Chapter XXI: Part 21

Definition. Increase of connective tissue, decrease of gland
parenchyma. Causes: in man, alcoholism; in animals, chronic heart
disease, chronic recurrent perihepatitis, biliary obstruction, toxins.
In horses: age, emphysema, unwholesome fodders, vegetable alkaloids,
infection. Symptoms: prostration, hebetude, impaired appetite, colics,
constipation, later diarrhœa, unthriftiness, emaciation, dropsy,
icterus, ascites, intestinal catarrh, tender hypochondrium, early
fatigue. Lesions: increase of connective tissue, compression and
absorption of parenchymatous tissue, greatest around portal vessels,
thickening of fibrous stroma between capillaries of acini, shrunken,
granular, pigmented liver cells. Treatment: salines, Glauber salts,
diuretics, sodium carbonate, or iodide, or salicylate, derivatives,
mineral acids, bitters, open air, laxative food, pure water. In
cattle: obstruction to circulation or the flow of bile; advances from
the vessels, causes absorption, caseated foci, adhesions, enlarged
liver. Symptoms: jaundice, yellow, red, albuminous urine, chronic
indigestion, tends to fatal though slow advance. Treatment: green
food, open air life, saline laxatives, alkalies. In dog: common
following heart disease, parasites, bacteria. Lesions: Congested
brownish red liver, fibroid increase from Glisson’s capsule,
compression of acini, their elevation above surface, fatty and
pigmentary degeneration of hepatic cells, increasing sclerosis.
Symptoms: as in parenchymatous hepatitis with slower advance, in time
tender loins, brownish or reddish urine, ascites, intestinal catarrh,
it may be icterus. Treatment: Correct cardiac troubles, digitalis,
strophanthus, and intestinal, careful diet, mineral acids, bitters,
pure water, saline laxatives, antiseptics, alkaline diuretics.
Potassium iodide. Derivatives. Draw off liquid. Laxative
non-stimulating diet.

_Definition._ An interstitial inflammation of the liver characterized by a great increase of the connective tissue and compression, atrophy and degeneration of the glandular elements.

The same final result may undoubtedly originate in various different primary morbid processes.

In man cirrhosis is looked upon as almost always the result of abuse of alcohol. In animals this cannot be the case, apart from a few kept in connection with breweries or distilleries.

In heart disease a long continued mechanical congestion of the liver causes compression and degeneration of the secreting cells in the centre of the acini (around the intralobular veins), while the peripheral portions undergo cell proliferation and increase of connective tissue.

In chronic or recurrent perihepatitis, a whole lobe may be compressed by the hyperplasia of the investing connective tissue, and the hepatic cells are degenerated and absorbed.

Overdistension of the biliary ducts from obstruction to the flow of bile (gall stone, catarrhal inflammation, constipation), leads to proliferation and hyperplasia in the walls of the biliary radicals throughout the entire liver.

The presence in the liver of toxic agents, ingested, or generated from microbian fermentation in the intestinal canal or liver is another recognized cause of connective tissue hyperplasia.

CIRRHOSIS IN THE HORSE.

Cirrhosis of venous origin has been observed mainly in old horses, while hypertrophic cirrhosis from biliary obstruction occurs rather in the young (Cadeac). Bruckmüller records a case of the first kind in a horse with extreme pulmonary emphysema. Walley gives a bad condition of fodders as the main cause, virtually implying, in many cases, infective catarrh and obstruction of the biliary ducts.

A form of the disease prevails at Schweinsberg in Hesse, and has been variously attributed to spoiled fodders (Nicklas), to vegetable alkaloids and other poisons in the food (Friedberger and Fröhner), to clover, to telluric poisons (Redner), to infection (Meminger), and to heredity (Neidhardt). It is a suggestive fact that it is confined to the valleys of the Ohm, Glon, and Zusam where the land is peaty or swampy and subject to inundations, while it is unknown on the dry table lands (Friedberger and Fröhner). This strongly suggests intoxication with microbes or their deleterious products. The gastric catarrh that frequently attends the disease may point in the same direction.

_Symptoms._ These are too often general rather than diagnostic. Dullness, prostration, hebetude, yawning, hot, sticky mouth, lost, irregular or depraved appetite, colics, constipation or diarrhœa, dry, harsh coat, emaciation, weakness, œdema of the limbs, vertigo and drowsiness may be among the symptoms. More characteristic are icterus, abdominal distension from ascites, or congestion of the liver, yellow or high colored urine, intestinal catarrh, indigestion, and tenderness in the region of the liver. The mucosæ are usually pale at first and not always icteric later. On exertion the horse shows early fatigue, tumultuous heart beats and oppressed breathing.

The Schweinsberg disease often lasts for months, with alternate improvements and exacerbations, but almost invariably ends in death, and sometimes completely depopulates a stable.

_Lesions._ These consist primarily in the great increase of the connective tissue and the relative decrease of the hepatic tissue. This is usually mostly around the divisions of the portal vein and the periphery of the acini, but also in the end around the hepatic veins as well. When it has formed around the biliary canals there is a great increase of the liver (often doubled) and its edges have become rounded. Within the acini the increase of the fibrous stroma is seen between the radiating capillaries, and the hepatic cells are contracted, granular, pigmented, and comparatively destitute of protoplasm around the still persistent nucleus.

_Treatment._ Glauber salts to clear the bowels of offensive matter, and deplete from liver and portal vein, bicarbonate of soda or iodide of potassium to eliminate the poisons through the kidneys and to lessen the induration, and finally salicylate of soda as a liver stimulant and intestinal antiseptic are suggestive of the line of treatment that may be pursued. The saline laxatives and diuretics, and antiseptics may be changed for others according to special indications, and bitters and mineral acids may be resorted to. Counter-irritants to the right hypochondrium should not be neglected in case of local tenderness. In the otherwise fatal Schweinsberg disease, Imminger, Künke and Stenert had a remarkable success from the free use of potassium iodide, which suggests a cryptogamic origin, as this agent is so valuable in polyuria which results from musty fodder. In all cases, gentle exercise in the open air and a moderate ration of laxative food (green) are of great value. Above all the old suspected diet should be carefully avoided, also any impure water supply.

CIRRHOSIS IN CATTLE.

