Chapter XIV: Part 14

Subacute endocarditis, which is the most common form, may not become appreciable for several days after its commencement. It is characterized by being confined to one or more anatomical divisions of the heart, and all the successive morbid changes follow each other in a comparatively slow process. Often we would not be led to suspect heart affection were it not for the distress in breathing, which it generally occasions when the animal is exercised, especially if the valves are much involved. When coagula or vegetations form upon the inflamed membrane, either in minute shreds or patches, or when formation of fibrinous clots occurs in the cavity affected, some of these materials may be carried from the cavity of the heart by the blood current into remote organs, constituting emboli that are liable to suddenly plug vessels and thereby interrupt important functions. In the great majority of either acute or subacute grades of endocarditis, whatever the exciting cause, the most alarming symptoms disappear in a week or 10 days, often leaving, however, such changes in the interior lining or valvular structures as to cause impairment in the circulation for a much longer period of time. These changes usually consist of thickening or induration of the inflamed structures. But while the effects of the inflammation in the membrane lining the walls of the ventricles may subside to such a degree as to cause little or no inconvenience, or even wholly disappear, yet after the valvular structures have been involved, causing them to be thicker, less flexible than normal, they usually remain, obstructing the free passage of the blood through the openings of the heart, thereby inducing secondary changes, which take place slowly at first, but ultimately seriously impair the animal's usefulness. What was but a slight obstruction to the circulation during the first few weeks after the subsidence of the cardiac inflammatory attack becomes in process of time so much increased as to induce increased growth in the muscular structure of the heart, constituting hypertrophy of the walls of the ventricles, more particularly of the left, with corresponding fullness of the left auricle and pulmonary veins, thereby producing fullness of the capillaries in the lungs, pressure upon the air cells, difficult or asthmatic breathing--greatly increased in attempts to work--until in a few months many of these cases become entirely disabled for work. Sometimes, too, dropsical effusions in the limbs or into the cavities of the body result from the irregular and deficient circulation. Derangement of the urinary secretion, with passive congestion of the kidneys, may also appear.

Endocardial inflammation is seldom fatal in its early stages, but in many cases the recovery is incomplete, for a large proportion is left with some permanent thickening of the valves, which constitutes the beginning of valvular disease.

_Symptoms._--Endocarditis may be ushered in by a chill, with sudden and marked rise in temperature. The pulse rapidly decreases in strength or may become irregular, while the heart beats more or less tumultuously. In the early stages soft-blowing sounds may be heard by placing the ear over the heart on the left side, which correspond in number and rhythm to the heart's action. Excessive pain, though not so great as in acute pleuritis, is manifested when the animal is compelled to trot; very often difficulty in breathing, or shortness of breath, on the slightest exertion develops early in the attack. When the valves are involved in the inflammatory process the visible mucous membranes become either very pale or very dark colored, and fainting may occur when the head is suddenly elevated. When the valves of the right side are affected we may find a regurgitant pulsation in the jugular vein. Occasionally it happens that the heart contracts more frequently than the pulse beats--that is, there may be twice as many contractions of the heart in a minute as there are pulse waves in the arteries. The pulse is always very fast. In some cases we find marked lameness of the left shoulder, and when the animal is turned short to the left side he may groan with pain, and the heart's action become violently excited, although pressure against the chest wall will not produce pain unless roughly applied. The animal is not disposed to eat or drink much; the surface of the body and legs are cold--rarely excessively hot--and frequently the body of the animal is in a subdued tremor. In nearly all cases there is partial suppression of the urinary secretion. The symptoms may continue with very little modification for three or four days, sometimes seven days, without any marked changes. If large fibrinous clots form in the heart the change will be sudden and quickly prove fatal unless they become loosened and are carried away in the circulation; then apoplexy may result from the plugging of arteries too small to give further transmission. If the animal manifests symptoms of improvement, the changes usually are slow and steady until he feels apparently as well as ever, eats well, and moves freely in his stall or yard. When he is taken out, however, the seeming strength often proves deceptive, as he may quickly weaken if urged into a fast gait, the breathing becomes quickened with a double flank movement as in heaves, and all the former symptoms reappear in a modified degree. An examination at this stage may reveal valvular insufficiency, cardiac hypertrophy, or pulmonary engorgement.

In fatal cases of endocarditis death often occurs about the fourth day, from the formation of heart clot or too great embarrassment of the circulation. Endocarditis may be suspected in all cases where plain symptoms of cardiac affection are manifested in animals affected with influenza, rheumatism, or any disease in which the blood may convey septic matter.

Acute endocardial inflammation may be distinguished from pleuritis by the absence of any friction murmur, absence of pain when the chest wall is percussed, and the absence of effusion in the cavity of the chest. It may be distinguished from pericarditis by the absence of the friction sounds and want of an enlarged area of dullness on percussion.

_Treatment._--The objects to be attained by treatment will be to remove or mitigate as much as possible the cause inducing the disease; to find a medicine which will lessen the irritability of the heart without weakening it; and, last, to maintain a free urinary secretion and prevent exudation and hypertrophy. So long as there is an increase of temperature, with some degree of scantiness of the urine, it may be safe to believe that there is some degree of inflammatory action existing in the cardiac structures, and as long as any evidence of inflammatory action remains, however moderate in degree, there is a tendency to increase or hypertrophy of the connective tissue of the heart or valves, thereby rendering it almost certain that the structural changes will become permanent unless counteracted by persistent treatment and complete rest.

