Chapter LIII: Part 53

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 {763} 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.

[Footnote 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 {764} 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.

[Footnote 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 {765} 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 {766} 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 {767} 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 {768} 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]

[Footnote 10: _Medical Electricity_, by Roberts Bartholow, M.D., LL.D., etc., Philadelphia, 1881.]

[Footnote 11: _Clinical Treatise on the Diseases of the Nervous System_, by M. Rosenthal, translated by L. Putzel, M.D., New York, 1878.]

[Footnote 12: Vide article entitled "Basedowsche Krankheit," in _Real-Encyclopedie_, Wien and Leipzig, 1880.]

{769}

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 {770} 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. Buist[1] 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]

[Footnote 1: _Charlestown Medical Journal and Review_, Jan., 1858.]

[Footnote 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.

[Footnote 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 {771} 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.

[Footnote 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.

[Footnote 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 {772} 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 {773} 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.

{774} 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]

[Footnote 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 statement[7] 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.

[Footnote 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 {775} 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. Rotch[8] 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.

[Footnote 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. Hayden[9] 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.

[Footnote 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 {776} 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.