Chapter XV: Part 15

But the heart is not always the primary source of such clots. Virchow and others have demonstrated by _post mortem_ examinations in cases of plugging and by a number of experiments on the lower animals, not only that such clots may have their place of nativity in some distant and diseased part of the body and proceed in the veins to the heart, and thence through the arteries to other distant parts of the body where they plug the vessels and induce a train of morbid changes; but that such embolism arteritis and abscesses can be produced at will by the introduction into the circulation of solid and insoluble (infecting) bodies. Fragments of decaying and suppurating tissue and the elements of tubercle and cancer may be thus equally carried onward in the current of the circulation, and reproduce themselves at those points where their course is arrested. This is a mode in which secondary deposits of these morbid matters are determined. Embolism and arteritis in the body and limbs occurring in this way necessarily have their point of departure in pre-existing disease of the lungs. The clots loosened from the capillaries or veins of the lungs are carried through the left side of the heart into the arteries of the body at large to be arrested in some of the smaller vessels. I have seen plugging of the digital arteries of the hind limbs, to occur in this way in a horse that had been suffering from inflamed lungs.

Microbes and toxins may pass harmlessly through healthy parts, including the pulmonic circulation, to establish colonies and embolism beyond where the tissues have become debilitated. Thus Gamgee records a case of embolism of the anterior mesenteric, right external iliac and right femoral arteries, supervening on an attack of strangles.

_Symptoms of acute arteritis._ These consist largely in impaired muscular power in the part, indications of acute local suffering, such as trembling and tenderness to the touch, if the obstructed vessel lies within reach it can be felt as an exquisitely tender cord-like mass, and the limb on the distal side of the embolism and dependent on the diseased vessel for its blood supply is anæmic and cold. In the distal portion of the embolic artery and its branches pulsation has ceased. If the lesion is extensive there may be more or less fever, but a limited arteritis in a small vessel may escape this complication. If the disease is of long standing there is atrophy of the tissues formerly supplied by the embolic vessels. The secondary derangement of nutrition and function are as varied as the organs affected and will be noted below in the special article on thrombosis and embolism.

=Chronic arteritis.= =Atheroma.= This is an indolent inflammation supposed to result mainly from strain and overwork, and manifested by thickening and clouding of the serosa, with cell proliferation, softening and fatty degeneration. The diseased substance becomes soft, pultaceous, slightly greasy, and under molecular degeneration it breaks up and is even in part washed on in the blood stream. Other degenerations may occur in the inflamed walls of the artery. The exudate may become organized, constituting fibrous thickening. It may become the seat of calcareous degeneration. It may yield to the blood pressure, becoming slowly attenuated (atrophy), and even dilated (aneurism by dilatation). As a cause of chronic internal arteritis in the horse should be named the presence in the vessels of the larva of the strongylus armatus. The posterior aorta and anterior mesenteric artery which are the most commonly infested by these parasites are frequently attenuated, dilated and calcified in this connection.

_Treatment._ Acute arteritis should be treated like any other local inflammation, by rest, soothing applications (fomentations, astringents, icebags), and alkaline salts. It has been proposed to manipulate the affected artery and contained thrombus, but this can only tend to block the smaller arteries farther on, and perhaps with even more injurious results. The liberal use of alkalies on the other hand, if effective in dissolving any portion of the clot, returns this to the blood stream in a condition that will not endanger further embolism. The agents usually employed are carbonates of ammonia, potash or soda, and iodide of potassium.

THROMBOSIS AND EMBOLISM.

Definition. Thrombosis—clotting in the vessel. Embolism, blocking
of the vessel. Thrombus may form in any bloodvessel. Embolism
occurs in arteries. Clot follows the blood current. Causes of
clotting—fibrinogen, paraglobulin, fibrine ferment; foreign
bodies; parasites; air; blood that has been exposed, transfusion;
ærial germs; disease germs; chemical coagulants; high and low
temperatures; breaches of endothelium; congestion or inflammation
of the serosa; stasis of blood and extension of clot; ligature
near a branch vessel: deoxidation and carbonization of blood,
marasmus; neoplasms; traumas of the vascular coats. Infarction,
causes of blocking; disintegration of clots, softening,
liquefaction, ulceration, action of microbes; excess of white
globules; air; fat; parasites. Pathogenesis; complete occlusion of
vessel; infarction; sequestrum; collateral circulation; embolism
of external iliac or femoral artery; effects on pulse; during
rest; atrophy; lameness comes on with exertion; disappears under
rest; circulation inadequate to sustain active function. Embolism
of internal iliac artery; effect on pulse; on tail and pelvic
organs. Embolism of axillary artery; effect on pulse, action,
nutrition. Embolism of mesenteric artery; verminous; effects on
innervation and circulation; spasms, congestions, paresis;
involution. Treatment: expectant; alkalies; gentle exercise, time.

_Definition._ =Thrombosis= is the blocking of a blood vessel by a clot formed in its interior by the deposition of layer above layer on its inner coat.

=Embolism= is the blocking of a bloodvessel by a clot or other solid body formed at a distant point of the circulation floated on in the blood stream, and arrested when it reaches a vessel too small to transmit it.

A _thrombus_ may be formed at any point of the circulatory apparatus (heart, arteries, veins) whenever the conditions are such as to determine coagulation of the blood. An _embolism_ on the contrary is a disease of the arteries since in these the blood current, proceeding centrifugally from the greater to the lesser, inevitably carries the moving solid to a point too narrow to allow of its further progress. Thus clots originating in the systemic veins or right heart pass to the lungs and produce embolism of the pulmonary arteries whereas those formed in the pulmonary vein or left heart are arrested in some part of the systemic arteries. Clots formed in the portal vein however are arrested in the hepatic vessels into which that trunk breaks up.

