. The prevalent idea that iron is not well tolerated is to be overcome by assurances, argument, and, if necessary, by stratagem. It is certain that in most, if not all, instances this idea is a delusion. The anæmia in this affection, as in other pathological connections, is only to be overcome by the long-continued, uninterrupted employment of chalybeates conjoined with the other measures of treatment. This should be clearly stated to patients in order to forestall discouragement and neglect of the treatment advised.

Hydropathic packing and the needle-bath have been highly recommended. A patient of mine who has recovered apparently derived benefit from daily sea-bathing. The propriety of these measures is to be determined by the glow and feeling of invigoration to which they give rise if they be useful. Should these effects not follow, daily sponging of the body with cold or tepid water, to which may be added sea-salt or alcohol, may be substituted. Mental diversion is an important hygienic measure. The patient should be urged to conquer the feeling of mortification which prevents social enjoyments and disposes to brooding over the malady.

The enlargement of the thyroid body naturally suggests the employment of iodine. This local affection, however, is very different from bronchocele or goitre occurring independently of Graves' disease. Experience shows that iodine employed either topically or for its constitutional effect is useless if not injurious. Many years ago a case was related to me by a non-medical friend in which thyroid enlargement had been treated by the application of iodine. Remarkable prominence of the eyes soon followed, which was attributed to the iodine, and the physician fell under censure which, as I suspect, he was not prepared to meet by an acquaintance with Graves' disease. If the thyroid enlargement be sufficient to occasion tracheal obstruction or give rise to great deformity, the injection into the gland of a solution of ergotin may be resorted to. William Pepper has effected a complete reduction of the thyroid enlargement by this measure, in addition to ergot given internally. He employed a solution of ninety-six grains of ergotin to an ounce of distilled water, of which from six to ten minims were injected weekly by means of a needle introduced from half an inch to an inch in depth.

For the relief of the exophthalmia, gentle compression upon the eyes by a compress and bandage during sleep has been recommended. Aside from this, the indications for local treatment relate to the inflammation which is liable to be produced by insufficient covering of the eyeballs by the eyelids and by the impaired consensual movements of the latter with the former. The patient should, as far as practicable, abstain from reading, writing, and other uses of the eyes which involve strain.

Insomnia and general nervous irritability may call for palliative treatment. Opiates should if possible be withheld, owing to their effect upon appetite and digestion, and also on account of the risk of forming the opium habit. Other hypnotics and nervines are to be preferred, but it is best to be chary in the use of these. The bromides are perhaps the least objectionable of the remedies given to tranquillize the nervous system and promote sleep, but their prolonged use is detrimental.

The most important part of the remedial treatment relates to the accelerated action of the heart. Cardiac sedatives are rationally indicated, and experience confirms their usefulness. All writers recommend digitalis in order to diminish the frequency of the heart's action. A difficulty pertaining to this drug is its liability to disturb the stomach, and the consequent necessity for discontinuing its use. It is proper to give it a fair trial. In my experience aconite has proved more satisfactory. In a case already referred to two grains of reduced iron and one minim of the tincture of aconite constituted the medicinal treatment. These remedies, without any increase of dose, were continued for three years. At the end of this period the patient was in excellent health and had gained in weight forty pounds; slight exophthalmia and goitre only remained. In another case the treatment consisted exclusively of the tincture of aconite in doses gradually increased to seven minims three times daily. Chalybeates were not given in this case, because the patient was not anæmic. The remedy was continued most of the time for two years. The recovery is complete except that the heart is irritable and moderate prominence of the eyeballs remains. The treatment has been discontinued in this case for the past two years. Of veratrum and gelsemium as cardiac sedatives, which have been recommended in this affection, I have no practical knowledge. In paroxysms of unusual violence of the heart's action German writers recommend the application of cold to the præcordia by means of the ice-bag.

Galvanization of the sympathetic is strongly advocated by German writers—namely, Eulenburg, Dusch, Guttmann, Von Chvostok, Meyer, Leube—and in this country by Bartholow and others, as not only useful, but sometimes effecting a cure. The following extract from a treatise by Bartholow embraces rules for the employment of this therapeutic agent: "Recent cases treated efficiently by galvanism are relieved permanently or their course and progress much modified. During exacerbations, which constitute a prominent feature of the clinical history, the passage of a sufficient galvanic current through the pneumogastric immediately lessens the cardiac excitement. In the treatment for curative results a mild current is held to be most efficient (Chvostok). An electrode—the anode—is placed in the angle behind the jaw, and the cathode on the epigastrium, and a stabile current is allowed to flow for three to five minutes. The cervical spine should also be galvanized. It may be included in a circuit by placing the anode over the vertebræ in turn whilst the cathode rests on the epigastrium. Stabile may be varied by labile applications. The faradic current may be used successfully. An instance of this kind has come under my notice. The first published cases illustrating the curative value of galvanism were those of Chvostok (1871), who followed with a series of examples the next year, when Meyer also reported several cases. In 1874, I read a paper before the medical section of the American Medical Association advocating this plan of treatment, and illustrated its advantages by the details of five cases. In 1878, Vizioli, in a paper on electropathy, amongst others narrated several cases of Basedow's disease cured. In making the claim for the curative power for electricity the reader should understand that uncomplicated cases only are referred to."¹⁰ Rosenthal gives the following directions: "The ascending stabile galvanic current, from one to ten elements, is passed through the cervical sympathetic (the anode in the mastoid fossa and the cathode upon the upper cervical ganglion) for eight to ten minutes at a time. The current is also directed transversely across the thyroid tumor, or an ascending current may be applied to the cervical and upper dorsal vertebræ."¹¹ Guttmann states that temporary reduction of the frequency of the heart's action is first produced, but by persisting in the electrical treatment the reduction becomes permanent, together with progressive improvement as regards the exophthalmia and the thyroid enlargement.¹²

¹⁰ Medical Electricity, by Roberts Bartholow, M.D., LL.D., etc., Philadelphia, 1881.

¹¹ Clinical Treatise on the Diseases of the Nervous System, by M. Rosenthal, translated by L. Putzel, M.D., New York, 1878.