This has been recorded by different observers and usually as the result of some obstacle to the circulation, or of catarrh and obstruction of the biliary passages. Morot saw it in young calves, which showed greatly enlarged liver (in one case 24 lbs.) and kidneys, the former containing numerous cysts and marked sclerous thickening around the vessels. This advancing thickening of the connective tissue, causes increasing firmness of the liver and absorption, distortion and diminution of the lobules. Albrecht describes a chronic interstitial hepatitis with caseated centres (nontuberculous) many of them an inch in diameter. The liver is brown or grayish with whiter callosities which extend into its substance and make points of attachment to the diaphragm or other adjacent organ. The contrast between the fibrous layers and the hepatic tissue has been likened to a checker board (Höhmann). The enlarged liver may weigh 30 lbs.; in one remarkable case it weighed 300 lbs. (Adam). The bile is of a light color and mixed with mucus.

_Symptoms._ The symptoms are indefinite: a gradually increasing jaundice, the passage of yellowish red urine becoming more and more red and albuminous, and finally coagulating on the walls of the urethra or on the litter, chronic indigestion, salivation (Schäffer), weakness, breathlessness and more or less fever may give indications of the disorder. Höhmann failed to find tenderness of the right hypochondrium. The disease is liable to go on to a fatal issue, so that it is often sought to prepare the animal for the butcher.

_Treatment_ will follow the same line as in the horse. Green food, pasturage, open air life, saline laxatives, and alkalies with a free use of potassium iodide to check the sclerosis will be indicated.

CIRRHOSIS IN THE DOG.

In the dog, cirrhosis is much more common than in the larger animals, in connection with idle pampered habits, the frequency of diseased heart and consequent disturbance of the circulation, and the presence of parasites in the liver or biliary ducts. Bacteria intoxication and infection are also common.

_Lesions._ The liver is at first tumefied, with hard consistency and rounded edges, and a deep brownish red color, but this is modified by the grayish fibroid hyperplasia which is especially abundant in and around the vaginal sheaths of the capsule of Glisson. In cases arising from diseased right heart or lungs the induration is rather concentrated around the hepatic veins. The contraction and shrinking of the fibroid hyperplasia as the disease advances causes the projection of the hepatic tissue in minute rounded elevations which give a peculiar uneven appearance to the surface of the organ. The fibroid growth gives a remarkable hardness to the liver which resists even the edge of a knife. The hepatic cells are the seat of fatty and pigmentary degeneration. Inflammation and tumefaction of the kidneys, and ascites are common features of the malady.

_Symptoms._ The general symptoms are as in parenchymatous hepatitis with a more tardy development. There are impaired or irregular appetite, dullness, sluggishness, in an obese animal short-windedness or palpitations on slight exertion, symptoms of disease of the heart, lungs or digestive organs, a spasmodic cough, constipation followed by relaxation of the bowels, nausea and vomiting. As the disease advances tenderness of the loins, the passage of brownish or reddish, albuminous urine, the formation of ascites and of gastro-intestinal catarrh may be noticed. Icterus may be entirely absent, but, with a flaccid abdomen, enlarged liver and spleen may be detected.

_Treatment._ The indications are to first combat the causes. Irregularities in the heart’s action may be met by digitalis or strophanthus; gastro-intestinal catarrh by a carefully regulated diet, with mineral acids and bitters; portal congestion by a free use of water and other diluents and by saline laxatives; intestinal fermentations by antiferments (salol, naphthol) and toxic matters in the blood by alkaline diuretics. For the liver hyperplasia, potassium iodide may be freely used. Blisters to the right side will occasionally prove useful. The ascitic fluid must be drawn off when it accumulates. A diet of milk, bread and milk, buttermilk and mush, or one in which albuminoid elements are in minimum amount and the action of which is laxative is to be preferred. Out door exercise is desirable.

CHRONIC ATROPHY OF THE LIVER.

_Chronic Atrophy_: In _old horses_: in right and spigelian lobes;
others show hypertrophy. In _ruminants_, omnivora and carnivora: in
areas compressed by tumors or parasites. Perihepatitis. Sclerosis.
Remedy causes if possible. _Fatty Degeneration_: Oil globules in liver
cells, pathological when they destroy the protoplasm. In ducks and
geese on forced feeding. Causes: poisoning by phosphorus, arsenic,
antimony, lead, phenol, iodoform, alcohol; excess of fat in food,
spoiled fodders, colchicum autumnale, yellow lupins, bacteria,
hemorrhages, inflammations, tumors, parasites; improved meat producing
breeds, old animals, hot stables. Lesions: liver enlarged, pale,
yellow, bloodless, knife in cutting is smeared with fat, oily stain on
paper, liver cells enlarged, protoplasm replaced by fat or oil; may be
circumscribed. Symptoms: obesity, over-fed in fats and starches, of
fattening breed, kept in confinement, in hot moist environment, if fed
certain poisons, with costiveness and indigestion, no endurance, short
winded, slight icterus, scanty urine, little urea, later, emaciation,
palpation of enlarged liver. Treatment: send to butcher, pampered
horses, cows from swill stable, a run at grass, with shade trees, a
poor pasture, salines, cholagogues, mineral acids, bitters, iron with
alkalies, currying, massage, douches.

Acute yellow atrophy has been referred to under parenchymatous hepatitis but a chronic atrophy is also met with in all domestic animals.

In _old horses_ it affects, by preference the right and spigelian lobes, the portal circulation of which is less direct because of the veins of supply leaving the parent trunk at right angles (Leblanc), and because these lobes are more exposed to compression by solid accumulations in the double colon (Kitt). In such cases a compensatory hypertrophy of the left and middle lobes is often observed.

In _ruminants_ the lesion is often circumscribed to the areas that have undergone compression by tumors or parasites (echinococcus, actinomycosis), and there may be compensatory increase elsewhere in the organ.

In _swine_, _dogs_ and _cats_ the same conditions are operative. In all alike perihepatitis may be a causative factor, and sclerosis (cirrhosis), with contraction of the fibrous hyperplasia may also operate.

_Symptoms_ are very obscure and _treatment_ unsatisfactory unless the active causes can be recognized and arrested.

HEPATIC STEATOSIS. FATTY LIVER. FATTY DEGENERATION.