_Causes of Thrombus._ The production of a thrombus may be due to the condition of the blood or of the vessels. The researches of Buchanan, Schmidt, Hammersten and others show that two albuminoid elements, fibrinogen and paraglobulin, present in the living blood, and a fibrine ferment mainly derived from the white corpuscles in process of change or destruction, determine powerfully the formation of fibrine and clot. Hewson, Brücke and Lister have shown that blood may be maintained fluid for many hours in an unimpaired vein, or turtle’s heart though it may have been removed from the body, the important condition being that the vein shall retain its vitality and suffer no derangement of its endothelium. Lister has even shown that blood may remain fluid for many hours in a sterilized glass tube which has been filled by passing the tube carefully into such a vein without disturbing its lining membrane, or imparting motion to the liquid. In such a case a thin film of coagulum only, forms on the interior of the glass tube. In healthy blood, without addition of any extraneous matter, and kept perfectly still, the plasma and globules retain their integrity, and the former its fluidity for a length of time. But if shed into a basin it coagulates at once.

a. _Changes in the blood._ Contact with foreign bodies generally determines this change and prompt coagulation. Transfixing the artery with a needle, even a silver one, the entrance of parasites (actinomycosis, strongyli, filaria), the presence of pus, and of certain infectious microbes and their products, the introduction of solid particles and even of air into the vessels, the transfusion of blood which has been exposed to receive ærial germs, or which contains microscopic clots, or the globules of which have become modified by contact with a basin or other vessel, even the transfusion of defibrinated blood may cause coagulation. The danger is always greater if the blood is drawn from a different genus and unfitted to live in the blood of the recipient. Disease germs are especially dangerous if adapted to colonize the serosa of the vessel and destroy its epithelium. A decrease of the density of the blood favors coagulation, a lowering of one thousandth rendering it syrupy, and various chemical agents induce or favor coagulation, thus acetic acid, valerianic acid, alcohol, the salts of iron, and above all the salts of lime act in this way. Very high and low temperatures throw down the fibrine as a grumous precipitate, but the clot remains soft.

b. _Changes in the vessels._ Any disturbance or alteration of the endothelium sets free the so-called fibrine ferment, and precipitates coagulation. Lister found that contact of ammonia with the interior of an otherwise living vein caused a thrombus. So in all endarteritis and phlebitis coagulation takes place on the serosa and quickly blocks the vessel. Even in the capillary vessels the same principle holds, and in inflammation minute coagula (thrombi) form in the capillary network throughout the whole inflamed area. This explains not only the capillary blood stasis but the thrombosis of inflamed arteries and veins. In these two latter the clot increases and extends in the direction of blood stasis:—in the artery toward the heart as far as the next colateral branch, and in the veins away from the heart as far as to the next colateral trunk. On the distal side of the arterial thrombus the blood flows off freely toward the capillaries, but on the proximal or cardiac side it is absolutely stagnant up to the next branch through which it can freely flow into the capillary plexus. Into this stagnant blood the fibrine ferment, produced by the altered white globules in the clot already formed, slowly extends until the whole has formed a firm coagulum. Beyond this the actively moving blood carries off and dilutes this ferment so rapidly that it can exert no appreciable effect on the fibrine-forming elements. The principle is an important one in surgery, as the clot formed entad of the ligature will be extensive in proportion to the distance from the first colateral trunk, and in inverse proportion to this clot will be the danger of secondary hæmorrhage. In veins the same rule holds, with this difference that as the blood is flowing toward the heart it empties the vessel on the cardiac side, and stagnates on the distal side up to the next colateral branch. Hence it is that a thrombus in a vein always extends away from the heart, while that of the artery extends toward it.

Another cause of coagulation is the deoxidation of the blood and the excess of carbon dioxide. This occurs in the stagnant blood in the vessels and above all in the capillaries. The normal trophic changes in the serosa, fail to take place in contact with blood in this state, and the resulting changes in the white and endothelial cells set free fibrine ferment and determine coagulation. Stasis of the blood from any cause (ligature, pressure, embolism), tends to this condition and the extension of the coagulum.

A thrombosis of marasmus has been observed in anæmic and debilitating diseases, and apart from the microbian invasions in a certain number of those affections, this may be looked on as due in part to the lessened density and other changes in the blood and to the debility of the serosa of the vessels.

The compression of the vascular walls or their penetration by neoplasms, tumors and ulcers, is another cause of coagulation and thrombus, also a varicose or aneurismal dilatation, with weakening of the vascular walls, or dilatation of the heart with structural changes in the endocardium as stated under that heading, or compression of the smaller vessels and capillaries by an exudate in process of organization, or a similar obliteration under the action of extreme cold. Injury to the serosa of the vessel by stretching, bruising, laceration or section determines a thrombus starting from the injured endothelium. In the smaller vessels the thrombus is usually deep red from the entangling of a large quantity of red globules, whilst in the larger arteries the greater part of the globules pass on and the coagulum is largely buff or straw colored.

Again in obstruction in the smaller arteries, the inactive capillary plexus and the tissue beyond are liable to become gorged with blood with excess of red globules, from the adjacent capillary network, constituting _infarction_, and ending in gangrene. In cases in which this is prevented by the action of intense cold the part may remain pale, as _white infarction_.

_Causes of Embolism._ As already stated embolism results from a detached portion of a thrombus passing to a smaller vessel and obstructing it. Such detachment is favored by molecular softening, liquefaction or suppuration in the clot or beneath it, by the destructive action of microbes, or by friction or manipulation of the obstructed vessel. Excess of white globules (leukæmia) favors the formation of minute coagula and embolism. Bubbles of air, globules of fat, or cholesterine crystals block the fine pulmonary capillaries, and the debris from atheromatous patches, ulcers, and tumors opening on the inner wall of the artery form emboli in various parts. Finally parasites, especially the larval strongyli in solipedes and filaria and spiroptera in dogs, themselves obstruct the vessels and determine coagulation.

