Chapter LIV: Part 54

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. Craigie[10] 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 Peter[11] 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.

[Footnote 10: _Elements of the Practice of Physic_, Edinburgh, 1837, vol. ii. p. 151.]

[Footnote 11: _Clinique Médicale_.]

Since pericarditis is frequently attendant upon certain classes of diseases, {777} 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 Hayden[12] very truly.

[Footnote 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.

{778} 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, Balfour[13] 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. Balfour[14] 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.

[Footnote 13: _Diseases of the Heart_.]

[Footnote 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 {779} 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 {780} 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.

[Footnote 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 {781} 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 {782} 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. Burrows[17] 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.

[Footnote 16: _Diseases of the Heart_, 1876, p. 299.]

[Footnote 17: _Disorders of the Cerebral Circulation_, London, 1846, p. 187.]

The pathological changes in pericarditis are such that it is quite impossible to determine by the special signs or symptoms of the affection between simple pericarditis and a pericarditis the result of transmission from diseases in adjacent organs, as pleurisy or pneumonia, or as a complication of rheumatism or Bright's disease, except by the history and the general features of the case. Yet the prognosis is vastly different. The prognosis of simple pericarditis without carditis is good. Pericarditis in acute articular rheumatism is generally favorable as to life, and is nearly as favorable as simple pericarditis. Balfour[18] states that he has records of 1968 cases of disease treated in the Royal Infirmary, 70 of which were cases of acute rheumatism, with but 1 fatal case of rheumatic pericarditis. My general experience of the favorable character of rheumatic pericarditis without marked involvement of the deeper structures of the heart corresponds with this. I except, however, the comparatively rare cases with high temperature. A temperature of 105° is always grave. The prognosis of pericarditis in Bright's disease is, speaking in general terms, as unfavorable as that of the pericarditis of acute rheumatism is favorable. The pericarditis of poisons, of pyæmia, or of scurvy is, as a rule, a very serious malady. In the exanthemata recovery is the rule, unless there be extensive pleurisy or pneumonia as a complication.

[Footnote 18: _Op. cit._, p. 288.]

In injuries, such as in rupture or puncture, the prognosis must depend upon the extent and the character of the injury, the condition of the patient, and whether or not the puncturing body has been removed from the wound. Generally, these must be regarded as unfavorable cases, although paracentesis of the pericardium is now accepted as a proper operation and is attended with comparatively little risk. The cerebral symptoms occurring in pericarditis can hardly in themselves be regarded as unfavorable to life, but they are unfavorable when associated with high temperature and when considered in connection with full recovery of the mental powers. Relapses and recurrences of pericardial attacks have strongly fatal tendencies. Age and sex contribute materially to the prognosis. The very young and the aged are unpromising subjects; and Sibson[19] has shown that while females are somewhat more liable than males to acute articular rheumatism, males are more often attacked with rheumatic pericarditis; also that endocarditis accompanies pericarditis more frequently in males than in females, while simple endocarditis is more frequent in the female than in the male. He also shows that while pericarditis affects the two sexes below the age of twenty-one in nearly equal proportions, after the twenty-fifth year males are three times oftener subject to it than females. The disease is greatly modified by occupation as well as by age. Thus, Sibson has pointed out that female domestic servants under twenty-one years of age are extremely prone to acute rheumatic pericarditis, endocarditis, and carditis, as they are often unequal to labor and fatigue, and are easily affected by draughts and by exposure to wet and cold.

[Footnote 19: _A System of Medicine_, by Reynolds.]

{783} The causes of death in pericarditis are various. Death may occur in a few hours after the attack by the rapid effusion of a large quantity of fluid, compressing and causing mechanical paralysis of the heart; or it may happen from syncope due to the patient making sudden exertion, as in getting out of bed, more especially if there be a large amount of fluid in the pericardium; or, again, it may be owing to paralysis of the heart from disturbance of the cardiac centres, or to fatty degeneration of the cardiac walls largely induced by the inflammatory condition. Again, a fatal termination may be caused by pneumonia or extensive congestion of the lungs, or by a large quantity of fluid in the pleura, having its origin really in the pressure exerted on the veins and the other structures by the pericardial effusion; or death may result from non-aëration of the blood and from general exhaustion.

