Chapter XIX: Part 19

_Prevention._ The hard worked or systematically exercised horse, which is at the same time heavily fed must not be left in a state of absolute rest in his stall for twenty-four hours. A fair amount of exercise must be given on every day in the week, and at the same time, the food should be restricted in ratio with the restriction of exercise. Turning for an hour or two daily into a yard may be a sufficient precaution. When from any cause, rest is imperative, the diet must be materially reduced and given in part in a laxative form (bran, roots), or a slight laxative (Glauber salts) or diuretic (saltpeter) may be added. Cleanliness and a free ventilation of the stable, are also of value in obviating at once auto-intoxication and the admission of poison through the lungs. In the same way a free allowance of drinking water is beneficial as favoring a general elimination from the various emunctories, and a dilution of the plethoric blood.

These precautionary measures are especially important in the case of horses which have passed through a first attack and which are in consequence strongly predisposed to a second. Horses fed liberally on highly nitrogenous food (oats, beans, peas, cotton seed meal), will also require specially careful oversight when at rest for a day or two only.

_Treatment._ The first and perhaps the most important consideration is absolute rest. If the subject is stopped instantly on the appearance of the first symptoms, the disease may be often aborted. It is better to avoid the exercise of walking to a stable until such time as the severity of the attack has somewhat moderated and then to move the subject only in the slowest and quietest possible way. If the patient is already down and unable to rise, he may be carried to the nearest stable in an ambulance or on a stone-boat, and there helped to his feet and supported in slings. Though he may be unable to continue in the standing position without the sling, yet if he can use his limbs at all for support, and is prevented from lying down, the breathing will be rendered so much more free and quiet, that it may greatly lessen the transfer of the poisonous elements into the general circulation and materially contribute to recovery. If, however, he cannot stand on his limbs at all, but must settle in the slings, the compression of the chest will so excite the breathing that it will induce dyspnœa, pulmonary congestion and a rapidly fatal result. In such a case a good bed must be provided and the patient made as comfortable as possible in the recumbent position.

In some cases in the earliest stages a full dose of sweet spirits of nitre or even half a pint of whiskey has seemed to assist in aborting the disease though the urine was already of a deep red color. It probably acted by supporting the already oppressed heart, and securing a prompt elimination by the kidneys.

Friedberger and Fröhner strongly recommend bleeding in all cases of dyspnœa and excited heart action, and considering the plethoric condition of the animal it would equally commend itself in other cases as well. This is the most prompt sedative of the nervous and vascular excitement, and the most speedy and certain means of removing much of the poisons accumulated in the blood, and of diluting what remains by reason of the absorption of liquids from every available source. This will more than counterbalance any temporary increase of poisons drawn from the portal system to fill up the vacuum in the systemic veins caused by the emission of blood. When the thick tarry condition of the blood seriously hinders a speedy abstraction both jugulars may be opened at once.

In some cases of great nervous excitement bromides may be useful in moderating circulatory and respiratory movement, but on the whole the advantage is greater from an immediate resort to eliminating agents.

One of the most effective agents is water. If the patient is thirsty he should have all he will drink, and if not, it may even be given from a bottle, or thrown into the rectum. A still more effective resort would be to introduce water intravenously in the form of a normal saline solution, or even to pass it into the trachea through a small cannula or large hypodermic needle. This serves to dilute the over dense blood, to stimulate the kidneys and other emunctories to active secretion, and to retain in solution the hæmoglobin, urea and other products which would otherwise cause greater irritation. This would be especially applicable after the blood tension had been diminished by phlebotomy.

Warm fomentations to the loins or croup are not without their influence. They tend to soothe the irritated parts and to solicit the action of the kidneys more particularly. The old resort of a fresh sheep skin, with the fleshy side in, may be used as a substitute.

Perhaps the most important indication is to secure depletion from the overloaded portal system and liver. Where nothing better offers, a pint or quart of castor oil, or a pound of Glauber salts, or a half drachm of podophyllin and four drachms of aloes may be given. If available 1 to 1½ grains of eserine, or 7 grains of barium chloride may be given hypodermically in distilled water or that which has been raised to the boiling point. This may be supplemented by frequent injections of hot soap suds or even of laxative saline solutions. If the bowels can be roused to free secretion the removal of toxic matters from the portal blood and the delay in the progress of similar matters through the liver will go far toward securing a favorable result. When free purgation has been secured recovery can usually be counted on.

The action on the bowels must be followed up by diuretics to eliminate the offensive matters from the general system. Colchicum has been recommended because of its action in increasing the solids of the urine, and this may be combined with saltpeter or other diuretic, or the latter may be used alone and repeated twice a day. If, however, the patient can, by the free use of common salt or otherwise, be induced to drink freely of water, the elimination through the kidneys will be sufficiently secured.

The muscular weakness and paralysis that remain after the acute symptoms have subsided must be met by stimulating liniments and even blisters to the loins or affected muscles, by the internal use of strychnia (2 grs. twice daily) until the jerking of the muscles indicates that its physiological action has been secured, and by an electric current daily for ten minutes at a time through the affected nerves and muscles. Animals that have been helpless for weeks have, in our hands, recovered under such treatment, and even cases of several months’ standing, with the most extensive atrophy of the triceps, and in which the animal could barely stand, have made a satisfactory recovery.

Any remaining nephritis must be treated according to its indications.

During recovery and in the convalescent animal the diet should be laxative and non-stimulating. Bran mashes, turnips, beets, carrots, green fodder, ensilage and scalded hay may be allowed. Oats, corn, beans, peas, vetches, etc., must be carefully avoided. If the food fails to maintain the bowels in a gently relaxed condition one, two or more ounces of sulphate of soda may be added daily.

In the mild cases a good dose of purgative medicine succeeded by a course of diuretics will serve a good purpose.