_Pathogenesis._ In the larger arteries (aorta, radical stump of the mesenteric artery) clots (as from strangles) rarely produce dangerous obstruction. In the smaller vessels stenosis is complete and anæmia and gangrene are liable to occur unless the blood supply is partially maintained by anastomotic vessels. When the embolism affects a number of smaller arteries or capillaries in a vascular organ like the lungs, the blood filters in from the adjacent capillaries, in which circulation is still carried on, and this passes through the softened and ruptured capillary walls so that the tissue is charged with globules and constitutes a _black infarction_. In the lung this usually affects one or several lobulettes, forming a pear shaped mass corresponding to the distribution of the obstructed vessel. The cut surface is black, compact and granular. The lymph thrown out around it forms an organized fibrous sac, and the unclosed sequestrum undergoes a slow necrobiosis, blanching and liquefaction into a pus-like fluid which is removed by absorption. Such results are met with in the parenchymatous organs (lungs, liver, spleen, kidneys, etc.) and less frequently in the limbs. The symptoms will correspond to the particular organ invaded.

In the fore or hind limbs the result is usually less radical. The vessels below the obstructed trunk are connected more or less freely by anastomosing branches, so that the circulation in the tissues below, though somewhat restricted, remains active enough to sustain a fair measure of nutrition. Apart from the suffering, attendant on the preliminary inflammation, the morbid phenomena are largely confined to the absence of pulsation in the lower part of the limb and the inability of the muscles to sustain active contraction.

=Chronic Embolism of the External Iliac or Femoral Artery.= In this condition the pulsations in the digital arteries are imperceptible, if it has been of long standing there may be obvious atrophy of the muscles of the thigh, but when standing quietly or walking there is usually no lameness. In continuous rapid walking and above all in the trot, however, he soon begins to halt on the affected limb, and this rapidly increases, the joints bending under his weight, the toe dragging and the animal threatening to drop altogether. If stopped and allowed to rest for ten or fifteen minutes he gradually recovers and may be led quietly back to his stable without a sign of lameness. But if again trotted fifty or one hundred paces the lameness develops anew and disappears in the same way when left at rest. The circulation in the muscles is enough for a moderate nutrition but altogether inadequate to sustain active work.

=Chronic Embolism of the Internal Iliac Artery.= In this case the control of the muscles of the limb may be perfect but there is some indication of paresis of tail, bladder, rectum and anus. Impaction of the rectum is liable to occur. By examination through the rectum the pulsations are felt to be strong in the aorta and external iliac, but imperceptible in the internal iliac blocked by the embolus.

=Chronic Embolism of the Axillary Artery.= Here there are the same general symptoms, the absence of the radial and digital pulsations, the wasting of the muscles of the forearm, and the intermittent lameness, developed rapidly by exercise and recovering promptly under rest.

=Acute Embolism of the Mesenteric Arteries.= This will be fully treated under the title of verminous colic in solipedes. The blocking of the branches, usually of the anterior mesenteric artery, leads to derangement of the innervation, congestions, spasms, involutions and other disorders. The presence of the strongyli in the fæces, the general symptoms of intestinal worms, and the recurrence of the indigestions and spasms would serve to indicate the nature of the complaint.

_Treatment of Chronic Embolism._ As affecting the arteries of the limbs the repair must be largely left to nature, and we must place the patient in condition, favorable to such repair. Except in the early stages absolute rest is not necessary. Gentle exercise stimulating to a freer circulation solicits a slow enlargement of the anastomosing vessels (arterial or capillary), and when this has reached a given stage, weak pulsations may again be felt in the vessels beyond and the muscles will once more stand moderate work without lameness. Alkalies and iodide of potassium may be given to solicit solution of the clot, but this can rarely be counted on to the extent of rendering the vessel once more pervious. A small paddock in which the patient can move around quietly is desirable, and in a few months a tolerable recovery may have taken place.

Embolism in other organs must be treated on the same general expectant method, and a considerable time is usually necessary to secure a fair recovery.

ANEURISM.

Definition. Divisions, true, false, dissecting, arterio-venous, mixed,
traumatic, spontaneous. Causes, violence, rupture, debilitated
vascular walls, strains, stretching, force of blood current,
overloaded intestine, strongyli, contiguous inflammation, embolism,
microbian invasion of the walls, arteritis, concussion. Symptoms, soft
tumor pulsating with the heart, a double rushing sound, diagnosis from
abscess, nervous disorders through pressure, cramps, palpitations.
Treatment, when desirable, rest, moderate, laxative diet, iodides,
bromides, icebags, compression, ligature, galvano-puncture, wire
coils, injections.

_Definition._ A pulsating swelling on an artery, consisting of a sac filled with arterial blood.

_Divisions._ =A true aneurism= (=aneurism by dilatation=, =arteriectasis=) is a simple dilatation of the artery, the tumor being surrounded on all sides by the distended arterial walls. It is usually fusiform or cylindroid, but may have the form of a more or less rounded sac.

=A false aneurism= is where the wall of the artery has been lacerated and the blood is enclosed in an adjacent sac of condensed connective tissue and communicates with the interior of the vessel. The same name has been given to cases in which the inner coat only has given way, and the middle and outer coats constitute the walls of the sac. From its liability to extend and separate the tissues this is further known as a =dissecting aneurism=. =Arterio-venous aneurism= in which an intervening sac communicates with both artery and vein, has been found in the human subject.

=Mixed aneurisms= are those in which a dilatation of the artery is complicated by the presence of an outside pouch.

A distinction has also been made according to origin into _traumatic_ and _spontaneous_. The former is of necessity _false_, whereas the latter may be _false_ or _true_.

