Applied Anatomy of the Lymphatics
F. P. Millard, D.O.
R. M. Ashley, D. O., Detroit, Mich., 1504 Broadway.

    “The Law of the Artery is Supreme * * * * * * *” -- Dr. A. T. Still

    Upon the principle that the blood is our curative agent, will this blood not give us the best indication of destruction going on within the body?  All the tissues of the body are bathed with blood and lymph, and it seems only natural to look to the blood for pathology within these tissues.

    If the blood contains an abnormal amount of one or more of its component parts, certainly some part of our anatomy is not functioning properly, and since we know where these various substances are formed, will not the blood analysis be a great aid to us in making our diagnosis?  A thorough blood examination seems to me to uphold the basic principles of Osteopathy.

    For years Blood Chemistry has been looked upon as belonging exclusively to experimental physiological chemistry, and not in the practical phase as is urine and gastric analysis.  Not until Folin came with his Blood Analyses as practical aids in diagnosis, did the professions consider them.  Since his introduction of the work, Benedict, Lewis, Denis, M. Myers, and Fine, deserve much credit in introducing reliable methods for clinical laboratory technique.

    With the more elaborate technique required for Blood Chemistry the question naturally arises, of what value is it over the ordinary urinalysis to the diagnostician?  Here I must hasten to add that it far surpasses the urinalysis; rather, I should say, that they should go hand in hand.  The Blood Chemical examination gives us an idea of the retained products of metabolism rather than the pathologically changed ingredients of a fluid, such as the search for albumin and sugar of the urine implies.  The blood tells just what the kidneys are doing and what they are not doing, and gives the exact status of the nitrogenous and cartohydrate equilibrium.

    The urine tells a great deal about the pathology of the kidney, but we find in conditions such as glycosuria, that a blood analysis is far better.  We may have a great retention of sugar in the blood before the kidney permits it to permeate through.  In such cases only a blood analysis would detect the hyperglycemia.  On the other hand, a pronounced glycosuria may arise with a relatively low grade hyperglycemia.  In renal diabetes we have no hyperglycemia, simply glycosuria.  Without chemical analysis of blood, how shall we differentiate between renal diabetes and diabetes mellitus?

    The threshold point, i.e., the time when the sugar increase in the blood results in a pouring out of sugar in the urine, is a matter of debate.  Many investigators have arrived at as many different threshold points, and it is for this reason tht the blood sugar determinations are so important.

    I have found an example of this in a patient showing 220mg of glucose per 100cc of blood, the normal blood sugar being from 85mg to 100cc of blood.  Up to that time the patient had shown no sugar in the urine.  Very often a diabetic will starve himself for a few days, and become sugar free so far as the urine is concerned, but upon examining the blood, it will be found that the sugar though reduced is far from normal.  The kidneys may be impermeable to sugar up to a very high point.  In such a case the blood sugar would be quite high, before it would appear in the urine.  Folin (Journal Biol. Chem. 1915, Vol. XXII, P. 327) states that he could demonstrate the presence of sugar in the human urine in nearly every case examined.  However, this is by delicate technique, but it shows that there is more often sugar in urine than ordinary negative findings record.

    It seems that authorities quite disagree as to what is normal and what pathological urine as far as sugar is concerned.  On the other hand there is little doubt as to what constitutes the normal blood sugar.  Aside from the liver, which Von Noorden aptly calls “a glycogen reservoir,” and the muscles which he calls the “glycogen depot” we find another source of sugar in the proteins.  The proteins are transformed into amino-acids, such as glycocoll alanine, aspartic, and glutamic acids, and these in turn go over into dextrose.  The most recent work bearing upon the derivation of glucose from protein is that of N. W. Janey (Janey, N. W., Arch. Int. Med. Nov 15, 1916, Vol. XVIII, No. 5, Page 584.)  Contrary to existing opinions it has been found that the animal and vegetable origin of proteins bears no relationship in their ability to produce glucose within the animal organism, this function being dependent almost entirely upon the sugar-yielding amino-acids constituting the various proteins.

    We must distinguish between renal diabetes and diabetes mellitus, although we have but little pathology up to the present time upon which to base our diagnosis.  Foster and Joslin, who have recently written books on diabetes mellitus, state that the diagnosis must rest upon the chemical blood analysis.  Since we have no increase in the blood-sugar, in renal diabetes, and since we do get a decided rise in blood-sugar in diabetes mellitus, we will have to base our diagnosis on these points.