The tincture of digitalis, in 20-drop doses, repeated every hour, is perhaps the most reliable agent we know to control the irritability of the heart, and this also has a decided influence upon the urinary secretion. After the desired impression upon the heart is obtained the dose may be repeated every two or three hours, or as the case may demand. Tincture of strophanthus, in 2-dram doses, will quiet the tumultuous action of the heart in some cases where the digitalis fails. Bleeding, blistering, and stimulating applications to the chest should be avoided. They serve to irritate the animal and can do no possible good. Chlorate of potassium in 2-dram doses may be given in the drinking water every four hours for the first five or six days, and then be superseded by the nitrate of potassium in half-ounce doses for the following week or until the urinary secretion becomes abnormally profuse. Where the disease is associated with rheumatism, 2-dram doses of salicylate of soda may be substituted for the chlorate of potassium. To guard against chronic induration of the valves, the iodid of potassium, in 1 to 2 dram doses, should be given early in the disease and may be repeated two or three times a day for several weeks. When chronic effects remain after the acute stage has passed this drug becomes indispensable.

When dropsy of the limbs develops, it is due to weakened circulation or functional impairment of the kidneys. When there is much weakness in the action of the heart, or general debility is marked, the iodid of iron, in 1-dram doses, combined with hydrastis, 3 drams, may be given three times a day. Arsenic, in 5-grain doses twice a day, will give excellent results in some cases of weak heart associated with difficult breathing. In all cases absolute rest and warm stabling, with comfortable clothing, become necessary, and freedom from work should be allowed for a long time after all symptoms have disappeared.

PERICARDITIS, OR INFLAMMATION OF THE SAC INCLOSING THE HEART.

_Causes._--Pericarditis may be induced by cold and damp stabling, exposure and fatigue, from wounds caused by broken ribs, etc. Generally, however, it is associated with an attack of influenza, rheumatism, pleuritis, etc.

_Symptoms._--Usually the disease manifests itself abruptly by a brief stage of chills coincident with pain in moving, a short painful cough, rapid and short breathing, and high temperature, with a rapid and hard pulse. In the early stages of the disease the pulse is regular in beat; later, when there is much exudation present in the pericardial sac, the heartbeat becomes muffled, and may be of a double or rebounding character. By placing the ear against the left side of the chest behind the elbow a rasping sound may be heard, corresponding to the frequency of the heartbeat. This is known as a friction sound. Between the second and fourth days this sound may disappear, due to a distension of the pericardium by an exudate or serous effusion. As soon as this effusion partly fills the pericardium, percussion will reveal an abnormally increased area of dullness over the region of the heart, the heartbeats become less perceptible than in health, and in some cases a splashing or flapping sound may become audible.

If the effusion becomes absorbed, the friction sound usually recurs for a short time; this friction may often be felt by applying the hand to the side of the chest. In a few cases clonic spasms of the muscles of the neck may be present. In acute pericarditis, when the effusion is rapid and excessive, the animal may die in a few days or recovery may begin equally as early. In subacute or in chronic cases the effusion may slowly become augmented until the pressure upon the lungs and interference with the circulation become so great that death will result. Whether the attack is acute, subacute, or chronic, the characteristic symptoms which will guide us to a correct diagnosis are the friction sound, which is always synchronous with the heart's action, the high temperature with hard, irritable pulse, and, in cases of pericardial effusion, the increased area of dullness over the cardiac region. When the disease is associated with influenza or rheumatism, some of the symptoms may be obscure, but a careful examination will reveal sufficient evidence upon which to base a diagnosis. When pericarditis develops as a result of or in connection with pleuritis, the distinction may not be very clearly definable, neither will many recover. When it results from a wound or broken rib, it almost invariably proves fatal.

_Pathology._--Pericarditis may at all times be regarded as a very serious affection. At first we will find an intense injection or accumulation of blood in the vessels of the pericardium, giving it a red and swollen appearance, during which we have the friction sound. In 24 to 48 hours this engorgement is followed by an exudation of sero-fibrinous fluid, the fibrinous portion of which may soon form a coating over the internal surface of the pericardial sac, and may ultimately form a union of the opposing surfaces. Generally this adhesion will only be found to occupy a portion of the surfaces. As the serous or watery portion of this effusion is absorbed, the distinctness of the friction sound recurs, and may remain perceptible in a varied degree for a long time. When the serous effusion is very great, the pressure exerted upon the heart weakens its action, and may produce death soon; when it is not so great, it may cause dropsies of other portions of the body. When the adhesions of the pericardial sac to the body of the heart are extensive, they generally lead to increased growth, or hypertrophy, of the heart, with or without dilatation of its cavities; when they are but slight, they may not cause any inconvenience.

_Treatment._--In acute or subacute pericarditis the tincture of digitalis may be given in 20 to 30 drop doses every hour until the pulse and temperature become reduced. Whisky or carbonate of ammonia may be given regularly as stimulants. Bandages should be applied to the legs; if the legs are very cold, tincture of capsicum should be first applied; the body should be warmly clothed in blankets, to promote perspiration. When the suffering from pain is very severe, 10 grains of morphin may be given by the mouth once or twice a day; nitrate of potassium, half an ounce, in drinking water, every six hours; after the third day, iodid of potassium, in 2-dram doses, may be substituted. Cold packs to the chest in the early stages of the disease may give marked relief, or, late in the disease, smart blisters may be applied to the sides of the chest with benefit. If the disease becomes chronic, iodid of iron and gentian to support the strength will be indicated, but the iodid of potassium, in 1 or 2 dram doses, two or three times a day, must not be abandoned so long as there is an evidence of effusion or plastic exudate accumulating in the pericardial sac. Where the effusion is great and threatens the life of the patient, tapping by an expert veterinarian may save the animal.

VALVULAR DISEASE OF THE HEART.