_Causes._ Apart from rupture of the arterial coat by direct violence, the common cause is a debility and loss of resistance in the walls. In horses a far larger proportion of aneurisms are deep-seated than in man, in whom forced muscular effort is less common. Yet even in horses the most common seat—the posterior aorta—is liable to overstretching and to inflammation and softening by reason of contiguity to dorsal sprains. The posterior aorta too, from its size and direction on leaving the heart, is in the direct line of the strongest blood current, and under long continued, forced and violent efforts (as in racing, hunting, and heavy uphill draughts), has to sustain an extraordinary blood pressure. Bouley claims as an additional cause the pressure of a loaded colon. This is also the point of all others where the vessels suffer from the presence of the larval strongyli. From whatever cause originating, congestion of the arterial coats leads to more or less attenuation, softening or lack of cohesion, and they tend to yield under the blood pressure. Similar conditions operate on the smaller vessels in different parts of the body, and thus overstretching, contiguous inflammation, and excessive blood pressure cause such lesions in the chest, trunk and limbs.

Another cause is embolism which by blocking an artery at once increases the tension in the vessel on the cardiac side of the obstruction, and develops inflammation in the arterial coats, robbing them of their cohesion and resisting power.

Eppinger has shown the importance of infectious microbes in weakening the arterial walls and predisposing to aneurism.

The larval strongylus armatus already referred to is the most potent factor in solipedes. They accumulate in the anterior mesenteric artery, leading to clotting of the blood, inflammation of the serous coat, and dilatation, so that in some verminous localities nearly every old horse shows a lesion of this vessel.

All forms of arteritis, and disease of the vascular walls which entail attenuation or weakening, predispose to aneurism.

Of direct traumatism may be mentioned an aneurism of the arch of the aorta in a horse struck by a wagon pole, during a sharp descent (Jacob), and two with aortic aneurism after violent blows on the back with shafts of wagons.

_Symptoms._ An aneurism within reach of the hand is to be recognized primarily by the pulsation of the swelling synchronously with the beats of the heart, and by a double rushing sound with each beat of the heart, observed on auscultation. An abscess over a large artery lying on a bone may pulsate but it is to be distinguished by the presence of a single in place of a double rushing sound on auscultation, by the possibility of causing more or less complete collapse under pressure, and by the history of an active phlegmonous inflammation followed by softening which steadily extends from the centre of the previously dense mass. In a case of aneurism of the gluteal artery of the horse reported by King and in one observed by the author the symptoms were unmistakable. Other similar examples on the popliteal artery and other failed to be recognized during life though attended by lameness.

In internal aneurism the symptoms are mostly indefinite. Ollivier found tympany and vomiting in a goat which at the necropsy showed an aneurism of the anterior aorta as large as the closed fist and enclosing a sewing needle. A more careful diagnosis should have detected a retarding of the maxillary pulse and a double rush over the carotid with each beat of the heart. Pressure on the vagus doubtless led to the symptoms noticed. In aneurism of the posterior aorta there have been noticed a loss of life and energy, dulness, lack of appetite and stiffness of the loins. Torpor of the bowels, expulsion of fæces with effort and groaning, intermittent colics, lameness in one or both hind limbs, and finally cramps in the hind limbs, and palpitations. In one case Maillet was able to reach the aneurismal tumor through the rectum.

_Treatment._ The treatment of internal aneurism will be seldom called for in the lower animals, as the disease is seldom diagnosed, is beyond reach of mechanical applications, and survival without certain power of endurance would seldom be desirable. In some valuable breeding animals it might be worth while to seek prolongation of life. The most promising measures are absolute rest, and low, non-stimulating diet of a laxative nature and in small bulk. Iodide of potassium is often useful in man, and although in the lower animals there is not the excuse of specific disease, yet the rest to the circulation and reduction of blood tension are not to be undervalued. Bromides may be given with the same object.

Other measures applicable only to aneurisms, within reach and essentially of a surgical nature include: Ice bags and compression. The compression should as a rule begin at the distal end of the limb and be concentrated by suitably shaped pads on the swellings. Ligature of the diseased artery above or below or both above and below the tumor. Galvano-puncture of the aneurism with the object of inducing coagulation. The introduction of coils of fine wire through a hypodermic needle with the same object in view. In both horse and dog the persistent compression with the finger seconded as it is by the plasticity of the blood has succeeded in checking the flow from large arterial orifices, and offers great encouragement in the application of this measure to aneurisms. The injection into the sac of tincture of chloride of iron with firm compression to prevent motion of the blood is another available resort.

ARTERIO-SCLEROSIS.

Fibrous thickening of the arterial coats and calcification are well known lesions in the posterior aorta particularly of the horse. Commencing in congestion or degeneration which lessens the resistance of the vascular walls, the condition tends to dilatation, and if this is checked by compensatory thickening, the condition of sclerosis is induced. The combination of a slight fusiform dilatation and fibrous or calcareous sclerosis is well known in the posterior aorta of the horse. Unless it advances to marked aneurismal dilatation the condition is not often recognized. If diagnosed, rest and quieting of the circulation are especially indicated. Should it occur in other parts of the body the symptoms would correspond to the organ invaded.

ANGEIOMA. CIRCOID ANEURISM. ANEURISM BY ANASTOMOSIS. VENOUS TUMOR.
NŒVUS.

These are forms of dilatation and elongation of the network of small arteries, or veins, and even of the intervening capillaries. In man these constitute the unsightly red patches and swellings that appear on the face and hands. In animals with dark skins and hairy covering they can only be recognized by the swelling, the feeling as of a bag of worms when the hand is passed over it, and by the rushing sound when auscultated. The trouble is usually subcutaneous and is essentially a surgical one. The most promising treatment is by persistent pressure, by electric current supplementing the pressure, by electro-puncture, and by injections of muriate of iron. When the nœvus is not too extensive a double thread drawn by a needle through beneath the tumor at short intervals, then cut and each point tied separately, so as to completely stop circulation is most effective.

PHLEBITIS.