    An instance of renal diabetes is the glycosuria of pregnancy.  We find no increase in the blood sugar, and following the puerperium the sugar in the urine disappears.  Yet should these women become pregnant again they would again show glycosuria.  However, in passing we might say that cases of renal diabetes are extremely rare, and in glycosuria a thorough and exhaustive study of the blood should be made before coming to any decision.

    The data necessary for the diagnosis of renal diabetes is quite definite:

    1.  A glycosuria running at a general level and not influenced materially by the carbohydrate intake.

    2.  A normal percentage of blood sugar in contrast to the increase of sugar urine.

    A routine examination of the blood, chemically, will some day be required in clinical examinations.  The methods of the day are both accurate and easy to perform to one qualified to do chemical work.

    In the so-called alimentary glycosuria (Jour, Am. Med. Assn. Sept. 2, 1916, Pg. 748) we have a condition within the patient in which his capacity for utilizing glucose is lowered.  In other words, the sugar shows in the urine by an over-indulgence of carbohydrate food.  This condition we do not find in a normally healthy individual, for the healthy liver can store up the excess of sugar as fast as it is produced from the digestion of starches.  The rate of entry of sugar into the blood taken per mouth, depends upon a wide range of physical, physiologic, and pathologic conditions, and it will not be possible to force sugar into the blood faster than it can be absorbed.  When a certain concentration is reached in the blood no quantity of sugar given per mouth, subcutaneously or intraperitoneally, can raise it higher.  Joslin states that one per cent of all individuals in the United States have diabetes.  This is apparently a rapid increase over several years, according to statistics.  However, it merely means that through the routine examination of urine today many more cases are discovered.

    Using the latest methods of Myers and Bailey (Jour. Bio. Chem. 1916, Vol. XXIV, pg. 147) we find that the amount of sugar is practically the same in blood, plasma, and cells.  It was thought by the earlier physiologists that blood sugar was in loose combination with other substances in the blood.  This idea of course is now obsolete, for it is known conclusively that the blood sugar is in a state of solution.

    In conclusion, let us not forget, in cases of diabetes, that even though the sugar disappears from the urine under treatment we may have a hyperglycemia.  The rigid diet should be kept up and blood analysis made at intervals until the blood-sugar is normal.  Also that a routine blood analysis may discover sugar excess in the blood, long before it shows in the urine, thus giving the physician an opportunity to arrest further progress of the diabetes.


    The spleen and the stomach from the earliest times have been supposed to possess some close inter-relationship.  Stukeley, in 1723, assigned to the spleen the function of stimulating gastric digestion.  His first argument in favor of this statement was the relative position of the two organs, and the intimate inter-communication by means of their common veins, arteries and nerves.  One is forced to ask himself why the principal blood vessels of the stomach arise from the splenic artery in its direct route to the spleen, and why vessels return to the stomach direct from the spleen, as does the vasa brevia.  It has been justly called “the heart to the stomach,” as it seems always to have a supply of blood ready to furnish the stomach when the call comes, and later, when the supply is not needed, the spleen can recall it.

    It has been suggested by Aristotle, Graccus, and Galen that the spleen assists in warning the stomach against the injection of cold foods, liquids, etc.  They based their claim upon the fact that animals that drank great quantities of water had large spleens, the size of the organ being regulated by the warmth needed to the stomach.  As early as 1868 Bacceli, at Rome, demonstrated a definite gastro-splenic circulation.  He found that the veins of the basa brevia form five or six rectilinear canals, with inter-communicating smaller vessels from the spleen to the cul-de-sac of the stomach, which are devoid of valves so that the blood can pass in either direction.  The largest number of gastric glands are situated in the cul-de-sac at the area supplied or drained by these veins.

    The splenic artery in the adult is the largest of the three branches of the coeliac axis, and is remarable for the extreme tortuosity of its course.  After crossing in front of the upper part of the left kidney, and on arriving near the spleen, it divides, some of the branches enter the hilum of that organ, some to the pancreas and others to the greater curvature of the stomach.  (Gray, 661.)

    Thus we see that our osteopathic friend, the spleen, has some function in connection with gastric digestion that still remains hazy in the minds of science.  We are told by some that it aids in the pepsin secretion to the stomach; others, that the removal of the spleen has no effect whatever upon gastric secretion.  Whatever scientific men may think, I am inclined to believe that the general osteopathic idea is in favor of the phagocytic action arising in this organ.

