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alcohol, red, deeply injected, and “presenting at certain points a
black coloration due to effused blood.” This fact they regard as
worthy of note, because in their experiments the toxic agent was
introduced, not by the mouth, but hypodermically, and they explain it
by the supposition—which appears to me warrantable—that it is due
to elimination by the mucous glands. Hence the congestion,
softening, and hemorrhage.24 These observers also found that the
symptoms were more acute and the lesions more marked when
poisoning was caused by propyl, butyl, or amyl alcohol than when it
was produced by ethyl alcohol.
23 An Experimental Inquiry concerning the Presence of Alcohol in the Ventricles of the
Brain after Poisoning by that Liquid, together with Experiments illustrative of the
Physiological Effects of Alcohol, London, 1839.
24 Chatin and Gublier have emphasized the fact that certain poisons introduced by
intravenous injection or by absorption through the respiratory tract are eliminated by
the intestines, with the production of the same local symptoms as when administered
by the mouth (Bulletin de l'Académie de Médecine, Séance du 6 Novembre, 1877).
26 Cited by Blyth.
There is little doubt that the view now generally held, that acute
yellow atrophy is due to the action of some unknown toxic principle,
is correct. Alcoholic excess must therefore be regarded merely in the
light of a predisposing influence. Acute yellow atrophy of the liver is
an exceedingly rare disease.