TREATMENT.--In the treatment of acute pericarditis the first thing to insist upon is absolute rest--rest of body, rest of mind; all effort, all fatiguing conversation, is to be avoided. The diet should be of an easily-digested kind, nourishing, but given in small quantities at a time, so as not to distend the stomach. Milk, eggs, animal broths, with occasionally just enough solid food to gratify the wish of the patient, constitute the best diet. Further, from the very outset the cause of the malady should be clearly kept in view and the treatment directed in accordance. As so many cases have their origin in rheumatism, an antirheumatic treatment has usually to be carried out. But here let me at once record the more than uselessness of the salicylates. They have no influence when pericarditis has arisen, and if salicylic acid or its compounds are being given, they should at once be stopped. The alkalies have a far better action. Again, speaking in general terms, opium in moderate doses, to keep the nervous system quiet and to moderate the general discomfort, is of wide applicability and signal use; few are the cases which its steady, judicious employment will not benefit. Especially is this witnessed in the earlier stages and before marked effusion occurs.

The treatment of acute pericarditis is much influenced by the stages of the malady--whether it is seen in the stage with plastic exudation; whether this exudation markedly persist and but little liquid effusion takes place; whether the effusion is copious. Now, in the earlier stages and before decided effusion bloodletting was at one time much in vogue, but it has been by general consent abandoned, at least general bloodletting has. Local bloodletting is still employed by some, and I am sure I have known a few cups to the præcordial region or leeches there applied relieve the pain and make the action of the heart more regular. It is, I think, in robust subjects and in the early stages decidedly to be recommended. Mercurials, like general bloodletting, have fallen into disuse. Cases of pericarditis have been seen to originate in those whose gums were touched by mercury, and it does not prevent effusion. Certainly, in pericarditis with Bright's disease the remedy must not be thought of; but under other circumstances, in lingering cases with extensive plastic deposits, or in effusions that remain uninfluenced, it is worth a trial.

The application of cold to the cardiac region, either in the shape of cold compresses frequently changed or of a bladder of ice, is very much lauded by some of the French and German physicians. Gendrin's method consists in keeping a bladder of ice over the heart for from one to three hours until the pulse and temperature come down to about a normal condition. As these rise it is from time to time reapplied, although for a shorter period; and it is thought to influence both the pain and the inflammation. I have not seen the latter effects from it; and for the pain it is less trustworthy than the more commonly employed hot-water applications and poultices. Digitalis is in the earlier stages an admirable remedy. Its use in small, frequently-repeated doses will render the action of the heart more regular and reduce {784} its frequency. Friedreich[20] and Bauer[21] both recommend its employment in large doses, to be suspended when the pulse becomes slower or irregular. Notwithstanding it might be thought particularly valuable in marked effusions alike from its tonic action on the heart and its diuretic powers, my clinical experience is against it under such circumstances. It is far inferior to the free use of stimulants.

[Footnote 20: _Die Krankheiten des Herzen_.]

[Footnote 21: "Diseases of the Pericardium," _Ziemssen's Cyclop._]

When there is decided effusion diuretics are our main dependence, and squills and tartrate or acetate of potassium are most employed. The acetate of potassium is very serviceable--half an ounce or more in twenty-four hours in broken doses. Nor need we wait for the occurrence of the effusion to begin with this remedy. An occasional hydragogue cathartic is also indicated where the strength of the patient permits; but care must be enjoined not to let him rise to go to stool. In lingering effusions iodide of potassium, not less than forty grains daily, and repeated blisters are employed. The latter remedy may also be used early in the case where the friction sound is extensive, and a large blister then is better than a small one.

A state of things is at times met with in which the pulse is weak, the extremities cool, the effusion large, the impulse of the heart very faint, the heart evidently struggling. There is but one remedy for this--the free use of stimulus, whiskey or brandy or wine, whichever is best taken. Nor do cerebral symptoms contraindicate--on the contrary, they more decidedly indicate--stimulants. Tonic doses of quinine and hypodermics of brandy aid in this stage. Should the symptoms still prove unyielding and the effusion large, the question of puncturing the pericardium will arise; and as a means at least of gaining time the operation is strongly indicated. Its manner of performance and its general results have been carefully studied by John B. Roberts, and to his remarks in this volume the reader is referred. We cannot be too careful to be on the lookout for the pulmonary complications, pleurisy or pneumonia, which are so apt to be found in acute pericarditis. They require prompt treatment, but they ill bear depressants. They demand, among other means, often quinine, and the greatest attention in sustaining the action of the heart and in keeping the kidneys actively at work. When the dyspnoea is very great, and there is considerable pleural as well as pericardial effusion, it is best to tap the pleura. I have several times given this advice in cases in which it was under discussion to tap the pericardium, and after the relief afforded to the lung the pericardial affection has yielded to remedies.