Acute valvular disease can not be distinguished from endocarditis, and chronic valvular affections are generally the result of endocardial inflammation. The valves of the left side are the most subject--the bicuspid or mitral and the aortic or semilunar. The derangement may consist of mere inflammation and swelling, or the edges of the valves may become covered by the organization of the exudation, thus narrowing the passage. Valvular obstruction and adhesions may occur or the tendinous cords may be lengthened or shortened, thus obstructing the orifices and permitting the regurgitation of blood. In protected cases the fibrous tissue of the valves may be transformed into fibro-cartilage or bone, or there may be deposits of salts of lime beneath the serous membrance, which may terminate in ulceration, rupture, or fissures. Sometimes the valves become covered by fibrinous, fleshy, or hard vegetations, or excrescences. In cases of considerable dilatation of the heart there may be atrophy and shrinking of the valves.

_Symptoms._--Valvular disease may be indicated by a venous pulse, jerking pulse, intermittent pulse, irregular pulse; palpitation; constant abnormal fullness of the jugular veins; difficulty of breathing when the animal becomes excited or is urged out of a walk or into a fast trot; attacks of vertigo; congestion of the brain; dropsical swelling of the limbs. A blowing, cooing, or bubbling murmur may sometimes be heard by placing the ear over the heart on the left side of the chest.

Hypertrophy, or dilatation, or both, usually follow valvular disease.

_Treatment._--When the pulse is irregular or irritable, tonics, such as preparations of iron, gentian, and ginger, may be given. When the action of the heart is jerking or violent, 20 to 30 drop doses of tincture of digitalis or of veratrum viride may be given until these symptoms abate. As the disease nearly always is the result of endocarditis, the iodid of potassium and general tonics, sometimes stimulants, when general debility supervenes, may be of temporary benefit. Very few animals recover or remain useful for any length of time after once marked organic changes have taken place in the valvular structure of the heart.

ADVENTITIOUS GROWTHS IN THE HEART.

Fibrous, cartilaginous, and bony formations have been observed in some rare instances in the muscular tissue. Isolated calcareous masses have sometimes been embedded in the cardiac walls. Fibrinous coagula and polypous concretions may be found in the cavities of the heart. The former consist of coagulated fibrin, separated from the mass of blood, of a whitish or yellowish white color, translucent, of a jellylike consistence, and having a nucleus in the center. They may slightly adhere to the surface of the cavity, from which they can easily be separated without altering the structure of the endocardium. They probably result from an excess of coagulability of fibrin, which is produced by an organization of the lymph during exudation. They are usually found in the right auricle and ventricle.

Polypous concretions are firmer than in the preceding, more opaque, of a fibrous texture, and may be composed of successive layers. In some instances they are exceedingly minute, while in others they almost fill one or more of the cavities. Their color is usually white, but occasionally red from the presence of blood. They firmly adhere to the endocardium, and when detached from it give it a torn appearance. Occasionally, a vascular communication seems to exist between them and the substance of the heart. They may be the result of fibrinous exudation from inflammation of the inner surface of the heart or the coagulation of a portion of the blood which afterwards contracts adhesion with the heart. These concretions prove a source of great inconvenience and often danger, no matter how formed. They cause a diminution in the cavity in which they are found, thus narrowing the orifice through which the blood passes, or preventing a proper coaptation of the valves, which may produce most serious valvular disease.

_Symptoms._--These are frequently uncertain; they may, however, be suspected when the action of the heart suddenly becomes embarrassed with irregular and confused pulsations, great difficulty of breathing, and the usual signs dependent upon the imperfect arterialization of the blood.

_Treatment._--Stimulants, whisky, or carbonate of ammonia may be of service.

PALPITATION OF THE HEART.

This is a tumultuous and usually irregular beating of the heart. It may be due to a variety of causes, both functional and organic. It may occur as a result of indigestion, fright, increased nervousness, sudden excitement, excessive speeding, etc. (See "Thumps," p. 225.)

_Symptoms._--The heart may act with such violence that each beat may jar the whole body of the animal; very commonly it may be heard at a short distance away from the animal. It can usually be traced very readily to the exciting cause, which we may be able to avoid or overcome in the future and thereby obviate subsequent attacks. Rest, a mild stimulant, or a dose or two of tincture of digitalis or opium will generally give prompt relief. When it is due to organic impairment of the heart it must be regarded as a symptom, not as a matter of primary specific treatment.

SYNCOPE, OR FAINTING.

Actual fainting rarely occurs among horses. It may, however, be induced by a rapid and great loss of blood, pain of great intensity, a mechanical interference with the circulation of the brain, etc.

_Symptoms._--Syncope is characterized by a decrease or temporary suspension of the action of the heart and respiration, with partial or total loss of consciousness. It generally occurs suddenly, though there may be premonitory symptoms, as giddiness, or vertigo, dilated pupil, staggering, blanching of the visible mucous membranes, a rapidly sinking pulse, and dropping to the ground. The pulse is feeble or ceases to beat; the surface of the body turns cold; breathing is scarcely to be perceived, and the animal may be entirely unconscious. This state is uncertain in duration--generally it lasts only a few minutes; the circulation becomes restored, breathing becomes more distinct, and consciousness and muscular strength return. In cases attended with much hemorrhage or organic disease of the heart, the fainting fit may be fatal; otherwise it will prove but a transient occurrence. In paralysis of the heart the symptoms may be exactly similar to syncope. Syncope may be distinguished from apoplexy by the absence of stertorous breathing and lividity of the visible mucous membranes.

