Chapter XVI: Part 16

At a more advanced stage the mucosæ, especially the buccal, are pale and thin, the muscles are soft, flabby and weak, fatigue and perspiration are easily induced, the feet are advanced more nearly in the median line of the body, and the toes strike on any obstacles, the pulse is weak, small and quick, and the heart easily excited even to palpitation, and with an occasional anæmic murmur with the first heart sound. Arterial and venous murmurs may be present. The hairs are easily detached. Appetite and digestion fail, there is costiveness, a full secretion of urine of a clear aspect, the subcutaneous fat disappears and the skin feels thin and limp (paper skin in sheep), the hair dry and lusterless, the wool flattened (clapped). The weakness and emaciation go on increasing and dropsies appear in the limbs, under the trunk and jaw and in the internal cavities.

_Pathology._ _Lesions._ Apart from the causes, the morbid conditions are mainly found in the blood. The watery state of the blood, the lack of red globules (even to but 2,000,000 per cubic millimeter), the absence of albumen (76 per 1000 in place of 83), the loose coagulum with excess of buffy coat, and the excess of serum are characteristic. The presence of large, nucleated (myelogenous) red cells, of spherical bodies smaller than the normal red cells (microcytes), and of irregularly shaped red cells (poikilocytes) is characteristic, the latter especially of pernicious anæmia. As the disease advances fatty degeneration of heart, liver, kidneys, and other organs are complications and tend to aggravate the disease, by counteracting repair of the globules—thus establishing a vicious circle. All the organs are pale and flaccid, the arteries empty, the veins contain a little blood, forming pale clots. In the cases considered, all the result of another disease, the lack of blood and of the solid and vital elements in that which remains, entails imperfect function in all the vital processes, including sanguification itself, and in this way an anæmia once established tends to perpetuate and aggravate itself.

_Treatment._ The anæmia above considered being largely symptomatic, or resultant from other diseases, the first consideration as regards both prevention and treatment is to prevent or cure such diseases. Where dietetic or hygienic, a liberal diet, and good hygiene will meet every demand in the early stages. In the warm season an open air life is most important. In case of a drain by over-secretion (milk) this must be judiciously checked. In bitches it will often be needful to wean several of the puppies. A rich and very digestible diet (oats, beans, linseed, oil meal, milk, gruel), in small compass, and suited to the genus and individual, with iron and bitters, and in the herbivora carminatives, will suit many cases. Muriate of iron, with strychnine or nux vomica; iron sulphate, sodium chloride and nux; or dialysed iron, or some other soluble ferruginous salt, with quinia, gentian, or some other bitter will serve a good purpose. For the dog saccharated carbonate of iron or citrate of iron and ammonia with quinia or strychnine, in pill form, is convenient. With poor digestion muriatic acid and pepsin may replace the iron at first. Beef teas may often be given with advantage, even to the herbivora, and injections of defibrinated ox blood night and morning have proved of service. In extreme anæmia, as from hæmorrhage, transfusion, or its equivalent, must be resorted to. A normal saline solution (0.6 per cent. NaCl), boiled, may be thrown into the peritoneum or subcutaneous connective tissue, or defibrinated blood, may be injected into the peritoneum. Transfusion is the dernier resort.

PROGRESSIVE PERNICIOUS ANÆMIA. IDIOPATHIC ANÆMIA.

Definition. Causes, obscure, faulty diet, hygiene, microbes,
glycerine, pyrogallic acid, hæmoglobin, deranged sanguification,
parasitisms. Symptoms, of anæmia of obscure origin. Treatment as for
anæmia, special measures, for intestinal fermentations, dietetic.

_Definition._ Anæmia which is without any pre-existing appreciable cause.

_Causes._ As in the corresponding disease in man the real starting point of pernicious anæmia is unknown. Faults in diet and in general hygiene have been adduced, and while in Berne this appears to be sustained, in Ireland, in the poorest classes, the disease is little known, and in Montreal, it find its victims largely in a class of well to do artisans (Osler.) In the domestic animal it is described on all soils, and on the most varied dietary (Bouley and Reynal). Zschokke and Friedberger and Fröhner in cases occurring enzootically in stables, found a minute bacillus in the patients, which would remove these cases into the list of symptomatic anæmia. The same is true of the anæmia (Surra) of horses and mules in India and Siberia, in which Evans, Burke, Steele and Ignatovsky, found a motile spirilloid organism which destroys the red globules. Other forms that are apparently purely idiopathic have been attributed to a failure in the cytogenic processes in the bone marrow especially. Back of this we know only of the various debilitating causes in food, hygiene, building, location, work, etc., operating on a specially susceptible system, in which, once started, the morbid process tends to perpetuate itself and increase.

Ponfick induced anæmia experimentally by the intravenous injection of glycerine, pyrogallic acid, solutions of hæmoglobin, etc., which dissolve the blood globules. This suggests the probable pathogenesis by the production of unidentified blood solvents in cases of deranged sanguification, but it still leaves us in the dark as to the exact seat of such derangements (liver, blood glands, bone marrow, etc.) and as to the cause, parasitic or otherwise, which determines such disorder. Pathological investigation has enabled us to differentiate, according to their respective causes, a number of diseases (distomatosis, lung worms, ankylostomiasis, internal acariasis, chronic trichinosis, strongyliasis, etc.,) which were formerly classed as anæmias, and it seems altogether probable that the onward progress of medicine will enable us to go farther in the same direction and to allot the remaining unclassed anæmias to their proper etiological places. Some may be unrecognized helminthiasis, others microbian disorders, and still others, disorders in nutrition and sanguification from different causes.

The _Symptoms_ are those of other forms of anæmia, but being more obscure in origin and therefore less open to corrective treatment, it is more likely to grow to an extreme development and fatal issue. The weak pulse, irritable heart, debility, unsteady walk with the hind limbs, hurried breathing and sweating under exercise, watery, puffy eyes, dropsies in limbs and dependent parts of the body, progressive emaciation, and weakness are even more marked than in symptomatic anæmia.