¹² Vide article entitled "Basedowsche Krankheit," in Real-Encyclopedie, Wien and Leipzig, 1880.

DISEASES OF THE PERICARDIUM.

BY J. M. DACOSTA, M.D., LL.D.

Pericarditis.

The diseases of the pericardium, with a few exceptions, belong to the inflammatory variety, and, as a rule, are the consequences or accompaniments of other inflammatory diseases of the circulatory system or of parts near the heart. The most common of the pericardial affections is pericarditis, which may be simple or secondary, and acute or chronic.

Pericarditis may occur upon either the visceral or the parietal layer of the membrane, and may attack any portion or several or all parts at the same time, being thus circumscribed or general. Usually, the whole or a large part of the pericardium is affected. Pericarditis is further characterized by effusions or exudations, which may be either fluid or semi-solid, and in consequence of the varied character of these exudations subdivisions are often made, such as the serous, fibrinous, sero-fibrinous, purulent, sero-purulent, and hemorrhagic forms. Pericarditis is generally marked by an effusion of fluid, the exception being designated as dry pericarditis, in which serum or other thin exuded material is almost or entirely absent.

Simple acute or idiopathic pericarditis is comparatively rare, and some authorities doubt its existence, believing that the pericardial inflammation is always secondary, plausibly supposing that the primary affection has escaped detection. Bamberger and Hayden, for instance, are of this opinion. I am, however, certain that I have met with several instances of true acute idiopathic pericarditis. Cases of so-called simple pericarditis are really often due to injury. It may not be easy in many cases to determine the traumatic or other condition in which the apparent simple acute pericarditis originated. The weight of evidence is so much in favor of traumatism as a preceding and efficient cause of simple acute pericarditis that a diligent search should always be made for the same. But even these doubtful examples are comparatively rare; and pericarditis is in the vast majority of instances secondary, and not difficult to identify as such. By some, traumatic pericarditis is classed with simple pericarditis as a variety, although not idiopathic.

Inflammation of the pericardium is governed by all the laws which control inflammatory processes elsewhere, being either acute, subacute, or chronic. The subacute form probably exists frequently, but escapes detection on account of the latency of the symptoms. The acute form is the most readily recognized. If not relieved, it passes into the chronic disease, which may be of long duration. The passage from one kind to the other is so gradual as to make it almost impossible to determine when one stops and the other begins, though it may be stated that after an acute attack has continued for from two to three weeks the chronic form is established. The chronic affection may begin, however, insidiously, or develop out of the subacute variety.

CAUSES.—The causes of pericarditis are numerous, and range from simple cold and injuries to the thorax to those diseases of which it becomes a companion, whether the seat be remote from, or in immediate juxtaposition to, the pericardium. Simple cold as a cause of pericarditis is, as has already been indicated, very much questioned. Though a very rare, I believe it a possible, cause. Other causes of simple pericarditis may be blows upon the breast, as with the fist; crushing or compression, as in railway accidents; penetrating wounds, as from gunshot or knife; and injury from foreign bodies in the oesophagus, such as pins, false teeth, etc. Buist¹ records a case of a man who swallowed a plate with artificial teeth attached. The plate, becoming lodged in the oesophagus, finally penetrated the pericardium posteriorly and produced fatal pericarditis. A similar case is recorded by Flint.²

¹ Charlestown Medical Journal and Review, Jan., 1858.

² Diseases of the Heart.

By far the most common form of pericarditis may be termed secondary, which, like simple pericarditis, may be divided into the acute and chronic forms. It is termed secondary or consecutive, because it follows as a result either of impoverishment of the system or a pre-existing disease, constitutional or local. There are, however, exceptions to this rule; for we meet with cases of secondary pericarditis in which pericarditis preceded the onset of, and then continued associated with, the other manifestations of the disease which determined it. We see this sometimes in the history of acute rheumatism.

The disease of the pericardium is often the result of contiguity, but is much oftener determined by constitutional causes. Why the pericardium should be the particular membrane selected to take on inflammation as a complication to other affections has baffled the best endeavors of the most careful inquirers to determine. The diseases affecting the pericardium by continuity or contiguity of texture are chiefly myocarditis, tubercle of the lung and mediastinal glands, cancer of the same structures, pleurisy, pneumonia, and cancer of the oesophagus. On fibroid disease of the heart pericarditis is a frequent attendant.³ The diseases affecting the pericardium by a special election, and which are remote from the membrane, are, principally, acute articular rheumatism, Bright's disease, inflammation and other diseases of the liver, phlebitis, typhus, typhoid and eruptive fevers, scurvy, and acute alcoholism. Without doubt, by far the most frequent cause of pericarditis is acute articular rheumatism. Pericarditis does not occur in chronic rheumatism, and it is doubtful whether it may be occasioned by gout, notwithstanding the decided and weighty opinion of Hayden that this is an efficient cause.

³ It was found in more than half the cases published by Fagge in Transactions of the Path. Soc. of London, vol. xxv.

Acute pericarditis resulting from acute articular rheumatism has some peculiarities which it is well to bear in mind. It comes on early in the disease. We also know of its great frequency as a result of rheumatism, although the rheumatism be mild; for the intensity of the rheumatic inflammation is no measure of the extent or severity of the pericarditis. Nor does the number of joints involved nor their location give any idea of the greater or lesser liability of the pericardium to participate in the inflammatory action. Neither does the frequency of the rheumatic attacks bear any direct relation to the pericardial involvement; although experience has shown that the first attack usually is the one most likely to be the cause of pericarditis, while succeeding ones may or may not produce fresh seizures of pericarditis, or an aggravation of the disease where it has remained as the result of previous attacks of rheumatism.