_Treatment._--Dash cold water on the head; administer a stimulant--4 ounces of whisky or half an ounce of carbonate of ammonia. Prevent the animal from getting up too soon, or the attack may immediately recur. Afterwards, if the attack was due to weakness from loss of blood, impoverished blood, or associated with debility, general tonics, rest, and nourishing food are indicated.

HYPERTROPHY OF THE HEART, OR CARDIAC ENLARGEMENT.

Hypertrophy of the heart implies augmentation of bulk in its muscular substance, with or without dilatation or contraction of its cavities. It may exist with or without other cardiac affections. In valvular disease or valvular insufficiency hypertrophy frequently results as a consequence of increased demand for propelling power. The difficulties with which it is most frequently connected are dilatation and ossification of the valves. It may also occur in connection with atrophied kidneys, weak heart, etc. It may be caused by an increased determination of blood to the organ or from a latent form of myocarditis, and it may arise from a long-continued increase of action dependent upon nervous disease. All the cavities of the heart may have their walls hypertrophied or the thickening may involve one or more. While the wall of a ventricle is thickened, its cavity may retain its normal size (simple hypertrophy) or be dilated (eccentric hypertrophy), or it may be contracted (concentric hypertrophy). Hypertrophy of both ventricles increases the length and breadth of the heart. Hypertrophy of the left ventricle alone increases its length; of the right ventricle alone increases its breadth toward the right side. Hypertrophy with dilatation may affect the chambers of the heart conjointly or separately. This form is by far the most frequent variety of cardiac enlargement. When the entire heart is affected, it assumes a globular appearance, the apex being almost obliterated and situated transversely in the chest. The bulk may become three or four times greater than the average heart.

_Symptoms._--In hypertrophy of the heart, in addition to the usual symptoms manifested in organic diseases of the heart, there is a powerful and heaving impulse at each beat, which may be felt on the left side, often also on the right. These pulsations are regular, and when full and strong at the jaw there is a tendency to active congestion of the capillary vessels, which frequently give rise to local inflammation, active hemorrhage, etc. If the pulse is small and feeble at the jaw, we may conclude that there is some obstacle to the escape of the blood from the left ventricle into the aorta, which has given rise to the hypertrophy. In case of hypertrophy with dilatation, the impulse is not only powerful and heaving, but it is diffused over the whole region of the heart, and the normal sounds of the heart are greatly increased in intensity. Percussion reveals an enlarged area of dullness, while the impulse is usually much stronger than normal.

Dropsy of the pericardium will give the same wide space of dullness, but the impulse and sound are lessened. An animal with a moderate degree of enlargement may possibly live a number of years and be capable of ordinary work; it depends largely upon concomitant disease. As a rule, an animal affected with hypertrophy of the heart will soon be incapacitated for work, and becomes useless and incurable.

_Treatment._--If the cause can be discovered and is removable, it should be done. The iodid of potassium, in cases of valvular thickening, may be of some benefit if continued for a sufficient length of time; it may be given in 2-dram doses, twice a day, for a month or more. The tincture of digitalis may be given, in cases where the pulse is weak, in doses of 2 teaspoonfuls three times daily. This remedy should not be continued if the pulse becomes irregular. General tonics, freedom from excitement or fatigue, avoidance of bulky food, good ventilation, etc., are indicated.

DILATATION OF THE HEART.

This is an enlargement, or stretching, of the cavities of the heart, and may be confined to one or extend to all. Two forms of dilatation may be mentioned--simple dilatation, where there is normal thickness of the walls, and passive, or attenuated, dilatation, where the walls are simply distended or stretched out without any addition of substance.

_Causes._--Any cause producing constant and excessive exertion of the heart may lead to dilatation. Valvular disease is the most frequent cause. General anemia predisposes to it by producing relaxation of muscular fiber. Changes in the muscular tissue of the heart walls, serous infiltration from pericarditis, myocarditis, fatty degeneration and infiltration, and atrophy of the muscular fibers may all lead to dilatation.

_Symptoms._--The movements of the heart are feeble and prolonged, a disposition to staggering or vertigo, dropsy of the limbs, very pale or very dark-colored membranes, and difficult breathing on the slightest excitement.

_Treatment._--General tonics, rich feed, and rest.

FATTY DEGENERATION OF THE HEART.

Fatty degeneration may involve the whole organ, or may be limited to its walls, or even to circumscribed patches. The latter is situated at the exterior, and gives it a mottled appearance. When generally involved it is flabby or flaccid, and in extreme cases collapses when emptied or cut. Upon dissection the interior of the ventricles is observed to be covered with buff-colored spots of a singular zigzag form. This appearance may be noticed beneath the pericardium, and pervading the whole thickness of the ventricular walls, and in extreme cases those of the fleshy columns in the interior of the heart. These spots are found to be degenerated muscular fibers and colonies of oil globules. Fatty degeneration is often associated with other morbid conditions of the heart, such as obesity, dilatation, rupture, aneurism, etc. It may be connected with fatty diseases of other organs, such as the liver, kidneys, etc. When it exists alone its presence is seldom suspected previous to death. It may be secondary to hypertrophy of the heart, to myocarditis, or to pericarditis. It may be due to deteriorated conditions of the blood in wasting diseases, excessive hemorrhages, etc., or to poisoning with arsenic and phosphorus.

_Symptoms._--The most prominent symptoms of fatty degeneration are a feeble action of the heart, a remarkably slow pulse, general debility, and attacks of vertigo. It may exist for a long time, but is apt to terminate suddenly in death upon the occurrence of other diseases, surgical operations, etc. It may involve a liability to sudden death from rupture of the ventricular walls.