In all cases alike work must be resumed very gradually. At first the animal may be walked a few hundred yards, and the pace or load and duration of exercise may be increased day by day until full work can be safely endured. In an animal that has once suffered the same gradual inuring to labor should be followed, after any short period of rest on a fairly good ration.

JAUNDICE, ICTERUS, THE YELLOWS.

Symptomatic. Causes: Mechanical obstruction of bile duct, gall-stones,
hydatids, distomata, extraneous bodies, inflammation, stricture,
obliteration, absence, ulceration, spasm, tumor, enlarged lymph
glands, gastric tumors, pancreatic, kidney or omental tumor, aneurism,
fæcal accumulation, pregnancy, ovarian tumor: Without mechanical
obstruction, ptomaines and toxins, animal venoms, mineral poisons,
hepatic atrophy, fear, other emotions, cerebral concussion, imperfect
oxidation, excess of bile, hepatic inflammation, constipation and
reabsorption of bile, experimental jaundice, balance of tension in
gall ducts and blood vessels, duodenitis, compression of aorta,
hæmatoidin and bilirubin, destruction of blood globules by hydroæmia,
taurocholate of soda, chloroform, ether, freezing, heat, electricity,
alkalies, nitrites. Hæmoglobin: Its solubility in horse. Bile acids
and blood pigment. Summary of causes. Gravity of icterus. Symptoms:
Coloration, yellow, orange, brown, of tissues and secretions: Tests,
staining white paper, Gmelin’s test, nitric and sulphuric acids,
rainbow hues: Pettenkofer’s test for bile acids, syrup and sulphuric
acid, dark violet: Stranburg’s test syrupy paper and sulphuric acid,
dark violet; clay colored fœtid stools; gravity.

The terms icterus and jaundice are applied to a yellowness of the mucosæ, urine, skin and tissues caused by the presence in them of the coloring matters of bile. The condition is a symptom of many different affections rather than a disease _per se_, yet the phenomenon is so characteristic that it has been hitherto accorded a special place and article in systematic works.

Jaundice is either associated with _mechanical obstruction of the bile duct_ or ducts, or it is _independent of such obstruction_. The following enumeration of its causes slightly modified from Murchison, is equally applicable to the lower animals as to man:

A. Jaundice From Mechanical Obstruction of the Bile Duct.

_I. Obstruction by foreign bodies within the duct_:

1. Gall stones and inspissated bile.

2. Hydatids and distomata.

3. Foreign bodies from the intestines.

_II. Obstruction by inflammatory tumefaction of the duodenum or of the lining membrane of the bile duct with exudation into its interior._

_III. Obstruction by stricture or obliteration of the duct._

1. Congenital deficiency of the duct.

2. Stricture from perihepatitis.

3. Closure of the orifice of the duct in consequence of ulcer of the
duodenum.

4. Stricture from cicatrization of ulcers in the bile duct.

5. Spasmodic stricture.

_IV. Obstruction by tumors closing the orifice of the duct or growing in its interior._

V. Obstruction by pressure on the duct from within, by:

1. Tumors projecting from the liver itself.

2. Enlarged glands in the fissure of the liver.

3. Tumor of the stomach.

4. Tumor of the pancreas.

5. Tumor of the kidney.

6. Post peritoneal or omental tumor.

7. An abdominal aneurism.

8. Accumulation of fæces in the bowels.

9. A pregnant uterus.

10. Ovarian and uterine tumors.

B. Jaundice Independent of Mechanical Obstruction of the Bile Ducts.

_I. Poisons in the blood interfering with the normal metamorphosis of bile._

1. The poisons of the various specific fevers (Anthrax, Texas fever,
Hog cholera, Swineplague, Petechial fever, Pyæmia, Septicæmia, etc.).

2. Animal poisons: snake poison.

3. Mineral poisons: phosphorus, mercury, copper, antimony, etc.

4. Chloroform, ether, etc.

5. Acute atrophy of the liver.

II. Impaired or deranged innervation interfering with the normal metamorphosis of bile.

1. Severe mental emotions: fright, anxiety, etc.

2. Concussion of the brain.

III. Deficient oxygenation of blood interfering with the normal metamorphosis of bile.

IV. Excessive secretion of bile, more of which is absorbed than can undergo the normal metamorphosis.

Congestion of the liver: _a._ Mechanical, _b._ Active, _c._ Passive.

V. Undue absorption of bile into the blood from habitual or protracted constipation.

Mechanical obstruction, by tying the bile ducts in a dog, caused in two hours yellow coloration of the contents of the hepatic lymphatics and thoracic duct, and also of the blood in the hepatic veins (Saunders). That this jaundice is due to reabsorption and not to suppressed secretion of bile, already present in the blood, may be fairly inferred, from the complete absence of icterus, where, from general disease of the liver, the secretion of bile has been entirely suspended, and in which the gall ducts and bladder contain only a little gray mucus (Haspell, Frerichs, Budd, Murchison), also from the fact that after complete extirpation of the liver in frogs not a trace of biliary acids nor pigment can be detected in the blood, urine, or muscular tissue (Müller, Runde, Lehmann, Moleschott). Bile acids and bile pigment are formed in the liver by disintegration of blood globules, and when present in excess in the blood it is by virtue of reabsorption.

This reabsorption will take place under the slightest favoring influence. The obstructions in the bile duct, above referred to, cause the tension in these ducts to exceed that of the blood in the capillaries of the liver and at once osmosis of bile into the blood vessels sets in. This may occur from so slight a cause as the congestion and swelling of the duodenal mucosa around the opening of the bile duct. Again reabsorption of bile may be determined by a lessening of the normal fullness and tension of the hepatic capillaries as when the aorta is mechanically compressed by abscess, neoplasm, ingesta, or otherwise, just behind the diaphragm (Heidenham, Brunton). The cause is the same in both cases, namely, the want of balance between the fullness and tension of the bile ducts, and the hepatic blood vessels. There is increased fullness of the hepatic biliary ducts, or decreased plenitude of the hepatic capillaries and lymphatics.