The presence of oil globules in the liver cells is normal and physiological, the liver acting to a certain extent as a store-house for fat. This is always a marked feature, in healthy animals on high rations, and taking little or no work, but so long as the protoplasm and nuclei of the cells retain the normal characters and functions the condition is not a morbid one. It may, however, become excessive, with great enlargement of the liver, and with the substitution of fatty granules for the protoplasm of the cells as in ducks and geese subjected to forced feeding, and the condition becomes a distinctly pathological one.

In true fatty degeneration the protoplasm of the hepatic cells is destroyed and replaced by fatty granules, the resulting condition being a permanent destruction of the cell for physiological uses.

_Causes._ The liver cells undergo fatty degeneration under the action of certain poisons like phosphorus, arsenic, antimony, lead, phenol, iodoform and alcohol. According to Neyraud oxide of antimony is given daily to fattening geese to hasten the development of fatty liver.

An excess of fatty elements in the food leads to the same result as shown first by Majendie in dogs, in which not only did the liver undergo this degeneration but the sebaceous glands of the skin secreted an excess of volatile fatty acids.

The cryptogams and their products on musty fodders determine a gastro-enteritis in herbivora, accompanied by fatty degeneration of the liver.

Colchicum Autumnale, and poisonous yellow lupin both determine this degeneration.

The products of a number of pathogenic bacteria have a similar effect. This has been noticed in the cat with bacillus pyocyaneus (Charrin), the cholera spirillum, pyæmic and septicæmic infection, contagious pneumonia of the horse, strangles, and ulcerative endocarditis. It has been long noticed to be a complication of pulmonary tuberculosis, the result in this as in other affections of the lungs having been attributed to lessened oxidation in the tissues. It occurs also in hæmorrhages, ruptures and inflammations of the liver and in passive congestions of the organ, the impairment of the normal functions (in the altered conditions of nutrition, or under the influence of poisons,) proving an important factor in the process. The same remark may apply to the fatty degeneration which complicates most other liver diseases, cirrhosis, catarrh of the bile ducts, distomatosis, echinococcus, carcinoma, and epithelioma.

Certain other factors must be taken into account. The inherited disposition to the production of fat which characterizes the improved breeds of butcher animals, and particular individuals of all breeds, mature age which predisposes to the deposit of fat in internal organs, old age which lessens the vitality of the cells, and hot, damp climates or stables, all operate more or less in determining the fatty change.

_Lesions._ In fatty degeneration the liver is enlarged, pale, bloodless, yellowish, its cut surface exudes an oily fluid which smears the knife, and it is so light that it floats on water. If scraped and the material drawn across a sheet of paper it forms a transparent oily stain. Under the microscope the liver cells are seen to be enlarged and to have their protoplasm and nuclei replaced by fat or oil. If due to obstruction in the heart or lungs the degeneration is greatest toward the centre of the acinus, if due to an infectious disease it is usually greatest towards its periphery. In infectious diseases too the liver is not pale yellow, but usually of a deep brownish or yellowish red. The degeneration may be local or general. McFadyean found a circumscribed lesion in an ox’s liver, of a bright ochreous color, and the cells completely transformed into fat cells, while the rest of the liver was sound. In the dog fatty areas, up to an inch in diameter, are not uncommon. The swollen cells pressing on the adjacent vessels, account for the bloodless condition, and favor the degenerative process.

Neyraud records a fatty liver of 28 ℔s. weight from the horse, and Kitt one of 10 ℔s. from the pig.

_Symptoms._ Like as in most chronic liver diseases the indications are uncertain. The conditions may, however, suggest fatty degeneration; if the patient is very obese; if it has had an abundant food, rich in hydrocarbons and carbohydrates, and little exercise; if it has received in food or water continuous doses of phosphorus, arsenic or antimony; if it has lived in a hot moist climate or stable; if there has been a tendency to costiveness and indigestion; if the patient is weak, easily fatigued and short-winded; if there is a slightly yellowish red tinge of the conjunctiva and if the urine is scanty and contains little urea. If the disease is more advanced and the animal emaciated, it may be possible in the smaller animals at least to manipulate the liver to make out its increase, its smooth surface, and its absence of tenderness.

_Treatment._ When met with in meat producing animals the best resort is to turn these over to the butcher. When in an animal which is mainly valuable for breeding purposes, or in horses or carnivora, something may be done to check the progress of the malady, and maintain at least the present condition. The value of this will of course depend on how far the disease has already progressed. Cows that have spent a winter in a hot swill stable are of little use afterward for breeding or dairy uses and advanced cases of fatty degeneration in the horse or dog hold out little hope of a satisfactory issue. For cases in the earlier stages, nothing can be better than a run at grass, where there is opportunity for shelter from the noonday sun. If the pasture is short and the animal has to exercise to secure a living, so much the better. If kept indoors the patient should have a clean, roomy airy box stall, with a moderate allowance of easily digested food, and laxatives and cholagogues daily such as Glauber salts, aloes, calomel, podophyllin or cream of tartar. Mineral acids, especially nitro-muriatic acid, and bitters may also be given. The preparations of iron are sometimes useful in maintaining the tone of the digestive organs and counteracting anæmia but they must be conjoined with diuretic doses of bicarbonate of soda.

There is great advantage in stimulating the skin, and active brushing, currying, hand-rubbing, and even cold douches may be resorted to.

AMYLOID DEGENERATION OF THE LIVER.

Degeneration of basement substance of connective tissue, swollen,
transparent, homogeneous, colored mahogany brown by iodide. In wasting
diseases, tubercle, cancer, malaria, dysentery, leukæmia, suppuration,
ulceration, pleurisy, pericarditis, peritonitis, chronic catarrh,
broncho-pneumonia, orchitis, biliary calculi, nephritis. Chronic.
Lesions: Affected part swollen, sinks in water, bloodless, clear,
smooth, homogeneous, yellowish or reddish gray, under compound
solution of iodine becomes mahogany brown, under sulphuric acid dark
violet. Extends from vessel walls to adjacent connective tissue.
Symptoms: Of wasting diseases, but not diagnostic. Treatment:
Unsatisfactory, directed to causative disease.

