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.