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.