This is a condition in which the basement substance of the connective tissue, and especially of the walls of the vessels, becomes swollen and composed of a transparent, homogeneous substance, albuminous in character, and which stains of a deep mahogany brown on the application of a solution of iodine. The degeneration is usually associated with severe wasting diseases, in the human being with tuberculosis, syphilis, malignant tumors, malarial infection, dysentery, leukæmia, and chronic suppuration or ulceration, especially of the bones.

In the _lower animals_ (horse, dog, ox, sheep, rabbit, poultry) it has been seen to attend or follow on similar cachectic conditions. In the _horse_ it has been seen in connection with the effusions of pleurisy, pericarditis and peritonitis (Rabe), in chronic bronchial catarrh (Fischkin), in chronic broncho-pneumonia, and dilated right heart (Trasbot), in orchitis, phlebitis and cachectic states (Caparini), and in calculous obstruction of the biliary duct (Burgoin). In _cattle_ it has accompanied chronic nephritis (Brückmüller), tuberculosis, leukæmia, etc. In _lambs_ kept in confined stables, though well feed on oats (Werner). In long standing suppurations and in animals fed on distillery swill it has been observed.

It may last for months or years, and predispose to other disorders, functional and structural. It does not, however, interrupt secretion as bile continues to be formed.

_Lesions._ The affected part of the liver is enlarged, the entire organ in the horse may amount to 32 lbs. It is smooth and even, though thick and rounded at its inferior border, yet occasionally on the posterior aspect there may be hyperplasia and a rough irregular surface. The diseased liver is heavy and sinks in water, unlike the fatty liver. In the horse it is soft and friable or even pasty whereas in man it is firm and resistant. The cut surface is bloodless, smooth, clear, homogeneous and grayish, yellowish or reddish gray. When treated with a solution of iodine and potassium iodide it changes to a deep mahogany brown; if dilute sulphuric acid is then used it changes to a deep violet, almost black color. If the iodine solution is brushed over the smooth cut surface the mahogany color of the amyloid stands out in marked contrast with the bright yellow of the healthy hepatic tissue. The amyloid commences in the walls of the smallest arteries, in the media and intermediary layers of the intima, and thickens the walls so as to obstruct their lumen more or less completely and render the part comparatively exsanguine. It may extend to the connective tissue of the organ, but it is not certain that the hepatic cells are involved in the process. The cells are, however, pressed upon by the diseased vessels and stroma and undergo consequent fatty degeneration. The amyloid may be confined to but a small part of the liver or to its smaller blood-vessels or it may extend to the whole. In fowls it is always in multiple centres (Leisering). It may be found in other important organs, kidneys, spleen, lymphatic glands, intestinal mucosa, etc.

_Symptoms_ are not diagnostic. If with an old standing, exhausting disease, paresis, weakness, emaciation and unfitness for work, there is loss of appetite, dryness of the mouth, congestion of the rectal mucosa, yellowish, whitish, or dark tarry fæces, and a slightly brownish or yellowish tinge of the visible mucous membranes (Rexante) it may be suspected. In fowls Leisering noticed, weakness, lameness, ruffling of the feathers and attacks of vertigo. Icterus, ascites and tenderness over the region of the liver may all be absent. In the absence of ascites, tympany, or an excess of fat in the smaller animals, manipulation may detect the considerable enlargement of the liver, and the characteristic smoothness, of its surface. In other cases some indication may, at times, be had from the increased area of dullness on percussion.

_Treatment_ is essentially unsatisfactory even if a correct diagnosis can be made. The most hopeful course would be to correct the debilitating disease in which the amyloid seems to have originated. Diseased bones, ulcers, chronic suppurations, and catarrhs may be done away with, and at least any further advance of the degeneration arrested. Open air exercise and a green or otherwise laxative diet would be indicated. The amyloid in lambs fed on oats was corrected by a change of diet (Werner). As medication the alteratives, potassium iodide and potassium arseniate have been mainly resorted to. Bitters and iron may also be of use to build up the strength. The latter should be given with potassium bicarbonate.

BLACK PIGMENTATION OF THE HEPATIC CELLS. BROWN ATROPHY.

_In horse._ With melanoma and atrophy, or without, pigment granules
fill hepatic cells, liver becomes brown or black. In calves. In sheep.
Apart from melanosis, the real cause unknown.

The accumulation of granules of black pigment in the hepatic cells has been noticed in old and worn out horses (Louis Blanc, Cadeac, Bruckmüller), in calves (Degive, Cadeac), and in sheep (Siedamgrotzky, Barrier). In _horses_ it has been found in connection with atrophy, or in other cases, with melanotic tumors in other parts. In atrophic cases the liver is small, puckered, brown and dull, with a leathery appearance on section, and with the hepatic cells charged with pigment granules so that each acinus has a stellate appearance from the radiating lines of cells. This constitutes _brown atrophy_.

The second form which may be called _melanotic liver_, is not associated with atrophy, but is characterized by the crowding of the hepatic cells with black pigment granules, which fill up the protoplasm and crowd the still pale nucleus to one side. The affected portions become of a deep black.

In _calves_ the pigmentation may be confined to the superficial portion of the liver (Degive).

In _sheep_ pigmentation may be in the peripheral cells only of the acinus (Cadeac) but is about equally distributed on the surface, and throughout the interior of the liver, and may extend to the stroma of the gland (Siedamgrotzky).

Apart from the general causes of melanosis, benignant or malignant, no definite reason for this pigmentation has been assigned. The development of melanæmia and tissue pigmentation in man from malarious microörganisms suggests that other germs and their products may have a similar effect in the lower animals but nothing certain is known as to the true cause.

Apart from melanosis, it is not known that this pigmentation of the hepatic cells is of any essential pathological importance. It is important however for the veterinarian to be acquainted with the condition, that he may intelligently deal with such lesions whether seen in ordinary post mortem examinations, or in the course of meat inspection.

DILATATION OF THE GALL BLADDER AND BILE DUCTS.

Causes: obstruction of common bile duct, distoma, round worms, tæmiæ,
gall stones, encrustations, inflammations, tumors, cicatrices,
hydatids. Congenital absence. Ducts stand out on liver. Symptoms of
colic, icterus, bile poisoning, marasmus. Treat the causative
conditions.

This may occur in all our domestic animals except solipeds in which latter there is no gall bladder.