It must be added, however, that the coloring matter of the bile is apparently produced, in the liver, from that of the blood, and that the pigment (hæmatoidin), found in old extravasations of blood, is probably identical with bilirubin, and that any agent or condition which causes liberation of the coloring matter of the red blood globules, will cause a staining of the tissues, like that of jaundice. The following agents are known to have this effect on the blood globules: water, in hydroæmic states of the blood (Hermann); taurocholate of soda from absorption of bile (Frerichs, Kuhne, Feltz, Ritter); chloroform (Chaumont); ether (Burdon-Sanderson); freezing (Rollet); a high temperature +60° C. (Schultze); frictional and induction currents of electricity (Burdon-Sanderson); the alkalies (ammonia, potash and soda) and nitrites when present in excess.

The injection of hæmoglobin into the veins of dogs has been followed by the appearance of bile pigment in the urine, but Naumyn, Wolff, Legg and Brunton failed to obtain the same result in rabbits.

It is noticeable that the hæmoglobin of horses’ blood is very soluble at all temperatures and that of dogs very slightly so (Burdon-Sanderson). This may serve to explain the great prevalence among solipeds of diseases, associated with dusky brown or yellow discoloration of the mucosæ, with petechiæ, and with the passage of blood pigments in the urine. It may further explain the usually benignant course of jaundice in the horse and its extreme gravity in the dog.

There is further reason to believe that the bile acids, when in excess, may be transformed into bile pigment in certain conditions of the blood, as occurs under the action of sulphuric acid out of the body (Stœdler, Meukomen, Folwarcyny, Röhrig). Moreover, in the healthy state, the greater part of the bile secreted, including acids and pigment, is re-absorbed from the intestinal canal, but is oxidized and decomposed in the blood so that it cannot be detected, in blood or urine. But let the transformation be interrupted, as in certain diseases of the lungs, with imperfect oxidation, and the bile circulates in the blood, stains tissues and urine, and in short causes jaundice.

To sum up: it may be said that icterus is probably never due to simple inactivity of the liver: it may, however, be caused by excessive secretion of bile which is re-absorbed from obstructed bile ducts or bowels:—it may result from imperfect transformation, in the blood, of the bile which is normally re-absorbed from the intestine: or it may possibly be caused by the formation of pigments in the blood from the abnormal transformation of bile acids, or by solution of the hæmoglobin of the blood corpuscles.

The gravity of jaundice varies as much as its causes. It is well known that the system may be saturated with bile, and the tissues and urine deeply stained without much constitutional disorder. The pigment alone is not an active poison. But there may be much attendant suffering from obstructed biliary ducts or bowels, from diseases of the lungs, or from disintegration of the blood globules and imperfect nutrition, or there may be profound nervous prostration and disorder from uræmia, or from the presence in the blood of an excess of effete and partially oxidized albuminoids (See Azotæmia). According to our present knowledge, constitutional disorder, prostration and suffering in cases of jaundice, are mainly due to the presence in the circulation of these albuminoids, and of taurocholic acid which latter has a most destructive effect on the blood corpuscles.

The _symptoms_, therefore, are not characteristic apart from the yellow coloration of the tissues and urine and the chemical reactions of the bile acids and bile pigments furnished by the latter.

The coloration of the tissues may be a simple tinge of yellow especially noticeable in the eye (conjunctiva), or it may amount to the darkest shades of orange and brown. It may or may not be complicated by the presence of spots or patches of blood-staining (ecchymosis) on the visible mucous membranes but especially in cases complicated by poisoning with taurocholic acid or effete nitrogenous products.

The urine may be similarly colored in all shades of yellow or orange brown, and may leave a correspondingly deep stain on white paper.

The _test_ for _bile pigments_ (Gmelin’s) is simple and beautiful. Pour a little nitric acid into a test tube held obliquely and then add a few drops of sulphuric acid, and finally a little urine, so slowly, that it will remain on the surface. Soon at the point of junction appear in succession the various colors of the rainbow: yellow, green, blue, violet, red and lastly a dirty yellow. It is open to this objection that the characteristic play of colors may be produced by alcohol in the absence of bile pigments. Indican also will produce the green and yellow with blue between but never the violet nor red, nor all in their regular order.

A _second mode_ of applying this test is by spreading a few drops of the urine on a white plate and letting fall a drop of nitric acid in the centre. The play of colors is very characteristic.

The _test for bile acids_ (Pettenkofer’s) is to place a portion of the urine in a test tube, and after adding a drop of syrup, to add cautiously, drop by drop, two-thirds of the amount of sulphuric acid. Shake the mixture and set aside for some minutes. If sufficient heat is not produced by the mixing of the acid and urine warm slightly. The mixture becomes of a dark violet color which is destroyed by a temperature a little above 140° Fah.

A convenient application of this test (Stranburg) is to add a little cane sugar to the urine, dip a piece of filtering paper in the mixture, dry it thoroughly, pour a drop of sulphuric acid on the paper and allow it to run partially off. In a quarter of a minute a beautiful violet color is produced, best seen by holding up the paper to the light and looking through it (Brunton).

In cases due to obstruction of the bile ducts the dung is destitute of bile, whitish, often clayey and fœtid, while in cases due to reabsorption without obstruction the fæces have their natural color and odor.

It is needless to enumerate all the concomitant symptoms of jaundice which will be better noticed under the different disorders which determine it, for a list of which see the _causes_.

The gravity of the affection will depend on the dangerous nature of these concurrent diseases, and the destructive changes in the liver and blood rather than on the depth of color in the textures.

CATARRHAL ICTERUS (JAUNDICE) OF SOLIPEDS.

