CHAPTER VII. - INFLAMMATORY AFFECTIONS OF THE HEART.PERICARDITIS. Acute pericarditis-Anatomical characters-Division into three stages or periods-White spots on the heart-Pathological relations and causation of pericarditis-Connection with acute rheumatism, with albuminuria or Bright's disease, with endocarditis, etc.Symptoms of acute pericarditis-Symptoms referable directly to the heart, to the circu lation, to the respiratory system, to the digestive system, to the countenance, position, etc., to the nervous system-Notable disorder of the brain and spinal cord in connection with pericarditis-Physical signs of acute pericarditis-Signs furnished by percussion, by auscultation, palpation, inspection and mensuration-Summary of the physical signs of acute pericarditis-Diagnosis of acute pericarditis-Prognosis in acute pericarditis Treatment of acute pericarditis-Bloodletting, mercurialization, sedatives, revulsives or counter-irritants, opium, stimulants and eliminatives-Treatment prior to liquid effusion, during the period of liquid effusion, and after absorption of liquid effusion-Treatment when complicated with notable disorder of the nervous system-Subacute and chronic pericarditis, with and without liquid effusion-Symptoms, physical signs, and treatment-Paracentesis of the pericardium-Pneumo-pericardium and pneumo-pericarditis-Pericardial adhesions-Effects upon the heart and circulation Diagnosis. INFLAMMATION affecting the heart may be limited to one of the anatomical structures which compose this organ. The investing serous membrane may be alone inflamed, constituting the affection called pericarditis. When the membrane lining the cavities, or the endocardium, is the seat of inflammation, the affection is called endocarditis. Inflammation of the substance or muscular tissue of the organ is distinguished as carditis or myocarditis. Although these different inflammatory affections may exist, each independently of the others, they are often associated. In a large proportion of the cases of pericarditis, endocarditis coexists; and myocarditis very rarely occurs save in connection with inflammation of the investing or lining membrane of the heart. The intrinsic importance of these affections renders their study highly important. They are seated in an organ entitled to be called, par excellence, a vital organ. They involve, not infrequently, great suffering and imminent danger to life. They derive importance from their remote consequences. The organic affections which have been considered in previous chapters, originate, in the majority of instances, in cardiac inflammation. The study of this class of affections has been rendered highly interesting and important by the developments of modern researches as regards their pathological relations, especially to rheumatism and renal disease, and by the improvements in diagnosis arising from the successful application of physical methods of examination. PERICARDITIS. Inflammation affecting the investing membrane of the heart, or pericarditis, is less frequent in its occurrence than endocarditis, but is a more serious affection as regards immediate danger, and, perhaps, also in view of its remote effects. This membrane is analogous in structure to serous tissue in other situations; and pericarditis does not differ essentially from pleuritis or peritonitis. The points of difference pertaining to the symptomatic phenomena and the dangers peculiar to it, depend on the comparatively small size of the pericardial sac, the fact that the substance of the heart consists of muscular tissue, the function of the organ and its physiological relations. In treating of pericarditis, the morbid changes incident to the disease, or its anatomical characters, are to be first considered. Its pathological relations and causation will next be most conveniently noticed. The symptoms, physical signs, diagnosis, prognosis, and treatment, will severally receive distinct consideration. This, like other inflammatory affections, is presented in an acute and a subacute or chronic form. I shall treat, in the first place, of acute pericarditis under the foregoing heads, treating separately of subacute or chronic pericarditis; and, finally, the subject of pericardial adhesions will claim. some attention. ANATOMICAL CHARACTERS OF ACUTE PERICARDITIS. The morbid changes found after death in fatal cases of pericarditis, do not differ essentially from those which belong to the post mortem history of other serous inflammations. The appearances vary according to the stage of the disease at which death takes place. Death rarely occurs at the very commencement of the inflammatory action. In some instances in which the disease has proved rapidly fatal, the serous surface has been found more or less reddened, mainly from injection of the vessels situated in the subjacent areolar tissue. The redness is arborescent and in specks or patches, the latter giving to the surface a dotted or mottled aspect. Mere redness, however, and vascular injection are not reliable as the sole evidence of inflammation. The latter may be due to various causes which impede the circulation in the heart shortly before, or at the time of death; and the former may be produced after death by extravasated serum colored with the hæmatin of the blood globules. On the other hand, the redness which belongs to inflammation, here, as in other situations, may have existed during life and disappeared after death. Opacity of the membrane, alteration in its consistence, or the presence of lymph, are essential to constitute proof positive that inflammation has existed. Abnormal dryness of the membrane has been supposed to be an effect of incipient inflammation, and, immediately succeeding this, a glutinous or sticky sensation, communicated to the finger when passed over the surface. The latter condition, from its resemblance to that of some fishes when they have been several hours out of water, has been called by French writers, poissonneux. These signs, however, as well as vascularity and redness in specks or patches, are not, in themselves, sufficient anatomical evidence of