_Causes._ Any serious obstruction to the discharge of the bile into the duodenum may cause it. The presence of trematodes, nematodes, or even tæniæ in the ducts, gall stones, incrustations, occlusion of the ducts by inflammatory swelling, tumors of the liver or adjacent parts, echinococcus, cysticercus, or cicatrices may be cited. Cadeac mentions a case of congenital atresia of the bile duct in the calf. Vigney records a case in the cow in which the greatly dilated gall bladder formed a hernial mass in the epigastric region which was, however, easily reduced by manipulation.

In all such cases the distended bile ducts stand out as white branching lines on the back of the liver converging toward the portal fissure. The walls of the ducts may be attenuated or thickened and it is alleged calcified. They are usually lined by a deposit of cretaceous consistency precipitated from the retained bile. The contents of the distended ducts and bladder are variable. They may have the color (yellow, green) and consistency of bile; they may be thick, dense and albuminous; they may be thin and serous from inflammatory or dropsical exudation; they may be granular, or purulent.

Though there is no gall bladder, in the soliped, a similar condition of the biliary ducts may be produced in the same way.

According to the degree of obstruction there may be more or less acute symptoms of biliary colic, icterus, marasmus, poisoning by bile acids, etc.

_Treatment_ must be directed toward the removal of the special cause of dilatation.

DOUBLE GALL-BLADDER.

As a congenital formation the gall bladder is sometimes divided into two at its fundus, and in other cases the division extends throughout, forming two complete sacs. This has been found in the sheep, cat, ox (Gurlt, Goubaux) and pig (Goubaux). Such a redundancy does not interfere with normal functions.

CHOLELITHIASIS. BILIARY CALCULI. GALL STONES.

In ruminants, omnivora, and carnivora, less often in horse, 1 to 1000,
or more, biliary sand to marble or more, casts; nucleus, bile pigment,
blood mucus, etc., with concentric layers of cholesterine, pigment,
salts and lime. Causes: idleness, overfeeding, dry feeding, thickening
of bile, colloids, bacteria, wintering in stable. Colloids induce
globular deposits. Parasites. Inflamed biliary epithelium secretes
excess of cholesterine and lime. Age. Acid bile, constipation.
Diseased liver. Lack of bile salts. In _solipeds_: all sizes and
numbers, green, brown, yellow or white. Liver disease. Symptoms: colic
with depression, prostration, yellow or red urine, icterus, sudden
recovery. Treatment: sulphate of soda, olive oil, antispasmodics, warm
drinks, fomentations, salicylate of soda, chloroform, pasture, or
succulent food, and open air exercise. In _cattle_: musk odor; calculi
dark green, yellowish green, whitish or orange, dry red, all sizes and
numbers. Causes: dry winter feeding, etc. Lesions: dilated biliary
ducts and bladder. catarrh, thickening, rupture, septic peritonitis.
Symptoms: relapsing colic, with icterus, prostration, and tender right
hypochondrium, in stalled animal on dry feeding. Suggestive: not
pathognomonic. Treatment: as in horse: succulent spring pasturage. In
_sheep_: rare, musky odor; concretions and casts common in
distomatosis. Hypertrophied ducts. Symptoms of distomatosis.
Treatment: for distomatosis and calculi. In _swine_: rare: circular.
In _carnivora_: round, dark green, pin’s head to hazel nut. Symptoms:
colics, constipation, emesis, icterus, tender right hypochondrium,
concurrent catarrh of bowels, heart disease, dyspnœa, sudden relief.
Mode of relief. Treatment: olive oil, bile, sodium sulphate, or
salicylate, antispasmodics, alkalies, enemata, fomentations. Laxative
food, exercise, open air.

Gall stones are most frequent in animals having a gall bladder. Some medical writers say they are formed in the gall bladder only, but the soliped which has no gall bladder has in particular instances furnished hundreds of gall stones. Yet the ox, dog, sheep and pig are the common victims of biliary calculi among our domestic animals. In these the calculi appear to be mostly deposited from the stagnant bile in the gall bladder, yet concretions on the biliary ducts and hollow casts inside the ducts are by no means uncommon.

A gall stone may be single, or they may be multiple up to hundreds or even thousands, and when very numerous they are individually small, perhaps no larger than a pin’s head. They may, however, attain the size of a marble or more, and by mutual pressure and wear they assume various polygonal forms. If they lie apart in the gall ducts or bladder they are regularly rounded. They are sometimes mulberry shaped as if conglomerate. In other cases the solid masses are so small as to have secured them the name of biliary sand. Casts and incrustations in the ducts are not necessarily made up of smaller globular masses.

On section a calculus shows a nucleus, composed of bile pigment, blood, mucus, with the debris of parasites or bacteria. Around this nucleus the calculus is deposited in concentric layers, of a hard material consisting largely of cholesterine, but containing also bile coloring matter, bile salts, and lime, in short all the constituents of bile.

_Causes._ Various conditions contribute to the precipitation of biliary solids in the form of calculi or encrustations. The most prominent causes are: lack of exercise, overfeeding, dry feeding, concentration of the bile, the presence of colloids and bacterian infection.

_Idleness_ is especially operative in cattle, which are quite subject to biliary calculi and concretions, when shut up in the stall on _abundant, dry feeding_ for a long winter. They are not noticed in stalled animals, that are fed watery or succulent rations, such as green fodder, distiller’s or brewer’s swill, ensilage, brewer’s grains, mashes, roots, potatoes, apples, pumpkins, and in case a tendency to their formation is developed on the dry feeding of winter, the concretions may be re-dissolved and entirely removed by the succulent spring grass. A similar influence is noticed in the human family, as the female sex living mostly indoors, and males pursuing sedentary occupations furnish the greatest number of gall stones.

_Concentration of bile_ results in part from muscular inactivity and hepatic torpor, but also from overfeeding which loads the portal blood and indirectly the bile with an excess of solids, and from dry feeding which lessening the secretion of water leaves the bile more dense and predisposed to precipitate its solids. The density of the liquid, however, developed from a rich and dry ration and a prolonged inactivity, may continue for a length of time, without the occurrence of actual precipitation. It usually requires some additional factor to make this predisposition a direct cause.