Causes: infection from duodenum through biliary duct. Suppression of
bile favors. Musty, heated, mow burnt fodder, over feeding, irregular
feeding, or watering, over work, worms, fatigue, damp stables,
duodenal congestion, gall-stones, concretions, pancreatic tumor,
ascaris in bile ducts, distoma, infection through portal vein, toxins.
Symptoms: of duodenal catarrh, icterus, yellow, viscous, odorous
urine, dullness, weakness, somnolence, tardy pulse and breathing,
costiveness, or diarrhœa, pale, fœtid stools. Duration: 2 to 3 weeks
or longer. Lesions: duodenitis, distended biliary and pancreatic
ducts, calculi, enlarged softened liver and kidneys. Diagnosis:
icteric symptoms in absence of fever. Prognosis: usually favorable.
Treatment: laxative diet, pasture, soiling, ensilage, roots, fruits,
water freely, exercise, antisepsis, elimination, laxatives,
cholagogues, diuretics, calomel, salines, nitro-muriatic acid,
podophyllin, castor oil, aloes, tartar emetic, bitters, sodium
bicarbonate.

_Causes._ This may be said to be an extension of infection from the duodenum through the bile ducts. The microbes of the intestinal canal become acclimatized by living in the bile-charged contents of the duodenum until they acquired the power of survival and multiplication in the biliary ducts themselves. The well known antiseptic qualities of the bile, constitute a powerful barrier to this, yet the power of adaptation on the part of certain germs is greater than the defensive action of the bile. The attack is however mostly in connection with indigestion or muco-enteritis, and a more or less perfect suspension of biliary secretion, so that this defensive action is reduced to its minimum and the germs can ascend the bile ducts in the mucous secretion as a culture medium, and by interference with the resumption of a free hepatic secretion, they succeed in safely colonizing themselves in the mucosa and hepatic parenchyma. Whatever, therefore, interferes with the integrity of the duodenal functions directly contributes to the extension of infection from bowel to liver. Old, heated, musty, cryptogamic, dusty fodder, grains that have been badly harvested in wet seasons, feed that has been damp and fermented, overloading of the stomach, irregular feeding and watering, giving drink after a feed of grain, underfeeding, overwork, worms, excessive fatigue, damp, dark stables, etc., tend to induce indigestions and to lay the bile ducts open to infection. Blocking of the bile duct and stasis of its contents may be a sufficient cause. The swollen mucosa around the orifice of the duct not only blocks the passage but favors the formation of a mucous plug as recorded by Benjamin of an equine patient. Wolff found obstruction of the duodenum in the horse by a mass of ingesta, and blocking of the gall duct, with jaundice.

Gall stones and concretions are very direct causes of biliary obstruction and jaundice. Though less common in horses than cattle, these are not unknown in idle, pampered animals when on dry winter feeding.

Tumors of the pancreas or adjacent organs pressing on the gall duct are recognized as causes of equine icterus, (Megnin, Nocard).

With any obstruction to the bile a disturbance of balance of pressure between the bile ducts and the hepatic veins is brought about by respiratory movements. On the one hand the aspiratory power of the chest empties the hepatic veins, lessening blood pressure, and in expiration the contraction of diaphragm and abdominal muscles compresses the gall ducts increasing their tension and favoring absorption of bile.

The entrance into the bile duct of the ascaris megalocephala is at once a cause of obstruction and of the transference of duodenal microbes, and the presence of trematodes (fasciola hepatica, or distoma lanceolatum) will also favor obstruction. Other parasites, like the echinococcus or actinomycosis, may press on the biliary ducts and determine jaundice.

Another mode of infection is by way of the portal vein, the microbes entering from the intestine and becoming arrested and colonized in the liver (Dieckerhoff).

Whether from the presence of the microbes or from the absorption of ptomaines and toxins from the intestines, the radical biliary ducts become inflamed, swollen, and even blocked, and the hepatic cells degenerated or even completely devitalized, so that they fail to take an aniline stain. In such cases the remaining sound hepatic cells go on producing bile, but as this cannot any longer escape through the partially obstructed interlobular biliary radicles, it is largely absorbed and produces icterus. Cadeac mentions a case of this kind in a mare in which the toxic matters had not only led to hepatic disease, but also to structural changes in the eliminating organ (the kidney).

_Symptoms._ In the horse the disease is mostly attendant on subacute duodenitis, and even when this is associated with infective catarrh of the biliary passages the kidneys remain mostly sound and active, and eliminate alike the bile pigments and the more toxic matters so that the disease is not often grave. Beside the essential feature of yellow mucosæ, and urine, the latter viscous and smelling strongly, there is profound depression, sluggishness, weakness and somnolence. Imperfect muscular control and even slight paresis may be present. Tardy pulse and breathing are at times noticeable. At others these, like the temperature, are normal. The mouth is hot and dry. The urine may be slightly albuminous. The bowels incline to costiveness from lack of their customary stimulus, yet this in turn may give rise to diarrhœa. In either case, as the disease advances, the defecations lose the healthy yellowish brown color, becoming pale and fœtid.

_Duration._ The attack may last one, two or three weeks, and generally ends in recovery. With irremediable structural lesions, it is of course permanent and even fatal.

_Lesions._ The most common feature is duodenitis with thickening around the orifice of the common bile and pancreatic duct. The biliary ducts may be distended and their contents more than usually viscid and glairy from the presence of pus. Their mucosa may show ramified redness, or concretions as casts or calculi. The liver is enlarged, soft and friable giving way readily under the pressure of the finger. Enlargement of the kidneys is usually present, the cortical substance having a brownish red and the medullary portion a yellowish pink hue.

_Diagnosis._ The absence of hyperthermia in jaundice, serves to distinguish it from the acute febrile affections (pneumonia, influenza, contagious pneumonia, petechial fever, etc.,) which are marked by yellowness of the mucosæ and skin.

_Prognosis._ The merely functional forms of icterus in solipeds usually end in recovery.

