Calcified roundish nodules, in groups, under capsule. Mostly in
solipeds. Theories of origin: parasites, microbes, emboli, omphalitis,
intestinal disease, biliary obstructions. Calcification of liver with
large abdominal aneurisms. Cszoker’s case, Diagnosis and specific
treatment impossible.
In the domestic animals in general the liver may become the seat of
imperfectly spherical nodules of a white, yellow or brownish white
color, varying in size from a millet seed to a pea or hazel nut, and of
a gritty consistency and feeling, from the deposition of earthy salts.
These may be seen in groups under the proper capsule, the adjacent
hepatic tissue being healthy, or atrophied, sclerosed or pigmented.
These lesions have been found most abundantly in solipeds.
_Pathogenesis._ The most varied doctrines have been advanced as to the
origin of these lesions. They have been attributed to the previous
presence in the liver of linguatula, echinococcus, cœnurus, oxyurus,
distoma, and other parasites (Cadeac, Mazanti, Olt, Ostertag, Gripp,
Leuckart, Ratz), to glanders, to microbian attacks (Dieckerhoff), to
minute embolic infarcts in omphalitis in the foal, or intestinal disease
in the adult (Kitt), and to obstructions by the eggs of distomata in the
biliary ducts (Galli-Vallerio). It is not improbable that the lesion may
be due to any one of these in a specific case, and this may be
ascertained by the existence of certain definite features and
conditions. Linguatula, echinococcus and cœnurus can only be suspected
in districts where these prevail, and a careful examination of the
central mass of the nodule should reveal the presence of the
indestructible hooklets, as certified for given cases by Olt, Ostertag
and Gripp. In case of nematoid worms or distomata, the eggs may possibly
be found as in the cases of Villach and Ratz, or the embryos (Mazanti).
Or there may be traces of channels formerly hollowed out by the worms in
the vicinity of the nodules, as seen by Leuckart. Coincident tumors of
the intestinal mucosa from larval nematodes, or aneurism or emboli in
the anterior mesenteric artery would corroborate this conclusion. If
distomata had started the lesions, the distension of the gall ducts and
the thickening of their walls would be likely to indicate their former
presence. Glander nodules might be suspected from the absence of a
distinct rounded or oval outline, from the lack of a distinct, clear
line of demarcation between the nodule and the adjacent liver tissue,
and by the manifestation in the periphery of the nodule and around it of
free cell proliferation, showing the mode of progression by the invasion
of new tissue. If still active, the bacilli should be discoverable in
stained scrapings or sections. There should also be distinct indications
of the lesions of glanders in the lymph glands of the portal fissure, of
the mediastinum, of the submaxillary region and of other parts.
Heiss records an interesting case of general calcification of the
horse’s liver, with large aneurism of the abdominal aorta, mesenteric
and renal arteries. The liver was thirty-two pounds, puckered on the
surface and showed calcic degeneration of the walls of the vessels and
hepatic tissue, to such an extent that when the organ was dried it did
not add materially to its hardness. Microscopically the diseased centres
indicated minute blood clots (thrombi), with fibrinous development and
cretifaction. The lesions in this case were attributed to multiple
emboli in connection with the aneurism. It might suggest further,
microbian infection of both the aneurismal and hepatic vessels. In
another case of extensive cretifaction of the horse’s liver reported by
Cszoker, the calcified masses tended to assume rounded forms like
tubercle, and had a clear glistening surface.
These lesions are mainly interesting in a pathological sense, and unless
they are very extensive do not give rise to appreciable symptoms.
_Treatment_ could only be prophylactic and directed to the removal of
the special conditions, in which the calcification originated in a given
locality.