The _treatment_ is in the main as for the other form alike in its hygienic and medicinal bearing. In man recoveries have taken place under arsenic combined with the iron. Arseniate of potash and ferrum redactum in pill form, or tincture of chloride of iron, and Fowler’s solution in food or water, continued for a length of time. Phosphated pepsin, and peroxide of hydrogen have seemed to do well in some instances, and phosphorated oil is another resort. W. Hunter attributes idiopathic anæmia to toxins derived from microbes in the alimentary canal, as Sir Andrew Clark ascribes chlorosis to a similar cause. He prescribes beta-naphthol as the least soluble and best antiseptic, in a dose of 5 grains daily in mucilage for man (1 drachm for horse or ox). Hunter further found that a farinaceous diet protected the globules against destruction while a nitrogenous diet favored this. It may be noted that long ago Delafond attributed anæmia in animals to the extension of the use of artificial fodders of the natural order leguminosæ which are rich in nitrogen.

CHRONIC ANÆMIA. DROPSY IN CATTLE AND SHEEP.

Definition. Causes, parasitic and microbian. Symptoms. Treatment.

_Definition._ A progressive anæmia in ruminants and other animals, resulting in general anasarca, and dropsies of the internal cavities.

In veterinary works published on the European Continent this affection is given a special place apart from the same train of symptoms which mark distomatosis, taeniasis, and strongyliasis. The disease is described as prevailing in wet years, after inundations, when the vegetation is rank and aqueous, and of course largely aquatic, in animals that are turned out in early morning before the dew has evaporated, in the conditions, in other words, that favor the ingestion of parasites. It prevails also in work oxen fed on the refuse of sugar factories (beets, turnips) in which the nitrogenous materials are held to be deficient, but in Great Britain where cattle are often fattened on an exclusive diet of turnips, containing even a larger proportion of water, this non-parasitic disease is unknown. It is also ascribed to close, ill-ventilated, unwholesome buildings, and to over-kept and tainted fodder, and so far as a separate disease exists, it seems more reasonable to charge it to the toxins produced by bacterial ferments or cryptogams than to causes which elsewhere appear to be inoperative.

The _symptoms_ are essentially those of distomatosis, and the _treatment_, apart from the parasiticides, is the same. When helminthiasis can be certainly excluded _prevention_ would include the avoidance of the factory refuse, especially when in a state of decay.

MELANÆMIA. BLACK PIGMENT IN BLOOD.

Definition. Melanin, in normal tissues, abnormal. Melanosis.
Bisulphide of carbon subcutem. Decomposition of hæmoglobin in
leucocytes. Coloration of tissue.

_Definition._ Accumulation of granules and scales of blood pigment (melanin) in the circulating fluid, and in various organs (spleen, liver, bone marrow, brain, etc).

=Melanin=—C_{44.2}, H_{3}, N_{9.9}, O_{42.6}—or black pigment (a close relative of hæmatin) occurs physiologically in epithelium (choroid, retina, iris, in the deeper layers of epidermis, and on the surface of the dog’s lung and of the sheep’s brain) and in connective tissue corpuscles (lamina fusca of the choroid).

Pathologically it is found in the blood of the victims of malarious fever, often in great abundance, and in the spleen, liver, bone marrow, brain, lymph glands and some other organs. It is formed abundantly in the black pigment tumors (melanosis) of man and animals, and in extensive melanosis is present in the blood of both man and horse (Schimmeln). So far it has not been found in connection with the extensive destruction of red globules which takes place in anæmia. Schwalbe has developed malanæmia experimentally by the hypodermic injection of bisulphide of carbon in rabbits.

According to one view the melanin is produced in connection with the destruction of red globules in the liver, spleen, etc., and is thence carried into the blood. This is in keeping with the local formation of the pigment in melanosis. Arnstein however urges that in malarious cases the destruction of the red cells takes place in the blood, and that the hæmoglobin, absorbed into the leucocytes, is transformed into melanin, and finally deposited in the tissues by the migrating white corpuscle. Why the hæmoglobin set free in anæmia is not similarly transformed, does not appear. The pigmented organ may be quite black in the immediate vicinity of the blood vessels, and in its general aspect in chronic cases reddish brown, dark gray, or dark olive.

LEUKÆMIA. LEUCOCYTHÆMIA.

Definition. Nature. Result of other morbid processes. Leucocytes
polynuclear. Lymphatic leukæmia. Spleno-myelogenous leukæmia.
Leucocytes in each. Loss of amœboid movement. Charcot’s crystals.
Hæmatoblasts. Cell increase in bone marrow. Myelocytes. Enlarged
spleen and lymph glands. Hæmorrhages. Lymphoid growths. Susceptible
genera. Causes obscure. Symptoms, pallor, listlessness, weakness,
apnœa, sweating, thirst, emaciation, weak circulation, anæmic murmur,
enlarged spleen, bleedings, diarrhœa, dropsy, excess of white
globules, reduction of red globules, buffy coat, beaten fibrine is
granular, china-white mucosæ, hurried breathing, stertor, deranged
digestion, marasmus. Duration. Not inoculable. Treatment, not hopeful,
as for anæmia, good hygiene, tonics, stimulants, antiseptics.

_Definition._ An excessive and persistent increase of the white blood globules, and associated with enlargement of the spleen, lymph glands or bone marrow.

_Nature._ This must be distinguished from the leucocytosis which occurs during digestion, or that which attends on tuberculosis, glanders, pneumonia, and other extensive inflammations and profuse suppuration. These forms are transient and the cells are of the polynuclear variety. The cells of leukæmia are various in character, but bear some relation to the particular organ which is the seat of hypertrophy or morbid process.