_Treatment._ The first consideration is a laxative diet. A run at pasture will usually meet every indication. Fresh cut grass, ensilage, turnips, carrots, potatoes, beet, apples, or other succulent diet may be given as substitute. Bran mashes and hay cut and moistened may be allowed in the absence of the above. Abundance of water and especially cool water will stimulate bowels, liver and kidneys, favor the elimination of the bile by contraction of the biliary ducts, and hasten the expulsion of the poisons through the kidneys. Regular exercise an hour after meals stimulates both bowels and liver to action.

Medicinal treatment is largely directed to antisepsis of the bowels and the arrest of the production of injurious toxins; elimination from the bowels and incidental depletion from the portal vein and liver; antisepsis and stimulation of the liver; and stimulation of the urinary secretion.

The preparations of mercury fill several of these indications. Calomel 2 drs., or blue mass 1½ dr., is not only a soothing laxative and antiseptic, but seems to operate as a calmative and antiseptic to the liver as well. It may be continued in 5 to 10 grain doses two or three times a day, according to the size of the animal and the condition of the bowels, and associated with ½ dr. belladonna extract to each dose together with a bitter (quassia, gentian, nux vomica). Or 4 or 5 ozs. sulphate of soda may be given three times a day, with 2 drs. salicylate of soda as an antiseptic. Or, to increase the hepatic action, nitro-muriatic acid largely diluted may be given in sixty drop doses thrice a day in the drinking water. These are especially valuable for their antiseptic action, cutting off at once the source of nervous irritation from the attendant indigestions, and duodenal congestion, and arresting the flow of the irritant toxins and other products through the portal system. Podophyllin, castor oil, aloes, rhubarb, often act well by depletion from the portal vein, and expulsion of indigestible and irritant matters from the intestines, but there is more danger of resulting swelling of the duodenal mucosa than with the mercurials or aqua regia. Goubaux recommends 2½ drs. of tartar emetic.

Siedamgrotzky has had good results from an electric current sent through the region of the liver, but in the horse this is rarely demanded.

A course of bitters, with bicarbonate of soda in small doses, may be demanded to re-establish the healthy tone of the stomach and intestines, and a run at pasture, or at least an open air life, exercise, and a laxative diet with abundance of good water should be secured. Any undue costiveness should be counteracted at once by a saline laxative.

CATARRHAL ICTERUS (JAUNDICE) IN DOGS.

Pampered artificial life of dogs as predisposition. Eating carrion.
Chills especially when heated and exhausted. Infection from bowels.
Obstruction of gall duct by inflammation, calculi, neoplasms.
Catarrhal exudate as a protector of microbes. Toxins from intestines,
food or water. Youth, lack of acclimation, mental shock, blocking of
bowel, blood effusion in gall bladder, incubation. Symptoms: signs of
gastro-enteritis, prostration with invasion of the liver and
especially of the kidney. Icteric urine without jaundiced mucosa.
Gravity of icterus with suppression of urine. Hypochondriac
tenderness, arched back, dullness, irregular bowels, excited
circulation and breathing, preliminary fever tends to subside,
tympany, colic, trembling. Death in one or two days or more. Lesions:
congestion, degeneration, ecchymosis, ulceration of gastro-duodenal
mucosa, extending into liver ducts and acini, bile inspissated, liver
enlarged, yellowish brown, softened, fatty, shrunken, distorted
hepatic cells. Kidneys congested, ecchymosed, cortical part with
necrotic foci; lymph glands congested. Diagnosis: by icterus of
tissues and urine tests. Prognosis: grave in acute cases, more hopeful
in tardy ones. Treatment: antiseptics, cholagogues, salol,
salicylates, alkalies, carbonates, tartrates, iodides, laxatives, cold
enemata, aloes, electricity, water freely, pilocarpin, strychnia, aqua
regia, digitalis, bitters, muriatic acid, convalescent diet.

_Causes._ The dog is much more subject to jaundice than the horse, and the affection is liable to be much more severe, than in solipeds. He leads a more artificial life, especially in cities, where the lack of open air exercise, and of the facility for attending to nature’s wants, together with an excessive, varied, stimulating diet predisposes him to constipation, indigestion, and disorders of the stomach, bowels and liver. In other cases the devouring of decomposing food and foul water proves a cause of direct microbian infection, and of poisoning by ptomaines and toxins generated out of the body. Exposure manifestly has something to do with the prevalence of canine icterus, which is more common in spring and especially in autumn than at other seasons. In hunting dogs, out of condition, the suddenly induced over-exertion and fatigue, and the succeeding chill in cold air or water, become accessory factors.

It appears to be most commonly the result of the transference of germs from the intestine, either by way of the bile ducts, or with the blood through the portal vein. The first form is usually the sequel of muco-enteritis affecting the duodenum, with swelling of the walls of the common bile and pancreatic duct at its orifice, or from obstruction by gall-stones, concretions, impacted bowels or neoplasms. With the arrest of the biliary flow the intestinal ferments gain an entrance into the common duct and the sac of Vater, finding protection from the antiseptic bile in the resulting catarrhal exudate, and in this way they reach the gall-bladder, the biliary radicles and the acini. With the entrance of bacteria or toxins by the portal vein on the other hand, there is first a troubled condition of the acini and hepatic cells, an over-secretion of thick bile, and blocking of the passages so that little is passed into the intestine, the greater part being absorbed into the hepatic veins. Fermentation microbes in the stomach and intestines, the germs of suppuration and septicæmia, and saprophytic germs from outside the body are held to be causative of icterus. Cadeac lays much stress on the putrefactive germs in water, and traces different attacks to marshes and foul ponds.

As in other infecting diseases, early age has a predisposing influence. The older subject has presumably been already exposed to the microbe and acquired some measure of immunity. Animals coming new to the locality and poison, are equally susceptible with the young. Trasbot found that 14 out of 17 dogs thus attacked were between three and eighteen months.