Chronic Pericarditis.

Chronic pericarditis, as such, requires but little consideration here, since its main features have been discussed in this article under other heads.

Chronic pericarditis is divided from the acute by a very shadowy line: a few hours of the acute disease may terminate in the chronic form, as in acute inflammatory affections elsewhere, or the malady may follow an attack of acute pericarditis of several weeks' duration, or it may be chronic from the beginning. In the first case the pericardium is the organ primarily affected, generally from cold, or the lesion is dependent upon some acute inflammatory disease adjacent or remote, as carditis, pleurisy, mediastinitis, or upon rheumatism. In pericarditis the result of the exanthemata, of Bright's disease, of scurvy, of tuberculosis of the lungs or elsewhere, of profuse drainage from abscesses or injuries--of, in fact, any wasting disease or fault in the economy associated with malnutrition--the pericarditis may be subacute at first, and is then apt to become chronic.

{785} The symptoms are slow of development, and are not usually rapidly productive of discomfort. They are in the main the same as those of the acute affection, although less decided, and the thermometer may mark a normal degree or but little above the normal. The physical signs of effusion of fluid, the presence of pus and blood or of adhesions, have all been discussed under their proper heads. The prognosis is, generally speaking, not as favorable as in the acute form; it depends very much upon the cause, the duration of the case, and the character of the fluid. In the treatment great attention must be paid to the cause as well as to getting rid of the effusion and relieving any direct oppression of the heart the result of the pressure of the fluid. If this cannot be done by medical means, or if there be reason to believe that the collection is purulent, paracentesis is indicated. Adhesions are not, or are but very seldom, removed by any special treatment directed to them. Indeed, it is by adhesions that most of the cases of pericarditis with lymphous effusion get well. When adhesions have disappeared after these attacks of inflammation, it has been through the efforts of nature, and nothing is left but the milk spots to testify to the previous condition of the membrane. But these, it must be remembered, are also the result of altered nutrition in the membrane, and do not in themselves bespeak a chronic pericarditis.

Adherent Pericardium.

Early in this article adhesions were mentioned as one of the results of pericardial inflammation, and it was stated that the exudation may appear in spots or extend over the visceral or parietal layers of the pericardium or over both, and become organized tissue filled with blood-vessels, gluing the walls together, and completely obliterating the sac. Limited adhesions are much more common than those which are extensive or complete. The intensity of the inflammation offers no indication of the probability of the formation of adhesions. The position of the body will materially assist in the adhesion of one point in preference to another, more especially if the body should retain a certain posture for any length of time; for the heart naturally gravitates to the most dependent part, and these portions coming into apposition will form attachments. If these are not too large and firm they may become broken, their torn ends being absorbed or remaining as pendent shreds or patches.

When the adhesions are long and flexible, the motion of the heart is not interfered with; but when they are short, firm, and extensive, the heart labors to perform its duties, without hope of relief. If the adhesions do not contract, the heart retains its shape, and diastole is easy; but in its systole the difficulty is marked, for besides the effort to expel the blood there is restraint of motion, with great loss of energy in drawing to itself the unyielding pericardium. If the pericardium be adherent to the pleura and other surrounding parts, the obstacle is increased and the sternum and costal cartilages are drawn inward and the diaphragm upward. It is to this effort of the heart in systole that the hypertrophy which is often found with pericardial adhesions has been attributed; and in the main I believe this view to be correct. But a number of distinguished observers have denied that the pericardial adhesion is the cause, and think that the cardiac hypertrophy is more probably accidental or dependent upon valvular disease the result of endocarditis, or upon a condition of myocarditis which, however slight, may coexist and lead to inflammatory deposit in the walls, and consequent hypertrophy. It is not difficult to understand how with altered walls dilatation, another consequence of pericardial adhesion, may be caused. Adhesions to the more resisting chest-wall and diaphragm prevent the approximation of {786} the cardiac walls and also the complete closure of the valves. The weakened cardiac walls begin to yield: this will be assisted by the traction of the adhesions on the walls and by the persistent engorgement of the cavities of the heart resulting from inability to empty themselves as completely as when in the normal condition. Another element will be that of shrinkage of the heart-walls, which comes on when the adhesions become so firm and produce so much pressure by contraction that the nutrition of the organ is materially interfered with. But the problem is by no means an easy one to solve, and it seems to me that there is more than one factor influencing it, and that in cases with predominant dilatation the altered heart-walls play, most likely, the prominent part.