“In =lymphatic leukæmia= the increase in the number of leucocytes is due to the mononuclear lymphocytes, especially of the small form. As many as ninety-five per cent. of the colorless cells may be of this form. In =Spleno-Myelogenous leukæmia= the eosinophile cells may be especially increased in number, and there are also large leucocytes coming apparently from the marrow of the bones, and called myelocytes. These most nearly resemble the larger lymphocytes of normal blood, but they are usually larger. They have a single large nucleus which stains feebly and their bodies may show neutrophile granules. Larger and smaller nucleated red blood cells may be found in spleno-myelogenous leukæmia. The leucocytes are frequently in a condition of fatty degeneration, and there may be a decrease in the number of red blood cells.” (Delafield and Prudden). In splenic leucocythæmia blood plates may be absent and in lymphatic leucocythæmia they may be in excess.

Cafavy claims that many of the leucocytes have lost their active amœboid movements.

Bright white crystals in the form of elongated octahedra are found not only in the blood but in the diseased glands, spleen or marrow (Charcot’s crystals). Clusters of discoid hæmatoblasts (blood plates) are present in the blood in variable numbers (Schultze’s granule masses).

The bone marrow is marked by an accumulation of spheroidal cells, which tend to pass into a condition of fatty degeneration. Most of them are colorless, larger than the lymphocytes of normal blood and have one large often vesicular nucleus, staining less highly than the lymphocyte nuclei, and with neutrophile granules in the protoplasm (=myelocytes=). There are besides, nucleated red blood cells, spheroidal cells, containing red blood cells, and Charcot’s crystals. The marrow may be uniformly red, mottled gray and red, gray, grayish yellow, or puriform (Delafield and Prudden). This may affect one or many bones. The affected spleen is usually much enlarged, at first uniformly, later unevenly, firm or softened, and with thickened white capsule. The cut surface is smooth, brownish red, or yellow, with white lines (thickened trabeculæ) and indistinct Malpighian corpuscles. It contains glutin, glycocoll, hypoxanthin, zanthin, leucin, tyrosin, and lactic, acetic, or formic acids.

The affected lymph glands are somewhat enlarged, red or gray, exceptionally, softened or caseated and otherwise contain an excess of leucocytes.

Slight hæmorrhages may appear in any of these structures. Lymphoid growths may appear in a number of other organs as the liver, heart, lungs, kidneys, bowels, tonsils, the different blood glands, the serosæ and the retina.

_Genera affected._ It has been seen mainly in dogs, but also in horse, ox, pig, cat and mouse. Nocard has collected the following cases: horse 9, cattle 6, pig 5, dog 22, cat 1.

Leisering found a horse’s spleen weighing 28 kilogrammes. Johne found a pig’s spleen of 2.4 kilogrammes.

_Causes._ The primary causes of leukæmia are unknown. As in anæmia all unhygienic conditions are invoked as causes. That it is not due to simple hypertrophy or irritation of the leukogenic centers is plain, as it does not follow on ordinary diseases and injuries of these parts, but what is the precise nature of the morbid cause has so far eluded us.

_Symptoms._ Pallor of the visible mucous membranes, listlessness, lack of energy and endurance, breathlessness and perspiration on the slightest exertion, ardent thirst, rapidly advancing emaciation, unsteady gait, stiffness or lameness, lies most of the time, walks with pendent head, and jaws open, small, weak pulse, anæmic murmur in the heart, enlarged lymph glands, or spleen felt beneath the left lumbar transverse processes in the ox, or in the left hypochondrium in the horse. Bleeding from the nose or elsewhere, slight hæmorrhage into the conjunctiva, irritable conditions of the bowels, diarrhœa and dropsies are suggestive. The blood when obtained in epistaxis or drawn by a needle prick may be pale rose, brownish or grayish brown instead of red, and under the microscope shows the enormous excess of leucocytes—the ratio to the red being sometimes 1: 2, or even more, in the human subject. In the domestic animals the following ratios have been made by actual count: 1: 85 (Leblanc and Nocard), 1: 50, 1: 45 (Mauri), 1: 20 (Nocard), 1: 15 (Siedamgrotzky), 1: 12 (Forestier and Laforque). The normal average for the domestic animal according to Nocard is 1: 900. This great relative excess of white globules serves to distinguish this malady from anæmia, and its persistency is a means of diagnosis from transient leucocytosis.

The red globules are always reduced in number in the horse and dog to 5,082,000, and even 2,050,000 per cubic millimetre, while the normal is 7,500,000 (Nocard).

In clotting, the blood forms an extensive buffy coat, and in solipedes which normally show this, the blood set in a test tube forms three strata, the upper slightly yellow, semi-transparent and formed of fibrine; a median of a dull, opaque white color and formed mainly of leucocytes and blood plates, and a lower of a violet red and formed mainly of red globules.

The amount of fibrine is variable. It becomes granular when beaten. Albumen is variable but usually reduced.

The visible mucous membranes are bloodless and of a clear porcelain white. The walk becomes weaker, fore feet wide apart and the hind limbs partly flexed, head and neck extended, and breathing labored. The breathing may be with constant stertor, the bowels torpid and tympanitic, or loose and fœtid, dropsies and hæmorrhages ensue, and the patient dies in complete marasmus.

_Duration._ The disease may prove fatal in less than a month, or it may last for three, six, or eight months. It is mostly fatal.

_Not inoculable._ Many attempts have been made to transmit it by inoculation, but in no case with success.

_Treatment_ is not successful. All hygienic measures should be adopted, as for anæmia; open air and sunshine, with protection against chills; the treatment of all complications; iron, bitters, phosphorus, arsenic in particular, electricity to the spleen, massage; oxygen inhalation; and locally, iodide of potassium or mercury, generally and locally.

LYMPHADENOMA. HODGKIN’S DISEASE.

Definition. Relation to leukæmia. Causes. Mainly accessory. State of
lymph glands, spleen, liver, bone marrow, intestine, tonsils, thymus,
kidneys, liver, lungs, bronchial mucosa, pleura, pericardium, nervous
system. Symptoms, as in leukæmia, with adenoid hyperplasia, but little
leucocythemia. Relation to glanders. Uric acid, low density, no
hippuric acid. Tuberculin and mallein tests. Treatment, as in
leukæmia. Excision in cases not constitutional. Phosphorus, phosphide
of zinc.