Divisions, traumatic and idiopathic. Causes, punctures, defective
blood supply in walls, debile coats, thrombus, infection,
overstretching, injury or disease of serosa, irritants in blood,
microbic infection. Lesions, exudation, cell growth, breaches in
serosa. Adhesive phlebitis, desquamation, granulation, occlusion.
Suppurative phlebitis, infection, pyæmia, erysipelas, metritis,
ulceration, neoplasms, phlebolites. Symptoms, local, firm, corded,
swollen vein, extends entad, venous congestion, dropsy, gangrene,
diagnosis from lymphangitis. Fever, venous congestion in vicinity.
Treatment, germicide, rest, cold, antiseptics, blisters.

Inflammation of veins as seen in the lower animals has usually been a sequel of bleeding and is hence a purely surgical lesion. Animals as well as man however are subject to idiopathic phlebitis which as affecting the deeper seated veins may be held to be a medical subject.

The _causes_ of =idiopathic phlebitis= are varied. Injury to the walls like the punctures made in bleeding; if they result in the exposure of a raw, and above all an inflamed, surface to the blood, tends to the formation of a thrombus, and of local inflammation. Even the inflammation of the outer coat tends in the same way to thrombosis and phlebitis, and the experiment of Nicasse showed that the dissection of its sheath from a vein, thus robbing it of its vascular and nervous supply promptly induced coagulation of the blood in the denuded part. The debilitated or devitalized walls evidently give off fibrinogen and fibrine ferment in amount that is incompatible with the maintenance of fluidity. All other forms of direct injury to the veins, leading to disturbance of the endothelium or cell enlargement or exudation in the intima, will operate in the same manner. Sometimes as in puerperal phlebitis the inflammation extending from the adjacent tissue to the walls of the veins, determines thrombosis, and the invasion by pus microbes determines suppuration. Bruises, overstretching, pressure with overdistension, and the circulation in the blood of irritant matters may lead to changes in the wall, thrombus, and inflammation. Such irritants may be septic or other bacterial products, or they may arise from the colonization of bacteria on or in the venous coats with the same final result.

The _lesions_ in the vein are often primarily of the nature of exudation and cell growth in the coat, without at first any change in the serosa or endothelium. Later the changes implicate those, thrombosis follows and one of various ulterior processes.

In =adhesive phlebitis= which is most frequent as the result of purely mechanical injury, the endothelium is desquamated and granulations from the denuded surface extend into the clot and finally occlude the vein. A recovery takes place by the organization of this new product and the contraction of the vessel into a simple fibrous cord.

In =suppurative phlebitis=, which occurs especially in connection with infection (erysipelas, metritis), the inflammation, though starting in the same way in the vascular coats, advances rapidly to suppuration, and the intima, lying in contact with the resulting thrombus may become itself the seat of the suppurating process. Cases of this kind are almost of necessity in the nature of an infection and the danger is greatly enhanced. Small abscesses formed in the vascular coats may burst into the vein and passing on with the blood produce general infection (pyæmia). Even when the pus enters the vein at a point covered by the thrombus, it may escape by the partial loosening of the clot from the serosa, or through the interior of a honey-combed coagulum and thus lead to general infection. This is especially liable to follow in erysipelas and metritis, in which the tendency as in the solid tissues is to diffuse suppuration without any investing limiting membrane. There are other forms of bacterial colonization of the vascular walls, of ulceration, and of the extension of morbid growths into or through the venous walls, producing inflammation more or less localized, and leading or not to general infection. The presence of phlebolites in the vein is a conceivable source of phlebitis, though no such case has been so far recorded.

The _symptoms_ in localized cases of simple adhesive phlebitis may be purely local. The vein if within reach may be felt like a firm, rounded cord, which extends in a direction from the heart. If there are no free anastomosis with neighboring veins on the distal side of the thrombus, venous congestion and dropsy of the tissues ensue, and in some cases moist gangrene. When, however, such anastomosis is abundant these peripheral symptoms may be absent, especially if the affected vein returns blood from a higher level than the heart, and then the symptoms are confined to the vein and its immediate surroundings. From lymphangitis which shows similar hard cords, it is distinguished by the absence of an extended network of diseased vessels, by the lack of a diffuse, doughy swelling, and by the fact that the adjacent lymph glands remain free from inflammation, pain and swelling. In the more extended cases there is fever, which may be of a very high type and may merge into pyæmia. In deep-seated cases it may be difficult to identify the disease, but it may be suspected if in the course of erysipelas or metritis there is a sudden increase of fever with pain and swelling, and distension of veins leading into the part.

The _treatment_ of idiopathic phlebitis is largely that of the particular infecting disease on which it depends. In simple cases due to trauma absolute rest and the application of ice and antiseptic solutions, or where these cannot be applied, the use of antiseptics internally, will be indicated. Hyposulphite of soda and sulphide of calcium are especially indicated. From the early days of veterinary medicine, flying blisters of Spanish flies, over the inflamed vein or veins have proved very successful, and under the lead of Nonat the same was in 1858 and since adopted with gratifying success in the human subject. Abscesses formed in accessible situations should be promptly opened and treated antiseptically, and swelling of the affected part should be checked by elevated position, or if that is impossible, by a smoothly applied bandage. Rubbing and active movement are dangerous, as tending to detach clots which float off to start new emboli and inflammations in the lungs.

VARICOSE VEINS. DILATED VEINS WITH ALTERED WALLS.

Rare in animals. Angioma Varix. Superficial. Deep. Causes, obstructed
circulation, compression, congestion. Symptoms, enlargement,
elongation, tortuosity of veins, stiffness, lameness, complications.
Treatment, compression, coagulants, cauterization, ligature.

Varix is not so common in the lower animals as in man, and is generally observed in the superficial veins, so that it comes under the domain of surgery. In the form of angioma, which affects the veins, there is extensive dilatation and elongation, but it involves a large group of connecting and anastomosing veins, whereas varix usually affects but one or a few connecting vessels. In the horse the most common seat of varix is in the saphena vein, as it passes obliquely over the inner side of the hock. Less frequently it appears on the flank or other superficial part. In cattle the mammary veins are the most frequent seat. Varices, however, occur also in deep-seated veins and in connection with normal venous plexuses, as in the buccal, palatal, and peneal. Anatomically they may be simple fusiform dilatations, as in the saphena; dilated, elongated and tortuous, branching trunks, as in the mammary veins; or dilated veins with thickened walls and pouch-like dilatations.

