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 muffled 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, chorea, 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 classification 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 classification 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 chorea, 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 practitioners to be wise.
A chronic endocarditis with permanent lesions of the valves may become an acute inflammation with an infectious provocation.