26 "U. d. wiederkehrende Fieber," Arch. f. path. Anat. u. klin. Med., Bd. xlvii. p. 170.

Attention has already been called to the variations presented in the amounts of urea, but more extended observations are required to show the precise relations of these variations to the graver nervous phenomena. It will be found, we venture to opine, that, while in one group of relapsing-fever cases of grave type, cerebral symptoms are dependent upon the retention and accumulation in the system of urea and other effete nitrogenous products, owing to interference with renal activity from pre-existing organic disease of the kidneys or from an exceptional degree of congestion of those organs, there are other groups where similar typhoid cerebral symptoms are more directly dependent upon the specific toxæmia, upon the hyperpyrexia, upon exhaustion of the nerve-centres by intense peripheral irritation, or upon congestion or other morbid conditions of the nerve-centres themselves.

In all cases where cerebral symptoms manifest themselves in relapsing fever the daily examination of the urine—which here, as in other zymotic diseases, is a duty in all cases—becomes of extreme importance. Three conditions should be borne in mind in such examinations. In the first place, the attack of fever may have occurred in one already the subject of organic kidney disease, and, considering the classes from which the majority of the cases of relapsing fever are drawn, this possibility cannot be of rare occurrence. Out of eighteen post-mortem examinations in which the kidneys were studied with especial care we found positive evidence of pre-existing organic disease four times. In these cases the albuminuria was marked and persistent, though tube-casts were rarely found, and severe cerebral symptoms of typhoid type were prominently present. In another highly interesting case the patient, who had amyloid disease of the liver, spleen, and kidneys, contracted severe relapsing fever; he had increased albuminuria during both febrile stages, suppurative parotitis, but no grave cerebral symptoms, and apparently recovered. After an apyretic period of six weeks, during which the symptoms of the amyloid visceral disease persisted, a sudden and rapidly fatal pyrexia occurred. Unfortunately, the existence of spirillar infection of the blood was not known at the time.

In the second place, the attack of fever may become complicated with acute nephritis from special localization of the poison, as in Obermeier's cases, or from vulnerability of the kidneys. In such cases careful study of the urine should indicate the event, and the prognosis, though grave, is not so hopeless as in the first instance. An interesting example of this occurred under our observation, where the patient, who had apparently an ordinary attack, was seized with acute catarrhal nephritis, with temporary uræmia, during the relapse, but after a dangerous illness recovered without any organic renal disease as a sequel.

In the third place, may be found the more usual and more readily-determined condition of slight and transient albuminuria (with variations in urea excretion) which has already been discussed, and which has no serious prognostic significance.

The following very interesting case deserves special mention: The patient, a man aged thirty-six, was admitted on the fifteenth day of an attack of acute catarrhal nephritis, with slight ascites, marked oedema of the feet and legs, and highly albuminous urine. In the course of ten days the oedema and albuminuria were much diminished, when on the thirteenth day after admission he was attacked with relapsing fever, the ward in which he lay containing a number of persons ill with that disease. The initial paroxysm was severe, but without any grave cerebral symptoms; the urine grew scanty, dark, and bloody, and the oedema increased and invaded the pelvis. Crisis occurred on the fifth day, temperature falling 9°, sweating copious, urine 473 ccm. in twenty-four hours, color of porter, highly albuminous, and depositing blood, renal epithelium, hyaline, granular and epithelial casts, all stained reddish. Two days later, urine 1600 ccm., light colored, with only a small amount of albumen.

A slight and brief relapse (101° for two days) occurred after an interval of four days; a second imperfect relapse (100.5° for three days) after a further interval of six days; and finally, after a further interval of only two days, a violent relapse (temperature rising rapidly to 106°) with crisis (fall of 8° in twelve hours) at close of fifth day. The oedema gradually diminished from the time of the first crisis, did not increase in the relapses, and disappeared completely and finally about ten days after the last relapse. The urine was very free after the first paroxysm, averaging from 2000 to 2300 ccm. During the subsequent febrile periods it did not decrease, and indeed on the second day of the last relapse, with the temperature at 105°, the amount in twenty-four hours was 3200 ccm. Four days subsequently, during crisis, the amount was only 350 ccm.

The albumen disappeared entirely from the urine in two weeks from the close of the last relapse; there had then been no tube-casts for some days, and the patient was discharged entirely well a short time afterward. The treatment consisted of hot vapor-baths, repeated dry cupping over the kidneys, infusion of digitalis with acetate of potash during pyrexia, and Basham's iron mixture in the intermissions. It seemed that the occurrence of the relapsing fever interfered wonderfully little with the recovery from nephritis.

Hematuria is a comparatively rare and very grave complication. It may occur as an additional evidence of the dyscrasia of the blood in connection with hemorrhages from other surfaces, or as in the case we have before referred to or in that reported by Murchison,27 it results from intense engorgement of the kidneys. In Murchison's case hematuria, with much albumen and tube-casts, occurred in both paroxysms without any uræmic or typhoid symptoms, and was followed by satisfactory recovery.

27 Op. cit., p. 370.