Clinical literature is notably deficient in the reports of pericarditis ending in recovery, while the recorded cases of death from the disease as verified by autopsies are most numerous. Yet, although pericarditis is a serious malady, it is not commonly fatal; and this is especially true of the pericarditis of acute rheumatism. But it is a frequent disorder. Sibson,⁴ with large experience and patient observation, has collected and tabulated facts from many sources. In that particular variety of pericarditis which is the accompaniment of acute articular rheumatism he found that in 326 cases of acute rheumatism admitted into St. Mary's Hospital, about one-fifth of the cases (63) had pericarditis, which was accompanied in 54 cases by endocarditis; and only in one-fourth of the whole number (79) was there neither pericarditis nor endocarditis. One-third of the whole number of cases (108) had endocarditis, and a fourth (76) had threatened endocarditis, the signs being transient or imperfect. It is notable that the majority of the cases, regardless of sex and occupation, occurred prior to the twenty-fifth year of age; and what is equally notable is that the severity both of the joint and the heart affections was greatest at or before the same year. Of the 63 cases of pericarditis in rheumatism, there were 35 males and 18 females; of these, 11 males and 14 females were from sixteen to twenty years of age, and the fatal cases were all under the twentieth year.

⁴ Reynolds's System of Medicine, vol. iv.

Pericarditis happens most frequently between the first and second weeks of acute rheumatism, although there are instances in which it occurs later, and occasionally it follows a sudden subsidence of the disease. It may be observed coincident with the onset of the rheumatic attack, and even preceding it by several hours. Latham has pointed out how acute pericarditis is more to be looked for when acute rheumatism is shifting and inconstant in its seat than when it is fixed and abiding.

Having now looked at rheumatic pericarditis, we may examine the pericarditis of some other disorders. In that class of affections known as Bright's disease of the kidney the serous membranes are liable to take on inflammatory action. A particular preference for the pericardium seems to exist, and the affections are the cause of pericarditis next in frequency to acute rheumatism. The tendency varies, however, with the particular kind of disease of the kidney which may be present. Pericarditis is common in the contracted kidney; in amyloid degeneration it is rare.⁵ Where uræmia happens, it is apt to be developed. In warm climates it is less usual as an accompaniment than it is in cold and damp. But whether this be the full explanation of the varying frequency of pericarditis as an attendant upon Bright's disease in different countries is doubtful. There is, however, certainly, as we learn from the elaborate inquiry of Sibson, a varying ratio. The complication is, he proves, more frequent in Germany than in England, least frequent in France.

⁵ Ziemssen's Cyclopædia, vol. xv. p. 629.

Let us now take into consideration other diseases which in their course have strong, although less-marked, tendencies to involve the pericardium. As a class, the eruptive fevers, especially scarlet fever, may present a pericardial lesion. This is owing to the fact that the serous membranes generally are liable to become inflamed in these conditions; but another element in the production of acute pericarditis may probably be found in the congestion of the kidneys which is apt to occur. Pericarditis is not commonly present early in these diseases, but rather in their later stages, when the body is enfeebled by the specific poison and the skin is susceptible to the slightest variation of temperature. It is then that the weakest and most vulnerable part will be attacked, and the pericardium may prove to be the most vulnerable part.

Other diseases which will cause pericarditis are those dependent upon dyscrasia of the blood, as in the diatheses, injuries attended by shock, and those conditions in which there is a great drain from the system. Perhaps the diathesis most apt to induce pericardial inflammation is the scorbutic, in which the impoverished and relaxed state of the system frequently manifests itself by inflammatory lesions of a low grade. In injuries or diseases where there is excessive suppuration the system is so weakened that a low form of pericarditis is prone to develop itself. Diseases of the respiratory organs, as phthisis, pneumonia, or pleurisy, also enteric inflammations, will sometimes produce pericarditis. Indeed, any disease dependent upon or attended by a greatly deteriorated condition of the blood may cause pericarditis; for the health of the heart itself is determined by the quality of the vital fluid from which it draws its own sustenance in common with all other structures of the body, and any vitiated state of the blood seems to make a special impression upon the heart itself, its membranes as well as its structure.

MORBID ANATOMY.—In acute pericarditis the serous membrane first becomes injected with blood, and the injection, starting at a single or at several points, may become diffuse. If the engorged vessels do not relieve themselves, infiltration of lymph into the transparent serous layer follows, producing thickening and opacity as well as slight roughness. Consequent upon this there is further congestion, the membrane becomes red, with possibly here and there points of inflammation of greater intensity than that surrounding the original lesion; and at these places the vessels may give way and cause a hemorrhage into the sac or there are little spots of ecchymosis in the membrane. Usually there is a drying up or a partial suspension of the serous secretion from the turgid membrane, but before long the secretion generally recurs, and is even increased in quantity. Upon the surface of the serous membrane patches of coagulable lymph, more or less extended, are at the same time exuded. Under the microscope the bundle of fibres of connective tissue of the membrane appear swollen and broken up, and the proliferation starts which, as it progresses, determines the new growth and the villosities. Portions of the exuded lymph may be washed off and be found as shreds in the serum. The appearance of the lymphous deposit, as just indicated, is not always that of a plain smooth layer, but may be velvety and villous, like the lining of the small intestine, or it may be more roughened, or it may be honeycombed, as the interior of the stomach of the calf, or be in ragged shreds of varying sizes, either single or in bunches. Again, it may assume a lace-like texture, as of fibres coarsely woven together, or it may appear as if the threads were attached at one end to the pericardium and at the other floating free. All of these various forms are largely due to the heart, which in its action presses and rubs the lymph-covered surfaces together and keeps the softish exudation in constant agitation. One layer of lymph may be superimposed upon another until the deposit becomes very thick. It is this lymph which, existing before fluid is effused to any extent, determines what clinicians recognize as the dry or plastic stage of pericarditis.

Generally, however, there is effusion of considerable liquid, occasioning what is termed the stage of effusion. The fluid poured out is serous, alkaline, and albuminous, of a pale-yellow color, and transparent, but it may be opaque and milky. It may have flocculi floating in it, be stained any shade of color from red to brown by the coloring matter of the blood or by exuded blood-corpuscles, and may also contain pus. The quantity of fluid varies from a few ounces to several pints, but the latter amount is rare. The fluid is usually composed of the watery and saline elements of the blood, with a small quantity of albumen and a trace of fibrin. If the amount of fluid be small, the opposing surfaces of the pericardium come together, and the lymphous layer, becoming more or less organized by the presence of blood-vessels in it, makes attachments to the opposite wall; in this manner adherent pericardium is produced. The adhesion may vary in extent from the slightest filamentous attachment to complete obliteration of the pericardial sac; and it may be readily peeled off, or it may be so closely united as to become a part of the tissue upon which it lies. As the disease progresses the serum and, in exceptional cases, the fibrinous deposits may be entirely reabsorbed and leave but little evidence of the previous inflammation. The white milky-looking spots often found in autopsies are regarded by many as the remains of cured pericarditis, but they are more likely the result of nutritive changes and consequent tissue-alteration. Fibrinous deposits are not always entirely removed. In complete adhesion of the pericardium they may be considerably reduced, but the sac never regains its normal appearance, and when the adhesions are partial they remain permanently.