pericarditis. They derive their claim to be included among the anatomical characters of the disease, from their association with the ante-mortem history, and with other post-mortem appearances which are unequivocal in their significance. Acute inflammation speedily leads to the exudation of coagulable lymph. This exudation takes place sufficiently to give rise to the characteristic solid deposit, in most cases, probably, within a few hours from the commencement of the inflammatory attack. The deposit, at first, of a jelly-like consistence, adheres slightly to the membrane, forming a thin layer, either limited to the base of the organ and about the roots of the large vessels, or extending, more or less, over the pericardial surface. The heart, at this stage, covered with thin, soft lymph, presents an appearance which has been compared to hoar frost, or to a "layer of liquid gelatine spread upon the parts with a camel's hair pencil." The process of exudation goes on, and the uncoagulable or serous portion forms a liquid which accumulates within the pericardial sac. If the disease do not prove fatal during this period, the liquid is gradually resorbed, and adhesion of the pericardial surfaces brought into apposition follows. It suffices to divide the disease into three stages, the division being based on the series of morbid events just mentioned. The brief period during which the membrane is supposed to be dry, or when a glutinous exudation is appreciable by the touch and not by the eye, is by some reckoned as the first or dry stage. Practically, this division is, to say the least, superfluous. The first stage may be considered as extending to the time when the accumulation of liquid is sufficient to be determinable during life by symptoms and physical signs. The second stage will embrace the period during which an appreciable amount of liquid continues. The third stage comprises the duration of the disease after resorption of the liquid. These stages may be called, respectively, the stage of exudation, of liquid effusion, and of adhesion. These terms, however, are open to criticism, and a more simple mode is to speak of the disease as consisting of three periods, viz., before, during, and after liquid effusion, the latter expression being understood as applying to a quantity of effused liquid sufficient to distend, more or less, the pericardial sac. If the disease end fatally during the first period, or before much accumulation of liquid takes place, the heart presents a coating of lymph, varying in different cases in its thickness and extent of diffusion. The deposit is more apt to be present and is more abundant at the base than over the other portions of the organ. It may be situated on both the visceral and parietal surfaces of the pericardium, or it may be limited to the former. It is very rarely, if ever, found exclusively on the parietal surface. The lymph is soft, slightly adherent, being very easily removed, and presents, in different cases, diversities of appearance which subsequently become more marked, and will be presently noticed. The membrane is more or less opaque, and may present the arborescent and dotted redness already mentioned. The latter, however, are often wanting after death. In some instances, when the deposit of lymph has been removed, the general aspect of the organ is not, in a marked degree, morbid; in some instances, the membrane covering the heart is studded with prominences resembling the enlarged papillary bodies on the tongue; in other words, it presents a mammillated aspect. The opacity is due to infiltration beneath the membrane; and this infiltration loosens the attachment of the membrane, so that it is detached from the heart with greater facility than in the normal condition of the organ. The exudation within the sac, in some instances, consists almost entirely of coagulable lymph, and an amount of liquid sufficient to be determinable does not occur during the progress of the disease. The affection in these cases is analogous to dry pleurisy; and they have been called cases of dry pericarditis. It is, however, rare for inflammation diffused over the pericardial surfaces, in other words, general pericarditis, to run its course without giving rise to considerable liquid effusion. When this effect does not occur, the inflammation is generally partial, that is, limited to a circumscribed portion of the membrane. This remark holds good equally with respect to pleurisy. The accumulation of liquid sufficiently to be manifested by signs and symptoms, takes place at a period from the commencement of the disease, varying in different cases. The quantity becomes sometimes large enough to occasion distension of the pericardial sac in twenty-four or thirty-six hours from the date of the attack. In the majority of cases, three or four days elapse before this occurs. As just stated, in some exceptional cases it does not take place during the whole career of the disease. The amount of effusion also varies greatly in different cases. From four to six ounces of liquid may be determinable in some cases; and the quantity which may accumulate beyond this amount ranges from a few additional ounces to as many as eight pounds. A case is reported by Corvisart, and also one by Dr. Swett,' in which the accumulation attained to the maximum just stated. The distension in these cases was enormous, exceeding several times the limit to which the healthy sac is capable of being dilated by forcible injection of a liquid after death. Experiments made by Dr. Sibson to determine the latter point showed that, in the adult male at fifty years of age, the injection of twenty-two ounces of liquid dilated the sac to its utmost capacity. Very great accumulation belongs rather to chronic than acute pericarditis. The quantity in the latter rarely exceeds two or three pints. The effused liquid is more or less turbid. It is sometimes transparent at the surface, resembling clear serum, but muddy and thick at the bottom. The turbidity proceeds from the admixture of lymph, and detached Lectures on Diseases of the Chest. 2 Bellingham, op. cit., Part I., p. 22. |