Leblanc and Trasbot claim mental shock as a cause of icterus in the dog. The disappointment and weariness caused by the master’s absence, the excitement of a fiercely contested fight, and brutal punishment are adduced as cases in point. Abuse of emetics and purgatives, in connection with a pre-existing hepatic or duodenal disorder or as a supposed prophylactic of canine distemper has induced jaundice.

Obstruction of the small intestine has proved a factor, partly by the reflex irritation through the splanchnic nerves, and partly through obstruction to the common bile and pancreatic duct.

Walley records a case of obstruction of the cystic duct by extravasation of blood in the gall bladder.

Icterus not infrequently supervenes during canine distemper in which the early gastric and duodenal irritation becomes an occasion of the extension of the catarrhal infection to the common bile duct. Even apart from this Trasbot has seen the majority of cases ushered in by a gastro-duodenitis. In this connection it is interesting to quote the remark of Pfuhl that 26 out of 27 persons using the foul baths of a given establishment contracted icterus, while the soldiers bathing in another branch of the Elbe entirely escaped.

The fact that icterus usually sets in several days after such an exposure, whether in man or dog, indicates a period of incubation, and thereby sustains the theory of infection.

_Symptoms._ In the majority of cases, gastro-enteritis constitutes the first step of this affection and the early symptoms are characteristic of that disease. Frequent vomiting, at first of food, and later of a glairy fluid which may be discolored by bile, redness of the tongue, especially along its margins, bloodshot, watery eyes, lying down with the nose on the right side of the abdomen, or standing with the abdomen tucked up and the back arched, halting movements of the limbs, wincing if manipulation is made of the spine or the epigastrium, elevated temperature, accelerated pulse and breathing, anorexia and perhaps purging, mark the onset. So long as the liver is unaffected prostration is not a marked feature.

Even when the liver is invaded, a fair measure of life and activity may often be retained so long as the kidneys remain sound and active. The bile pigments and salts, and the toxins generated by the invading microbes are alike eliminated in large part in the urine, and the profound poisoning and prostration of the nervous system are in a measure prevented. In many cases therefore the urine is strongly jaundiced without much or any discoloration of the mucosæ and in such cases the prospects are usually good for an early and complete recovery. It must not, however, be inferred that such a happy issue will always follow, as the pigments are by no means as toxic as are other hepatic products and fatal results may ensue with very slight jaundice of the tissues.

As a rule, however, the jaundice of the tissues (eyes, nose, mouth, white portions of the skin) is to be accepted as a grave manifestation, indicating either an excessive production and absorption of bile, or a suppressed secretion through the kidneys, or both. Then the poisoning by biliary salts and bacterial toxins is shown in profound dullness, prostration, muscular weakness, indisposition to rise, moving stiffly and only when dragged by the collar, the limbs trembling and the back arched. The tender back is arched, the right hypochondrium sensitive, the expression dull, stupid and listless, and constipation or a fœtid diarrhœa is liable to set in. The heart beats may be strong and irregular, the breathing is easily disturbed and hurried. The temperature at first 104° to 107° may descend to the normal as the system becomes charged with the toxic products, and does not usually exceed 99.5° after two or three days of jaundice of the tissues.

The icterus is shown in the eye or mouth, or on any white portion of the skin, and in the urine it will be detected by the eye or by the tests above given.

In the worst cases the urine is very scanty and of a deep yellowish brown color, prostration is extreme, tympany, colic, obstinate constipation or bloody diarrhœa may set in, the breathing, hurried or not, is trembling, the pulse small, and the temperature at first high may descend to 95° or even much lower before death.

The _course_ of the disease varies according to its gravity. If there is complete retention of bile, and abundant production of toxins, the animal dies in one or two days in a state of collapse. If there is general progressive degeneration and destruction of the hepatic tissue without at first absolute suppression of the discharge of bile into the duodenum, the patient may last till the fourth or fifth day, or later.

_Lesions._ There are usually congestion, tumefaction, friability, ecchymosis and even ulceration of the gastric and duodenal mucosa. The organs are empty, but show a reddish brown exudate of a glairy consistency, and containing red blood globules and pus corpuscles. The same inflammatory lesions are to be traced into the common bile duct, the cystic duct and bladder, the biliary ducts, and the acini. The mouth of the common duct is usually blocked with a plug of tenacious mucus, the gall bladder having been unable to expel this and the inspissated bile into the intestine. The liver is slightly enlarged, yellowish, with patches of brownish yellow more or less deep, and the acini contain an abundance of oily globules, and yellowish brown granules. The acini have no clear line of delimitation, and the contained hepatic cells are shrunken and distorted, standing apart from each other in a dropsical or watery medium.

The kidneys are congested and ecchymosed; the cortical substance brown, friable, and with numerous areas of necrosis of a bluish white color, and even abscesses. The medullary substance is yellow and the uriniferous tubes contain an abundance of yellowish brown granules.

The lungs have a yellowish red color, with patches of ecchymosis.

The lymph glands generally are congested and many of them gorged with blood, of a dark red color, and lacking in consistency and cohesion.

_Diagnosis._ The characteristic icterus is lacking in the early stages, and active treatment gives good hope of success. When indigestion, persistent vomiting and tenderness of the epigastrium, and right hypochondrium, are associated with diarrhœa, it is highly important to examine the urine for even slight traces of bile. When the jaundice is due to impaction of a biliary calculus, the symptoms may increase slowly, and yet reach a sudden climax with acute colicy pains and tenderness of the right hypochondrium.

_Prognosis._ In acute rapidly developing cases a fatal issue is to be expected. In those which develop more slowly, recovery may be hoped for if early treatment is instituted.

_Treatment._ Cases due to biliary calculus must be treated for that lesion.