_Treatment._--Confinement in feed to oats, wheat or rye bran, and timothy hay. Twenty drops of sulphuric acid may be given in drinking water three times a day, and hypophosphite of iron in 2-dram doses, mixed with the feed, twice a day. Other tonics and stimulants as they may be indicated.

RUPTURE OF THE HEART.

This may occur as the result of some previous disease, such as fatty degeneration, dilatation with weakness of the muscular walls, etc. It may be caused by external violence, a crushing fall, pressure of some great weight, etc. Usually death follows a rupture very quickly, though an animal may live for some time when the rent is not very large.

WEAKNESS OF THE HEART.

This may arise from general debility, the result of exhausting disease, overwork, or heart strain, or loss of blood. It is indicated by a small, feeble, but generally regular pulse, coldness of the body, etc.

Treatment should be directed to support and increase the strength of the animal by tonics, rest, and nutritious feed. Carbonate of ammonia may be given to stimulate the heart's action and to prevent the formation of heart clot.

CONGESTION OF THE HEART

Congestion, or an accumulation of the blood in the cavities of the heart, may occur in consequence of fibrinous deposits interfering with the free movements of the valves, usually the product of endocarditis or as a result of excessive muscular exertion.

Symptoms are great difficulty of breathing, paleness of the visible mucous membranes, great anxiety, frequently accompanied by a general tremor and cold perspiration, followed by death. It usually results in death very quickly.

CYANOSIS OF NEWBORN FOALS.

This is a condition sometimes found in foals immediately after birth, and is due to nonclosure of the foramen ovale, which allows a mixture of the venous with the arterial blood in the left cavities of the heart. It is characterized by a dark purple or bluish color of the visible mucous membranes, shortness of breath, and a general feebleness. Foals thus affected generally live only a few hours after birth.

DISEASES OF ARTERIES, OR ARTERITIS AND ENDARTERITIS.

Inflammation of arteries is rarely observed in the horse as a primary affection. Direct injuries, such as blows, may produce a contusion and subsequent inflammation of the wall of an artery; severe muscular strain may involve an arterial trunk; hypertrophy of the heart, by increasing arterial tension, may result in the production of a general endarteritis. Septic infection may affect the inner coat and ultimately involve all three, or it may be the result of an inflammation in the vicinity of the vessels, etc. Inflammation of arteries, whatever the cause may be, often leads to very serious results in the development of secondary changes in their walls. Arteritis may be acute, subacute, or chronic; when the inner coat alone is affected it is known as endarteritis.

_Symptoms._--Arteritis is characterized by a painful swelling along the inflamed vessel, throbbing pulse, coldness of the parts supplied by the inflamed vessel, sometimes the formation of gangrenous sloughs, suppuration, abscess, etc. In an inflammation of the iliac arteries we find coldness and excessive lameness or paralysis of one or both hind limbs.

_Pathology._--In acute arteritis we find swelling along the vessel, loss of elasticity, friability, and thickening of the walls; a roughness and loss of gloss of the inner coat, with the formation of coagula or pus in the vessel. Subacute or chronic arteritis may affect only the outer coat (periarteritis), both the outer and middle coat, or the inner coat alone (endarteritis); and by weakening the respective coats leads to rupture, aneurism, or to degenerations, such as bony, calcareous, fatty, atheromatous, etc. It may also lead to sclerosis or increase of fibrous tissue, especially in the kidneys, when it may result in the condition known as arterio-capillary fibrosis. Chronic endarteritis is fruitful in the production of thrombus and atheroma. Arteritis may be limited to single trunks or it may affect, more or less, all the arteries of the body. Arteries which are at the seat of chronic endarteritis are liable to suffer degenerative changes, consisting chiefly of fatty degeneration, calcification, or the breaking down of the degenerated tissue, and the formation of erosions or ulcerlike openings in the inner coat. These erosions are frequently called atheromatous ulcers, and fragments of tissue from these ulcers may be carried into the circulation, forming emboli. Fibrinous thrombi are apt to form upon the roughened surface of the inner coat or upon the surface of the erosions.

Fatty degeneration and calcification of the middle and outer coats may occur, and large, hard, calcareous plates project inward, upon which thrombi may form or may exist in connection with atheroma of the inner coat. When there is much thickening and increase of new tissue in the wall of the affected artery it may encroach upon the capacity of the vessel, and even lead to obliteration. This is often associated with interstitial inflammation of glandular organs.

_Treatment._--Carbonate of potassium in 1-dram doses, to be given in 4 ounces liquor acetate of ammonia every six hours; scalded bran sufficient to produce loosening of the bowels, and complete rest; externally, applications of hot water or hot hop infusion.

ATHEROMA.

Atheroma is a direct result of an existing chronic endarteritis, the lining membrane of the vessels being invariably involved to a greater or less degree. It is most frequently found in the arteries, although the veins may develop an atheromatous condition when exposed to any source of prolonged irritation. Atheroma may affect arteries in any part of the body; in some instances almost every vessel is diseased, in others only a few, or even parts of one vessel. It is a very common result of endocarditis extending into the aorta, which we find perhaps the most frequent seat of atheroma. As a result of this condition the affected vessel becomes impaired in its contractile power, loses its natural strength, and, in consequence of its inability to sustain its accustomed internal pressure, undergoes in many cases dilatation at the seat of disease, constituting aneurism. In an atheromatous vessel, calcareous deposits soon occur, which render it rigid, brittle, and subject to ulceration or rupture. In such vessels the contractility is destroyed, the middle coat atrophied and beyond repair. Atheroma in the vessels of the brain is a frequent cause of cerebral apoplexy. No symptoms are manifested by which we can recognize this condition during life.

CONSTRICTION OF AN ARTERY.