Now, even as to the fact of hypertrophy occurring there is far from unanimity. To cite, by way of illustration, the opinion of a few observers. This condition has been asserted by Chevers[22] and by Barlow[23] to be the usual and normal result of complete adhesion of the pericardium to the heart and consequent obliteration of the sac. Hope[24] very emphatically states: "I have never examined, after death, a case of complete adhesion of the pericardium without finding enlargement of the heart, generally hypertrophy with dilatation." Stokes,[25] on the other hand, writes: "Without denying that generally adhesion may induce hypertrophy and dilatation, experience leads me to doubt that such an effect necessarily or even commonly follows the condition indicated. I have often found the heart in a perfectly normal condition with the exception of an obliterated pericardium." He adds: "It has been stated to me by Smith that he has found general adhesion of the pericardium coinciding with atrophy or with hypertrophy of the heart in nearly equal frequency. In some of the cases of atrophy the change was simple, consisting essentially in a diminished volume, with perhaps a paler color of the heart, while in others a true fatty degeneration had commenced." Bauer[26] records that "as a rule the heart is found in a more or less marked condition of degeneration and atrophy. The bundles of muscular fibres show evidences of fatty degeneration, or even of hyalin and pigment degeneration, or the appearances are those of an interstitial myocarditis, with its results." To my mind, I repeat, the state of the muscular walls seems of great importance, and it may explain the varying condition of hypertrophy and dilatation found in association with the pericardial adhesions in such a differing manner.

[Footnote 22: _Guy's Hospital Reports_, vol. vii. p. 421.]

[Footnote 23: "Gulstonian Lectures," _London Med. Gazette_, 1844, pp. 755, 756.]

[Footnote 24: _Diseases of the Heart_.]

[Footnote 25: _Diseases of the Heart and Aorta_.]

[Footnote 26: _Ziemssen's Cyclopædia_, vol. vi. p. 634.]

It is strongly held by some that hypertrophy is occasioned more by the valvular disease that may coexist than it is by adherent pericardium. Sibson[27] tells us that "when pericardial adhesions are associated with valvular disease the heart is always enlarged. It was so in twenty-five out of twenty-six cases, and in the remaining instance, a case of mitral constriction, the heart was rather large." Undoubtedly, this combination is not unusual, but there may be the most marked hypertrophy with adherent pericardium without valve affections. I have met with several such instances, and Blache[28] has recorded three of striking character.

[Footnote 27: _A System of Medicine_, by Reynolds, London, 1877, vol. iv. p. 440.]

[Footnote 28: _Maladies du Coeur chez les Enfants_, Thèse de Paris, 1869.]

Adherent pericardium may occur at any age. It has been found by Behier as the result of chronic pericarditis in an infant of eleven months.[29]

[Footnote 29: Constantin Paul, _Maladies du Coeur_, Paris, 1883.]

The SYMPTOMS of adherent pericardium are uncertain; the physical signs are the only means we have of determining its existence, and even these signs are far from invariable or well defined. In marked cases, on inspection of the præcordial region, it will be noticed that there is more or less complete {787} absence of the heart's impulse against the chest-wall. This is due to the fixed or restrained condition of the heart, particularly of its apex, and to the interposition of a layer of plastic lymph, and possibly of some fluid. There is sometimes a prominence of the costal cartilages over the heart, and the organ itself may be abrupt and jogging in its motion. The intercostal spaces to the left of the sternum are indented, and there is a drawing in of the lower portion of the sternum and attached cartilages with each systole of the heart, giving rise to a wavy movement in the epigastrium.

The application of the hand over the heart detects the impulse, but this is diminished in force and extends over a larger area than in health. The pulse is usually accelerated and irregular in its rhythm. When palpitation of the heart occurs--and this is far from a constant sign--it is dependent upon pressure at the origin of the great vessels. In some cases there is pulsation in the liver, also pulsation in the epigastrium, and venous pulsation in the vessels of the neck. The regularity of form of the chest in its rise and fall during the acts of respiration will be interfered with if the adhesions be extensive.