    At least, it is a great field for our osteopathic research laboratories to work on, and I am sure they can and will give us some information in the near future that will be helpful to us individually, and as a profession.

    Dr. M. A. Lane told us that within the spleen we have the antibodies to fight off disease.  He showed us how to stimulate them to action, but did he tell us why they acted thus?  Nevertheless, it is an osteopathic organ, left for osteopaths to discover, and make use of.  In Hodgkin’s disease we find splenic involvement with hyperplasia of the lymphatic glands, and general anemia.
Hodgkin’s Disease

    The blood counts in Hodgkin’s disease are unsatisfactory.  We do get an increase of eosinophiles, but it is believed that the extensive cutaneous lesions may influence these.  Levin makes an interesting explanation with regard to the increase of lymphocytes.  He believes that the terminal lymphcytosis is due to the crowding full of all the lymphoid tissues and an overflow of lymphocytes into the blood stream.  However, he admits tht the blood count is usually normal in Hodgkin’s disease.  He says nothing of the chemical analysis.  The lymphoid tissue is involved throughout the body generally, and the advised treatment is Roentgen Ray.  In fact, scientific writers have been telling us for some time that the X-Ray offers most in mediastinal complications.  It results in a replacement by connective tissue and a diminution in the size of the glands.

    My experience with blood chemistry in connection with Hodgkin’s disease has been limited through lack of such cases; however, an early diagnosis is the greatest advantage to both the patient and the doctor and I think through the blood we will arrive at our conclusions, aided by physical examination, and accomplish as much or more than by any other treatment.  Osteopathy most certainly will build up the Opsonic index of the blood, and this alone will be a great recommendation for it.

    The Laboratory Age will be the Golden Age in osteopathic diagnosis.  While we are as yet far from being an exact science, we have eliminated much of the inexactness and have located some of that which remains.  Such an age as that through which we are now passing forces many hardships upon those who must keep pace with advancements in all fields of science.  With new discoveries we find many opportunities for improving our technique.

    With the preponderance of laboratory study and facts, however, some will minimize the non-laboratory side of our diagnosis.  We cannot overestimate the significance of laboratory findings, but we must not underestimate the non-laboratory side.  Our patient, too, is a laboratory in which actions are followed by reactions, and if we can stimulate the proper chemical reaction within this human laboratory we have accomplished our purpose.  The time is near at hand when the practice of Osteopathy will be based on an understanding which comes from a combination of facts derived from both laboratory investigation, and acurate observation of the patient, interpreted by a doctor who KNOWS HIS PATIENT as he knows the disease, and who refuses to shirk one method in favor of another.


    In acidosis of the blood we do not mean an actual acid reaction, for this is impossible in life.  It is only in the very last stages of life practically “in extermis” that an acid condition occurs.  The neutrality of the blood depends upon the mixture of carbonic acid, carbonates and phosphates.  Carbon dioxid is thrown off by the lungs, and the urine in health is acid in reaction thus helping to maintain the alkalinity of the blood.  Any excess of acids in the blood seems to stimulate the respiratory centers in such a way that more CO2 is thrown off.  There is also a quick call on the ammonia, from the liver.  It is only when the ammonia is being used up that acidodis supervenes.  In the course of normal metabolism we know that the ammonia of the body is converted into urea and eliminated as such, but the supervening acidosis takes up some of this ammonia and keeps the blood alkaline.  Our analysis in such a case would show a reduction in the urea of the urine as well as a reduction of the ammonia of the blood.

    Respiration lowers the concentration of CO2 within the lungs, thus allowing the CO2 of greater concentration to pass from the blood through the alveoli to the plane of lower concentration, namely, the lungs and be removed.  It is merely an exchange of different concentrations going on continually, the greater displacing the lesser through osmotic pressure.  The sodium bicarbonate occurring in the plasma and the cells, as well as alkaline phosphates of sodium and potassium found in the red cells, are one of our first line defenses against acidosis.  Thus we have the alkaline compounds of blood; the kidneys excreting an acid urine form an alkaline blood; the production of ammonia and the proteins combining with the acids of the blood; all lines of defense aginst the supervening acidosis.

