ENDOCARDITIS.
Definition. Pathology and lesions, congestion of the endocardium covering the valves, valves liable through friction and strain, exudation in or on the serosa rendering it opaque, coagula of fibrine on the surface, secondary endocarditis mycotic, microbes, changes in serosa, distortions and degenerations of valves. Symptoms, as in pericarditis, with violent heart impulse of varying force, clear metallic sound, blowing murmurs, weak pulse decreasing in force, irregular, intermittent, absence of local tenderness, no friction sound, no increase in area of dulness, if lesions are in right heart—venous pulse, venous congestion, dropsies. Valve lesions, in mitral valve—general heart symptoms and murmur with 1st heart sound, 2d sound may be repeated and exceptionally a venous pulse—in tricuspid valve—same with constant venous pulse, venous congestion and dropsy; narrowing of the mitral orifice—general heart symptoms and blowing murmur before the 1st sound; narrowing of the tricuspid orifice—same with murmur sometimes audible on the right side; insufficiency of aortic valves—general heart symptoms and murmur with 2d heart sound, double rushing sound in arteries and delay of pulse beat at jaw; lesions in pulmonary valves—same but without double rush in arteries, or delay of pulse beat at jaw. Loose coagula. Embolism. Causes, as in pericarditis and strain on valves, and poisons and microbes in the blood. Prognosis grave. Treatment, as in the early stages of pericarditis, antirheumatics and germicides more, and diuretics less desirable. For clots iodides, alkalies.
Definition. Inflammation of the serous membrane lining the chambers and covering the valves of the heart.
Pathology and Morbid Anatomy. The causes and symptoms will be better understood after the diseased conditions have been comprehended. The earliest changes are the reddening and thickening of the lining membrane of the heart but above all of that covering the valves. The valves are particularly exposed to inflammation by reason of the friction of the blood when violently forced through the narrow opening in excited conditions of the heart, by the strain thrown upon them from the violent contractions of the heart or the recoil of blood in the arteries, and by their susceptibility in common with all other fibrous structures to rheumatic inflammation. The redness is of the ramified or branching kind characteristic of inflammation, and is neither removable by washing the surface nor does it correspond in position with the colored portion only of a clot which the cavity in question may contain, as seen in bloodstaining occurring after death.
There is further exudation of plastic lymph into and beneath the serous membrane, rendering it opaque, white and thick, or on its surface forming granular elevations, and in the case of the valves becoming moulded into ridges or festoons by the mutual pressure of the different flaps on each other. The inflamed surfaces are further liable to be covered by masses of blood clot in successive layers, deposited by the action of the fibrinogenous matter developed in the inflamed part. These clots sometimes accumulate in considerable masses, firmly adherent to the heart’s walls or valves by their attached surface, but soft and filamentous on their free aspect. These clots or polypi, as they have been called, are soft and loose on their free surface, and become firmer toward their points of attachment. In other words their consistency is in direct ratio to their age. If of old standing they are usually pale yellow or white and streaked with red, while if recent they are mostly red throughout. They vary in size from a thin film to a mass filling up nearly the entire cavity in which they are lodged, and as they frequently extend through the auriculo-ventricular openings or become applied against this or the opening of the great artery, they seriously and sometimes fatally interfere with the circulation. Leblanc asserts that large masses of this kind may be deposited in a few days or even hours, causing sudden deaths, and especially in dogs. He has found other circumstances than endocarditis to cause these fibrinous deposits, and especially the absorption of pus, or the sudden suppression of a long standing discharge, as in catarrh of the air passages. If death does not immediately ensue, these fibrinous deposits may become vascular, as is the case with false membranes in the pleuræ, becoming organized into fibrous tissue, or even degenerating into calcareous matter, necrotic debris, or pus, several instances of which as occurring in horse and cow are on record.
These cases illustrate endocarditis by infection (mycotic, malignant, or ulcerative endocarditis), which occurs independently, or as an extension of a bacteridian disease, primarily localized elsewhere in the system. Thus it is a secondary lesion in infectious omphalitis, pneumonia, pleurisy, arthritis, abscess, pyæmia, etc. Beside the general lesions of endocarditis and a great tendency to molecular death of the new formations and the underlying tissues, there is the presence of specific germs which have been the occasion of the disease. Among these the staphylococcus pyogenes aureus, the streptococcus pyogenes, and the diplococcus pneumoniæ, have been particularly noted. In case the valves were already diseased, they become especially liable to be colonized by any such bacteria that may be circulating in the blood.