The formation, density, and organization of the lymph depends largely upon the cause of the pericarditis. The more acute the attack and the greater the constitutional disturbance, the more likelihood there is of rapid effusion of lymph and of its speedy organization, whether it form adhesions or not. Where the fibrin is exuded under the influence of a subacute or chronic disease, the formation will be slow, paler, less highly organized, softer, and if adhesions form they will be less strong.

The heart participates in the inflammation of the pericardium, and if it be for any time subjected to the presence of the fluid effusion its walls degenerate and a granular atrophy occurs. Besides this, in extensive and firm adhesions there is likely to be primary hypertrophy followed by dilatation, the walls being enfeebled by degeneration, and, it may be, becoming thinner. At first, the effort to overcome the pressure of the pericardial effusion produces the hypertrophy; then the more or less complete binding down of the walls of the heart, preventing complete systole and weakening their inherent elasticity, and the pressure upon the coronary vessels, depriving the heart of the blood necessary for its healthful existence, are the causes of the degeneration and wasting of the walls and of the dilatation of the cavities.

Pus in the pericardium, as a result of pericarditis, may appear very early in the inflammatory attack, or it may occur after the effusion of lymph and serum. It may happen but in small amounts smeared over the surface of the membrane, or be profuse in quantity. Pus may also arise from small abscesses in the tissue of the heart bursting through the pericardium. It may be the result of injuries to the pericardium or to the inflamed membrane, or it may originate in the migration and proliferation of the leucocytes of the blood. The microscope in doubtful cases gives us the best idea of their prevalence and quantity, as well as of the amount of blood-corpuscles present. Where pus alone exists it is yellow and creamy; but with an excess of serum or fibrin it may be thinner or thicker in consistence, the entire heart being bathed in the fluid.

The lesions of chronic pericarditis differ but little from the acute, except as to their inception or the initial stage. The change from the acute to the chronic form may occur in a very few days, or even in less time, and an autopsy would not reveal anything to determine the fact. Pericarditis in any form is apt to be associated with pleurisy, and adhesions between the pericardium and adjacent pleura are common. In some instances the distended sac is adherent to the back of the chest. By its pressure on the lung and the oesophagus it may produce secondary lesions in them as well as in the phrenic nerves.

SYMPTOMS.—The symptoms of pericarditis may be so slight as not to attract attention. Where they are noticeable we find pain or a sense of uneasiness or of pressure, with or without tenderness in the pericardial region. The pain or uneasiness is not infrequently accompanied by pain or tenderness in the epigastric region when pressure is made upon it. This arises from the contiguity of the part and the pressure of the diaphragm against the inflamed and tender pericardium. The pain is sometimes preceded by a chill of varying severity, and is followed by febrile symptoms of greater or less intensity; but these may be so slight as to escape observation altogether except by taking notice of the markings of the thermometer.

Yet the thermometric record, although indicative of fever, has nothing characteristic. It is, I think, more influenced by the conditions under which pericarditis happens than by the pericardial inflammation itself. Often the fever-curve is marked by decided remissions, and as the result of the pericarditis alone does not attain a high degree. In the aged, Charcot has pointed out that the temperature of the body is lowered in some instances of acute pericarditis. The setting in of pericarditis in acute rheumatism was observed by Lorain to depress the thermometric marking, and Brouardel has noted the same effect at the onset of pericarditis in typhoid fever.⁶

⁶ Constantin Paul, Maladies du Coeur, Paris, 1883, p. 130.

The action of the heart is increased in frequency and force, as indicated by observing the impulse and the pulse at the wrist. There may be present, in different degrees, difficulty of breathing or a sense of suffocation; difficulty in swallowing; also cerebral disturbance, as headache, dizziness, sleeplessness, mental depression, fear of impending death. Besides these we may meet with hiccough and nausea and vomiting. But any or all these symptoms may also occur in myocarditis and in endocarditis, and are therefore not of themselves diagnostic; they only serve as indicators of the direction in which to seek the cause of disturbance. Some of the latter symptoms may be so aggravated, particularly those manifested by the nervous system, that attention is absolutely diverted from the seat of the disease. Indeed, they are often very misleading; and I cannot even agree to Hayden's statement⁷ that with few exceptions the symptoms of pericarditis take precedence of the physical signs, though they cannot be regarded as sufficiently distinctive to warrant a positive diagnosis. Doubtless these symptoms, however suggestive of pericarditis, may be found to depend upon other causes. With so little, then, of a positive nature to assist us in our search, we should be always at great loss were it not for the physical signs.

⁷ Diseases of the Heart and Aorta.

PHYSICAL SIGNS.—The chief of these are determined by inspection of the chest, by palpation, by auscultation, and by percussion.

Inspection.—In inspection of the chest the age of the patient is to be regarded in the interpretation of the appearances. In pericarditis with effusion we are apt to find a change in the shape of the chest—a bulging in the region of the heart, even though the effusion be somewhat small in quantity. This change is more apparent when it occurs in young persons, where the chest-walls are very elastic. In those advanced in years, in whom the costal cartilages are more or less ossified and the elasticity of the rib materially altered, or where the chest-walls are bound down by pleuritic adhesions, the shape of the chest may be materially altered and yet not be very apparent. The intercostal distension is in any case a matter for investigation. The chest shows a bulging in the pericardial region, slightly diminished by a dorsal decubitus and but little influenced by the acts of respiration.

