PARENCHYMATOUS HEPATITIS, ACUTE YELLOW ATROPHY OE THE LIVER.

The characteristic morbid lesion in this disease is the degeneration of

the liver cells, loss of their protoplasm and nuclei and of their normal

functions. It may be circumscribed to limited areas, or may affect the

liver, generally. As the hepatic functions, are so intimately related to

those of the bowels and kidney, the affection is usually accompanied by

inflammations of these organs as well.

_Causes in horses._ The same general causes which produce congestion,

may also determine the further morbid stage of inflammation. Cadeac

mentions a case which developed in a horse kept alone and idle in the

stable. He makes no mention of condition, food, cleanliness nor

ventilation. Haubner and Franzen have traced it to a diet of malt or of

hay harvested from inundated meadows. Zundel records a case following

exposure to extreme cold. More commonly the disease is secondary to the

overtaxing of the liver, by heavy feeding in warm moist climates, or in

hæmoglobinæmia, or to the arrest of the micro-organisms of the food, or

of infectious diseases.

_Causes in Cattle._ These suffer rarely, but from essentially the same

conditions. It has followed aphthous fever (Eletti), and arisen under a

forcing ration, in hot weather (Callot, Cruzel), or under overwork

(Cruzel).

_Causes in Dogs._ Most cases result from infection by way of the stomach

and intestines, or by the transfer to the liver of the ptomaines and

toxins of such infections. It is thus related in its origin to catarrhal

jaundice and hyperæmia.

_Lesions._ In the earliest stage with albuminoid exudation into its

substance the liver may be greatly enlarged, its sharp edges rounded,

and its consistency softened. After a week’s illness atrophy may have

set in and the organ appears shrunken and of ocherous yellow. In the

early stages there may be sanguineous engorgement, the cut surface may

bleed freely, and small extravasations may show throughout the liver

substance, later the clay yellow hue, the granular aspect and the

absence of blood on the cut surface are characteristic. The margins of

the adjacent acini are indefinite or lost, and under the microscope the

hepatic cells are charged with granules (albuminoid, fatty and

pigmentary), while the nuclei are no longer demonstrable.

In _cattle_ the liver may be double the normal size and at first of a

deep purple red, which may change later to the earthy yellow.

In _dogs_ the liver is tumid and yellow, and marked by small pea-like

centres of softening. There is marked softening and the microscope

reveals the characteristic degeneration of the hepatic cells.

_Symptoms in the Horse._ These resemble those of congestion rendered

more intense and therefore somewhat less obscure. The attack is usually

sudden, there may be rigor followed by hyperthermia, dullness, pendent

head, drooping eyelids, injected conjunctiva with a yellowish tinge,

unsteady gait and slight indications of colic. There is anorexia,

partial suppression of urine, and what is passed is thick, glairy and

brownish red, fæces are passed with pain, and groaning, probably from

compression of the liver, the heart beats violently, while the pulse is

small, breathing accelerated and perspiration abundant. The temperature

rises (101° to 106°) and remains high throughout unless lowered through

biliary intoxication. Percussion over the liver and especially on the

right side shows increased area of dullness and marked tenderness. On

the second or third day the icterus usually increases, and a slight

fœtid diarrhœa may set in with marked fœtor of the pale or colorless

discharges. The jaundice is not, however, a criterion of the danger, as

it may become less marked or entirely disappear because of the extensive

degeneration of the hepatic cells and the arrest of the formation of

bile.

_Diagnosis in the horse._ The disease is recognized by the coincidence

of fever, with great depression, icterus, painful defecation,

constipation followed by a fœtid diarrhœa with lack of color in the

stools and by increased area of dullness and tenderness in the region of

the liver and especially on the right side. From influenza which it

resembles in many respects, it is distinguished by the absence of watery

discharge from the eyes, and by the entire absence of all indication of

contagion. The cases occur one at a time.

_Prognosis in the horse._ The disease is exceedingly fatal. When the

kidneys remain active, the poisons are eliminated and there may be hope

of recovery, but when urine is suppressed an early death by poisoning is

to be expected.

_Treatment in the horse._ A most important indication is to secure

depletion from the portal system. Calomel 1 dr., aloes 4 drs., ipecacuan

1 dr. may be given in bolus, and followed by small daily doses of

sulphate and nitrate of soda with bitters, with or without the

ipecacuan. Action on the kidneys is essential to secure elimination of

the poisons which threaten a fatal poisoning if retained. To favor the

same action fomentations may be applied to the loins. The frequent

presence of pathogenic microörganisms either in the bowels or liver

suggests the use of germicides (salol, salicylic acid, salicylate of

soda, naphthalin, naphthol, beta-naphthol, etc.) as in catarrhal

jaundice. Sinapisms or blisters applied to the right side of the chest

and over the short ribs may be useful, and after the subsidence of the

more violent symptoms, dilute mineral acids and especially

nitro-muriatic acid may be resorted to in combination with diuretics and

bitters.

When appetite returns succulent, laxative, non-stimulating food in small

quantity should be given. Wheat bran mashes, carrots, turnips, potatoes,

apples, fresh grass, ensilage may be adduced as examples. Throughout the

disease the ingestion of an abundance of pure water should be

encouraged.

_Symptoms in the ox._ These may appear more tardily than in the horse,

loss of appetite, staring coat, dullness, pendent head and ears,

unsteady movements, rigors, drivelling of saliva from the mouth and

grinding the teeth are usually noted. To these are added the more

diagnostic symptoms of slight (or severe) jaundice, constipation

followed by a fœtid light colored diarrhœa, a strong disposition to

remain recumbent, marked suffering attendant on rising, arching of the

back when up, and tenderness on percussion over the right hypochondrium.

The temperature gradually rises, though more slowly than in the horse,

and may again descend under a profound poisoning.

_Course._ The disease reaches its acme in four to six days, and

generally has a fatal issue.

_Treatment_, is on the same lines as for the horse only as a purgative,

sulphate of soda may advantageously replace the aloes.

_Symptoms in the dog._ The symptoms are those of congestion in an

exaggerated form. There are muscular tremors, erection of the hair,

followed by rising temperature up to 105° or 106°, an icteric hue of the

mucosæ, the pulse is accelerated, strong, irregular, respiration rapid,

panting, fœtid breath, ventral decubitus, and prostration extreme.

Appetite is completely lost, the bowels become relaxed, the stools

fœtid, the right hypochondrium painful on pressure or percussion, and

the urine greatly reduced and icteric or suppressed. This feature of

urinary suppression, determines a rapid poisoning and death in two or

three days.

_Treatment_ must follow the same lines as in other animals, a purgative

of calomel and jalap, followed by diuretics, laxatives, derivatives, and

above all germicides. In case of survival mineral acids, aqua regia,

bitters, and a carefully regulated diet will be in order.

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