In the early stage there may be a mere swelling of the valves, with as yet a smooth, unbroken surface, but with enlargement and increase of the connective tissue cells, later fungous vegetations start out from the surface, and on these the fibrine of the blood is deposited in layers.
Besides the formation of clots on their surfaces other changes occur on the cardiac valves as the result of inflammation. The organization of the exuded lymph within and upon them leads to rigidity, loss of elasticity, unevenness of their surface, contraction and puckering so that they can no longer approximate to each other, but leave the orifice imperfectly closed. They may, moreover, have gristle or bone deposited in their substance. The osseous degeneration of such new products appears to be the most common cause of those ossifications of the heart, of which specimens are to be found in nearly all veterinary museums.
Chronic valve disease is thus found to be a common result of endocarditis, and from the obstacle presented to the flow of blood through the different cardiac orifices by the rigid, inelastic and distorted valves, hypertrophy of the heart frequently supervenes.
In our domestic quadrupeds ante-mortem clots and fibrinous polypi have been chiefly formed in the right side of the heart, and diseased valves in the left.
Symptoms. The general symptoms agree in many respects with those of pericarditis. There are the same general symptoms of fever (temperature 102° to 106°), the same pinched, anxious countenance, the same shortness of breath and oppression when moved, the same violent heart’s action, and the same rapid, excitable pulse tending to be irregular and intermittent. Among the more specific symptoms are a very violent impulse of the heart against the left side, varying in force, however, in successive beats; a metallic tinkling accompanying the impulse and sometimes heard at some little distance from the body, a blowing murmur as soon as the changes in the valves render them insufficient to close the orifices, and, if the obstruction exists on the right side, venous pulse, general venous congestion, and dropsical swellings.
The pulse may at first have considerable force but, as insufficiency of the valves ensues, it becomes small and weak, its weakness forming a most marked contrast to the violence of the heart’s impulse against the side. The irregularity and intermission of the pulse is to be ascribed at first to the impaired nervous energy of the heart though later it is often due to the obstacle presented by clots to the flow of blood from the heart, so that a beat sometimes takes place without a corresponding pulsation. It may reach 80 or 160 per minute in horse or ox.
The blowing murmur when heard is one of the most characteristic symptoms but must be carefully distinguished from other allied heart sounds. If very loud it may be confounded with the friction sound of pericarditis, but may be differentiated by its invariable coincidence with some particular portion of the heart’s beat. The absence of local tenderness is another distinctive symptom. Again in pericarditis effusion takes place early annulling friction sound, and diminishing alike the impulse and the sounds of the heart.
It is of less practical value to be able to distinguish the precise seat of the murmur, yet the following data will guide to such a conclusion.
Simple induration or insufficiency of the Left Auriculoventricular (Mitral) valve. Paroxysms of palpitation, oppression, and difficulty of breathing; vertigo with loss of control over the limbs and vacillating gait; stupor, coma; slight tremor and blowing noise with the first sound of the heart; heart’s impulse, violent, but irregular in force, sometimes double; pulse feeble, irregular, unequal, or intermittent; sometimes though not at all constantly a venous pulse in the lower end of the jugulars. In chronic induration of this valve, or in osseous, or cartilaginous degeneration the same symptoms are shown. The more general symptoms may, however, require exercise to develop them.
Induration, etc., of the Right Auriculo-Ventricular (tricuspid) valve. The symptoms are almost identical with the last. Venous pulse is constant, and, particularly after exertion, the veins generally are distended. Dropsies are more common.
Narrowing of the Mitral orifice. In addition to the same general symptoms as the last named lesions, there is a sighing, blowing, purring or rasping sound, according to the degree of narrowing, heard before the first sound of the heart. It is the noise of the blood rushing through the narrowed orifice between auricle and ventricle. It is usually loudest behind the middle of the shoulder on the left side. Feeble pulse, frequent imminence of suffocation and filling of the limbs, etc., are nearly constant.
