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THE CHICAGO CLINIC

VOL. XII-No. 8.

TWELFTH YEAR.

The Clinical Significance of Variations in the Amount of Urinary Solids.

By J. H. SALISBURY, A.M., M.D. Professor of Medicine in Chicago Clinical School.

The importance of the renal excretion is recognized by all physicians, and the detection and determination of its various components have been carried to a high degree of perfection. In practice, however, the difficulties of making exact quantitative analyses are such as to deter most physicians from attempting it. The estimation of the amount of total solids is, on the other hand, both simple and easy, and would seem to offer a means of estimating the aggregate of the renal functions, which is more useful than single determinations, because it includes the excretion of substances which we have no exact means of estimating by themselves.

The determination of the amount of solids is very simple. The methods which require much time, and aim at great accuracy, are not regarded as at all preferable to the simple plan of calculating the total solids from the specific gravity. The last two figures of the specific gravity, multiplied by 2.2 or 2.33, give the proportion of solids per 1,000. This, multiplied by the numbers of liters passed in twenty-four hours, will give the number of grams of solids excreted by the kidneys. For those who still use the fluid ounce and grain, the very simple formula that the number of grains per ounce is equal to the last two figures of the specific gravity, multiplied by 1.1, is sufficiently accurate.

In such estimates the necessity of a normal standard is paramount. Text-books of physiology give the average amount of solids, but the quantity is subject to such wide variations that unless the quantity falls below a very low minimum it is impossible to say that the renal excretion is deficient.

The variations in urinary solids correspond to several factors which must be

AUGUST, 1899.

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taken into consideration before take the amount passed as a valuable indication in the diagnosis of disease. The factors usually considered are age, sex and body weight. The usual statement with reference to age is that the amount excreted in infancy and childhood is absolutely smaller, but relatively greater, in proportion to body weight than in adult life. In old age it is absolutely and relatively less. The excretion of urea is normally about one-half of the total solids. Harley gives the following as the excretion of urea in children aged eighteen months, as compared with that of adults aged twenty-seven years:

Boy.. 18 mos. Girl.. 18 mos. Man. 27 yrs. Woman. 27 yrs.

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93-139 grains 5.4

387.5-542.5 grains 3.8 310-465 grains 3.I

If we multiply these figures by 2 for the proportion per pound of total solids, we have in infancy 12.4 grains per pound as compared with 7.6 in the adult.

According to Camerer the daily excretion of urea per kilo of body weight in children from two to eleven years amounts to 1.12-0.8-0.64 grams. In an eleven-year-old child it is not essentially higher than in an adult.

Males excrete somewhat more than females. In relation to body weight a ratio of 1.1 per 1,000, or 7.7 grains per pound, is given. This must be modified by the age of the individual. Ralfe adopts the following as the normal standard of urea in proportion to body weight:

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The amount of fat should be taken into consideration, for there is no reason to suppose that adipose tissue takes as active a part in nitrogenous metabolism as muscular and glandular tissue. Such a table as the above, however, gives only the average and is subject to wide variations. Thus, in five cases which I took from healthy individuals, it varied from 5 grains per pound to 10.5 grains. The variations are also great in individual cases. Thus in my own case, when in good health, the ratio varied from 5.9 grains to 7.6 grains a variation of over 22 per cent. With a considerable reduction of diet the ratio fell to 3 grains per pound. These extreme variations make the ratio of 1.1 per 1,000 very unsatisfactory for determining the normal amount of excretion. As urea forms about half the total solids of the urine we may assume that the total solids will vary with variations in the amount of urea. Numerous experiments show that the amount of urea varies directly in proportion to the amount of proteids contained in the food. According to Voit, the amount of urea is equal to the amount of urea which can be formed from the nitrogen which the system receives in the form of nourishment, and Bouchard has drawn the conclusion that 100 grams of meat increases the excretion of urea by six grains.

Lehman gives the solids in urine under various diets as follows:

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On the first day I excreted 648 grains of solids.

On the second day I excreted 858 grains of solids.

On the third day I excreted 825 grains of solids.

On the fourth day I excreted 729 grains of solids. (On this day I took only 60 ounces of milk.)

On the fifth day, ordinary diet, 750 grains of solids.

I next experimented with one quart of milk. I lived on this one day without measurement of the urine, and the next day, continuing the same diet, I passed 520 grains of solids.

The next day I increased my diet to two quarts of milk, one pound of crackers, onehalf pound of rice and one pound of meat.

