dropsy and uremia are of value chiefly for the immediate prognosis and have only a limited significance in regard to ultimate. recovery. Their usefulness in prognosis is limited, because many cases of Bright's disease may be discovered and cured before either dropsy or uremia appear.

In prognosis, the urinary signs are the most important. These have been studied from the time of Bright and Bostock* with a slowly increasing understanding of their meaning. At first, it was all a question of albumin. To the general medical mind, in the years from 1827 to 1868, the presence of albumin in the urine. was the beginning and the end of Bright's disease, generally the end, for as Fothergill describes it," When albumin was discovered, the patient was condemned straight off, and if medical men found it in their own urine, they took to their beds and waited for the advent of the King of Terrors. Often they lived to laugh at their fears." Now we, who see patients live along for months and even years while passing two to four grammes of albumin daily, when others become uremic, and die while passing only one-half gramme; we, who see albuminuria where there is no Bright's disease and nephritis with no albuminuria, no longer regard the changing amounts of albumin as of great value in the ultimate prognosis. We are forced to search for a more reliable prognostic sign.

It was Christison, in 1839, who showed the importance of the specific gravity in prognosis. While studying cases of chronic interstitial nephritis, he noted that the specific gravity progressively declined to 1010 or 1006 or even lower. All observers can confirm this statement in regard to interstitial nephritis and in the late stages of any nephritis; but, in the early and curable stages of Bright's disease, the specific gravity may be normal, 1018 to 1025, and thus useless as a sign of returning health.

We come now to two factors which I regard as absolutely reliable in the prognosis of chronic Bright's disease. These are the amount of urea and the amount of phosphates excreted in twentyfour hours. I mean the amount of phosphates as demonstrated by accurate estimation of the phosphoric acid passed in twenty-four hours. Here a common error should be mentioned. It is well known that many urines of weak acidity deposit the earthy phos

1887.

*Reports of medical cases, Guy's Hosp. Reports, 1827. +Vaso-Renal Change versus Bright's Disease. New York and London,

On Granular Degeneration of the Kidnies, Edinburgh, 1839.

phates either spontaneously or when the urine is heated. This deposit is often referred to as an excess of phosphates. The conclusion is not warranted; in fact, as I have often demonstrated to physicians in my laboratory, such urines are frequently deficient in total phosphates. So, then, if it is understood that I refer only to the accurate chemical estimation of the phosphoric acid passed in twenty-four hours, I will make the statement that this amount of phosphates is the most delicate indication of the health of the kidney and of the state of the blood that underlies the development of chronic Bright's disease. In all cases of nephritis, in all cases of the Brightic diathesis, the amount of phosphates passed in twenty-four hours is much reduced, and not until recovery is complete do the phosphates in the urine increase to the normal amount. In Bright's disease, the excretion of urea is generally parallel with the excretion of the phosphates, but the phosphates generally constitute the more delicate sign; for urea can often be made to rise and fall by drugs and diet, while the phosphates are seldom influenced by anything but tissue recovery.

I have notes of a case of Bright's disease in which the patient was passing 22 grammes of urea, and 1.0 gramme of phosphoric acid. Under the influence of digitalis, the quantity of urine increased and the urea rose to 30 grammes, but the phosphoric acid remained sullenly at 1.0 gramme, and even declined to .75 gramme. That patient did not recover.

In another Brightic patient, with marked dropsy and uremic symptoms, apparently a more serious condition than in the former case, under the influence of iodine, the urea gradually rose from 22 to 30 grammes, and the phosphoric acid from 1.3 to 2.8 grammes. That patient recovered, not straight away, but after the vicissitudes attendant on every recovery from a chronic disease.

In a third patient, dropsy and uremia disappeared, and the albumin vanished under milk diet and rest in bed. The patient - felt perfectly well, but the urea remained down at 18 grammes, and the phosphoric acid at 1.5 for a long time. After many months under iodine, the urea slowly crept up to 28 grammes, and the phosphoric acid to 1.8, but perfect recovery is not yet established. In a fourth patient, with much dyspnoea, albumin is scanty and infrequent, and casts are few and hyaline. are few and hyaline. Between the dyspnoeic attacks, the patient feels well, but the persistence of the phosphoric acid below two grammes is a constant but silent warning of returning uremia, and the prophecy is fulfilled by an occasional return of the dyspnoea.

In a fifth patient, under the long-continued administration of iodine, the specific gravity rose from 1010 to 1018, the albumin disappeared, and dropsy and gastric symptoms vanished. The urea became normal in four weeks, and remained so. Casts persisted in the urine for six months, and not until casts were no longer demonstrable did the phosphoric acid rise to the normal and remain there.