The position of the heart is but little changed from the normal, though of necessity the organ is more or less fixed in its position by the adhesions. No matter what posture the patient may assume, the apex-beat of the heart remains unchanged where bound by the adhesions; this is especially the case if the adhesions have extended to the pleura. The apex-beat may be entirely masked; but if it be in its normal site, a depression of the intercostal space during the systole of the heart occurs, caused by traction upon the intercostal muscle at that point. If the pleura be implicated, greater expansion of the upper and outside portion of the left side of the chest in inspiration takes place. In a certain proportion of cases the position of the heart is more oblique than normal.

On auscultation the sounds of the heart are found to be more distant and muffled, though generally less so than in effusions of fluid into the pericardium. They may be very faint; at least the first sound may be, on account of the degeneration of the walls of the heart, and murmurs may exist from attending valvular lesions. The sounds of the heart may be reduplicated. Skoda and Friedreich laid great stress on this. But reduplicated heart sounds are not pathognomonic of any affection.

It has been stated that partial adhesions may exist in such form as not to prevent the free surfaces of the pericardium from rubbing against each other, and friction sounds will result, but as the adhesions become general these sounds will disappear.

The cardiac percussion dulness is but slightly increased unless there be also hypertrophy or dilatation. The area of cardiac dulness is lessened during inspiration, because the anterior margins of the lungs extend nearly to the middle line over the front of the heart. This is so even in pericarditis with adhesions, unless the adherent pericardium be attached to the front of the chest and the pleura be also adherent; then the area of absolute dulness remains unchanged during the respiratory acts.

The cardiac impulse will be found at times to be increased by the traction of the adhesions in the pericardium and adjacent parts; at others the impulse is diminished. A disproportion between the marked beating of the body of the heart against the chest-walls and the feeble impulse of the apex has a diagnostic significance--one much greater than a double impulse. The point of cardiac impulse mostly remains unchanged. A depression at and near that point, noticeable during the systolic action of the heart, is among the more certain of the signs of adherent pericardium. When the adhesions extend to the pleura, this systolic dimpling is greater, and becomes often very marked; and it is questionable whether it occurs to any extent without pleural adhesions also existing. Often the apex-beat of the heart does not change {788} with the change of position of the patient. The chest remains normal in shape unless altered by extensive and strong adhesions to the adjacent parts. Under such circumstances there is depression of the fifth and sixth intercostal spaces, the epigastrium is sunken, and the sternum and cartilages are flattened or drawn in; this becomes most apparent during the systole of the heart. The inspiratory bulging is greatest on the right side in consequence of the fixation of the diaphragm.

Hypertrophy or dilatation and valvular disease, if associated with adherent pericardium, modify of necessity both the signs on percussion and auscultation. The aortic and mitral valves are the ones particularly affected. It is when these complications exist, rather than merely from the pericardial adhesion, that we find more or less dyspnoea or orthopnoea and a sense of faintness and dizziness, an anxious expression of countenance, imperfect aëration of the blood, lividity of the lips, dropsy, and difficulty of swallowing.

There is much uncertainty in the DIAGNOSIS of partially adherent pericardium; for the friction sound may be present, the impulse normal, the heart's action unrestrained, there may be no impeded respiration, and the patient may present none of the physical signs of adhesions. Indeed, under any circumstances the diagnosis of adherent pericardium is not a very trustworthy one. More than one of the physical signs mentioned must exist to warrant anything like a positive opinion, and the disease may be latent.

William H. Webb[30] has recorded a case of complete obliteration of the pericardial sac by inflammatory adhesions, associated with enormous hypertrophy of the heart and valvular disease, in which there were no symptoms nor physical signs to lead to a suspicion of the true state of things.[31]

[Footnote 30: I take this opportunity of acknowledging the valuable aid I have received from Dr. Webb in preparing this essay on affections of the pericardium.]

[Footnote 31: _Philadelphia Medical Times_, vol. ii.]

The PROGNOSIS of adherent pericardium depends rather upon the secondary consequences, upon the condition of the muscular walls, the hypertrophy, the dilatation, the coexistence of valvular disease, than upon the adherent pericardium itself. Yet there is a tendency to sudden death caused by it. In 115 instances of sudden death, Aran has recorded 9 of complete pericardial adhesion.

