companied by pain if the patient be at all anxious, perhaps by swelling, certainly by effusion. These inflammatory outbursts may occur anywhere, as if in fact by accident; in the peritoneum, in the pleura, in the tissue of the lungs, in the bronchial mucous tract, in the alimentary mucous tract, in the encephalon. They may vary in character; they may be acute in acute uræmia, or in chronic uræmia subacute and very gradual in progression. They may prove eventually the immediate cause of death. The day will come when all these forms of inflammatory lesion will be classified under one head, as derived from the primary uræmic diathesis. But to mention these inflammatory complications, to notice their symptomatic connection with the uræmic state, is sufficient for this moment. I shall treat in a subsequent section on their production.

PATHOLOGY OF URÆMIA.

In all cases of uræmic intoxication, whether preceded by chronic renal disease, or occurring suddenly during an acute inflammatory attack, or induced in an animal by removal of the kidney, the blood assumes various physical and chemical peculiarities, essentially characteristic of alkaline or alkaloidal toxæmia. In the first stages of the uræmic attack, the blood truly may assume the inflammatory cast; i. e. it may be buffed and cupped. I saw this markedly in one instance where uræmic coma came on in a harvestlabourer, who, after a night's exposure to a damp cold air, was seized with inflammatory dropsy, followed

quickly by uræmic coma; and I saw the same in a case of scarlet fever. But this inflammatory condition soon subsides, even if it occur; and the blood then undergoes what might very correctly be termed alkaline decomposition. The tendency of this blood is to remain fluid after it is removed from the body, or, if it separate at all, to separate into loose shreddy masses of fibrine. If to the fluid blood milk of lime or baryta be added, there is rapid coagulation with evolution of ammonia. The corpuscles of uræmic blood undergo also great modifications. They are crenate at the edge, they take an oval form, show little tendency to coalesce, and are reduced in number. This diminution of red corpuscles, first observed by Christison, I have been able to confirm in two cases on the human subject, and in an experimental case on an inferior animal. I have noticed the same diminution of corpuscles after poisoning by belladonna.

There is also an excess of serum in proportion to the solid constituents in uræmic blood; and often a low specific of the serum, owing to a deficiency of albumen. The fibrine in the later stages seems to become decreased; but whether this decrease is absolute or relative I am unable to say. Certain it is that uræmic blood, in which the fibrine is apparently so far absent that spontaneous coagulation is impossible, will coagulate readily enough on the addition of milk of lime, baryta, or a weak solution of potassa cautiously added. It is possible, therefore, that the fibrine is not actually deficient, but is held

in solution by the presence of an alkaline body, which is liberated as an ammonia on the addition of a displacing agent.

In a case recorded by F. Simon, the serum exhibited a remarkable milk-white turbidity. This colour, which was not caused by fat in a state of suspension, was found to depend on the presence of numerous minute solid granules, which on collection and inquiry were found to be insoluble in alcohol and ether, but soluble in dilute acetic acid, from which they were separable by ferrocyanide of potassium. Hence Simon concluded that they were particles of fibrine. The same experimentalist found hæmatoglobulin more abundant in the hæmatin in cases of uræmia, than in ordinary cases. It varied from 8 to 9.5 per

cent.

The amount of urea in the blood is increased. This fact, asserted by Christison, Simon, and all the earlier writers, but disputed by other succeeding authors, is now satisfactorily proved. The experiments of Hammond on the increase of urea in dogs, after extirpation of the kidneys, remove all doubt. In one of his carefully conducted inquiries, 100 grammes of blood removed from the jugular vein before extirpation of the kidneys yielded 0.026 gramme of urea whereas, twenty-four hours after extirpation, 100 grammes of blood from the same vein yielded 0.083 gramme of urea.

From these peculiarities of blood, we may pass to the pathology of other structures. Effusions are common during uræmia: they must be so, for, in condi

tions where the functions of the kidney are suppressed, and albumen is an excrete, not only is there accumulation of water in the tissues, but there is decreased specific gravity of blood, which, in proportion as it exists, induces exudation by incapacitating that fluid from eliminating its water. This result of uræmia-exudation-occurs in divers parts of the organism; in the cellular tissue, in the serous cavities, in the bronchial mucous tract, in the ventricles of the brain. With the mere serum thrown out, pseudo-plastic material is sometimes admixed; and, after death from uræmic coma, these exudative products may constitute a marked feature in the morbid representations. They are to be looked upon as sequences; and, although they may materially have influenced the course of a case, their secondary character should invariably be recognised by the philosophical student.

Whether effusion exist or not in uræmia, there is always more or less of congestion of the vascular organs. In the earlier stages this frequently leads to diseased states of special organs, inflammatory in appearance. In later stages the congestion becomes universal; for, as we shall see by and by, in comparing the mode of death in uræmia with asphyxia, that while the congestion commencing at the kidney is for a time partial only, extending to the lungs it is reflected through the whole of the soft tissues. Hence, after death from uræmic coma, we almost invariably find congestive enlargement of the liver and spleen, intense congestion of the lungs, with distension of the sinuses of the cerebral membranes, and congestion of

M

the minute vessels of the brain itself. For this same reason the muscles are often dark and filled with blood, and the inner surface of the arterial system is deeply stained.

It is worthy, too, of special remembrance, that the congestive condition above described may extend to the alimentary mucous surface in any part of its tract.

This fact, of which I have given one illustration (vide pp. 134-5), is important, inasmuch as the congestion of the alimentary tube is usually followed by exudation of serous fluid containing urea. Mixing now with the secretions natural to the canal, the urea is transformed partially or altogether into carbonate of ammonia, which acting in turn as an irritant, produces, when present in excess, distinct gastro-enterite with diarrhoea and vomiting as symptoms, and an inflamed mucous membrane as the visible morbid upshot. Thus in the train of acute uræmia we may have all the results of an irritant poison. We may have gastro-intestinal inflammation, or peritoneal effusion, or both combined. We may have congestion of lung, pleural exudation; cerebral congestion, ventricular effusion; deep staining of the endocardial membrane, and equally dark staining of muscular fibre. We may, I say, have all these obvious lesions, or we may have none of them; for if, on the one hand, the suppression of the kidney be immediate and perfect, death may take place purely from a rapid disorganisation of the blood, owing to accumulation of water with the urea; or if the arrest of the renal