I have made many interesting observations of the effects of different drugs on the elimination of urea and phosphates in the urine and can corroborate Fleischer's statment* that the inflamed kidney will usually refuse to excrete the normal amount of phosphates, even when these salts are administered freely as food. In other than nephritic cases, small doses of sodium phosphate given with the food, not only appear in the urine, but the presence of the phosphate increases the amount of urea excreted, bringing it speedily up to the normal if it has been deficient. Small material doses of iodine will raise both urea and phosphoric acid to the normal, and this drug is of great service in the cure of the anemia and the nephritis of Bright's disease. I have utilized the well-known therapeutic aphorism concerning croup, "When iodine fails, try bromine"; and, in one case, at least, have found that bromine acted nicely after the failure of iodine. Iodine and bromine are homoeopathic to the profound dyscrasia that is so frequently found in the Brightic case. I was first led to its use by the respiratory and heart symptoms, and found such a marked increase in the elimination of urinary solids that I made further studies of its action on urine formation. The symptomatology of iodine is paralleled by many a case of Bright's disease.

I have learned, then, in my work in urinalysis, to watch the amount of phosphoric acid excreted in twenty-four hours as the most important element in prognosis. In any case of chronic Bright's disease, when the urea and phosphates rise toward the normal, the patient is getting well; and, when, in the absence of medication, the phosphates are excreted in normal amount, the patient may be regarded as completely recovered. As a corollary, it may be stated that any therapeutic measure which raises the amount of urinary urea and phosphoric acid to the normal and keeps them there, is a curative measure in Bright's disease. We have strontium lactate and corrosive sublimate and fuchsin, all of which may reduce albumin, but we know, to our disappointment,

*Deutsche Archiv für Klinische Medicin, 1881, xxix., p. 129.

that the mere reduction of albumin does not indicate that the patient is getting well. A truer test of recovery will be found in the quantitative analysis of urea and phosphoric acid; and, of the two, the phosphoric acid is the more significant.

In conclusion, I wish to make acknowledgments to Dr. Clifford Mitchell, who first directed my attention to the prognostic importance of the phosphates, and to the venerable Dr. Howship Dickinson, who, in 1868,* published the first complete quantitative analysis of the urinary salts, and first pointed out the curious. deficiency of the phosphates in the urine of nephritis.

DISCUSSION.

We are greatly indebted to Dr. Laidlaw for his truly interesting, instructive and valuable paper. Valuable because it is the quintessence of his laboratory investigations, proven by his clinical observations. From a clinical ground, I fully agree with him in the usefulness of iodine and bromine in many of the chronic nephritis cases, and also in the importance of the fluctuations of the urinary solids for prognostic purposes, the urea and phosphates being to the prognosis what the albumin and casts are to the diagnosis. But there is one point which needs a little elucidation, or an error may be made as to the percentage of phosphates present in the urine of the adult male, who often has an associated catarrhal prostatitis, with over-activity of the prostate gland, and consequent over-production of prostatic fluid, which is composed largely of phosphates, and by its mixture with the urine, may cause a urine which is deficient in phosphates when emptied from the ureters into the bladder, to seemingly contain a normal amount of phosphates, or even give a laboratory evidence of a phosphaturia. To avoid this error, I would suggest that the urine for quantitative prognostic analysis be removed from the bladder by catheterization, to prevent the possible contamination by a prostatic fluid which may be discharged from the prostate, and mixed with the urine during micturition.-BUKK G. CARLETON, M.D., New York City.

*On the Pathology and Treatment of Albuminuria, London.

CLIMACTERIC INSANITY.*

By AMOS J. GIVENS, M.D.,

Stamford, Conn.

T is not my intention to analyze the different manifestations that are so frequently observed in women at the change of life, nor to enter into detail at all concerning the physiological conditions incident to ovarian involution, but rather to describe the psychosis known as Climacteric Insanity.

In every institution there is a large number of women patients who have become insane as the result of the changes which occur at this critical time of life.

In the New York State hospitals for insane, from Oct. 1, 1888, to Sept. 30, 1895, there were 19,237 patients admitted, of which 354 were cases of climacteric insanity. In six different English asylums, there are reported 5672 admissions of which nine per cent. were climacteric cases. Clouston reports 3154 cases of insanity, of which 196, or about six per cent., were of this class. Tilt reports 430 cases among 1320 admissions.

Of 200 patients admitted to the Royal Asylum at Edinburgh, 107 were cases of melancholia, and of fifty-seven cases analyzed by Dr. Conkling, of Ohio, forty-one cases were of melancholia, and five

acute mania.

It will therefore be observed that melancholia is the most common type of this disease, although epilepsy, hypochondriasis and hysterical mania and paranoia, are occasionally observed.

imme

With climacteric insanity one would naturally think that uterine disorders would be frequently present, that displacements, tumors or other abnormal pelvic conditions would be found, but this is seldom so. In many cases there does not even seem to be any diate relation between the disappearance of the menses and the mental disease. Sometimes the mental symptoms are not apparent for some months after the menstrual periods have stopped or the mental aberration may appear some time before the menses cease, or perhaps the mental condition may be aggravated once a month, and the physical indications of menstruation may not be present at

all.

Where there is a bad hereditary history, an inherited nervous temperament, or where the patient has been troubled with menor*Read before the Homeopathic Medical Society of the State of New York

at Syracuse, 1898.