A treatise on the principles and practice of medicine : designed for the use of practitioners and students of medicine / by Austin Flint.

  • Flint, Austin, 1812-1886.
Date:
1881
Catalogue details

Licence: Public Domain Mark

Credit: A treatise on the principles and practice of medicine : designed for the use of practitioners and students of medicine / by Austin Flint. Source: Wellcome Collection.

Provider: This material has been provided by the University of Massachusetts Medical School, Lamar Soutter Library, through the Medical Heritage Library. The original may be consulted at the Lamar Soutter Library at the University of Massachusetts Medical School.

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    There is no doubt that carbonate of ammonia may be absorbed by the blood from the intestine, and that, in certain cases, which are rai'er than was once supposed, it may be detected in the breath. It is true that the injection of carbonate of ammonia into the blood of animals produces more marked symp- toms than does the introduction of urea. The most constant of these symptoms are convulsions, followed often by coma, with infrequency of the pulse and res- piration. But while carbonate of ammonia always produces one and the same group of symptoms, mainly those of irritation, on the other hand the manifes- tations of uraemia are various, and only in a certain proportion of cases are they analogous to those produced by the ammonia-salt. Carbonate of ammonia has been detected in small quantity in the blood in uraemia, but it has also been found absent in many cases. Traube referred the uremic phenomena to cerebral oedema and consequent cerebral anosmia. The oedema he attributed to hydrfemia and high arterial pressure, conditions which are often, but not invariably, present in urgemia. Oedema and antemia of the brain are found when no ura^mic symptoms were manifested during life, and they are by no means constantly present after death from uraemia. Qildema of the brain may often be regarded with more propriety as the result, rather than as the cause, of convulsions. . It is held by some writers that urtemia is not always produced in the same way, but that, in ditFerent cases, the causes are different. Bartels was an eminent advocate of this eclectic view. Jaccoud attempts even to diagnosti- cate between urtemia due to toxaemia and that due to oedema of the brain. But no essential differences have been detected, as regards symptoms, between cases of uraemia in which the blood was loaded with urea, and those in which no excess could be determined ; between those in which carbonate of ammonia was found in the blood, and those in which it was absent, or between cases accompanied with hydriemia, and those without the latter pathological con- dition. It is only established with regard to the cause of ursemia, that this condi- tion is the result of an abatement of the function of the kidneys, and that this abatement is followed by an accumulation of excrementitious substances in the body. It is inconceivable that the accumulation in the blood and tissues of waste products should not have an injurious effect. Perhaps the following explanation of the ura^mic phenomena is most in harmony with clinical and experimental observations : The ura;mic symptoms are the result of the reten- tion in the system of excrementitious materials. It is the entire mass of waste products, and not any single element, which is the source of trouble. The nature of these waste materials is very imperfectly known. They probably consist mostly of nitrogenous substances in different stages of the metamor- phosis of which urea is the final stage. The non-elimination of the excretory products, causes an incomplete metamorphosis of the waste nitrogenous ele- ments. These are retained, not only in the blood, but, finally, in the tissues. The nutritive processes are thereby disturbed. As the ura^mic symptoms are chiefly of nervous origin, it is necessary to emphasize especially the disturbance of nutrition in the nervous system. A m m 0 n i 88 m i a. The occasional absorption of carbonate of ammonia produced from urea excreted by the intestine, has been mentioned already. Whether the amount of carbonate of ammonia, which thus gains access to the blood, ever suffices to produce poisonous symptoms, is uncertain. There is, at least, not sufficient ground lor believing that uraemia is, in reality, ammonifemia. An ammoniacal state of the blood has also been referred to the absorption of carbonate of