Palpation.—This gives us an idea of the amount and outline of the tenderness, which is often found to correspond with that of the inflamed pericardium. It also enables us to determine to some extent the limit of distension of the pericardium, the location of the heart, and the shape of the sac. We also ascertain the impulse of the heart. Now, at first this is somewhat increased, although it is apt to be irregular. As effusion of liquid takes place, the heart is displaced generally backward and upward, and the impulse becomes indistinct or imperceptible. A slight wavy, irregular motion diffused over considerable part of the cardiac region may take its place.

Percussion.—During the dry stage, unless a very considerable amount of lymph be extravasated, the natural percussion dulness in the cardiac region is not appreciably altered. When the pericardium becomes distended with fluid the cardiac dulness increases markedly, particularly in a transverse manner; and as the pericardium is conoidal in shape, but its position the reverse of that of the heart, its base resting upon the diaphragm, with its distension a roughly pyramidal outline of dulness is found, the apex being near the root of the vessels, the base upon the diaphragm. A great deal of stress has been laid on this shape of the percussion dulness—much more, I think, than in point of fact is warranted, for it is not always to be distinctly made out. Rotch⁸ has called attention to the dulness being early manifest in the fifth intercostal space of the right side, and in all large effusions it is sure to extend across the sternum. It may, when the sac is much distended, reach as high as the first rib, as low as the seventh rib, and below the ensiform cartilage, and the line of the lower dulness may become continuous with that of the displaced liver. The dulness may extend on the left side backward almost to the spinal column and across the sternum to the right nipple. The dulness is somewhat influenced by position; changing from side to side alters the line of the fluid.

⁸ Boston Medical and Surgical Journal, 1878, vol. xcix.

Auscultation.—Pericarditis is not discoverable without the signs by auscultation, and it is the interpretation of these signs which enables us to distinguish the various stages. We must bear in mind that, roughly speaking, there is first a stage of suspension of the serous secretion, and consequent dryness of the pericardium; secondly, effusion of lymph or fibrin; thirdly, effusion of serum or sero-pus. Now, the question arises whether we can distinguish the first effect of the inflammation on the serous membrane, which, indeed, may be exceedingly short in duration, limited to a few hours. From the fact of there being a suspension of secretion and absorption of that which has been normally secreted, it becomes evident that, the parietal pericardium coming into direct contact with the visceral layer, certain sounds will be caused by the friction of the heart in its action. Can we discern them? Great differences of opinion have been expressed with reference to this; indeed, it has even been questioned whether sounds would be or would not be produced. Stokes doubted the competency of simple dryness of the pericardium to generate friction phenomena. Collin, on the contrary, held that this is actually the condition of the pericardium indicated by the new-leather sound. To this Walshe makes assent. Hayden⁹ says: "I have never met with a case which would warrant me in asserting that a state of simple dryness and vascularity of surface may give rise in the pericardium to veritable friction sound. I do not, however, deny the possibility of an occurrence which, theoretically, would seem not improbable. In every instance, without exception, in which I have had the advantage of determining by post-mortem examination of the body the condition of the serous surface of the pericardium, where friction sound of indubitable pericardial origin had existed during the patient's last illness, I have found lymph in greater or less quantity effused upon the surface." My own experience is entirely in accord with this. Theoretically, I grant the possibility. Practically, I have never seen it; and in the suspected cases lymph has always been found, with the single exception of a case in which the friction sound had disappeared nearly a week before death, which resulted from kidney lesion, and where it was reasonable to infer that the lymph had been absorbed.

⁹ Diseases of the Heart and Aorta, Philada., 1875, vol. i. p. 327.

The friction sound, then, is the sign of exudation. Since it was originally described by Stokes in 1833 it has been likened by different observers to familiar objects, such as the crackling of parchment and the new-leather sound. It is generally most evident at the base of the heart, is considerably influenced by pressure, is more often double than single, frequently resembles a double cardiac murmur, and justifies the name of a to-and-fro sound given to it by Watson. The friction sounds change from time to time according to the character, quantity, and stage of the exudation, ceasing altogether when adhesions have taken place or fluid has been effused, to return again as the fluid is absorbed, and to cease when recovery has taken place. They exhibit an inspiratory rhythm very much intensified by full inspiration. Although, as the place of election of the inflammation is at the base of the heart, we are apt to find the friction there earliest as well as longest, this is not invariable; for, as above stated, the morbid process may begin anywhere in the continuity of the pericardium.

Next to the friction sound, the most valuable signs in pericarditis are derived from the muffling of the cardiac sounds. This is particularly valuable in the stage of effusion, for prior, notwithstanding the friction phenomena are somewhat obscure, they do not render the sounds of the heart fainter to any material degree. The cardiac sounds become less and less distinct as the fluid increases. The heart sounds cease to be audible, just as is the case with the friction sound, from below upward, beginning to be indistinct at the apex of the heart. Gradually and lastly, the sounds of the aorta and pulmonary valves are lost, but not entirely, unless there be a large amount of fluid pushing up the pericardium at its attachment around the roots of the great vessels, and the second sound at these valves is scarcely ever wholly gone. Sudden effusions of large quantities of fluid are so rare that the progressive extinction of the cardiac sounds becomes an important element in diagnosis and prognosis. It has already been noted that the friction sounds linger around the base of the heart; this may happen with even considerable effusion. As regards the character of the fluid influencing the distinctness of the cardiac sounds, I think it may in general terms be stated that if the effusion be dense, sero-purulent, or purulent, the sounds of the heart are, in proportion to the size of the effusion, relatively more obscured than when this is thin.