_Definition._ Hypertrophy of the lymphatic glands with little or no leucocytosis. There may further be lymphoid growths in the liver, spleen, bone marrow and other organs.

The visceral lesions in lymphadenoma do not differ in character from those of leukæmia, and as it does often apparently merge into that disease by the characteristic changes in the blood, it is denied by many that it constitutes a separate pathological entity. In his admirable monograph on leucæmia in the lower animals Nocard affirms their identity. The main excuse for keeping up an alleged distinction, is the frequent absence of leucocytosis, and this often supervenes after the lymphadenoma has existed for some time.

_Causes._ As in leucæmia, no definite cause can be found in the majority of cases. An accessory cause can sometimes be observed where a local irritation gives rise to swelling of the adjacent lymphatic glands and this goes on to distinct lymphadenoma.

=Lesions in the Lymph Glands.= The hyperplasia may affect but a single group of glands, more commonly a number of groups, and often nearly all. In one case only of leukæmia in the lower animals, a dog, has Nocard failed to find the lymph glands affected. In the horse he has found the sublumbar glands alone weighing 14.5 kilogrammes, 11 k. and 8 k. They compressed the posterior aorta and vena cava and had caused extensive ascites.

The enlarged glands are white, gray or in case of rapid growth veined or pointed with red; they may be soft or firm according as the hyperplasia has operated most on the trabeculæ or the cells; they are homogeneous throughout. The scraping of the cut surface gives a more or less thick milky juice containing a great number of nucleated or double nucleated lymphocytes, free nuclei and granules which stain strongly.

Hardened sections show an enormous development of the follicles at the expense of the medullary walls, and double nucleated white globules packed in a rich reticulum of adenoid tissue, whilst the bloodvessels in the connective tissue are crowded with white cells, and there are slight ruptures, old or recent.

=Lesions of the Spleen.= These are nearly always present. Leisering found a horse’s spleen over three feet long and 28 lbs. weight, and Nocard one of 13 lbs. Bollinger found a pig’s spleen 3½ lbs. Siedamgrotzky found dog’s spleens over 2 lbs. The consistency is usually firm (sometimes soft in dog). Capsule thickened and white, cut surface dry, reddish brown, granular, Malpighian bodies enlarged like a pea, hazel nut or walnut, with contents as in the lymph follicles. The capillaries are enlarged and crowded with white cells.

=Lesions in the Liver.= The liver is enlarged in one-half of the cases of leukæmia in the lower animals. It has been found to weigh 20 lbs. in the horse, and 4 lbs. in the dog. It is of a grayish brown, or yellowish brown hue, or light red spotted with yellow, or mapped out by anastomosing grayish white lines. There may be enlargement of the acini, or the formation of little nodes of adenoid tissue, or most commonly in the lower animals, there is an adenoid thickening of the bands of connective tissue extending in from the capsule. These are filled with white cells which stain deeply with carmine. There may also be slight extravasations of blood and infarcts.

_Lesions in the Bone Marrow._ These noticed in the pig by Fürstenberg, and in dogs by Siedamgrotzky, consist in increased vascularity, great cell hyperplasia, and formation of adenoid tissue as described under leukæmia.

=Lesions of the Intestine.= These commence in the agminated or solitary glands, which become enlarged, causing thickening of the mucous membrane, and later grow out into more or less rounded masses of lymph—adenoid tissue up to an inch in thickness. They are quite subject to ulcerations.

=Lesions of the Tonsils.= Bollinger, Nocard and Siedamgrotzky found these enlarged in dogs in connection with adenoma of the spleen. They were soft, friable, grayish, and consisted of a very delicate and fragile adenoid tissue.

In one case Siedamgrotzky found adenoid hypertrophy of the thymus in a cow, and adenoma of the kidneys similar to that of the liver has been noticed.

Similar adenoid hyperplasia has been found in the lungs, the bronchial mucous membrane, the pleura, the mediastinal and bronchial glands, and the pericardium. In man this has invaded the nerve centres, and it seems that at any point where there is a lymph gland or a lymph plexus this adenoid hyperplasia may localize itself.

_Symptoms._ The general symptoms of failing health are as described in leukæmia. The particular symptoms of this disease consist in the recognition of the adenoid hyperplasia in the absence of a marked leucocytosis. The submaxillary glands are usually the first attacked, and the disease may, in the horse, be confounded with glanders. There is, however, no pituitary discharge nor ulcer, the glands are enlarged symmetrically on the two sides, and a careful search will usually discover other groups with similar symmetrical enlargement. The parotidean, the pharyngeal, the prepectoral, the prescapular, the axillary, the popliteal, the prefemoral, the post and premammary, and the inguinal should be critically examined. The enlarged mesenteric glands may be reached and detected by the hand engaged in the rectum, or in the small animals by external palpation, as may also the enlarged spleen or liver.

The adenoid hyperplasia in the chest offers very obscure and uncertain symptoms. The enlarged bronchial and mediastinal glands may seriously interfere with the functions of the vagus nerve, causing, in cattle, disturbed digestion and rumination and tympanies, in horses stertorous breathing, and in the carnivora and omnivora a tendency to vomiting. In animals generally the pressure on the cardiac nerves leads to great irritability of the heart, and violent action under any exertion. The prominent dyspnœa in the advanced stages may be explained by these thoracic hyperplasiæ.

Nocard claims that the urine furnishes most important indications in its low specific gravity (horse 1010), its constant acidity, and in the almost entire absence in that of the horse of hippuric acid. When there is any suspicion of tuberculosis or glanders, the tuberculin or mallein test will decide.

_Treatment_ is essentially the same as in leukæmia, and equally unsatisfactory. Arsenic has in the main given the best results. In the very earliest stages when the granular hyperplasia is confined to one group, excision is advisable. This should be avoided in all cases in which the constitutional symptoms have developed. Phosphorus and phosphide of zinc have seemed beneficial in certain hands. Injections into the glands have so far proved useless.