_Causes._ There is usually some obstruction to the circulation through the affected vessel, it may be by pressure by a tumor, or a constrained position, obliteration by a phlebitis and thrombus, extension of inflammation from adjacent organs, increased blood pressure by gravitation, or from diseased heart or lungs. Whether from the extension of contiguous inflammation, from external pressure, or from blood tension, the morbid process has much in common; the circulation and nutrition in the vascular walls are interfered with, degenerations set in (softening, fatty, connective tissue), which predispose to dilatation under the blood pressure. The pouch-like dilatations of the jugular consequent on bleeding, are essentially traumatic. The impaired innervation which lessens the resistance of the vascular walls is not to be forgotten. Varix of the saphena is usually an attendant or sequel of tibio-tarsal synovitis, and is the result of combined pressure and congestion. Mammary varices are manifestly connected with the congestion and exudations which affect the udder and environment at the time of parturition, or with a casual mammitis.

The _symptoms_ in superficial vessels are visible enlargement, and often elongation and tortuous direction of the vein or veins, with or without tenderness. Deep-seated varicosities may be attended by stiffness of the part and a halting in progression with or without pain on pressure. These cases may recover spontaneously as the result of adhesive phlebitis, or they may develop phlebolites, suppuration, inflammation, ulceration and hæmorrhage.

_Treatment._ Superficial varices have been treated by compression, cauterization, coagulating injections, and ligature. It is not often that interference is demanded but in such cases, pressure with elastic bandage having failed, ligature with antiseptic precautions is indicated.

PHLEBOLITES. CALCAREOUS BODIES IN THE VEINS.

Nature. Location. Mode of formation. Calcareous plates in two inner
coats. Phlebotomy. Altered sanguification. Treatment. Extraction.

Calcareous bodies have been repeatedly found in the veins of man and several observations of the same kind have been made in the horse. Spooner found them in the abdominal veins and Simmonds in the jugular. Much difference of opinion has existed as to the mode of formation of these bodies whether by calcareous deposit in a coagulum or by degeneration of a neoplasm in the vascular wall. Andral held the latter opinion, and Tiedemann and Cruveilhier found the bodies connected to the inner coat of the vein by a fine membrane. Morton’s cut of one of Simmonds’ specimens (Calculus Concretions) shows a structure in successive layers having their centre at one end, evidently corresponding to a former connection by pedicle. Cornil and Ranvier says “sometimes there are seen in chronic varices, calcareous incrustations in the form of plates, nodules or spheres with concentric layers ... calcareous infiltration is seen in the form of spheres or phlebolites in the varicose diverticula. An extensive calcareous induration several centimetres in length, is also sometimes observed, the vein being transformed into a calcareous tube with the ramifications also varicose.

The calcareous plates of the vein are developed in the fibrous and internal portion of the middle coat. At the beginning they consist of granules deposited in the fasciculi of the connective tissue or between them; these soon unite and form transparent plates with granular striæ.”

Phlebolites in the jugular suggest a connection with the pouch-like dilatations, and transformations in the vascular walls that have been subjected to phlebotomy. It is probable however that there is usually a morbid condition of sanguification and nutrition which predisposes to their formation. In Simmonds’ case the jugular was impervious below the bodies, there was hepatitis and arthritis of the fetlock joint.

When recognized during life these may be extracted with due antiseptic precautions. If the vein can be dispensed with it may be ligatured above and below, if not an attempt may be made to preserve it, extracting through a clean cut longitudinal incision and securing as perfect coaptation of the edges of the wound as possible.

HÆMORRHAGE.

Arterial, venous and capillary hæmorrhage belong almost exclusively to the domain of surgery. Internal hæmorrhages will be considered in connection with the organs in which they take place.

HÆMOPHILIA.

Definition. Causes, lack of plasticity of the blood, thin walls, blood
tension, cardiac erethism, hypertrophy and neurosis. Sex. Heredity
through the female. Treatment, depletive, styptic, astringent.
Transfusion.

This is a constitutional infirmity, usually hereditary and characterized by the occurrence of profuse and continuous bleeding as the result of otherwise insignificant injuries or even apart from any recognizable lesion. It has been attributed to a slow coagulation of the blood, but at the start of a hæmorrhage the blood is rich in corpuscles and coagulates firmly. It has also been ascribed to extreme tenuity of the vascular walls, but this has only been met with in a certain proportion of the cases. Another potent factor is a permanent over-filling of the bloodvessels (Immermann, Delafield, Prudden). The same writers attach importance to cardiac erethism, cardiac hypertrophy, and certain neurotic influences which temporarily increase the habitually congestive diathesis. In man the majority of victims have been males, perhaps because most subject to traumatisms. On the contrary the hereditary transmission is mainly through the female members of the family. The families are very prolific, a condition counterbalanced by the death of the majority of the victims at an early age. Among the lower animals it has been observed in horses consequent on castration (Siedamgrotzky, Kohne, Friedberger and Fröhner), setoning (Kohne, Dieckerhoff), and an ulcer of the leg (Kohne).

_Treatment_ consists in combating plethora and constipation by saline purgatives. The subject should be carefully protected from injuries. Locally use styptics such as matico, muriate of iron, tannin, alum with pressure. Internally ergot, lead acetate, iron chloride, tannin, alum, or muriate acids. Transfusion is a dernier resort.

DISEASES OF THE BLOOD.

Obscurity of blood changes. Red globules, biconcave, embryonic.
Source. Escape of immature red globules. White globules, eosinophile,
neutrophile, uninuclear, multinuclear, lymphocyte, granular amœboid,
strap-nucleated. Conditions of increase. Relation to microbes and
their products. Blood plates. Destruction of red globules in the
liver. Numbers in animals, in different vessels and conditions.