DIAGNOSIS.—The diagnosis of pericarditis, as before remarked, cannot be determined by any but physical signs, and even these signs may not be sufficient for us to come at once to a positive conclusion: the refinement of perception necessary to detect and properly interpret the delicate changes which occur in some cases is still lacking to us. In reviewing the general diagnosis of pericarditis we must bear certain facts in mind. The acute malady has a very dissimilar origin. It usually sets in with a fever, ordinarily not of high grade, which may be preceded by a chill of differing intensity; the pulse is decidedly accelerated and of varying regularity, not uncommonly strikingly irregular; on the other hand, the nervous phenomena may be the most prominent. Craigie¹⁰ observed long ago in a case of pericardial inflammation in a girl of fourteen that the only prominent symptom besides the symptom of fever was constant tossing of the extremities and person, jactitation similar to the motions of the dance of St. Vitus. Roeser of Bartenstein observed the same symptom in a child of nine years. There is at times early delirium, very frequently considerable restlessness, with more or less of an anxious expression of countenance. Quickened rather laborious breathing is often early observed, and so is pain in the præcordial region directly under or near the sternum, perhaps extending to the left shoulder, acute, severe, and shooting, increased by pressure and motion, and, as Peter¹¹ has pointed out, associated with pain in the phrenic nerve, elicited by pressure between the two insertions of the sterno-mastoid and also found on each side of the xiphoid appendix. But the pulse may be regular, the breathing not perceptibly accelerated or laborious, and even the important symptom, pain, may be wanting from the beginning to the end of the disease. This occurs in the so-called latent cases.

¹⁰ Elements of the Practice of Physic, Edinburgh, 1837, vol. ii. p. 151.

¹¹ Clinique Médicale.

Since pericarditis is frequently attendant upon certain classes of diseases, as acute articular rheumatism, Bright's disease of the kidneys, the eruptive fevers, it behooves the physician to be on the alert and examine the heart, even though nothing point to its involvement. Reminded of this fact, we must seek for those signs which will enable us to diagnosticate early the cardiac disease. And in any case the first sign of importance detected will be, in all probability, the friction sound, generally, but not invariably, first heard at the base, and prone to mask the natural sounds of the heart. At all events, this is the case when the friction sound is localized at the apex of the heart, as it occasionally is, before there is very marked development of the lymph-deposit; it is then, too, that from its softness the friction may be mistaken for a regurgitant mitral murmur. The friction may at times be felt by applying the hand to the region of the heart. This friction fremitus is, however, far from constant, and can hardly be considered of much diagnostic value, notwithstanding the high authority of Stokes, who looked upon it as distinguishing pericarditis from valvular disease. Prior to the existence of the friction sound we may suspect pericarditis by the sense of general distress and the dropping of pulse-beats or the otherwise altered cardiac rhythm. But the diagnosis is presumptive; the friction phenomena make it positive. Until the quantity of fluid is sufficient to separate the two walls of the sac the rubbing sound will be apparent. The friction sound never disappears suddenly, and this gradual disappearance points to the formation of fluid and may be regarded as a truly diagnostic sign. The fluid, following the laws of gravitation, seeks the most dependent portion of the sac, which it more or less fully distends; in consequence, the disappearance of the friction begins at the bottom of the sac and at the apex of the heart and gradually extends upward to the base. Adhesions of the pericardium will modify and may entirely prevent the formation of the friction sounds. If the adhesions be local, and if no lymph-deposit be present between them, there can be no friction; so also where the adhesion is general the friction sound is destroyed. Where local adhesions and portions of free surface more or less covered by the lymph exist, the heart, being allowed sufficient motion, produces friction sounds which may be found anywhere over its surface except at the points of adhesion. From the character of these sounds the location and the extent of the adhesions and of the cardiac movements may be determined, for "the rhythm of the pericardial friction sound is as the natural movement of the portion of the heart engaged and the mobility of the opposed surfaces," says Hayden¹² very truly.

¹² Diseases of the Heart and Aorta.

In weighing the value of friction sounds in diagnosis, especially in determining whether they are produced in the pericardium and not in the adjacent pleura, we have the simple, though not infallible, method of discrimination of letting the patient cease breathing for a moment and then ausculting the heart: they persist if pericardial. This test will fail, however, in case a portion of the pleura adjacent to the pericardium also be covered with lymph: then the heart's motion, transmitted through the pericardium, may produce pleuritic friction even while the lung is at rest. In such a case if a friction fremitus be felt it will pass beyond the cardiac area, while in pericarditis without associated pleurisy it will not be likely to extend farther than the normal limit of cardiac dulness. The pericardial friction sound may be sometimes noticed more or less extensively over the whole chest in children, and also in adults with hypertrophy of the heart, but this is far from being usual. There may be a friction sound produced by the action of the normal heart in an inflamed roughened pleura. This is very difficult to distinguish except by the attending symptoms. The sound is perceived near the apex of the heart. It is not apt to occur with each beat of the heart, and may be absent in held expiration.

In the diagnosis of pericardial effusion, when at all extensive, we have, in judging of the amount of fluid in the pericardium, to take into account the increasing dyspnoea with a decided suffocative tendency, the dizziness, the pallor or lividity of the countenance, the swollen cervical veins, the bluish nails, the heart flutterings, the weak, rapid, and irregular pulse, the drowsiness or tendency to mental wandering. But the physical signs of the effusion above detailed are of the greatest value, although they give us but little information as to the character of the fluid. Even in large effusions the friction sound may not disappear from the base. Indeed, Balfour¹³ records as the result of his observation that "however large may be the effusion, basic friction, if it have once existed, is never effaced." It is stated that when the amount of fluid does not entirely fill the pericardium there may be a splashing sound, and the location of the sound, as well as that of the percussion dulness, will be changed by changing the position of the patient's body. I have never observed this splashing sound. The extent of percussion dulness is no absolute sign of the extent of effusion. The area of cardiac dulness may be materially influenced by the following circumstances: the anterior margins of the lungs which overlap the front of the heart may, from emphysema, give rise to percussion resonance over the heart, even though considerable effusion have taken place; the anterior margin of the lungs, becoming solidified and having strong pleuritic attachments to the pericardium and anterior chest-wall, may increase the dulness over the heart and prevent the recognition of the effusion in the pericardium; effusion in the pleural cavity of one or both sides may produce similar results. Balfour¹⁴ in fact mentions a case of his own in which the pericardial dulness was merged in the pleuritic dulness, and careful auscultation failed at any time to detect friction sound; the coexistence of pericarditis was surmised, but could not be detected. After death the pericardium was found to be distended with reddish serum, and both its surfaces were coated with shaggy, blood-stained lymph. Such cases are unusual, yet I have met with a similar instance. Lastly, a growth in the anterior mediastinum may be the means of masking or being mistaken for pericardial effusion by changing the dulness in the cardiac region and altering the cardiac sounds, or it may, by obstructing the circulation, cause effusion. When an effusion of fluid takes place into a partially adherent pericardium, the area of cardiac dulness may be irregular or restricted, or both, the shape and size depending on the length and strength of the adhesions.

