Part 9 (1/2)
Acute endocarditis can probably not occur without some inyocarditis, and myocarditis probably does not occur without some endocardial disturbance and perhaps some pericardial irritation. This is especially true in endocarditis which occurs during any acute infection, even in rheumatism. The greater the amount of pericarditis, the more serious is the acute condition. The greater the amount of myocarditis, the more doubtful is the heart strength in the near future. The greater the amount of endocarditis, the greater the doubt of freedom from future permanent valvular lesions.
Endocarditis may be divided into: acute mild (simple) endocarditis, acute malignant (ulcerative, infective) endocarditis, chronic endocarditis and valvular disease.
ACUTE MILD ENDOCARDITIS
This inflammation of the endocardium is generally confined to the region of the valves, and the valves most frequently so inflamed are the mitral and aortic. There may be a slight inflammation or actual ulceration and loss of tissue. Vegetations more or less constantly occur on the inflamed surfaces, with more or less danger of particles becoming loosened and moving free in the blood stream, causing embolic obstruction in different parts of the body. There is also more or less probability of serious adhesions or contractions occurring from the healing of the ulcerated surfaces. The future health and welfare of the valves depend on the fact that the inflammation has healed without contractions or adhesions.
It is often difficult to decide when acute endocarditis has developed; but with the knowledge that the endocardium often becomes inflamed during almost any of the acute infections, the physician should repeatedly examine the heart for murmurs, for m.u.f.fled closure of the valves, or for other evidences of endocarditis or myocarditis during the acute infective process.
It has been shown positively that acute endocarditis is due to micro-organisms, generally streptococci, staphylococci or pneumococci, and, more frequently than once believed, gonococci. The most frequent causes are acute rheumatic fever, diphtheria, pneumonia, cerebrospinal meningitis, scarlet fever, erysipelas, influenza, ch.o.r.ea, gonorrhea, sepsis and typhoid fever. It may also follow a follicular tonsillitis or some infection of the mouth or throat with or without arthritis. Tuberculosis may also occasionally cause an endocarditis. Organisms may be found in a terminal simple endocarditis due to a chronic disease, as tuberculosis or cancer; such inflammations may have been caused by circulating toxins.
It will be noticed by the foregoing cla.s.sification that the terms ”mild” and ”malignant” endocarditis are used. The purpose is to convey the fact that there may be no etiologic distinction between the two forms, and it is impossible to decide clinically in the beginning of an endocardial inflammation which form is present. In the malignant form the infection is probably more serious or the infective germs are more active, the ulcerations deeper, and the likelihood of emboli and the seriousness of such embolic infarcts more serious and more dangerous. The differences in inflammation in the two cases is really one of degree, and the cla.s.sification is made to coincide with this probable fact. it is, of course, clinically recognized that endocarditis following certain diseases, especially rheumatism, is of the simple or mild type, while that termed ulcerative endocarditis may occur apparently as a primary or general infection, and the causative bacteria, as a rule, are readily discovered in the blood. The Streptococcus viridans is one of the most dangerous of these bacteria.
A SECONDARY AFFECTION
Mild endocarditis is rarely a primary affection, and is almost invariably secondary to one of the diseases named above. Nearly 75 percent of secondary endocarditis occurs as a complication of acute articular rheumatism and ch.o.r.ea, or subsequently. On the other hand, about 40 percent of all patients with acute articular rheumatism develop endocarditis, sometimes perhaps so mild as to be hardly discoverable. This complication is most likely to occur during the second or third week of rheumatic fever. It is not sufficiently recognized that a subacute arthritis, recurring tonsillitis, open and concealed infections in the mouth, and even a condition of the system with acute, changeable and varying joint and muscle pains may all develop a mild endocarditis, even with subsequent valvular lesions. Therefore in all of these conditions the decision can be made only as to how much rest the patient must have or how serious the condition is to be considered by careful examination of the heart in every instance.
Children are more liable than adults to this complication, especially with rheumatism. Therefore, acute mild endocarditis with future valvular lesions occurs most frequently during childhood and adolescence, and if one attack has occurred, a subsequent infection, especially of rheumatism, is liable to cause another acute endocarditis.
PATHOLOGY
The part of the heart most affected is the part which has the most work to do--the left side of the heart--and of this side the left ventricle and therefore the mitral and aortic valves; the most frequent valve to be inflamed and to stiffer permanent disability is the a mitral valve, the valve which in its inflamed condition is subjected to the greatest amount of pressure and therefore irritation. Not infrequently soft systolic murmurs are heard at the pulmonary and tricuspid valves during acute endocarditis. It is rare, however, that these valves are so affected during childhood or adult life as to be permanently disabled.
Whether a diminished alkalinity of the blood in rheumatism has anything to do with the cause of the frequent complication of endocarditis has not been determined. Whether the administration of alkalies to the point of increasing the alkalinity of the blood is any protection against the complication of endocarditis has also not been positively demonstrated, although clinically such treatment is believed by a large number of pract.i.tioners to be wise.
A chronic endocarditis with permanent lesions of the valves may become an acute inflammation with an infectious provocation.