=Presence of Colloids.= This may be found in the presence of solid or semi-solid particles. Just as the introduction of a thread into a concentrated solution of sugar or salt will induce an instant crystallization on the filament so the presence of solid bodies determines a similar condensation in solid form of the solids of the bile. But this tendency is increased materially if the solid body is itself of a colloid or non-crystallizable material. Rainey and Ord have shown experimentally that colloid bodies like mucus, albumen, pus, blood, epithelial cells, not only determine the precipitation of crystallizable salts from a strong solution, but that they cause the precipitate to assume the form of globular or spherical particles, which by gradual accretions on their surfaces tend to grow into calculi. They found that salts which are deposited by mere chemical reaction, without the intervention of colloids, appear in the form of sharply defined angular crystals. The very fact that a precipitate assumes a spherical form suggests the presence of colloids as an active factor in the precipitation. Heat appears to intensify this action, though probably the normal body temperature operates mainly through the more active proliferation of bacteria.

_Bacteridian infection._ In connection with the action of colloids it has been observed that when such bodies are in a condition of fermentation they are much more potent as precipitants than if inactive and sterile. But as all fermentations are the work of microörganisms we are at once brought to the conclusion that bacterial infection is one of the most potent causes of calculous formations. The invading microbes operate upon the dissolved solids, causing changes in their condition which reduce their solubility, and thus determine the separation of calculi and concretions in a manner allied to the precipitation of nitrates in the soils.

But the same microbes operate in producing the colloids which coöperate so effectively in the formation of calculi. The catarrhal biliary ducts, or bladder, shed their epithelium, and transude white and red globules, and form pus and an excess of mucus, all tending to the separation of the biliary solids or forming nuclei on which these solids may condense. The calculi and concretions tend in their turn to maintain and advance the inflammation.

The access of the microbes to the biliary duct or bladder may be effected through the blood of the portal vein or hepatic artery, or in the new-born, through the umbilical vein from an infected navel. As other modes of access may be named, a gradual advance from the duodenum through the common bile duct, or more speedily on or in the bodies of parasites (ascaris, strongylus, stephanurus, tænia, echinococcus, distoma, fasciola, coccidia), etc.

_Changes in the chemical composition of the bile_ have been invoked as a cause of gall-stones, and Naunyn has found that the inflamed biliary epithelium secretes an excess of cholesterine and salts of lime. Thomas has also observed a great increase of cholesterine in connection with a catarrhal angiocholitis in the dog.

Among other alleged causes of biliary calculi are _advanced age_ (Rigot, Hering), _acidity of the bile_ (Zundel), _constipation_, and any _organic disease of the liver and bile ducts which interferes with excretion of bile_.

Age is supposed to act by inactivity, lessened secretion, hepatic torpor, and the greater presumption of liver disease, acidity by the precipitation of cholesterine and the dissolving of lime present in the tissues, and constipation through hepatic inactivity, obstruction of the flow of bile, and the tendency to infection through intestinal fermentations.

It may be added that any diminution of glycocholate or taurocholate of soda or potash, decreases the solubility of cholesterine and bile acids and favors their precipitation.

GALL STONES IN SOLIPEDS.

_Characters._ The biliary calculi of solipeds are of all sizes and shapes. When numerous they are mostly the size of a pin’s head (Lucet). Birnbaum found in one animal 400 like peas. Dieckerhoff has repeatedly found four or five of the size of a hazelnut. Verheyen found one as large as an apple and says one exists at the Berlin Veterinary College which weighs several pounds. Rigot found 90 in the biliary ducts of an old horse, and Zundel records the death of a stallion of twenty-six years from multiple gall stones.

The calculi may be little larger than grains of coarse sand. When larger and solitary they are mostly globular or mulberry shaped; if many are together they have become polygonal by friction. In other cases notably with distomata they form hollow tubular incrustations on the bile ducts, and contain a thick grumous bile. They are usually of a green color, but may be yellowish brown, yellow, or whitish. When cut across they present a nucleus enclosed in successive layers, each successive one often differing from the last in color. Their specific gravity is low, some will even float in water when taken from the ducts, and all float when dried. Their composition is variable but chiefly cholesterine, bile acids, resin and pigments, an albumoid matter, with lime salts, etc. The nucleus may be the remains of a dead parasite, epithelial cells, blood, pus, mucus, etc. The outer layers are usually the hardest.

There may be attendant hypertrophy of the liver, cirrhosis, amyloid and other degenerations, catarrh of the biliary ducts, and distension or (according to Birnbaum) rupture of the portal vein.

_Symptoms._ There are no reliable diagnostic symptoms apart from the colics which accompany the obstruction of a bile duct by a passing calculus. These in the main resemble the colic of ordinary indigestion, but they may be complicated by unusual depression and nervous prostration. There may be drooping of the head, ears and eyelids, watery eyes, resting the head on the manger or pushing it against the wall. The urine is liable to be red or reddish (Jobelot), and if it or the mucosæ show a yellowish tinge it is strongly suggestive. There may be constipation or diarrhœa. The colics are severe and may last for several days (Seaman, Lucet, Burgoin) without fever and recover abruptly when the stone passes into the duodenum. They recur, however, with the impaction of another stone, and this intermittent feature, with the marked prostration, and the access of slight jaundice with each colic furnishes the best means of diagnosis.

_Treatment._ During the access of colic give a full dose (1 to 2 lbs.) sulphate of soda in warm water along with some active antispasmodic (belladonna, lobelia, chloroform, ether), and foment the loins and hypochondriac regions. Olive oil in large doses (1 to 2 quarts) has been found effective. Salicylate of soda in full doses is beneficial in stimulating the biliary secretion, diluting the bile, and securing some measure of antisepsis in both bowels and liver.

In the intervals between the colics, sodium salicylate, sodium or potassium carbonate, or olive oil in continuous doses may assist in disintegrating the calculi or passing them on. Chloroform tends to break them up by dissolving the cholesterin. But any such treatment must be accompanied by the abundant ingestion of water, and this is often best secured by a run in a rich green pasture. In the absence of pasturage, succulent fruits, and roots, ensilage, mashes, and gruels may be advantageously substituted, and conjoined with systematic exercise in the open air.

GALL STONES IN CATTLE.

_Characters._ The biliary calculi of cattle are characterized by a faint odor of musk, which becomes stronger on the addition of potassa and the consequent disengagement of ammonia.