The next day I consumed two pounds of meat and one-half pound of crackers, and continued the same diet for the third day. Under this increased diet the solids were:

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It is evident that increase or diminution of the solids of the urine can only be taken as evidence of disease when we take into account the various factors which influence the excretion in a normal state. Not only must the quality, but also the quantity, of food be considered. If we determine the urinary solids in a person taking little food we will almost certainly find them below the normal, as expressed by the average proportion in relation to body weight. But the diminution is only evidence of lack of appetite, and not of faulty metabolism or retained excreta. The expressions animal and vegetable diet are certainly very loose, since they do not take into consideration the amount of food consumed. If we can put the patient upon a fixed diet we may determine from the amount of food taken

whether the excretion of solids corresponds to the amount normally produced from the same amount of food.

The food should be varied enough so that the appetite may continue as nearly normal as possible. The amount of food should be sufficient for nourishment, because if this is not the case the albuminous compounds of the tissues are likely to be broken up and the urea derived from these will increase the solids so that the amount derived from the food cannot be properly estimated.

The following remarks of Salkowski in reference to the clinical estimation of urea seem equally applicable to the determination of the total solids:

"For the estimation of pathological states the knowledge of the normal amount of urea is only of secondary importance. It is seldom that a quantitative estimation is made with the view of learning how much nourishment the patient absorbs. Such a conclusion can only be drawn in diseases unaccompanied by fever or wasting, in which nitrogenous equilibrium can be assumed as in healthy individuals. In other

cases it would be erroneous, because the urea in disease arises not only from the food, but also from the tissues of the body. The morbid organism does not find itself in nitrogenous equilibrium, but gives out urea continually from its own tissue and would continue so to do with ever so abundant ingestion of albumen, if such a thing were possible.

"What we seek to learn from the investigation of the excretion of urea in disease is how much albumen or muscle the patient's body itself loses. To obtain an estimate of this we must subtract from the amount of urea found the amount which corresponds to the nitrogen in the food ingested.'

A few words with regard to the collection and measurement of the urine may not be out of place. The specific gravity and quantity of the mixed urine for twenty-four hours should in all cases be taken. It seems to me best to begin the collection of the urine in the morning, rejecting the urine first passed in order that the influence of food ingested the previous day shall be as far as possible eliminated, and continue until the following morning, including the urine passed on rising. Since the solids vary less than urea, it is evident that if only one can be determined the estimation of the

quantity of solids will yield more valuable

conclusions than that of urea alone.

Pathologically, an increase of urinary solids above that due to the food taken and not due to sugar must mean an abnormally increased metabolism of the albuminous constituents of the tissues with a corresponding increase in urea phosphates, sulphates, etc. This occurs in fevers and other wasting diseases in which the albuminous material of the tissues are broken down, probably to furnish material with which to keep up the

fever.

It is to the diminution in urea and in urinary solids, below the amount proportional to the food, that the greatest interest attaches. This occurs in structural disease of the kidneys in consequence of their failing function. In cases where there is no organic disease such a diminution must be due either to insufficient functional activity of the kidneys or to imperfect digestion, by which the materials of the food are not absorbed. Another condition must be mentioned, in which we should expect that the urinary solids would not correspond to the food consumed, viz., in growing children

and in adults convalescing from fevers or other wasting diseases.

It is generally accepted that there are various pathological states due to deficient elimination by the kidneys, and it has been assumed that the functional activity of the kidneys can be measured by the solids excreted. It is to be feared that many of the observations that have been made with reference to this matter are inexact, because the amount of the food has not been taken into consideration.

Further investigation of the relation of the amount of urinary solids to pathological states would be very desirable. As. however, the estimation of the amount of solids can give us no exact information as to the relative proportions of the various constituents, too much reliance ought not to be placed upon it.

A Plea for Radical Treatment of Hay Fever.

By CHAS. E. CLARK, M.D., Kansas City, Mo. Professor of Clinical Laryngology, Kansas City Medical College.

My only apology in offering a paper upon such an important subject without attempting to offer any new ideas is that, in judging of the prognosis frequently offered to patients by the profession, there must yet be much misapprehension regarding the true status of this disease.

Without entering into historical details, I wish to recall to your minds that the first lucid account of the disease was given by John Bostock in 1819, who described "a periódical affection of the eyes and chest," from which he was himself a sufferer. In 1828 he wrote another paper upon the subject, calling the affection "summer catarrh."

In 1862 Phoebus, of Giessen, Germany, published a paper reciting one case; following which he directed circular letters of inquiry to the medical profession of the world, containing a list of questions touching every phase of the disease. As a result of the information thus acquired considerable progress was made, and the pollen theory of etiology was evolved.

In 1875 Blackley of Manchester contributed the most scientific paper yet written upon the subject, in which he corroborated the pollen theory of etiology and fur

ther asserted that the severity of the disease bore a direct relation to the amount of pollen present in the atmosphere. In 1876 Beard of New York published information which he had gathered in the treatment of a considerable number of cases, and by correspondence with over two hundred hay fever sufferers. In his statistics he also confirmed the pollen theory, and elicited the additional information that a very large per cent of the cases so affected were of a nervous temperament, and that nerve tonics had an important place in treatment. So fixed had Blackley and his followrs become in their belief in the pollen theory that this intrusion of a new etiological factor was met with the observation that its author was a member of two neurological societies, and hence his views must be received with a due degree of caution.

