(b) Acetonuria and Acetonemia.—The former sometimes follows chloroform anesthesia, and occurs especially in diabetes (particularly after removal of the pancreas in experimental animals). Acetone per se is nearly or quite harmless, but its congeners, diacetic and beta-oxybutyric acids, are very toxic. The danger in so-called acetonuria is from acid intoxication by these acids, which has been described as “excessive acidosis,” and its co-existence with glycosuria makes diabetes certain, while prognosis is grave in proportion to its presence. Prominent among the symptoms produced by it are delirium and coma.
When either or all of these three substances are present in the blood its alkalinity is reduced and its ability to absorb carbon dioxide impaired; hence, acetonemia is evidenced by carbon dioxide poisoning. To the brain symptoms above noted is added a peculiar odor in the breath—sweetish or ethereal. This has been noted in pyemia. This condition may set in after various operations, but whether due to disease, the traumatism itself, or to chloroform may not always be determined.[3]
[3] See paper by Brewer, Annals of Surgery, 1902, vol. xxxvi, No. 4, p. 481.
(c) Cystinuria.
(d) Coma of cancerous cachexia (coma carcinomatosum).
(e) Exophthalmic goitre, from excess of thyroidal activity (thyroidism).
Besides the above there is auto-intoxication proceeding especially from the gastro-intestinal and hepatic systems. Of the former, the best surgical examples are seen in the tetany which occasionally takes its rise from a dilated stomach, and which may be cured by a pyloroplasty or a gastro-enterostomy; in the nephritis which follows stercoremia of intestinal obstruction; and in oxaluria, with its painful, serious, and often deforming or crippling joint affections. Of the latter we have examples in the cholemia of acute atrophy or of biliary obstruction, and in the uremia of hepatic origin which occasionally terminates a surgical case.
In addition to the above there should also be mentioned the auto-intoxications of pregnancy, with the consequent salivation, peripheral neuritis, pigmentations of the skin, icterus, and pruritus, which are mainly attributed to perverted action of the liver or kidneys.
The practice of preparing patients for operation by a course of purgatives, emetics, etc., is based upon the recognition of certain principles. The general symptoms included under the name enterosepsis, stercoremia, copremia, are due to the activity of the colon bacillus, which seems to be made more virulent by certain conditions of diet or retained fecal excretions, and to such an extent that it wanders widely from its normal habitat and may be found in distant parts of the body. Enterosepsis may be mistaken for surgical fever, and is to be distinguished from it, perhaps, only by the study of the excretions of a case and establishing the fact that they are free, and that consequently pyrexia, etc., cannot be due to diminished elimination. Aside from the migrations of the colon bacillus, it is also possible for auto-intoxication to occur. Thus that which is stercoremia one day may later become a genuine septicemia, vital resistance being so lowered as to permit of local infection. The various conditions are so often merged that it is difficult to separate and identify them. Nevertheless, enterosepsis differs from sapremia in that in the one instance the putrefying material is contained within a normal cavity, whereas in sapremia it is contained within an abnormal cavity, in either case corresponding to a septic suppository, varying, however, in the place of insertion, also in the nature of the surrounding tissues, which in the latter case are more capable of absorption and of becoming infected than in the former.
A determination of indol and indican is often of the greatest value, both in determining the extent of infection and the presence of pus. Indol is set free under the following circumstances: (a) Suppuration in a closed cavity. (b) Continued suppuration in a cavity with an outlet. (c) Ulceration or necrosis of tissue. The degree of indicanuria will depend on the length of time pus has been present, the possibility of absorption from the tissues surrounding it, and its degree. When pus is fully formed in a serous sac the indican reaction becomes intense according to the length of time pus has been present. This is particularly true in the empyemas of childhood. In continued suppuration with a free outlet the production of indol will be great; but the amount finally eliminated will depend upon the character of the surrounding tissue. When solid tissue, like bone, becomes affected, the elimination of indol is intense. Rapid biogenic degeneration of tissue causes an increased amount of indol to be deposited in the liver, and it is possible at postmortem, by simple extraction with absolute alcohol, to take from the liver this excess deposit in the shape of its oxidation product, indigo blue. Lardaceous degeneration is characterized by marked and persistent elimination of indol, which seems to be a product of tyrosin. It occurs frequently in the liver, in which indol is notably deposited. Its primary factor is deposited by the blood, in which latter indol circulates and is oxidized. Lardaceous material gives a red or blue color with oxidizing agents, which latter yield with indol an indigo red or blue.