This is usually the result of arteritis, and may partly or wholly be impervious to the flow of blood. When this occurs in a large vessel it may be followed by gangrene of the parts; usually, however, collateral circulation will be established to nourish the parts previously supplied by the obliterated vessel. In a few instances constriction of the aorta has produced death.

ANEURISM.

Aneurism is usually described as true or false. True aneurism is a dilatation of the coats of an artery over a larger or smaller part of its course. Such dilatations are usually due to chronic endarteritis and atheroma. False aneurism is formed after a puncture of an artery by a dilatation of the adhesive lymph by which the puncture was united.

_Symptoms._--If the aneurism is seated along the neck or a limb it appears as a tumor in the course of an artery and pulsating with it. The tumor is round, soft, and compressible, and yields a peculiar fluctuation upon pressure. By applying the ear over it a peculiar purring or hissing sound may sometimes be heard. Pulsation, synchronous with the action of the heart, is the diagnostic symptom. It is of a slow, expansive, and heavy character, as if the whole tumor were enlarging under the hand. Aneurisms seated internally may occupy the cavity of the cranium, chest, or abdomen. As regards the first, little is known during life, for all the symptoms which they produce may arise from other causes. Aneurism of the anterior aorta may be situated very closely to the heart or in the arch, and it is very seldom that we can distinguish it from disease of the heart. The tumor may encroach upon the windpipe and produce difficulty in breathing, or it may produce pressure upon the vena cava or the thoracic duct, obstructing the flow of blood and lymph. In fact, whatever parts the aneurism may reach or subject to its pressure, may have their functions suspended or disturbed. When the tumor in the chest is large, we generally find much irregularity in the action of the heart; the superficial veins of the neck are distended, and there is usually dropsical swelling under the breast and of the limbs. There may be a very troublesome cough without any evidence of lung affection. Sometimes pulsation of the tumor may be felt at the lower part of the neck where it joins the chest. When the aneurism occurs in the posterior aorta no diagnostic symptoms are appreciable; when it occurs in the internal iliac arteries an examination per rectum will reveal it.

There is one form of aneurism which is not infrequently overlooked, affecting the anterior mesenteric artery, primarily induced by a worm--_Strongylus vulgaris_. This worm produces an arteritis, with atheroma, degeneration, and dilatation of the mesenteric arteries, associated with thrombus and aneurism. The aneurism gives rise to colic, which appears periodically in a very violent and often persistent type. Ordinary colic remedies have no effect, and after a time the animal succumbs to the disease. In all cases of animals which are habitually subject to colicky attacks, parasitic aneurism of the anterior mesenteric artery may be suspected. (See p. 92.)

_Pathology._--Aneurisms may be diffuse or sacculated. The diffuse consists in a uniform dilatation of all the coats of an artery, so that it assumes the shape of a cylindrical swelling. The wall of the aneurism is atheromatous, or calcified; the middle coat may be atrophied. The sacculated, or circumscribed, aneurism consists either in a dilatation of the entire circumference of an artery over a short portion of its length, or in a dilatation of only a small portion of one side of the wall. Aneurism may become very large; as it increases in size it presses upon and causes the destruction of neighboring tissues. The cavity of the aneurismal sac is filled with fluid or clotted blood or with layers of fibrin which adhere closely to its wall. Death is produced usually by the pressure and interference of the aneurism with adjoining organs or by rupture. In worm aneurism we usually find large thrombi within the aneurismal dilatation of the artery, which sometimes plug the whole vessel or extend into the aorta. Portions of this thrombus, or clot, may be washed away and produce embolism of a smaller artery. The effect in either case is to produce anemia of the intestinal canal, serous or bloody exudation in its walls, which leads to paralysis of the intestine and resultant colicky symptoms.

_Treatment._--The only treatment advisable is to extirpate or ligate the tumor above and below.

RUPTURE OF AN ARTERY.

Endarteritis, with its subsequent changes in the walls of arteries, is the primary cause of rupture in the majority of instances. The rupture may be partial, involving only one or two coats, and will then form an aneurism. If complete, it may produce death when it involves a large vessel, especially if it is situated in one of the large cavities permitting an excessive escape of blood. Rupture may be produced by mechanical violence or accident.

_Symptoms._--In fatal rupture, associated with profuse bleeding, the animal becomes weak, the visible mucous membranes become blanched, the breathing hurried or gasping, pupils dilated, staggering in gait, syncope, death. When the hemorrhage is limited the symptoms may not become noticeable; if it is near the surface of the body a round or diffuse swelling or tumor may form, constituting a hygroma. If the rupture is associated with an external wound, the bleeding artery should be ligated, or where a bandage is applicable, pressure may be applied by tight bandaging. As a secondary result of rupture of an artery we may have formation of abscess, gangrene of a part, etc.

_Treatment._--When rupture of a deep-seated artery is suspected, large doses of fluid extract of ergot may be given to produce contraction of the blood vessels. Tannin and iron are also useful. The animal should be allowed to have as much water as he desires. Afterwards stimulants and nourishing feed are indicated.

THROMBUS AND EMBOLISM.