ACUTE LYMPHANGITIS OF PLETHORA IN HORSE. ANGEIOLEUCITIS.

Definition. Symptoms and causes. Genera affected. Causes of plethora.
High feeding. Work followed by rest. Fever, hurried breathing, strong,
rapid pulse, anorexia, stiffness and swelling in a hind limb, inguinal
glands, connective tissue engorgement, corded lymphatics, suppuration
rare. Mild forms. Lesions, in lymphatic vessels and glands. Chronic
cases. Nature, plethoric, lymph excess, stasis, excess of cells and
fibrine, immunity of the fore limb. Season of prevalence. Climate.
Diagnosis, from farcy, erysipelas, etc. Treatment, exercise, friction,
resolvents, purgative, bleeding, diuretics, astringents, iodine,
pressure, diet. Prevention. Treatment of chronic cases.

_Definition._ Inflammation of the lymphatic vessels and glands of one limb usually in connection with rest.

_Symptoms._ This affection is common in heavy draft horses of a lymphatic temperament and kept on high feeding and at hard work. It rarely develops however while the subject is kept at steady work. But if, in the midst of such work, the horse is kept at rest in the stall over one, two, or more days on the same generous diet, he is found shivering violently, with rapid, labored, breathing, high pulse and elevated temperature, symptoms which have been frequently mistaken for those of pneumonia. There is complete anorexia, and often ardent thirst. The patient is indisposed to move and if forced to it shows lameness in one hind limb with an extraordinary abduction of the limb at each step, and sometimes so severe as to prevent his putting his full weight upon it. If an examination is now made high up in the groin close outside the inguinal ring, the lymphatic glands will be found to be swollen, hot and tender, so that under even moderate pressure the leg will be lifted and abducted until the patient threatens to fall on the other side.

A little later the shivering may have given way to the hot stage, with it may be general perspiration, and the swelling may have extended down the course of the saphena vein and lymphatics, as a distinct ridge and the lower part of the limb from the foot to the hock may be filled, dropsical and hot. Unless checked the swelling goes on increasing till the lower part of the limb is two or three times its natural thickness, and the swelling has extended well up on the thigh. The swelling has a soft œdematous feeling, easily receiving and retaining the imprint of the finger and is not only hot, but excessively tender. From the margin of the swelling, firm, tender, rounded cords are found to emerge passing upward along the line of the saphena vein and its branches toward the inguinal glands. These represent the swollen and gorged lymphatic trunks, and may often be traced for some distance into the substance of the general engorgement.

When the inflammation is violent, suppuration may ensue at one or several centers, but more commonly the engorgement goes on increasing and when the febrile attack has subsided the limb is left permanently enlarged and correspondingly liable to a second attack.

Milder cases are met with which are perhaps even more misleading. There may be little or no rise of temperature, loss of appetite or general constitutional disturbance, but under some change of regimen and particularly after one or two days of rest the subject becomes lame in one hind limb, without any of the usual injuries to account for it. Examination of the groin shows swelling and tenderness of the external inguinal glands, with or without, a tender cord-like swelling running down from them.

Between these two types may be found all grades of lymphatic inflammation with a varied degree of attendant constitutional disturbance.

_Lesions._ The coats of the inflamed lymphatic vessels are thickened by exudate and the outer coat is the seat of ramified redness with minute spots of blood extravasation. The inner coat is dull, opaque, or even thickened. The vessel is dilated and its walls friable. The contained lymph in the intervals between the valves has coagulated into a very thin diffluent jelly-like clot, which in old standing cases may have become granular. The connective tissue from which these vessels lead is infiltrated with liquid and the lacunar spaces distended. Red patches from blood extravasations are numerous. The external inguinal glands and often the internal and sublumbar are swollen, congested, and the seat of active cell hyperplasia. Abscesses are exceptionally seen.

In chronic cases the lymphatic vessels of the affected limb and especially of the lower part which is permanently swollen, are enormously increased in calibre (lymphangiectasis), and have their walls correspondingly thickened. The connective tissue is the seat of extensive fibrous hyperplasia, and its interstices are greatly enlarged.

_Causes._ _Nature._ This disease has not been sufficiently studied to ascertain what toxic agents are produced in the plethoric condition, under the torpid processes of nutrition and sanguification entailed by absolute compulsory rest. A consideration, however, of the relations of the lymph and lymph vessels and glands to other parts will in part explain the pathology of the malady. The lymphatics take their origin in the nuclear spaces of the various tissues, the anastomosing canals of such pericellular spaces together with the latter forming the actual radicles of this set of vessels. They receive, therefore, the surplus plasma which is not used up by the tissue cells in performing their trophic, secretory and other functions. This lymph carried on by the _vis a tergo_, muscular compression and other movements, is delayed in the adenoid tissue known as lymph nodes, and especially in the lymph glands, in which the proliferation of lymph cells is mainly carried on. Thus the lymph cells are very scarce in the lymph radicles of the connective and other tissues, and are found in greater numbers after passing through the lymph nodes, and in still greater after passing through the lymph glands. But the increase of cells is also in inverse ratio with the rapidity of the circulation of the lymph. When this is rapid the cells are hurried on and there is little time for their reproduction. When slow on the other hand, there is time for cell growth and division in the glandular detention cavities, and the ratio of cells to the plasma is materially increased. Consider next that the multiplicity of cells determines an increase of the fibrine factors, so that the more cells the lymph contains there is the more material for fibrine (Landois), and we have one good reason why under enforced rest the overcharged and congested gland may become the seat of fibrinous coagula or lymphatic embolism. Any overdistension, toxic element, or other cause of disturbance, which deranges the functions of the cell or causes its rapid multiplication by division—as in inflammation—at once sets free the fibrine ferment and determines the coagulation. In the disease before us we have the overfeeding of an animal having a strong digestion, we have an absolute compulsory inactivity, with a suspension to a large extent of the functions of nutrition, sanguification, secretion, and elimination; we have in consequence an increase of the blood pressure, and of the solids of the blood and of the plasma of the lymph; we have a suspension of the great motor force of lymph circulation, namely, the muscular contraction, and we have the consequent tardy movement of the lymph, the great increase of lymphocytes, and the distension and engorgement of the lymph glands. As soon as this has reached a certain stage the congestion and incipient inflammation of the gland determines the precipitation of fibrine, the obstruction of the gland, and of the entire circulation of lymph in the lower part of the limb. The fever, the local swelling, and the subsequent steps follow as a matter of course. This view is sustained by the fact that incipient cases can be cured by muscular movement alone. The rarity of the disease in the fore limb may be ascribed to the greater force of the _vis a tergo_, the lesser height of the lymph column, and the stronger action of the aspiratory power of the chest on the lymphatic vessels.