¹³ Diseases of the Heart.

¹⁴ Ibid.

Some of the results of large effusions show themselves on other organs. The backward pressure of the fluid upon the bronchi, trachea, aorta, and oesophagus interferes with their functions and actions. There may be bronchial or blowing respiration heard over the lung, due to compression of the parenchyma. The fluid around the heart prevents free motion of the organ, although not to so great an extent as in adherent pericardium; complete diastole does not occur; the auricles and ventricles are not completely filled; the systemic and pulmonary circulations become engorged, and pressure is exerted upon the coronary arteries, thus disturbing the nutrition of the heart. The irregular action of the heart occasions at times a vibration which is more or less apparent to the touch. Percussion of the liver shows enlargement of the viscus; this is due to the obstruction of the ascending vena cava, which prevents a free emptying of its blood into the right auricle, and consequently causes a backing up of the blood in the gland. If the pericardial effusion press upon the anterior portion of the chest, it may produce pain and aggravate all the other symptoms, such as the pulmonary oppression, the dizziness, the hurried respiration, the increase of pulse. Water, blood, or pus in the pericardial sac gives rise to the same physical signs as serous effusion, and cannot be distinguished from it with any degree of certainty, although a careful consideration of the general symptoms presented may enable us to make a guess which can only be proved or disproved by an autopsy.

Having endeavored to show the most prominent features characterizing pericarditis in its various stages and bearing in a general way on its diagnosis, we shall examine some of the special maladies which are liable to be confounded with it. The diseases most likely to be mistaken for the acute inflammatory stage of pericarditis are inflammation of the pleura and of the endocardium. They are liable to occur from the same causes, and may be—indeed, often are—concurrent. Pleurisy gives rise to many of the symptoms of pericarditis. The chief difference is in the physical signs, some of which, however, are alike in kind, although different in locality; for in pericarditis they are confined to the region of the heart: in pleurisy they are spread over the whole side of the chest and are most perceptible at the back. This is true of the dulness, and for the most part of the friction sound, which when of pericardial origin is very rarely heard posteriorly. Then stopping the act of breathing if the sound be pleural suspends it. At times, however, as above described, we meet with cases in which a friction sound discovered over the heart may in reality be produced in the adjoining pleura. To confound the dulness on percussion caused by liquid in the pericardium with that due to liquid in the pleura is, from the different site of the liquid, not likely to happen unless the effusion be extremely large; for ordinarily a pericarditis uncomplicated with pleurisy or with pleuro-pneumonia does not change the clear sound at the back of the chest nor enfeeble or abolish there the breath sounds and the vocal fremitus. Besides, effusion into the pleura, if it give rise to a flat sound anteriorly, does not occasion the special præcordial bulging, and shows the sounds of the heart unaltered unless the pericardium contain fluid also.

Acute pericarditis is likely to be confounded with acute endocarditis. The chief difference consists in the physical signs—the friction sounds and signs of effusion in pericarditis, the blowing sounds, the slight alteration of percussion dulness in endocarditis, and the fact that in this disease the abnormal murmurs are often transmitted beyond the cardiac region and heard in the carotids and subclavian, and are far less changeable in character and in pitch.

There are other affections with which pericarditis is likely to be confounded, such as gastric irritation and acute inflammation of the brain. When pericarditis resembles gastric disorder the thoracic symptoms may be latent, but the disease produce the manifestations of extreme gastric irritation or inflammation. There are nausea and vomiting, and tenderness on pressure in the epigastric region, yet no disease of the stomach may be present. An examination of the cardiac region for the physical signs of pericarditis should be made in every case of persistent vomiting or of hiccough.

Where the symptoms are chiefly cerebral, the cardiac disease may be overlooked; indeed, in both endocarditis and pericarditis the insomnia and the active delirium may throw all the other symptoms into the shade. The violent disturbance of the brain may have its origin, in part at least, in the contaminated state of the blood which occurs in the affections, as rheumatism or Bright's disease, with which pericarditis is often associated. But it is possible also that it may be due to a coexisting endocarditis of which the products are washed into the brain. In ulcerative endocarditis cerebral manifestations are especially common, and there may be acute mania of the most violent type, as in the case reported by Sioli.¹⁵ Sibson in his exhaustive analysis points out what I have known to happen in more than one instance, that the desponding and taciturn—or, as he calls it, sombre—delirium of pericarditis lasts from two to three weeks to as many months. Indeed, it may terminate in confirmed insanity. Any form of nervous disturbance having its centre of disorder in the cerebro-spinal axis and of any degree of intensity may be seen in cases of pericarditis, whether produced as a consequence of rheumatism, of albuminuria, or by other causes. The cases with marked nervous symptoms are apt to present high temperature, 105° or more.

¹⁵ Archiv für Psychiatrie, Bd. x.

The diagnosis of pericarditis from hypertrophy of the heart is made by remembering that in pericarditis we find friction sound, præcordial bulging, peculiar enlargement of percussion area, enfeebled impulse and heart sounds, besides the presence of pain, of fever, of dyspnoea. In hypertrophy the area of percussion dulness is enlarged, but the shape is normal; the impulse and heart sounds are strong; no pain or fever, no friction sounds exist. The chance of mistaking dilatation of the heart for pericarditis is much greater. In the early stage of pericarditis the area of percussion dulness is generally similar in size and shape to the dulness in dilatation. But soon the difference both in size and shape of the cardiac area becomes marked, the shape being pyramidal or pyriform in pericardial effusion, while in dilatation the increase is lateral and does not extend beyond the point of impulse. There is no friction sound in dilatation; and if the first sound be weakened, though it may be also sharp and short, the second sound is everywhere distinct, unlike the muffling of the cardiac sounds, except at the base, in pericardial effusion.