They are distinguished according to their color as dark green, yellowish green, and orange, brownish or white. There are also the sedimentary deposits (biliary sand).

The _dark green calculi_ are the most frequent, and being found in the gall bladder and larger bile ducts, they attain a larger size than the others. Those in the gall bladder may be pear-shaped, and those in the ducts, round, ovoid or cylindroid. They are often rough and uneven on the surface with deep cracks and holes penetrating deeply into their substance and often filled with cholesterin. The pigments may change to a blood red when dried. The consistency of these calculi varies, some being hard, resistant and heavy, while others are soft and friable. All are composed of concentric layers around a central nucleus as in those of the horse. They vary in weight up to seven ounces in exceptional cases. They contain cholesterin, fat, resin, pigments, and lime and magnesia salts.

The _yellowish green calculi_ are usually spherical unless moulded into polygonal shapes by mutual contact. In the last case they have flattened surfaces. These have a firm consistency and are composed of successive layers of nearly equal color and density surrounding the central nucleus. They are on an average smaller than the dark green variety but individual calculi have been found of three ounces.

The _whitish or orange calculi_ are usually in the form of hollow casts of the bile ducts having a dull white color externally and a yellowish brown internally. They are usually thin, fragile and crystalline and contain relatively more earthy salts than the two first named varieties. From this cause also they have a higher specific gravity. One specimen weighed 8 ounces.

The _biliary sand or pulp_, is made up of granules of a yellowish, dark green or black color, forming with the bile a pultaceous mass but drying into a consistent mass. It may be firmly adherent to the mucosa of the gall bladder and require to be scraped off. These granules may be looked on as the first step in the formation of calculi or encrustations.

The _causes_ of biliary calculi in cattle are mainly close confinement, dry feeding, abundant rations, the presence of trematodes in the bile ducts and finally microbian infection.

_Lesions_ vary. With obstruction of the common bile duct or cystic duct, there are usually dilatation of the bile ducts with fibrous thickening of their walls so that they stand out as white branching lines on the back of the liver. In extreme cases the common duct may acquire the calibre of the small intestine. The gall bladder may participate in this thickening (Chassaing) or may even rupture (Proger, Shaw).

In connection with obstruction microbian infection extends upward into the liver, and in rupture of the bladder an acute, diffuse septic peritonitis follows (Chassaing). This only follows on infective inflammation of the gall bladder. Aseptic bile causes little or no irritation.

_Symptoms._ As in the horse, general symptoms of ill health or hepatic disorder are not pathognomonic. The presence of intermittent attacks of constipation, and colic, with icterus, tympanies and violent efforts at expulsion are the diagnostic symptoms of an acute attack. Pulsation and respiration are accelerated, and the urine dense, high colored, oily and slightly yellow. Reboul has noticed that symptoms are aggravated on exposure to cold; there are great prostration and dullness, frequent moaning and marked indications of tenderness when the right hypochondrium is percussed. Charlot has observed that the only symptoms may be persistent jaundice with scanty, high colored urine, containing some sediment.

_Treatment_ is essentially the same as in the horse. Vanswieten and Verheyen draw special attention to the fact that whereas biliary calculi are very common in cattle during winter, they are rarely found in animals that have been for even a short period on the spring grass. Spring pasture is therefore the best therapeutic agent. During paroxysms of colic, Glauber salts, or olive oil, antispasmodics and fomentations over the liver are to be tried. In the intervals salicylate of soda, sodium and potassium carbonate, olive oil, chloroform, and ether may be used. Abundance of water and aqueous rations are essential.

GALL STONES IN SHEEP.

Calculi are very rare. One described by Morton had a brownish yellow color on its surface, and a white color spotted with green internally; it had a bitter taste, colored saliva yellow, and melted when heated, diffusing the odor of musk. It weighed twelve grains and contained 70 per cent. of cholesterin, calcic phosphate and carbonate and the usual biliary elements.

But if spherical calculi are rare, concretions and casts of the bile ducts are common, especially in distomatosis. These are of a yellowish, reddish, greenish or blackish brown, and form granular plates, or veritable cylindroid casts often firmly adherent to the mucous membrane of the duct.

In such cases the walls of the encrusted ducts are hypertrophied and stand out on the back of the liver as white bands diverging from the portal fissure.

Apart from the usual _symptoms_ of distomatosis no special indications have been observed.

_Treatment_ is primarily that for distomatosis, to which the general measures advised for calculi may be added.

GALL STONES IN SWINE.

_Characters._ The calculi are spherical, rough or on their opposed surfaces flat, clear and glistening where they have become polished by friction. They are found as a fine sand or as calculi the largest of which have been 75 grains, and of a high density (1303 to 1484). Bruckmüller found that they contained carbonate of lime and biliary mucus. Verheyen found biliary resin, mucus, pigment, and a little fat. They are rare in fat hogs in America. No diagnostic _symptoms_ have been observed.

GALL STONES IN DOG AND CAT.

These are more or less spherical, dark brownish green, and usually found in the gall bladder or larger bile ducts. They may vary in size from a pea to a hazel nut. Their chemical analysis is wanting.

_Symptoms._ There may be evidence of biliary obstruction and if this occurs intermittently and is associated with colic, it becomes somewhat characteristic. Constipation, emesis, icterus, and sometimes tenderness of the right hypochondrium would indicate the source of the colic. A pre-existing and concurrent catarrh of the bowels corroborates these indications.

Cadeac explains that the obstructing calculus is called on to resist the impulse of the bile forced upon it by the spasmodic contraction of the bile ducts, which distends the bile duct immediately back of the stone to perhaps ten times its normal size. Then under a suspension of the spasm or even an antiperistaltic contraction of the duct, the calculus is forced back into the dilated portion or even into the gall-bladder, and the attack is relieved. Under repeated irritations of this kind the inflammation of the bile ducts extends into the liver and determines cirrhosis. The irritation further through the sympathetic produces a reflex constriction of the pulmonary capillaries, with the natural results of increasing tension of the pulmonary artery and right heart, and dilatation and degeneration of the walls of the latter even in the best nourished animals. Thus dyspnœa and modified heart sounds (murmurs) may be symptoms of biliary calculi.