Illustrative of the one idea zeal with which the pollen advocates adhere to their theory and seek to logically explain its action might be mentioned the ludicrous theory advanced by Mr. Wright Wilson, viz.: "That the pollen granule, being only onetenth the size of the red blood corpuscles, readily passes through the vessel wall and acts as a foreign body in the blood current." Dr. J. N. McKenzie comments on this theory as follows:

"Through ciliated epithelium, basement membrane, and vessel wall, the dreadful vitalized ameboid pest of the summer months is launched into the general circulation. Does it feast on the nuclei of the white corpuscles as its legitimate prey, or does it seek its pabulum in the more organized and nutritious protoplasm of their redder and more numerous companions? Is it carried into the more remote organs on the crest of the serous wave, or is it whirled through the circulation on the back of the red blood cell? Is the dyspnea of this disorder due to pollen emboli in the lungs or to granular invasion of the respiratory center? Are we at last to realize the poetic conception of

"Quick effluvia darting through the brain, Die of a rose in aromatic pain?"

In 1881 my friend and former associate, Dr. William H. Daly of Pittsburg, Pa., read a paper before the American Laryn

ological Association in which he showed by the recital of a series of cases that in at least a very large proportion of the

cases affected with hay fever there is local disease of the nose or naso-pharynx, varying from a simple hyperesthesia to pronounced structural changes, such as hypertrophic rhinitis, polypi, etc., without which the exciting, or, as he designates it, "extrinsic" cause, pollen, is innocuous; and the cure of the affection may be accomplished through the removal of the local, or "intrinsic" cause.

While the observations of Beard directing attention and treatment to the nervous system, thereby enabling constitutional treatment to mitigate to some extent the severity of the disease in certain individuals, and while the previous observations of the pollen theory suggested immunity from the disease by the removal from their customary place of residence during certain periods of the year, yet to Daly belongs the credit of promulgating the theory of a third etiological factor and outlining a treatment both practical and efficient.

Much has been written since the acceptance of the theory of a local cause, touching on the exact nature of such disturbance, and while it is undoubtedly a fact that almost any portion of the nasal mucous membrane may become the site of sensitive areas, yet it is also probably true, as observed by J. N. McKenzie, "that the area most sensitive to reflex producing impressions is represented by the portion of the mucous membrane which covers the turbinated corpora cavernosa, the most sensitive spots being in the mucous membrane covering the posterior extremity of the inferior turbinated body, and the septum immediately opposite, a zone corresponding to the distribution of the spheno-palatine branches of the superior maxillary nerve, which, derived through the spheno-palatine ganglion, probably contains the vaso-motor fibers which govern the erection of the turbinated tissue." In short, to have a paroxysm of hay fever there must be present three etiological factors as suggested by Sir Andrew Clark in 1887:

1. A neurotic habit.

2. An intra-nasal pathological condition.

3. An external exciting cause.

The latter expression (an external exciting cause) is preferred rather than "thc pollen," as this classification includes pollen as well as many other substances which are now recognized as being capable of

exciting a paroxysm of hay fever. The absence of any one of these factors breaks the chain requisite for the production of the paroxysm. The problem which confronts us, then, in the treatment of this affection is, which factor can be the most readily overcome?

All physicians, whether general practitioners or specialists, realize what it is to overcome a decided neurotic tendency in the treatment of any disease wherein it furnishes a complication.

To remove at all times the exciting cause is likewise difficult, and is generally effected by removing the patient from the cause, rather than the cause from the patient. Social and business duties, as well as circumstances in life, frequently render this extremely difficult, if not impossible. All things considered, then, the most practical method of relief, and the one whose beneficent results are within the reach of the most humble walks of life, is the removal of the local pathological conditions. Treatment to this end may be commenced either during the interval between attacks or during the height of the paroxysm, the result in either instance being almost invariably satisfactory and frequently almost magical. Local treatment may be either palliative or radical. Palliative treatment consists in the use of various sedative sprays, powders or ointments, the chief ingredients of which are generally cocaine, morphine, belladonna, etc., and at most can do no more than furnish temporary relief, and always with the possibility of establishing a drug habit much more terrible than the disease. Radical treatment consists in the complete removal of all abnormal conditions found in the nose or naso-pharynx by the use of such methods as may be required for each individual case. Polypi should be removed with the cold wire snare, and the pedicle thoroughly destroyed with the galvano-cautery. Marked vaso-paresis with distension of the turbinated corpora cavernosa should be incised with a fine cautery electrode from one extermity to the other and down to the bone, using care to destroy as little of the mucous surface as the requirements of the case will permit.

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