It has been shown that even in a few hours after endocarditis has started, little vegetations composed of fibrin, with white blood cells, red blood pigment and platelets, may develop. Practically in all instances such vegetations develop, and later become more or less organized into connective tissue. These little vegetations, generally minute, perhaps not exceeding 4 mm. in height, are irregular in contour like a wart. Some of these may have small pedicles, and as such, of course, are more likely to become loosened and fly off into the blood stream. It is of interest to note that these little vegetations are more likely to be on the left side of the heart than the right; on the valves than any other part, and on the mitral valve than on the aortic. The consequence is a more frequent permanent disability of the valves of the left side of the heart, and of these more frequently the mitral. Although these little vegetations and excrescences sooner or later become mostly connective tissue, still fibrin and white blood cells may form thin layers over them, more or less permanent. In this fibrin are frequently found bacteria, even when there has been no recent acute inflammation. The deeper layers of the endocardium during acute inflammation may become infiltrated with young cells, with resultant softening and destruction of the intercellular substance. This softening and some swelling of the lower layers of the endocardium allow the pus.h.i.+ng up of these extravasated blood cells which, being covered with fibrin, makes the little vegetations above described; and as just stated, the fibrin may form a more or less permanent cap. If this cap is disintegrated or lost and the cells under it washed away in the blood stream, ulceration takes place, which may be more or less serious, even to the perforation of a valve or actual erosion of one of its cusps, and the parts of the valves most seriously affected are the parts which strike against each other on closure; as previously stated, the parts subjected to the greatest strain and the greatest amount of friction during the inflammation are the parts most seriously affected afterward.
If a perforation has occurred, it may make a permanent leak. If an erosion of the edge of the valve has occurred, it may make permanent insufficient closure. If the valve has become thickened and stiffened during the cicatricial healing, it may not only be incompetent, but may not open perfectly, and a narrowed orifice may be the consequence. During the healing of these granulating ulcers there may be thickening of the part or shrinking of the tissue, and the valve may become shortened by adhesion to the wall, or the cusps of the valve may adhere together so that the valve becomes permanently unable to open properly or to close properly, or to do either.
Not infrequently and probably more frequently than we recognize, recovery without any of the pathologic lesions just described follows mild endocarditis. The occurrence of simple endocarditis is undoubtedly frequent during acute disease, and is unrecognized because there are no lesions of the heart at the time or subsequently; but valvular lesions only too frequently follow the endocarditis which occurs with rheumatism. Occasionally the ulcerations become serious, and ulcerative endocarditis or malignant endocarditis develops on the mild inflammation. In this form the little vegetations are liable to become loosened, fly off into the blood stream, and cause emboli in different parts of the body.
Recently Fraenkel [Footnote: Fraenkel: Beitr. z. path. Anat. u. z.
allg. Path., 1912, iii, 597.] concluded that the microscopic nodules which occur in endocarditis in the myocardium, and which consist of the several varieties of white blood corpuscles first referred to by Aschoff in 1904, are characteristic only of acute rheumatism.
Fraenkel found these nodules in the myocardium in a case of ch.o.r.ea, showing the close relations.h.i.+p between it and rheumatism.
While repeated careful examination of the heart during acute infections will generally show signs of endocarditis if it is present, even if there are no subjective symptoms, the disease may be so insidious as not to be noted until a valvular lesion occurs.
Often, however, during the course of the disease, especially in rheumatism, there is a slight increase in fever and there is a discomfort complained of in the region of the heart, frequently accompanied by slight dyspnea. Real pain is seldom present unless the pericardium is affected. If the myocardium is much inflamed at the same time, the heart becomes more rapid and the blood tension lowered, and the apex beat diminished in intensity and perhaps not palpable. If there is pain, with or without pericarditis, it is often referred to the epigastrium, especially in children. The patient is often nervous, restless and sleepless. In simple endocarditis emboli rarely occur. If they do, of course the signs will be in the part in which the infarct occurs. Besides the diminished intensity of the apex beat and its greater diffusion, the valve sounds may be m.u.f.fled, and sooner or later there may be systolic murmurs over the different orifices. Of course systolic murmurs may be due to a disturbed condition of the blood, but if they occur with the above-mentioned symptoms and signs, endocarditis should be diagnosed. If the heart becomes seriously weak and the patient suffers much dyspnea, myocarditis should be known to be present with the endocarditis. If there is a diastolic murmur, there can be no question of serious endocarditis having occurred.
Unexplainable palpation during acute illness liar been thought to be a distinct symptom of endocarditis.
TREATMENT OF ENDOCARDITIS
As mild endocarditis rarely occurs primarily but is almost always secondary to some acute disease, its immediate treatment is only a slight modification of that of the disease which is causing it. A complication which is so frequent should always be expected, and consequently warded off or prevented, if possible. Knowledge of the diseases which are most liable to cause endocarditis makes frequent heart examinations a necessity, to note when it arrives. While an extra heart tire, sleeplessness, and the circulation of unnecessary toxins from a bad condition of the bowels and from improperly selected food all make this complication more liable, its occurrence is, nevertheless, often unpreventable.