_Treatment._ Three or four ounces of olive oil were found to greatly increase the quantity and fluidity of the bile in from thirty to forty-five minutes. Bile, sulphate of soda and salicylate of soda are excellent cholagogues, and the latter at the same time an antiseptic. Anti-spasmodics are especially indicated to relieve the colics, but they must be used in relatively smaller doses than in the herbivora. Potassic and sodic carbonates or tartrates (Vichy) may be used as enemas if they cannot be administered by the mouth. Fomentations may be resorted to. The food must be laxative and aqueous, and exercise must be imposed as far as the animal can bear it.

FOREIGN BODIES IN THE LIVER.

In _horse_: spikes of leguminosæ, barley awns. Symptoms: of internal
hemorrhage, pallor, weakness, vertigo, death; jaundice, prostration,
stupor, weakness, crossing of fore limbs, tender right hypochondrium.
In _cattle_: bodies passing from rumen. In _swine_, sand. In _dog_,
sharp bodies from stomach. Treatment: laparotomy.

Foreign bodies are rare in the liver in our domestic animals. _Horse._ St. Cyr has found the spikes of leguminosæ and Megnin the beards of barley. St. Cyr believed that he traced the passage followed by the stalk through the walls of the duodenum, and portal vein where it divided to be distributed through the liver. At the point of supposed entrance the walls of the vena portæ were thickened and its lumen filled with clots. The further course of the portal vein and its branches showed similar thickening and clots, and on the branch leading to the right lobe was a large abscess containing 4 decilitres of pus. Clots extended into the splenic, omental and mesenteric veins, and between the folds of the mesentery of the small intestine were a number of minute ruptures and blood extravasations.

Megnin found traces of the passage of the barley beards through the gastric walls and into the substance of the liver close to the portal fissure. Around the centre where the barbs were implanted there was an irregular hæmorrhagic extravasation in the liver, and in the abdominal cavity an effusion of 8 or 10 quarts of blood.

_Symptoms._ In such a case the only definite symptoms are those of internal hemorrhage, pallor of the mucous membranes, gradually increasing weakness, vertigo, unsteady gait, and an early death. In more protracted cases slight jaundice, dullness, prostration, stupor, drooping of head, ears and eyelids, resting it on the manger or walls, muscular weakness, crossing of the front limbs, and it may be tenderness on percussion on the right side of the chest posteriorly. It resembles the _coma_ or _immobility_ of the horse but the patient backs more easily.

_Cattle._ In ruminants sharp pointed bodies passing from the rumen will occasionally penetrate the liver, and give rise to symptoms of hepatic disorder. Augenheister found in a cow dilatation of the larger bile ducts, which contained about 10 quarts of sand, that had apparently entered from the duodenum by the common bile duct which had an orifice of an inch in diameter.

_Pig._ The gall ducts of a pig’s liver, in the Veterinary College of Berlin contains a large amount of sand (Gurlt).

_Dog._ The liver is exceptionally perforated by sharp pointed bodies coming from the stomach. Cadeac and Blanc report three cases of needle in the liver. Blanc’s case had been killed because of old age; one of Cadeac’s showed symptoms resembling rabies.

_Treatment_ of these cases would be very hopeless as nothing short of laparotomy and the removal of the foreign body would promise success.

TUMORS OF THE LIVER. NEW GROWTH.

Largely secondary, from stomach, intestine, lymph glands, spleen,
pancreas; the hepatic tumor may be disproportionately large. In
_horse_: sarcoma rapidly growing soft, succulent, slow-growing,
fibrous, tough, stroma with round or spindle shaped cells and nuclei.
Symptoms: emaciation, icterus, enlarged liver, rounded tumors on
rectal examination. Melanoma, in old gray or white horses, with
similar formations elsewhere; not always malignant. Lymphadenoma.
Angioma. Carcinoma. Epithelioma, lesions, nodular masses, white or
grayish on section, and having firm stroma with alveoli filled with
varied cells with refrangent, deeply staining, large, multiple nuclei,
cancerous cachexia and variable hepatic disorder. In _cattle_:
sarcoma, adenoma, angioma, cystoma, carcinoma, epithelioma. In
_sheep_: adenoma, carcinoma. In _dog_: lipoma, sarcoma, encephaloid,
carcinoma, epithelioma. Wasting and emaciation, yellowish pallor,
temporal atrophy, ascites, liver enlargement, tender right
hypochondrium, dyspepsia, symptoms of primary deposits elsewhere.

The great quantity of blood which passes through the liver lays it open, in a very decided way, to the implantation of germs and biological morbid products. Hence tumors of the liver are largely secondary, the primary ones being found mostly in the stomach, intestine, abdominal lymph glands, spleen and pancreas. The primary neoplasm is often comparatively small, while the hepatic one supplied with a great excess of blood may be by far the most striking morbid lesion. The hepatic tumors are mostly of the nature of angioma, sarcoma, melanoma, adenoma, lipoma, cystoma, carcinoma, and epithelioma.

NEOPLASMS IN HORSES LIVER.

_Sarcoma._ This is usually a secondary formation from the primary tumors in the spleen and peritoneum, and it occurs as multiple masses throughout the substance of the gland. The liver is greatly increased in size, extending far beyond the last rib on the right side, and weighing when removed as high as 70 ℔s. (Mason), or even 88 ℔s. (Cadeac), in extreme cases.

The whole surface of the liver may show bulging, rounded masses, and the morbid growth may have involved the capsule and caused adhesion to the back of the diaphragm (Bächstädt). The cut surface of the neoplasm is smooth, elastic, yellowish and circular or oval in outline. It may have a variable consistency—friable or tough, according to the activity of growth and the relative abundance of cells and stroma. The portal glands are hypertrophied and thrombosis of the portal vein is not uncommon.

Microscopic examination of the dark red scrapings shows numerous blood globules, intermixed with the round or spindle shaped cells and nuclei of the tumor. Sections of the tumor show these cells surrounded by a comparatively sparse fibrillated stroma. The round cells may vary from .005 to .05 m.m. They contain one or more rather large nuclei and a number of refrangent nucleoli. The nuclei are often set free by the bursting of the cells in the scrapings. They become much more clearly defined when treated with a weak solution of acetic acid. Small grayish areas in the mass of the tumor represent the original structure of the liver, the cells of which have become swollen and fatty.