In addition to the causes mentioned above must be noted the following: The disease is an affection of heavy draft horses, in which the tissues are more lax, and the lymph plexus in the connective tissue of the hind limb is much more abundant. It is common in the heavy English, Scotch and Belgian draft horses, and rare in the English racer, the American trotter, and in the average light American horse. The malady is most frequent in spring and autumn, when the work is hardest and the feeding most abundant. It rarely attacks the horse in steady work, but appears after an idle Sunday spent in the stable (Monday morning disease), or after one or more days of compulsory idleness from heavy rains or other cause. The damp climate of western Europe has probably an exciting influence, as it has in producing the lymphatic constitution. In the same line of thought Zundel says that many cold weather attacks would be prevented by clipping off the heavy coat which keeps the entire system relaxed. In some cases a sudden change of food, and in others musty oats have been claimed as causes.

_Diagnosis._ Lymphangitis is distinguished from a simple dropsy of the limb by the acute fever, the great local tenderness especially of the inguinal glands, and by the tender corded lymphatics that enter these. From cutaneous glanders (farcy) it is diagnosed by the more acute fever, by the swelling of the inguinal glands in the early stage of the disease, followed by the swelling of the lower limb, and by the absence of the hard, comparatively insensible and prone to ulcerate, farcy bud. Farcy buds usually appear on the pastern or fetlock, with more or less swelling of the lower part of the limb, while the inguinal glands are as yet normal in size and without tenderness. From erysipelas, with which this has been confounded, it is distinguished, by the suddenness of the onset, under the circumstances above described, by the high type of fever, by absence of early cutaneous inflammation and the formation of vesicles, and by the fact that lymphangitis commences in swelling of the inguinal glands.

_Treatment._ In cases that are seen in the earliest stages, before the leg has become badly swollen, recovery will usually take place under active exertion continued for hours at a time. The pumping action inside the hoof during exercise, and the alternate compression and relaxation of the lymph vessels by the muscles, tend to establish a rapid current of lymph, to break up coagula and to re-establish a healthy condition. Friction from below upward on the lymphatic vessels and swollen limb will greatly assist in this restoration. Different agents are employed, such as camphorated spirits or oil, iodine, mercurial, and even blistering ointments. These should not replace exercise when this is possible.

When the fever has set in suddenly and runs very high, the abstraction of four or five quarts of blood, and the administration of a purgative (8 drs. aloes) will be in order. In cases occurring in the same stable and in all other respects apparently identical, the subjects of phlebotomy recovered without any permanent swelling of the limb, while those that were not bled recovered with thickened limb.

In cases so advanced that the limb cannot be used, cold irrigation, with friction, may be applied, and when the irrigation is intermitted one may apply some astringent (vinegar, alum, lead acetate), or an iodine lotion followed by an evenly applied bandage.

The purgative should be followed by full doses of diuretics (nitre, bicarbonate of potash or soda, colchicum, iodide of potassium) until fever and local inflammation have subsided.

As soon as the patient can use the limb, walking exercise should be kept up for several hours forenoon and afternoon.

Throughout the disease the food should be of a light and non-stimulating variety. When appetite returns give at first wheat bran, or roots, or sweet grass in small amount, and do not return to a grain diet until fully recovered and ready to go to work.

After one attack there is always an increased liability to a second, and great care should be taken to give the subject daily exercise, or where this is impossible, to reduce the feed, give a dose of saltpeter, and turn into a yard or roomy loose box on the idle day.

In chronic thickening of the limb, an evenly applied elastic bandage, extending from the hoof up, regular feeding and exercise, washing daily with a weak iodine lotion, and the internal use of iodide of potassium and other diuretics, with bitters and even iron tonics may be used.

INFECTIVE LYMPHANGITIS. TRAUMATIC LYMPHANGITIS.

Infection varied, through wounds, autogenous. Simple irritation,
simple lymphangitis. Causes, sun’s rays, bruises, other injuries,
lymph coagulation from heat, cold, chemical irritants, and coagulants.
Germs in blood act on debilitated tissues, lymphatic constitutions,
anæmic, overworked, or starved. Insect bites, claws, teeth of
carnivora, foul instruments, fingers or clothes. Bloodless wounds
dangerous. Distal parts of the limbs exposed. Fresh wound exposed,
granulating less so. Most microbes enter by the lymphatics. Symptoms,
extension from wound, swollen lymphatics, reticular lymphangitis,
tubular lymphangitis, farcy, tuberculous case, slough. Fever variable.
General infection. Joint infection. Chronic cases. Lesions. Diagnosis,
from phlebitis. Treatment, antiseptics, diet, eliminants,
antithermics, blisters, mercurial ointment, iodine, lancing, tonics,
massage, bandage.

Under this heading must be named not one specific disease but a group of infections entering by the lymphatic vessels and developing inflammation of their substance. They may be divided into two classes: those caused by infection through external wounds and those in which the poison already in the system becomes localized on a weak or exposed tissue.

A third class must be included, in which there is no recognizable poison but simply a local irritation which leads to coagulation or other alteration in the lymph, or disease of the lymphatic vessels.

This subject belongs rather to surgery than medicine but it seems necessary to contrast it here with the plethoric form of equine lymphangitis. Most of its forms pertain to infectious diseases and will be treated in connection with these.