The blood is the common medium through which all nourishment is conveyed to the tissues, all material to the glands for secretion, or transformation, and all effete matter to the various emunctories for elimination. It is beside the carrier of oxygen for the respiration of the tissues, and the seat of changes, as yet little known, effected through the white globules. The activities of the various processes, carried on by the fixed tissue cells and nuclei would suggest, that any disease or derangement of these processes would be at once cognizable in changes shown in the blood. Yet so perfect is the balance of sanguification and elimination on the one hand, and of the remaining vital processes on the other, that it has hitherto been impossible to detect in the blood such changes as would identify the great majority with morbid processes. Some morbid changes are however recognizable and it is important that the significance of these should be known.

The blood is a liquid, consisting of a plasma holding in solution serum albumen, serum globulin, fibrine-forming elements, sugar, urea, salts, and a variety of other soluble bodies, and floating a series of semi-solid organized bodies, the red and white globules.

The red globule is however seen in two distinct forms. 1st. The biconcave disc, non-nucleated, containing a colorless stroma, and the coloring matter—hæmoglobin. 2d. The embryonic red globule, large, nucleated and rarely biconcave. The latter is found in the blood of the fœtal man or animal and persists to a slight extent for some time after birth. These are believed to be formed from the embryonic cell and from the cells of the embryonic liver, spleen, and marrow, whereas after birth they are derived from the marrow cell, and in healthy conditions pass the nucleated stage before they escape into the blood. In pathological anæmia and after severe hæmorrhages they escape more rapidly, probably from both spleen and marrow, and appear in the blood, even of the adult, of the gigantic size and nucleated appearance of the embryonic red globule.

The white blood globules (leucocytes) are spherical, about twice as large as the red globules, and are readily divisible by the acid eosin stain into two kinds: 1st. Cells which are deeply stained by eosin—eosinophile; and 2d. Cells that do not take on the eosin stain—neutrophile (Ehrlich).

Howells further divides these white globules into uninuclear and multinuclear. Of the uninucleated he describes three varieties: _a._ The lymphocyte which is non-granular and without amœboid movement; _b._ The granular cell with a protoplasmic envelope and amœboid movement; and _c._ The granular with strap-shaped, horseshoe or spiral nucleus. Like Lovet he considers the multinucleated as on the way to disintegration.

We cannot as yet speak with confidence of the pathological significance of these respective forms of white globules, but they increase greatly in numbers in connection with certain diseases of lymph plexus, and glands, of the spleen and other blood glands, and in foci of inflammation, and they perform most important functions in connection with the resistance of microbian invasion and in elaborating the antitoxines which confer immunity from second attacks.

The next form of blood solids are the _blood plates_ of Bizzozero, the hæmatoblasts of Hayem. These are nucleated (Semmer) discoid, less than half the diameter of the red globules, and cluster together in granule masses when the blood is drawn. Their true significance is uncertain though it has been surmised that they are intermediate corpuscles (Semmer), that they are the disintegrated nuclei of the leucocytes, and that they furnish paraglobulin to the circulating blood (Schmidt, Howell).

The liver is one centre for the destruction of red blood globules and in the blood of the hepatic vein there may be a reduction of a million to a million and a half of red globules per cubic centimeter, as compared with the portal vein.

Malassez gives 4,500,000 as the number of globules in a cubic millimeter of blood (dog and horse 7,500,000, Nocard). The white globules are to the red in the proportion of about 1 to 300 (domestic animals 1:800, 1:1100, Nocard). The variation in different parts of the vascular system and at different times of the day is striking and suggestive.

In the blood of the splenic vein 1:60; in the hepatic vein 1:170; in the portal vein 1:740; in the morning, fasting 1:716; half an hour after breakfast, 1:347; in boys 1:226; in girls 1:389; in men 1:346; in old men 1:381; in menstruating woman 1:247; in pregnant woman 1:281, (Stricker).

PLETHORA. POLYÆMIA.

Definition. Transitory only. Causes, kidney disease, drinking freely,
rich feeding, profuse secretion, polycythemia, hyperalbuminosa, excess
of fibrine, sugar or fat. Ratio of blood to body. Variations of
globules. Symptoms, general, local. Appearance of blood. Prevention.
Treatment.

_Definition._ An excess of blood, of the blood globules, or of the albuminoids.

Formerly accorded an important place in pathology, plethora has been entirely eliminated from some recent works. The actual amount of blood varies greatly at different times, rising after a free consumption of food or drink, and falling during a period of abstinence. A healthy activity of the secretory and excretory organs secures a fair uniform average in the plenitude of the circulatory system. Moreover, large variations are not in themselves rapidly injurious. Worm-Müller and Cohnheim introduced into dogs ten to twelve per cent. of the body weight (fifty to eighty per cent. of their blood) of canine blood without inducing fatal results. More than this was fatal. In non-fatal cases a reduction to the normal standard is speedily secured.

But we cannot count on absolute immunity in all circumstances. Disease of the kidneys, or drinking water to excess, determines a surplus of water and urinary salts (serous plethora, polyæmia aquosa). In cases of rapid gain in condition from rich feeding, and above all after profuse watery secretion (diarrhœa, diuresis, perspiration), the red globules are relatively increased (plethora polycythæmica). After hearty feeding there is a large increase of albumins (plethora hyperalbuminosa). Fibrine-forming elements are apparently in excess during rheumatism, pneumonia and other acute inflammations. Sugar is in excess after a saccharine or farinaceous meal, fat in obese individuals, after consumption of fat, after injuries to the bone marrow, and after severe diseases with much destruction of albumen.

