§ 294. The kidneys exhibit alterations very similar and analogous to those of the liver. They are mostly enlarged, congested, and flabby, with extravasations under the capsule, and show microscopic changes essentially consisting in a fatty degeneration of the epithelium. In cases attended with hæmorrhage, the tubuli may be here and there filled with blood. The fatty epithelium is especially seen in the contorted tubes, and the walls of the vessels, both of the capsule and of the malpighian bodies, also undergo the same fatty change. In cases in which death has occurred rapidly, the kidneys have been found almost healthy, or a little congested only. The pancreas has also been found with its structure in part replaced by fatty elements.
Of great significance are also the fatty changes in the general muscular system, and more especially in the heart. The muscular fibres of the heart quickly lose their transverse striæ, which are replaced by drops of fat. Probably this change is the cause of the sudden death not unfrequently met with in phosphorus poisoning.
In the lungs, when the phosphorus is taken in substance, there is little “naked-eye” change, but Perls,[312] by manometric researches, has shown that the elasticity is always decreased. According to experiments on animals, when the vapour is breathed, the mucous membrane is red, congested, swollen, and has an acid reaction.
[312] Deutsch. Archiv f. klin. Med., vi. Hft. 1, S. 1, 1869.
In the nervous system no change has been remarked, save occasionally hæmorrhagic points and extravasations.
§ 295. Diagnostic Differences between Acute Yellow Atrophy of the Liver and Fatty Liver produced by Phosphorus.—O. Schultzen and O. L. Riess have collected and compared ten cases of fatty liver from phosphorus poisoning, and four cases of acute yellow atrophy of the liver, and, according to them, the chief points of distinction are as follows:—In phosphorus poisoning the liver is large, doughy, equally yellow, and with the acini well marked; while in acute yellow atrophy the liver is diminished in size, tough, leathery, and of a dirty yellow hue, the acini not being well mapped out. The “phosphorus” liver, again, presents the cells filled with large fat drops, or entirely replaced by them; but in the “atrophy” liver, the cells are replaced by a finely-nucleated detritus and through newly-formed cellular tissue. Yellow atrophy seems to be essentially an inflammation of the intralobular connective tissue, while in phosphorus poisoning the cells become gorged by an infiltration of fat, which presses upon the vessels and lessens the blood supply, and the liver, in consequence, may, after a time, waste.
There is also a clinical distinction during life, not only in the lessening bulk of the liver in yellow atrophy, in opposition to the increase of size in the large phosphorus liver, but also in the composition of the renal secretion. In yellow atrophy the urine contains so much leucine and tyrosin, that the simple addition of acetic acid causes at once a precipitate. Schultzen and Riess also found in the urine, in cases of yellow atrophy, oxymandelic acid (C8H8O4), but in cases of phosphorus poisoning a nitrogenised acid, fusing at 184° to 185°.
According to Maschka, grey-white, knotty, fæcal masses are found in the intestines in yellow atrophy, but never in cases of phosphorus poisoning. In the latter, it is more common to find a slight intestinal catarrh and fluid excreta.