_Causes of Simple Lymphangitis._ Formerly many forms of lymphangitis were ascribed to mere local irritation; a superficial form will occur from exposure to the rays of the sun, and an inflammation attendant on a bruise or other injury with unbroken skin, may cause local inflammation of the lymph vessels and enlargement of the adjacent lymph glands. As we have seen above coagulation of the lymph and fibrine embolism may induce local inflammation in the walls, and this may occur in connection with excessive heat or cold or the presence of chemical irritants and coagulants. These cases are however rarely serious and the tendency today is to trace nearly all cases to infection, from germs already present in the lymph or blood, or introduced through a wound or sore. The effect of germs already circulating was shown in the beautiful demonstrations of Chauveau in regard to calves subjected to castration by subcutaneous torsion (bistournage). In the healthy calf the simple operation gave rise to little disturbance. The healthy calf injected with septic liquids equally escaped visible trouble. But the calf injected with septic liquids and then subjected to bistournage had a fatal infecting inflammation. There is a strong presumption that, in lymphangitis, starting from an injury with no external sore, the germs were already present in the blood or tissues but were unable to do any serious damage until the injured and weakened part or organ offered an area of lessened resistance to their colonization. Following the same line of thought it has been noticed that animals of a coarse texture, and lymphatic constitution (heavy draft horses and animals raised for the butcher), and such as are debilitated by anæmia, overwork, or poor and insufficient nourishment are above all liable to be attacked by lymphangitis.

The insertion of the septic poison may take place through the bites of insects, the claws, or teeth of carnivora that have been devouring tainted or infecting meat, through the lancet or operating instrument of the surgeon, by his fingers or the dust from his hair or clothes. The wound is perhaps more likely to be infecting if it leads to no effusion of blood, but affects only the thickness of the epidermis, as there is less chance for the washing out of germs by the flowing blood, and there is less care to employ antiseptics. Wounds in the feet and lower parts of the limbs are specially liable to infection by reason of their frequent contact with manure and decomposing organic matter in the soil.

A fresh wound, in which the lymph spaces are exposed, is somewhat more open to infection than one that has advanced to the stage of granulation, the layer of unorganized lymph and cells acting as a slight barrier to the passage of the microbes.

Nearly all microbian diseases make their inroad by way of the lymphatics, where the sparse cells fail to establish as active phagocytosis as do the numerous moving cells of the blood. Hence a number of infectious maladies are primarily and pre-eminently diseases of the lymphatics, as glanders, strangles, tuberculosis, cancer, anthrax, swine-plague, etc.

_Symptoms._ The most common form is where lymphangitis extends from some pre-existing wound—as pricked or suppurating foot, fistula of foot, withers or poll, chafing of shoulder or back, cracked heels, boil, sloughing bruise, etc. The swelling around the sore or injury involves in fact the radical lymphatic plexus in the connective tissue (reticular lymphangitis). When the swelling extends and becomes more tense, with firm, painful sinuous cords running out of it in different directions, and especially toward the nearest lymphatic glands, and when these glands are slightly swollen and tender, tubular lymphangitis is diagnosed. No more striking example can be found than in skin glanders (farcy). The rigid cords extend from the side of the face, from the eye, and nose down toward the submaxillary glands and with more or less adjacent engorgement. Or on a hind limb, or some portion of the trunk, a more or less turgid swelling with one or more firm nodes (farcy buds) and painful, tortuous cords running towards the lymph glands is very characteristic.

A tuberculous case may show an indolent, hard, comparatively insensible cutaneous cord leading toward the jugular furrow, the prescapular, precrural or inguinal glands, and at long intervals softening, fluctuating, bursting and discharging a thick pus. In a carcinoma there is the old, hard, nodular, and finally ulcerating swelling from which the firm cords extend to the mass of steadily enlarging lymphatic glands.

A simpler form is where a bruise by the harness causes a hard, thick, slough, embracing the entire thickness of the skin, from which the firm corded lymphatics extend in different directions. After the slow process of detachment, the local lymphangitis usually subsides under simple cooling or antiseptic treatment.

But the grade of such lymphangitis is as varied as the particular germ or combination of germs present in the wound, and the susceptibility of the animal attacked, and there will be high, moderate or no fever, according to the severity of the case, and in some cases purely local trouble and in others general infection with purulent or septic localization in distant parts. There is always danger of extension to a neighboring joint with destructive results.

A curious outbreak is described by Wiart as attacking nearly every horse in the regiment that sustained a slight wound. A tubercle looking mass formed in the depth of the wound was slow to heal, and the lymphatics leading out from it became round, corded, turgid, and at long intervals developed along their course fluctuating centres which, whether opened spontaneously or by the lancet, showed the same indolent habit. A single attack would last from two to six months, and the actual cautery had to be used on the sores.

The _lesions_ are those already described in the last article for simple lymphangitis. For infecting cases they are those of the particular disease which may be present.

_Diagnosis._ The general diagnosis of lymphangitis is the distinction from phlebitis. In phlebitis the vein is blocked and cannot be raised by pressure on the side leading toward the heart; in lymphangitis it can be so raised. The swelling and tenderness are both greater in lymphangitis. The inflamed vein is more rectilinear, the lymph vessel somewhat sinuous. If suppuration ensues it is more diffuse in lymphangitis; more restricted and mixed with the elements of blood in phlebitis.

For identification of the particular forms of infecting lymphangitis, the reference must be made to the individual infectious diseases.

_Treatment._ In general the treatment of lymphangitis is the antisepsis of wounds. Further than this the treatment of each case is that of the particular disease which it represents. For all cases alike it is important to apply vigorous treatment early, so as to cut it short before it can attain a dangerous extension.