Tumor of the anterior mediastinum, whether solid or fluid, may become a source of perplexity in determining the diagnosis of pericarditis; for by the interposition of the morbid mass between the chest-wall and the heart the cardiac dulness is increased and the heart sounds are lessened in distinctness and perhaps in force; though if the tumor be solid and very dense the sounds may be intensified. Pericarditis may also be associated with a tumor, and a diagnosis under such circumstances is attended with great difficulty. A tumor of the anterior mediastinum is comparatively rare, and seems to be more frequent in females than in males, although the statistics are meagre and not conclusive. There may be displacement of the heart in any direction as the result of pressure from the growth. Should this be equable in front of the heart, the diagnosis becomes one of doubt, for the same alteration of the shape of the chest may be present as in pericarditis with effusion. If the tumor be malignant or scrofulous, tumors of a similar character may be found in the neck, axilla, or elsewhere, and aid us in arriving at a correct conclusion.

The differential diagnosis of pericarditis from inflammation of the anterior mediastinum will cause at times no slight difficulty. However, inflammation of the anterior mediastinum is infrequent. It may come on without assignable cause or as the result of injuries. It may be produced by extension of inflammation from adjacent parts, as in pericarditis; it does not appear in association with, or as a consequence of, other diseases, such as rheumatism, renal diseases, scurvy, or the exanthemata, as is so largely the case with pericarditis. The symptoms resemble those of pericarditis, and there is likely to be chill, followed by fever, substernal pain and weight, pain on pressure over the sternum, accelerated action of the heart. Respiration is more or less difficult and painful, on account of the movements of the cartilages and intercostal muscles. The disorder in respiration becomes the more decided when the inflammation has extended to the pleura; there is also pain on pressure in the epigastrium. The physical signs of mediastinitis may be precisely similar to those of pericarditis. The extension of the inflammation to the adjacent parts produces the characteristics of uncomplicated inflammation of these parts, and under such circumstances the distinction is far from being easily made; the pleuritic and pericardial friction sounds which are developed will naturally be ascribed to affections of the pleura and pericardium alone. In accumulation of pus in the mediastinum no little uncertainty will exist in determining the difference between this and pericardial effusion. The percussion dulness may extend beyond the area of the heart, and take the form of the area in effusion into the pericardial sac. It is true, however, that in purulent collections in the mediastinum the shape of the percussion dulness is often more elongated, extending upward to the sterno-clavicular articulation. Should the accumulation be large, we meet with difficulty of respiration and of deglutition from pressure, as in pericarditis with effusion or in hydropericardium; and there may be elevation of the sternum and intercostal bulging. Abscess of the mediastinum tends to point at an intercostal space; it may also do so in the scrobiculus cordis: the impulse of the heart is weakened or entirely lost and the heart sounds are distant and obscured. There is apt to be hectic, with headache, delirium, and syncope. In fact, there is no symptom of pericarditis or of hydropericardium which may not also be found in acute mediastinitis or in the accumulation of pus in the mediastinum. Where the inflammation can be traced to an injury, as a blow upon the sternum, or where there exists caries or necrosis of the sternum, the diagnosis is greatly facilitated. The inflammatory symptoms, while of all grades of intensity, are, as a rule, more intense in the forms of mediastinitis than in any of the acute stages of pericarditis. In cases of fibrinous mediastinitis associated with fibrinous or fibro-purulent pericarditis, Kussmaul has called attention to the diagnostic value of a pulse intermitting at regular intervals simultaneously with inspiration, the pulsus paradoxicus.

PROGNOSIS.—The prognosis of pericarditis is exceedingly variable, depending largely upon the primary cause, the intensity, the stage and duration of the attack, the prior condition of the individual, and his surroundings. The general prognosis is favorable to life: though some of the older writers were disposed to look upon it as a highly dangerous disease, it is clearly one from which recovery is frequent. In many autopsies of individuals who have subsequently died of other disease the evidences of cured pericarditis have been found. By cured it is not wished to convey the idea that the pericardium was restored to the condition it was in prior to the inflammatory attack, but that the inflammation had ceased without injurious consequences. There may be recurrent attacks, and they are frequently of a subacute character; even when fibrinous deposit and attachments continue to exist, it often happens that the movement and functions of the heart are not interfered with. Unless the disease be exceedingly severe in the acute stage, the prognosis is decidedly favorable. When the attack is very severe there are strong reasons for believing that the structure of the heart is also involved, and death ensues chiefly from the latter complication.

Should adhesions take place, the prognosis is unfavorable in proportion to their extent, though to this rule there are decided exceptions. If effusion rapidly develop, the prognosis becomes at once unfavorable, death resulting in a short time from sudden pressure upon the heart and its palsy. If, however, the effusion accumulate slowly, the parts become tolerant, and a large amount of fluid may be thrown out without fatal consequences. Where death occurs it usually comes on slowly, and the immediate cause is from the pressure of the large effusion upon the heart, preventing its free diastole. The lungs become engorged with venous blood, and asphyxia of the heart ensues. There is apt to be general dropsy in such cases, particularly oedema of the lower limbs and accumulation of fluid in the serous cavities, as in the pleuræ, and the patient becomes gradually exhausted. If effusion of serum be accompanied by pus or by blood, or if there be pericarditis with pus or blood alone, the prognosis is unfavorable. Balfour,¹⁶ however, states that recovery is not impossible in purulent pericarditis, "for the elements of pus are more or less present in every pericarditis, and pus may be only a transitional stage, and may result in the breaking down of cell-elements, the formation of a pathological cream, and its complete absorption, and the perfect cure of the disease." The caseous formation, or even the pathological cream, is rarely met with, and cannot be detected prior to death. Burrows¹⁷ records a case in which there was a layer of concrete pus over a small space in a pericarditis of seven days' duration. Pericarditis with large amount of membrane, whether this be coated with pus or not, and even without liquid effusion into the sac, is always of grave prognosis; so are cases with high temperature, cases complicated with pneumonia, cases in which the dyspnoea is of intensity disproportionate to the local symptoms, and in which the pulse is not in unison with the impulse of the heart.