The TREATMENT must be that of the consequences with careful attention to the state of the muscular walls. Digitalis is indicated in cases with dilatation and flabby walls. Early in the case repeated small blisters and a course of iodide of potassium may be tried. But it is doubtful whether any useful result will be accomplished.

Hæmopericardium.

Hæmopericardium, or blood or blood and serum in the pericardial cavity, is rarely met with except as a result of rupture of the heart, injury to the pericardium by perforation or crushing, aneurisms, and in pericarditis occurring in diseases of a low type with degeneration of the blood, as in scurvy and purpura hæmorrhagica.

In rupture of the heart the effusion of blood into the sac is rarely rapid, and death is not immediate unless the rupture be large. Rapid distension of the pericardium with blood speedily causes death by embarrassing the action of the heart and by producing anæmia of the brain. Thus the rupture of an aneurism into the pericardial sac is of necessity quickly fatal. Penetrating wounds may be the cause of a bloody accumulation in the pericardium and give rise to serious symptoms. But the injury is not always fatal, since large vessels are not likely to be cut; the {789} hemorrhage is slow, thus permitting the pericardium to accommodate itself to the fluid; and if the amount of blood be not very large, it may be ultimately absorbed. Crushing injuries to the chest may produce effusion of blood into the pericardium by lacerating small vessels, and may burst the coronary arteries if they be diseased. The foregoing are traumatic causes; the true hæmopericardium is due to the effusion of blood or blood and serum in diseases of malnutrition and in dyscrasias which have special tendencies toward the serous membrane, particularly to the pericardium. This does not take note of the bloody effusions or of a certain amount of blood in the serum which may occur in the course of acute pericarditis; but rather of those diseases, such as scurvy, purpura, and chronic alcoholism, in which the blood is broken down, the tissues weakened, the degenerated vessels rupture or are no longer able to contain their contents, and in which the blood or bloody serum accumulates speedily in the pericardium, without or with but slight previous inflammation.

The physical signs of hæmopericardium are the same as in other effusions into the sac, with this difference--that in the traumatic kind the area of cardiac dulness is rapidly increased, while at the same time the fluid never reaches the bulk of other effusions, for before this can happen death occurs. Friction phenomena are not perceived. There are as symptoms dizziness and faintness, drowsiness, difficulty of breathing, sense of præcordial oppression, weak pulse, and, when myocarditis exists, pain in the heart. The prognosis generally is unfavorable. Death, if not the direct result of the causes producing hæmopericardium, is due to the hemorrhage or to failure of the heart.

The TREATMENT consists in absolute rest, in giving readily-digested food, and in supporting the action of the heart; for this purpose stimulants may be required, unless something in the history of the case forbid. Of course it will also be important to keep the emunctories, especially the kidneys, freely at work, and to modify the condition of the blood in the cases associated with dyscrasias. The mineral acids and ergot are remedies to be borne in mind.

Hydropericardium.

Hydropericardium is the presence of serous fluid in the pericardium of greater quantity than the normal, not dependent upon inflammation--a pericardial dropsy. To constitute this it must be more than an ounce or two; it must be sufficient to be recognizable during life.

The fluid in hydropericardium very rarely reaches the extreme quantity effused in pericarditis. It is alkaline in its reaction and of a pale straw color, or it may be of a deeper yellow and opaque, the color and opacity depending upon the presence of hæmatin, biliary coloring matter, and epithelium. It is chiefly water. According to the analysis of Gorup-Besanez, there are of water, 95.51; albumen, 2.46; fibrin, 0.08; organic matter, 1.27; inorganic salts, 0.95.

Hydropericardium is apt to occur in conjunction with dropsies in other parts, particularly with hydrothorax. It may be the result of local stasis in the veins and lymphatics of the heart and pericardium or of neighboring parts; or it is more usually the sequela, forming part of a diffused dropsy, of certain general diseases, as of the exanthemata, particularly scarlet fever; or is the accompaniment of Bright's disease of the kidneys; or of obstructive diseases of the liver; or of affections of the thoracic viscera which impede the circulation of blood through the heart and lungs. The walls of the heart become soft and flabby, and are consequently weakened; the circulation in the coronary arteries and veins is sluggish.

It is almost invariably a chronic affection, coming on insidiously, and its {790} existence may not be suspected until the disorder is well advanced, when some symptom, suddenly developed, directs attention to the heart.