In purely infective icterus attempts must be made to arrest the intestinal and hepatic fermentation. As intestinal antiseptics, naphthol, benzo-naphthol, naphthaline, 5 grains four to six times a day. As hepatic antiseptics, salol 5 grains, salicylate of soda 8 grains, or calomel 1 grain four times a day. The salol and salicylate tend to increase biliary secretion and to render it more fluid. The same end is attained by alkalies (carbonates of potassa, or soda or lithia, bitartrate of soda, iodide of potassium). These are further valuable in hastening the elimination of toxic matters by the kidneys. The expulsion of bile, and of intestinal microbes and toxins may be sought by laxative doses of Glauber salts, or by cold enemas of the same. Verheyen recommends aloes in laxative doses for six days. Siedamgrotzky had good results from induction currents of electricity, sent through the region of the liver twice a day for ten minutes on each occasion. To assist in elimination abundance of pure water or of watery fluids may be used. The most effective eliminating agent is pilocarpin in ⅙ gr. dose hypodermically, repeated daily. In weak conditions frequent small doses of strychnia, ether, aqua regia, or digitalis may prove valuable.

In case of improvement a course of bitters is usually demanded, and these may be combined with hydrochloric acid or small doses of sodium bicarbonate.

Throughout the disease, gruels, beef tea, buttermilk, whey or any simple nutritive aliment which the animal relishes may be given, but both then and during convalescence fatty matters and indigestible materials should be carefully withheld.

JAUNDICE IN CATTLE AND SHEEP.

Usually with gall-stones or concretions, or distomata. In sheep from
decomposing vegetation. Symptoms: anæmia, emaciation, pallor, icteric
mucosæ. Digestive disorder and bilious stools suggest worms.
Treatment: as in horse, or vermifuge.

Though less common than in the dog icterus in ruminants occurs, but most commonly in connection with gall stones and concretions, or with trematodes in the gall ducts. These forms will be noticed under these respective headings. Verheyen describes an icterus of sheep which occurs enzootically in damp low undrained localities, and is attributed by shepherds to the consumption of dead and fermenting leaves. The symptoms are those of anæmia, emaciation, and increasing weakness, with a pallor and more or less dull yellow of the conjunctiva, and, later, of the other mucosæ. The loss of appetite, indigestion, yellow liquid fæces, suggest the possible presence of parasites as a cause, and the prescribed treatment by common salt, juniper berries and tonics strengthens the suspicion. Other forms must be treated according to cause on the lines laid down above.

JAUNDICE OF THE NEW-BORN. ICTERUS NOUVEAUX NÉS.

In mules; less frequently in horses and cattle. Bacteridian.
Predisposition from alleged miscegeneration. Offspring of lymphatic
mares. Spoiled fodders, foul buildings, exposure, infection by
umbilicus. From gastro-enteritis, diarrhœa, dysentery. Congenital.
Symptoms: refuses the teat, scours, red urine, palpitation, colics,
perspirations, inflammations, or abscesses of navel, arthritis, other
internal disorders. Death from exhaustion or in convulsions. Or
symptoms subside and pass in 15 days. Diagnosis: prostration,
palpitation, icterus, and bloody urine with omphalitis. Streptococci.
Prognosis: with hæmaturia nine-tenths fatal. Lesions: icterus, heart
soft, flabby, lungs congested, general ecchymosis, blood black, clot
diffluent, liver congested, enlarged, spleen, swollen, softened with
spots of brownish yellow, meconium bloodstained, kidneys swollen,
congested, points of infarction or necrosis, urine bloody, navel
lesions. Treatment: for congenital cases improve hygiene for dams; for
offspring, antiseptics to navel, shelter, warm box; aloes to dam, or
oil to colt, antiseptics internally, demulcents, stimulants,
derivatives, opium, water, alkalies.

This has been observed in cattle (Kitt), and in horses (Levrier, Bernadin, Lhomme) but above all in mules (Villa-Roya, Carrere, Levriere, Bernadin, Lhomme, Hartmann, Dieckerhoff).

The affection is a bacteridian disease, in which there is a great destruction of red globules, and liberation of hæmatin, with hæmaturia and yellow coloration of the tissues.

_Causes._ Carrere attributes much to a supposed congenital weakness induced by the unnatural generation of ass with mare. Cadeac noticed that the offspring of certain mares and horses remained sound, while the progeny of the same animals, and asses suffered largely from icterus. Levrier found it especially in the mules born of mares having a lymphatic temperament or suffering from canker, grease or chronic lymphangiectasis. Bernadin and Lhomme attribute much to bad hygiene, and especially to poor or spoiled fodders. Lhomme, Lafosse and Trasbot find accessory causes in cold and wet weather. Retention of the meconium is another cause. Dieckerhoff, Hartmann, Cadeac and Bournay trace the disease to bacterial infection as the essential cause. Many cases originate in septic infection and inflammation of the navel and umbilical veins. Others commence with mucous gastro-enteritis, attended by diarrhœa or dysentery. In other cases the germs appear to have reached the liver through the circulation as the animal is already affected at birth.

_Symptoms._ When not congenital, symptoms are usually seen in the first few days of life, usually before the fifth day.

In congenital cases the new born animal is unable to stand at all or for longer than a very short time, it lies listlessly and makes no attempt to suck even when held up to the teat. There is acceleration of pulse and respiration, the heart beats are tumultuous, the mouth is dry, the mucosæ of a straw yellow, the bowels are costive, and the urine, whether discharged in life, or found in the bladder after death, is bloody.

When attacked later, the animal becomes dull, weak, and stupid, refuses the teat, and has the bowels relaxed. The mucosæ become pale yellow, the breathing accelerated, the heart beats violent, and the pulse rapid, small and weak. The urine is passed slowly and with effort and has a red hue more or less deep according to the severity of the attack. Colics are not uncommon, causing uneasy shifting of the limbs and tail, cries, frequent lying down and rising, and partial or general perspiration. Complications on the part of the navel and umbilical veins are to be looked for, in open sores, swellings, abscess, phlebitis, and in arthritis and secondary abscesses in different organs. Death may occur quietly, as from exhaustion, while in other cases it is preceded by convulsions.