Narrowing of the Tricuspid orifice. Symptoms nearly identical with the last. Venous pulse more constant. Blowing murmur sometimes loudest on the right side of the chest.
Induration or insufficiency of the aortic valves. Blowing murmur with the second sound of the heart. Double rushing sound in the carotid with each heart’s beat. There is an appreciable interval between the beat of the heart and corresponding pulsation at the jaw.
Induration or insufficiency of the pulmonary valves. Blowing murmur with the second heart sound, but no corresponding double sound in the carotid, nor any marked retarding of the pulse.
Loose coagula in the heart or adherent ones (polypi) produce one or other of the above class of symptoms, according to the particular orifice they tend to block or the valves whose function they impair.
Anæmia and leukæmia may have blowing murmurs with the first or second heart sound.
Embolism. Plugging of arteries. Another class of symptoms sometimes supervenes because of loose clots being washed on into the arteries, and blocking them when they reach those that are too small to transmit them. These symptoms will be as varied as the organs whose arteries are plugged. If in the brain there may be dulness, stupor, vertigo, somnolence, delirium; if in the liver, biliary and digestive derangement; if in the lungs, cough with the other signs of pneumonia and abscess; and if in the limbs lameness and paralysis, (brought on or aggravated by exercise, and often removed by a few minutes’ rest), wasting of the muscles, etc. (See Embolism).
Causes. These are in the main the same as those of pericarditis. Weak health, exposure to extremes of weather, punctures with foreign bodies, but above all, the rheumatic constitution are common causes. Indeed rheumatism appears more prone to attack the serous membrane lining the heart cavities than that enveloping it externally. One reason for this is to be found in the great and incessantly recurring strain on the fibrous structure of the valves, and particularly in hard worked horses and hunting dogs in which the strain is often extreme. It has been argued that the increased blood pressure caused by digitalis is an appreciable cause. Its frequent connection with rheumatism is shown in the rheumatic lesions of joints and fibrous structures seen in carcasses dead of endocarditis.
Diseases in the muscular substance of the heart as cysts, abscess, etc., frequently extend to the endocardium.
Among other causes must be mentioned disease-changes in the blood. These may act on the valves directly as in the case of lactic acid injected by Dr. Richardson, into the peritoneum with the view of producing rheumatism and successfully as regards the lesions of the cardiac valves; or indirectly by determining coagulation and irritation of the lining membrane coming into contact with the clot. The very fibrinous and plastic state of the blood in extensive inflammations is a probable cause of the occurrence of clots in the heart, and the frequency of such clots in the dog has been ascribed to the plasticity of his blood (Leblanc). The injection of pus into the blood or the absorption of microbes from diseased surfaces will sometimes produce ulcerative disease of the valves. The same is true as regards the germs of omphalitis, pneumonia, arthritis and other infectious diseases.
Lafosse records certain cases of endocarditis due to extension of the disease from inflamed veins.
Prognosis. Endocarditis is always attended with great danger to life, but it is more likely to terminate in chronic valvular disease which quite unfits the animal for useful work. Mild cases may terminate in complete recovery.
Treatment. This is in the main the same as that adopted in the early stages of pericarditis. Absolute rest is of prime importance. Laxatives, sedatives and counterirritants are to be mainly relied upon. Belladonna and chloroform on the chest behind the left elbow may be used. As there is not the same danger from effusion, diuretics need not be pushed to the same extent. Digitalis must be avoided if possible until the high fever subsides. In infective cases, quinia, salicylate of soda, salol, or hyposulphite of soda may be given. Later give tincture of muriate of iron.
In rhemuatic cases, treat as for an acute attack of rheumatism. Frequent large doses of salicylate of soda or salol, large doses of acetate of potass and colchicum, warm clothing and counterirritants to the region of the heart are especially demanded. (See Rheumatism.)
When clots are suspected, and when endocarditis threatens to lapse into the chronic form, it is recommended to give iodide of potassium (horse and ox 1 drachm, dog 5 grains, twice daily) with carbonate of ammonia or of potass and bitter tonics. A lengthened rest after apparent recovery is essential to avoid permanent valve lesions.