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shall be vomiting as an early symptom, in the next no indication of such an effect. These distinctions, all of import, are nevertheless secondary; since, in every case, they are included in two common symptoms-excretion of albuminous urine, and coma. Differential Diagnosis. Uræmia simulates in some particulars so many of the diseases in which coma is the leading symptom, that an attempt to enter into the distinctions that mark it off from every analogous disorder would be interminable. In some instances, too, the task would be an exceedingly difficult one, unless considerations relating to the previous existence of albuminuria were admitted into the argument. Thus, for example, the diagnosis between uræmic poisoning and belladonna poisoning is so difficult, that, in a case where the history of the patient was unknown until the occurrence of coma, I for one, after having witnessed both classes of toxæmic disease, would scarcely be able to note a trustworthy sign on which to build a decided opinion. It is obvious, in fact, that the poisons producing the two classes of symptoms are well nigh identical in regard to their effects. Here, therefore, we must rest on the course which the symptoms take, and on such occurrences as the vomiting of suspicious matters, for a guide to diagnosis, rather than on any particular or exclusive symptom.

From epilepsy, uræmia is distinguished by the tendency to diarrhea, and, above all, by the suppression of urine. Distinctions may also be drawn at the time of the acute paroxysm; for the convulsion of uræmia is not of the same tonic character as in epilepsy; the asphyxia is not so marked, and the coma is more prolonged.

At one time in the history of medicine, uræmia constituted one of the varieties of coma called generically “apoplexy.” The unlearned as yet call uræmia apoplexy. From true cerebral apoplexy, however, uræmia is distinguishable by the facts that the skin is less hot, the stertor less marked, the blowing expiration less frequent, the convulsion more defined, determinate, and paroxysmal, and the suppression of urine more certain.

From poisoning by opium, uræmia is to be distinguished by the following particulars. In uræmia, the pupils are generally dilated; the patient may become quite sensible during the acute attack, and then profoundly relapse; the bowels are often free; the urine is scanty or absent; the breathing is free from stertor; and the convulsions are active. In opium poisoning the pupil is contracted; the patient remains unconscious, or, recovering his consciousness, remains conscious; the breathing is stertorous; the urine free; and the muscles paralytic rather than convulsed.

In fine, in establishing, in a doubtful case, a differential diagnosis between uræmic intoxication and its analogues, we must depend most on the previous history of the patient, and on a correct recollection of the absolute symptoms by which uræmia is manifested. The careful practitioner will then rarely be misled. If, however, a preceding history cannot be gleaned, if the symptoms be obscure, and if urine be not passed by the patient, it is an excellent point of practice to draw off by a catheter the urine that may be contained in the bladder, and test for albumen.

The presence of ammonia in the breath, looked on by many as a definitive indication of uræmia, is not, according to my mind, of any peculiar diagnostic value; inasmuch as ammonia is presented in the breath in the natural condition, and is expired in excess in many other diseased states than uræmia: thus, in the coma of typhus and of typhoid fevers, an excessive ammoniacal exhalation from the breath is a common symptom. Further, there are examples of acute uræmia where the ammoniacal exhalation, common to the patient antecedently to the attack, is suspended during the comatose state. Without going so far, therefore, as to say that the presence of ammonia in excess in the breath is not to be taken with other indications as a corroborative sign of uræmia, I should not let it rank as a positive symptom for differential purposes.

COMPLICATIONS OF URÆMIA. I have tried, so far, to give the diagnostic history of uræmia in its simple form; but it happens often that there are certain complications which present symptoms delusive in character, and calculated greatly to deceive him who has not his eye on the unities of diseased action. These complications consist generally of inflammatory or pseudo-inflammatory outbreaks, ac

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

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