In case of recovery, there is an improvement of the general symptoms, the heart and respirations become moderate, appetite is restored, the little animal sucking the teat, there are abundant, yellow, semi-solid defecations, the strength increases day by day, and convalescence may be fully established by the twelfth to the fifteenth day.

_Diagnosis._ This is mainly based on the extreme weakness and prostration, the violent heart action, the jaundiced hue of the mucous membranes, and the bloody urine. Confirmation may be sought in the presence of streptococci in the fresh urine, kidneys, liver and blood, and in the artificial cultures made from them. The presence of omphalitis is further significant.

_Prognosis._ Bernardin says that if hæmaturia is present nine out of ten cases are fatal, while in the absence of this feature nine-tenths recover.

_Lesions._ The jaundiced appearance of the conjunctiva and other tissues is constant. The heart is pale, soft and flaccid, with petechial patches of a deep red extending into the muscular substance; the lungs are congested with similar patches of blood-staining; the blood in the heart and larger vessels is dark, and fluid or only loosely clotted. The liver is congested to twice or thrice its normal size (10 lbs. in place of 3 or 4 lbs.); the spleen is enlarged, softened, and shows spots of brownish yellow. The small intestine contains a yellowish or dark red meconium, and it may contain effusions of dark blood, while its mucosa is inflamed, thickened, easily lacerated, and pigmented, or marked by petechiæ. The large intestines and especially the rectum are packed with hard dry balls.

The kidneys are enlarged, often to double their volume, and deeply congested, with infarcts, and patches of necrosis, of a pale brownish yellow hue. The urine in the bladder is deeply stained with blood coloring matter.

_Treatment._ For congenital cases it is manifest that treatment must be preventive and applied to the dam, before parturition. An open air life, moderate exercise, sound, easily digestible and nourishing food; grooming; in the stable, cleanliness, dryness and good ventilation; good water, are essential.

For the offspring, antiseptics (tannin, mercuric chloride lotion, copperas, calomel, iodoform), applied to the navel, and protection against cold winds and rains, and damp lairs. For mules and other young animals born in severe, winter weather a dry, warm, foaling box is desirable, and the little animal should be rubbed dry and covered with a warm woolen blanket. When the temperature approaches zero or the barn is cold, the smaller animals, as soon as they are dropped, should be placed under a box with a jar of hot water wrapped in woolen coverings, or with hot bricks similarly wrapped, and should only be let out for food when they are completely dried, or when the weather has moderated.

_Therapeutic treatment_ may be commenced by a dose of aloes given to the dam, or of olive or castor oil or manna given to the offspring. As a substitute sulphate of soda may be used. Antiseptics like salicylate of soda, salol, or the sulphites may be added. To act as a demulcent on the alimentary and urinary tracts, well boiled flaxseed tea is usually recommended. Weakness may be met by warm strong coffee, salicin, quinia, or other bitters, and more stimulating agents like camphor, angelica, assafœtida, or even oil of turpentine may be added. Diarrhœa may be checked by linseed tea, mustard plasters, or in obstinate cases, by opium. Elimination should be sought by administering abundance of pure water or watery demulcents, and even by the use of alkalies like bicarbonates of soda or potash. A moderately free action of the bowels must be constantly maintained.

Antiseptic treatment of the navel and umbilical veins must not be overlooked.

LUPINOSIS, ACUTE TOXÆMIC ICTERUS, ACUTE YELLOW ATROPHY OF THE LIVER.

Attacks sheep, goat, ox, horse, stag; and, experimentally, dog.
Causes: consumption of lupins, at a given stage of ripeness, from a
given part of a field, or from centre of a stack. Lupinotoxine,
conicine, methyl conicine, lupinine. Cryptogamic or bacterial poison.
Weak subjects, sheep and even ewes and lambs, suffer most. Symptoms:
Acute form: anorexia, fever, excited pulse and breathing, stupor, or
hyperæsthesia, vertigo, swellings on head. Poisonous lupins are first
rejected. Bloody nasal froth. In two or three days icterus. Urine may
be bloody. Fæces at first hard, coated, bloody, later dark brown and
often liquid. Emaciation. Death in 1 to 5 days. Chronic form,
gastro-enteritis, emaciation, anæmia. Nasal catarrh. Facial swellings
and sores. Lesions: hepatitis, nephritis, muco-enteritis, enlarged
spleen, icterus, blood extravasations; hepatic tissue, infiltrated,
cloudy, granular, fatty, later cirrhosis. Kidneys contain casts:
Spleen tumid, blood gorged. Prognosis: grave: acute cases die, chronic
may recover. Prevention: feed no lupins, avoid dangerous fields, wash
off poison from lupins with a soda solution. Ensilage with acid
producing fodder in alternate layers. Treatment: avoid alkalies, give
acids, purgative, castor oil, water. In horse, causes anorexia,
anæsthesia, dullness, stupor, colic, constipation, urinary irritation,
fever, slight jaundice, vertigo, orange nasal discharge, sores on
tongue and face, and lower part of limbs. Diagnosis. Prognosis
hopeful. Treatment as in sheep. Icterus from other fodders.

This affection has been noticed especially in sheep, but also in the goat, horse, ox and stag as the result of eating lupins. The dog has contracted the disease under experiment. It has been studied especially in Northern Germany where the lupin is largely cultivated as a fodder crop. The yellow lupin (Lupinus Luteus) is mainly to blame for the disease, but the Lupinus Albus and Augustifolius are also spoken of as factors.

The disease caused by altered seeds and straw of the lupin is mainly characterized by jaundice, fatty degeneration of the hepatic cells and hypertrophy of the connective tissue of the liver causing acute atrophy of the organ.