The ratio of blood to the body weight is: In birds 1: 12; in Guinea pig 1: 19; in rabbit 1: 20; in cat 1: 21; in dog 1: 17; in horse 1: 18; in sheep 1: 24; in pig 1: 26; in ox 1: 29 (Colin). As showing the variation under even different normal conditions of the system Bollinger found the blood but 2.2 per cent. of the body weight in a fat pig, whilst it was 13.5 per cent. in a draft horse. Colin found it 2.4 per cent. in the fat ox instead of the usual 3.4 per cent.

The excess of red globules and usually also of albumins is seen as a temporary condition, in lean but vigorous animals put suddenly on an abundant diet, rich in assimilable albuminoids, in working animals, put in confinement to feed, and above all in high conditioned cows after an easy parturition, when the uterine blood has been suddenly thrown on the general circulation and the emunctories have failed to establish a balance. Also in the lymphangitis occurring after a day or two of rest, in a horse that has been hard worked and heavily fed.

It should be borne in mind that the number of red globules varies considerably in the different animals. In the dog it was by weight 148.3 grammes per 1000; in the pig 105.7; in the horse 102.9; in the ox 99.71, and in the sheep 98.2 (Andral, Gavarret, Delafond). By count the horse has 5,500,000 per cubic millimeter (7,500,000, Nocard); and the dog 5,000,000.

_Symptoms._ Under a sudden dangerous increase of the volume or the organic elements of the blood, there are usually dulness, lassitude, dropping of the head, strong, full, hard pulse, extra force in the heart beats, thirst, elevated temperature, and redness of the visible mucous membranes. At first there is no indication of local disease, but unless relief comes by free secretion some local complication is likely to ensue. This may be epistaxis, congestion or apoplexy of the brain, parturition fever, lymphangitis, or congestion of some internal organ, etc. A drop of blood colors deeply the finger or other object, it clots firmly in three to five minutes, and shows more than usual of a buffy coat.

_Treatment._ As dangerous plethora is usually a very transient condition the main attention should be given to _prevention_, in keeping the diet low and the emunctories active in high conditioned parturient cows; in lowering the diet and securing free secretion, or in giving exercise to high fed, hard worked horses that have been laid off work; in changing only by slow gradations thin, vigorous animals to a rich diet, etc. When the danger is imminent prompt relief can be secured by the liberal abstraction of blood. Purgatives, diuretics, and restricted diet may be applied to less urgent cases.

HYDROÆMIA. ANÆMIA OLIGÆMIA.

Definition. Causes: bleeding, watery repair, hydroæmia, repair of
globules, changes in red globules, in bone marrow. Cause of
chronicity; profuse secretions; moplasms; parasites; chronic
exhausting diseases; defective diet or hygiene; diseases of jaws or
throat; overwork; toxic substances. Symptoms: pallid mucosæ, weakness,
perspiration, soft tissues, small pulse, palpitation, anæmic
heart—arterial and venous murmurs, depilation, indigestion,
costiveness, urine clear, abundant, emaciation. Lesions: blood poor in
globules, embryonic, and other abnormal red globules, fatty
degeneration, blood clot. Treatment: remove causes, diet, hygiene,
sunshine.

_Definition._ Bloodlessness; Deficiency of blood; Lack of red blood globules. The last named is the condition to which the term is habitually applied.

_Causes._ Anæmia is not so much a disease, as a result of a great many debilitating and exhausting conditions. =Hæmorrhage= the most direct cause of anæmia determines at first an actual lack of blood (oligæmia) and of blood pressure, which may be sufficient to cause fainting and death. In case of survival the amount of blood is rapidly made up by absorption from all available sources of liquid in the economy, but the blood so restored is essentially hydroæmic having an excess of water and a lack of globules and dissolved solids. If however the loss has been moderate the quality may be restored in a few days. Buntzen found that after moderate bleeding the volume is restored in a few hours; after a profuse hæmorrhage in 24 to 48 hours. After bleeding to 1.1 to 4.4 per cent. of the body weight the increase of the red globules may be noticed after 24 hours, and is completed in 7 to 34 days. It is noteworthy that during this repair the bone marrow becomes much redder and more cellular, and that new red cells found in the blood are nucleated (Neumann) and contain less hæmoglobin (Ott). The absence of hæmoglobin is nearly in proportion to the amount of the hæmorrhage (Bizzozero, Salvioli). If the hæmorrhage is slow and continuous this repair is counterbalanced and the anæmia is much more persistent.

=Profuse secretion= as of milk (cows, goats, ewes, bitches, on poor feeding), of liquid fæces, urine, or pus often determine a marked and even dangerous anæmia.

The rapid growth of multiple =tumors= as of _melanosis_ in gray horses has been noticed to cause profound anæmia (Bouley).

Perhaps no cause is more potent than the attacks of =parasites= and especially such as live by sucking the blood. The numerous strongyli of the lungs, stomach, and intestine, the tricocephalus, and allied round worms, the trematodes of the liver, and the cytodites of birds furnish striking examples of the bloodless and debilitated condition which they may produce. In man ankylostomata causes anæmia in Egypt, Italy (St. Gothard) and elsewhere, and bothriocephala in different countries.

=Chronic exhausting diseases= especially those which affect the digestive organs and mesenteric glands are prolific causes. So with Bright’s disease.

Connected with these are =defects in diet or hygiene=. Starvation, unsuitable, innutritions, or indigestible food, too laxative food, damp, dark, draughty or unventilated stables, and irregularity in feeding, watering and work are all potent factors in inducing anæmia.

=Diseases of the masticatory apparatus= (broken jaw, diseased teeth,) preventing the preparation of food, and pharyngeal troubles interfering with deglutition are other causes. Finally overwork is not to be forgotten.

=Toxic anæmia= may occur from the ingestion of lead, mercury, or arsenic.

_Symptoms._ These may be little marked at the outset in slowly developing cases. Extra pallor of the mucous membranes, fatigue and even breathlessness on slight exertion, a small, weak, pulse, with a tendency to become rapid, with violent heart beats, when excited.