By thrombosis is generally understood the partial or complete closure of a vessel by a morbid product developed at the site of the obstruction. The coagulum, which is usually fibrinous, is known as a thrombus. The term "embolism" designates an obstruction caused by any body detached and transported from the interior of the heart or of some vessel. Thrombi occur as the result of an injury to the wall of the vessel or may follow its compression or dilatation; they may result from some alteration of the wall of the vessel by disease or by the retardation of the circulation. These formations may occur during life, in the heart, arteries, veins, or in the portal system. When a portion of fibrin coagulates in one of the arteries and is carried along by the circulation, it will be arrested, of course, in the capillaries, if not before; when in the veins, it may not be stopped until it reaches the lungs; and when in the portal system the capillaries of the liver will prevent its further progress. The formation of thrombi may act primarily by causing partial or complete obstruction, and, secondarily, either by larger or smaller fragments becoming detached from their end and by being carried along by the circulation of the blood to remote vessels, embolism; or by the coagulum becoming softened and converted into pus, constituting suppurative phlebitis. These substances occur most frequently in those affections characterized by great exhaustion or debility, such as pneumonia, purpura hemorrhagica, endocarditis, phlebitis, puerperal fever, hemorrhages, etc. These concretions may form suddenly and produce instantaneous death by retarding the blood current, or they may arise gradually, in which case the thrombi may be organized and attached to the walls of the heart, or they may soften, and fragments of them (emboli) may be carried away. The small, wartlike excrescences occurring sometimes in endocarditis may occasionally form a foundation on which a thrombi may develop.

_Symptoms._--When heart clot, or thrombus, exists in the right side, the return of blood from the body and the aeration in the lungs is impeded, and if death occurs, it is owing to syncope rather than to strangulation in pulmonary respiration. There will be hurried and gasping breathing, paleness and coldness of the surface of the body, a feeble and intermittent or fluttering pulse, and fainting. When a fibrinous coagulum is carried into the pulmonary artery from the right side of the heart, the indications are a swelling and infiltration of the lungs and pulmonary apoplexy. When the clot is situated in the left cavities of the heart or in the aorta, death, if it occurs, takes place either suddenly or at the end of a few hours from coma.

_Pathology._--When a coagulum is observed in the heart it may become a question whether it was formed during life or after death. The loose, dark coagula so often found after death are polypi. If the deposition has taken place during the last moments of life, the fibrin will be isolated and soft, but not adherent to the walls; if it be isolated, dense, and adherent or closely intertwined with the muscles of the papillae and tendinous cords, the deposition has occurred more or less remote from the act of dying. Occasionally the fibrin may be seen lining one of the cavities of the heart, like a false endocardium, or else forming an additional coat to the aorta or other large vessels without producing much obstruction. Thrombi, in some instances, soften in their centers, and are then observed to contain a puslike substance. If this softening has extended considerably, an outer shell, or cyst, only may remain. The sources of danger exist not only in the interruption of the circulation of the blood, but also in a morbid state of the system, produced by the disturbed nutrition of a limb or organ, as well as the mingling of purulent and gangrenous elements with the blood.

_Treatment._--The urgent symptoms should be relieved by rest, stimulants, and the use of agents which will act as solvents to the fibrinous clots. Alkalis are specially useful for this purpose. Carbonate of ammonia may be administered in all cases of thrombus, and should be continued for a long time in small doses several times a day. In cases of great debility associated with a low grade of fever, stimulants and tonics, and nitro-muriatic acid as an antiseptic, may be beneficial.

DISEASES OF VEINS, OR PHLEBITIS.

Inflammation of veins may be simple or diffuse. In simple phlebitis the disease of the vein is confined to a circumscribed or limited portion of a vein; in diffuse it involves the vein for a long distance; it may even extend from a limb or foot to the heart.

_Causes._--Phlebitis may be induced by contusions or direct injuries, an extension of inflammation from surrounding tissue, such as in abscess, formation of tumor, or malignant growth. It is often due to embolism of infective material, gangrenous matter, etc. Blood-letting from the jugular vein is occasionally followed by dangerous phlebitis.

_Symptoms._--The symptoms vary according to the extent and severity of the inflammation. In most cases the vein is swollen, thickened, and indurated to such a degree as to resemble an artery. A diffused swelling, with great tenderness, may extend along the affected vessel and the animal manifest all the symptoms connected with acute fever and general functional disturbance.

_Pathology._--The disease is only serious when large veins are affected. The coats undergo the same changes as in arteritis; clots of blood and lymph plug the inflamed vessel, and, if the inflammatory process continues, these are converted into pus, which ruptures the vessel and produces a deep abscess; or it may be carried away in the circulation and produce metastatic abscess in the lungs or other remote organs. In mild cases the clots may become absorbed and the vessel restored to health. Phlebitis in the course of the veins of the limbs frequently leads to numerous abscesses, which may be mistaken for farcy ulcerations. A very common result of phlebitis is an obliteration of the affected portion of the vein, but as collateral circulation is readily established this is seldom of any material inconvenience.

_Treatment._--Phlebitis should be treated by the application of a smart blister along the course of the inflamed vessel; early opening of any abscesses which may form; the animal should have complete rest, and the bowels be kept loose with bran mashes. When the fever runs high, half-ounce doses of nitrate of potassium may be given in the drinking water, which may be changed in two or three days for 1-dram doses of the iodid of potassium. If the animal becomes debilitated, carbonate of ammonia, 1 dram, and powdered gentian, 3 drams, may be given every six hours.

VARICOSE VEINS, VARIX, OR DILATATION OF VEINS.

This may be a result of weakening of the coats from inflammatory disease and degeneration. It may also be due to mechanical obstruction from internal or external sources. It is sometimes found in the vein which lies superficial over the inside of the hock joint, and may be due to the pressure of a spavin. Occasionally it may be observed in stallions, which are more or less subject to varicocele, or dilatation of the veins of the testicular cord. Hemorrhoidal veins, or piles, are occasionally met with, generally in horses which run at pasture. Varicose veins may ulcerate and form an abscess in the surrounding tissues, or they may rupture from internal blood pressure and the blood form large tumors where the tissues are soft.