For the simpler forms of lymphangitis the wound should first be thoroughly cleansed and disinfected. Washing with soap suds, or carbonate of soda will remove any greasy agent which would prevent a thorough antisepsis. Then it may be washed with the antiseptic lotion:—carbolic acid solution (1:20), or mercuric chloride solution (1:500), or zinc chloride (1:400) or potassium permanganate (1:160). If the infection has been introduced by a small or punctured wound, the sting or bite of an insect, or the prick of a sharp instrument it should be freely cauterized to its depth with lunar caustic incising it if need be to reach the whole of the poison, and the surface afterward dressed with antiseptics.

The diet should be light but nutritious and laxative, and the free action of the bowels and kidneys should be maintained by salines. When fever runs high give quinine, or salicylate of soda. When a large wound has to be dressed it may be requisite to use a non-poisonous agent like acetate of aluminium or boric acid to irrigate it thoroughly. In some such cases packing the irrigated wound with iodoform gauze has often an excellent effect.

When there is a firm inflamed cord, hot and painful, a fly blister along its course followed by mercurial ointment often gives excellent results. Or they may be repeatedly painted with tincture of iodine.

Foci of suppuration must be promptly opened and thoroughly and persistently disinfected.

With suppuration in multiple abscesses or large open sores liberal feeding must be enjoined and iron and other tonics should be resorted to.

The persistent swelling of the part must be met by active rubbing or kneading, by exercise and by uniform compression by a flannel or elastic bandage.

LYMPHANGIECTASIS. DILATED LYMPHATICS.

Result of lymphangitis, of heart disease, of pulmonary arterial
thrombosis, of external jugular plugging. Causes, obstruction to lymph
flow, compression, increased venous blood pressure, fibrinous lymph
coagula, action of sensory nerves, of lymphadenitis, anæmia. Symptoms
like dropsy if in plexus, in large lymphatics, moniliform swelling,
sacculation, wounds discharge lymph, hyperplasia of connective tissue,
fatty deposits, lipomata. Treatment, elastic bandage, cold,
astringents, iodine, punctures, ligatures, cauterizations, tonics.

The most striking cases of dilatation of the lymphatics in the lower animals are met with in horses that have suffered repeatedly and severely from the lymphangitis of plethora. Then the lower part of the shank and the pastern are enormously thickened to perhaps two or even three feet in circumference, and skin and connective tissue are the seat of a general dilatation of the lymphatic plexus and vessels with great thickening of their walls. Nocard and Barrier record cases of general dilatation of the lymphatics in dogs in connection with heart disease, also the case of a horse with old standing thrombosis of the pulmonary arteries, hypertrophy of the right heart, and dilatation of the thoracic duct to the size of the arm and of the lymphatics of the mesocolon to the diameter of half an inch to nearly an inch. Nocard records two cases in the horse, one of a reticular lymphangioma of the sheath, and the other of dilatation of the lymph vessels accompanying the saphena vein on the inside of the thigh. This formed small, soft, fluctuating, extremely irregular tumors, completely covering the vein for a space of about four inches.

In both cases the dilatations were surrounded by a thick layer of connective tissue filled with liquid. Virchow records a case of a new-born calf in which a thrombosis of the external jugular vein caused obstruction of the mouth of the thoracic duct, and a consequent extreme distension of all the splanchnic lymph vessels with a slightly sanguinolent fluid. The intestines especially were covered everywhere with broad, bead-like canals, arranged so closely together that the intervening tissue could be scarcely recognized.

The _causes_ of lymphangiectasis appear to be generally some obstruction to the onward flow of the lymph. Any diseased condition, therefore, that causes compression of the larger lymph vessels may cause dilatation of the smaller ones leading into these. General distension may come from disease of the lungs or left heart and increased venous blood pressure, or from thrombus of the jugular, or a tumor obstructing the thoracic duct, while local engorgements may come from the pressure of tumors, or the occurrence of lymphangitis and formation of fibrinous coagula. In cases of partial obstruction of the lymph vessels the increased secretion of lymph may lead to distension and enlargement. It may be named in this connection that irritation of the sensory nerves in dogs has been shown to determine a larger production of lymph (Krause). Lymphadenitis and the obstruction of the passage of lymph through the glands is an obvious cause, and hence the disease is specially liable to appear in connection with diseases which show a predilection for the lymphatics (tuberculosis, glanders, strangles, carcinoma, etc.)

In his work on dilatation and occlusion of lymph channels Busey shows that in man the majority of cases are in hospital patients in whom blood and general health have been impoverished and reduced by unhygienic conditions. One case gave support to the theory of maternal impression, the pregnant mother having suffered from over-use of the right limb on a sewing machine, and the offspring having shown extensive lymphangiectasis in the right leg.

_Symptoms_ consist in enlargement of the lymph vessels or plexus, and often of the glands. If of the lymph plexus it may appear like a dropsical effusion in the part, with or without saccular dilatations at intervals. If of the larger vessels, their tortuous anastomosing trunks following largely the lines of the veins are usually characteristic. If the distension is slight it is usually moniliform, as the valves are still intact, and the intervals between them stand out as bladder-like masses. If the structure is wounded or if it ulcerates there is the discharge of a straw-colored fluid, often rendered milky by the presence of fatty granules, and at times tinged with blood. There is always a tendency to the increase and condensation of the connective tissue surrounding the vessels, and fatty degeneration and the formation of lipomata are not uncommon.

_Treatment._ Compression, by flannel or elastic bandage, from the foot upward, is the simplest and most promising treatment when the limb is affected. The local application of cold, astringents or iodine may be added. Punctures, ligatures, and cauterization have not given encouraging results. Ligature of the nutrient artery of the part, has succeeded in one or two cases, but has failed in others. Tonics are to be tried more particularly in cases due to specific debilitating diseases. Sometimes a spontaneous recovery has been noticed when the surrounding connective tissue has increased and contracted in connection with inflammation.

LYMPHORRHŒA. LYMPHORRHAGIA. DISCHARGE OF LYMPH THROUGH WOUNDS OR SORES.

Result of rupture of lymphatics. Milky, fatty lymph. Treatment,
ligature, excision, cauterization, of little avail. Compression.
Tonics.