_Treatment._--Stallions which manifest a tendency to varicocele should wear suspensory bags when they are exercised. Piles may often be reduced by astringent washes--tea made from white-oak bark or a saturated solution of alum. The bowels should be kept loose with bran mashes and the animal kept quiet in the stable. When varicose veins exist superficially and threaten to produce inconvenience, they may be ligated above and below and thus obliterated. Sometimes absorption may be induced by constant bandages.

AIR IN VEINS, OR AIR EMBOLISM.

It was formerly supposed that the entrance of air into a vein at the time of the infliction of a wound or in blood-letting was extremely dangerous and very often produced sudden death by interfering with the circulation of the blood through the heart and lungs. Danger from air embolism is exceedingly doubtful, unless great quantities were forced into a large vein by artificial means.

PURPURA HEMORRHAGICA.

Purpura hemorrhagica usually occurs as a sequel to debilitating diseases, such as strangles, influenza, etc. It may, however, arise in the absence of any previous disease in badly ventilated stables, among poorly fed horses, and in animals subject to exhausting work and extreme temperatures. The disease is probably due to some as yet undiscovered infectious principle. Its gravity does not depend so much upon the amount of blood extravasated as it does upon the disturbance or diminished action of the vasomotor centers.

_Symptoms._--This disease becomes manifested by the occurrence of sudden swellings on various parts of the body, on the head or lips, limbs, abdomen, etc. These swellings may be diffused or very markedly circumscribed, though in the advanced stages they cover large areas. They pit on pressure and are but slightly painful to the touch. The limbs may swell to a very large size, the nostrils may become almost closed, and the head and throat may swell to the point of suffocation. The swellings not infrequently disappear from one portion of the body and develop on another, or may recede from the surface and invade the intestinal mucous membrane. The mucous lining of the nostrils and mouth show more or less dark-red or purple spots. There may be a discharge of blood-colored serum from the nostrils; the tongue may be swollen so as to prevent eating or closing of the jaws. In the most intense cases, within from twenty-four to forty-eight hours bloody serum may exude through the skin over the swollen parts, and finally large gangrenous sloughs may form. The temperature is never very high, the pulse is frequent and compressible, and becomes feebler as the animal loses strength. A cough is usually present. The urine is scanty and high colored, and when the intestines are much affected a bloody diarrhea may set in, with colicky pains. Some of the internal organs become implicated in the disease, the lungs may become edematous, extravasation may occur in the intestinal canal, or effusion of serum into the cavity of the chest or abdomen; occasionally the brain becomes affected. A few cases run a mild course and recovery may commence in three or four days; generally, however, the outlook is unfavorable. In severe cases septic poisoning is liable to occur, which soon brings the case to a fatal issue.

_Pathology._--On section we find the capillaries dilated, the connective tissue filled with a coagulable or coagulated lymph, and frequently we may discover gangrenous spots beneath the skin or involving the skin. The lymphatic glands are swollen and inflamed. Extensive extravasations of blood may be found embedded between the coats of the intestines, or excessive effusion into the substance of the lungs.

_Treatment._--Diffusible stimulants and tonics should be given from the start. Carbonate of ammonia, 1 dram, fluid extract of red cinchona bark, 2 drams, and tincture of ginger half an ounce, with half a pint of water; thin gruel or milk should be given every four or six hours. But especial care should be exercised to avoid injury by drenching. If the horse has difficulty in getting the head up and swallowing, smaller doses must be given with a small hard-rubber syringe. Sulphate of iron in 1-dram doses may be dissolved in water and given every six hours. Chlorate of potassium, in 2-ounce doses, may be given every eight or twelve hours. Colloidal silver may be administered intravenously in doses of from 5 to 12 grains. Washings with lead and alum water are useful and may be repeated several times each day. If the swellings are very great, they may be incised freely and the resulting wounds should be washed at least twice daily with a warm 3 per cent solution of carbolic acid or other good antiseptic. Tracheotomy may be necessary. Complications, when they arise, must be treated with proper circumspection.

DISEASES OF THE LYMPHATIC SYSTEM.

The lymphatic, or absorbent, system is connected with the blood-vascular system, and consists of a series of tubes which absorb and convey to the blood certain fluids. These tubes lead to lymphatic glands, through which the fluids pass to reach the right lymphatic vein and thoracic duct, both of which enter the venous system near the heart. Through the excessively thin walls of the capillaries the fluid part of the blood transudes to nourish the tissues outside the capillaries; at the same time fluid passes from the tissues into the blood. The fluid, after it passes into the tissues, constitutes the lymph, and acts like a stream irrigating the tissue elements. Much of the surplus of this lymph passes into the lymph vessels, which in their commencement can hardly be treated as independent structures, since their walls are so closely joined with the tissues through which they pass, being nothing more than spaces in the connective tissue until they reach the larger lymph vessels, which finally empty into lymph glands. These lymph glands are structures so placed that the lymph flowing toward the larger trunks passes through them, undergoing a sort of filtration. From the fact of this arrangement lymph glands are subject to inflammatory diseases in the vicinity of diseased structures, because infective material being conveyed in the lymph stream lodges in the glands and produces irritation.

LOCAL INFLAMMATION AND ABSCESS OF LYMPHATIC GLANDS.

Acute inflammation of the lymph glands usually occurs in connection with some inflammatory process in the region from which its lymph is gathered. Several or all of the glands in a cluster may become affected, as in strangles, nasal catarrh, or nasal gleet, diseased or ulcerated teeth, the lymph glands between the branches of the lower jaw almost invariably become affected, which may lead to suppuration or induration. Similar results obtain in other portions of the body; in pneumonia the bronchial glands become affected; in pharyngitis the postpharyngeal glands lying above the trachea become affected, etc.