    In the prevention of acidosis the consumption of fats must be stopped, since the end product of fat metabolism, in the absence of proper carbohydrate balance, as in diabetes is oxybutyric acid and diacetic acid, instead of following the normal path and being transformed into butyric acid.  There is no further oxidation.  These organic acid derivatives of the fat and protein matter of the body furnish the basis for the so-called acetone bodies.  When these bodies appear in the urine we have an acetonuria or a ketonuria.  The acetone of the urine is excreted by the kidneys as diacetic acid which later changes to acetone by dropping the (COOH) radicle.

    CH3 -- CO -- CH3    - acetone.

    CH3 -- CO -- CH2 -- COOH    - diacetic acid.

    We find an acid condition of the blood very often in infancy and childhood, in severe diarrhoeas of infancy, and often alone, or rather, uncomplicated.  A difficulty of respiration usually bring such a condition to one’s mind.  Acidosis is such a fatal complication with infant diarrhoes that it is imperative that an early diagnosis be made.  Bicarbonate of soda should be administered to infants with severe diarrhoeas, as precautionary means, in quantities to keep the urine alkaline.  This is usually done intravenously or subcutaneously, intravenous being the method of choice since rapidity of action is always desired.

    The variation in acid base balance of the blood may be stated as follows: the blood bicarbonate may be high, low, or normal, and in each of these conditions the Ph (hydrogen ion concentration) may be high, low, or normal.  This would give nine theoretical conditions with, of course, only one being right, that is when the bicarbonate and the Ph are within normal limits.  At least six of these possibilities can be produced experimentally and some of them occur clinically.  I mention this to bring to your attention the wide range of the acid base balance within the body and the possibility of so many abnormal conditions.  Concerning the Ph of the body fluids, other than blood plasma, our knowledge is limited, but all indications are that all these fluids closely approximate the blood plasma in action, or rather reaction.  By the body fluids within the body proper we mean such fluids as the lymph, cerebrospinal fluid, transudates, exudates, but not secretions such as gastric juice or urine.

    The first effect of a CO2 retention on the blood is to increase the H2CO3 and the (H) of the blood.  Davies and Haldane observed, in 1920, that in breathing air containing up to 5% CO2, there was a doubling of the rate of ammonia and titratable acid excretion.  This increase in ammonia and titratable acid tends to raise the bicarbonate content of the whole body, and the blood plasma bicarbonate would normally rise with that of the other fluids.  The intercellular fluids, other than blood plasma, have, so far as studied, been found under normal conditions to approximate the blood plasma in bicarbonate and hydrogen concentration.  In the changes from normal the other fluids follow more or less promptly the blood plasma.  Van Slyke and Cullen (1917) found that when acid was injected into the circulation the fall of the blood bicarbonate was only about one-sixth as great as it would have been had the acid all remained in the blood; the other five-sixths of the acid must have gone into other body fluids and the tissues, or drawn alkali from them, thus neutralizing itself.  This gives us a good idea of the close relationship of the body fluids.

    In cardiac dyspnea it seems very likely that the predominant cause of the CO2 retention, resulting in an acidosis, lies in the lungs.  There is interference with the escape of the CO2 from the pulmonary circulation.  Possibilities arising from such a condition are: There may be portions of the lungs in which the circulation is more or less intact, but which contain no air, or there may be portions of the lung which are air containing, but immobile and not adequately ventilated by the respiration.  This latter is the view of Siebeck (Siebeck, R. Deutch. Arc. klin. Med., 1912, CVII, 253).  However, the present methods of measuring the lung volume has failed to answer these ideas, for we are capable of measuring only those portions of the lung which are air containing for respiratory purposes.  Whether or not there is a true CO2 retention in all cases of cardiac dyspnea, there is always interference with the limination of CO2 from the blood, and therefore, a compensated or potential acidosis, (John P. Peters, Jr. and David P. Barr, Jour. Bio. Chem. Vol. XIV, No. 3, Pg 537).

    In summarizing briefly, it is quite apparent that greater ventilation is necessary to effect the normal carbon dioxid elimination in cardiac dyspnea.  This lack of ventilation is largely brought about by the impairment of the pulmonary mechanism for the exchange of gases between the blood and the outside air.  In some cases the diminution of the circulation rate may be an additional factor in the production of carbon dioxid acidosis.  We also find in a certain number of cases a reduction of the available alkali of the blood.

    From well established facts regarding the process of acid excretion in man, it is absolutely incorrect to assume a depletion of the fixed alkali from an unusually acid urine.  The neutrality mechanism in man is remarkably extensible and is capable of neutralizing and conveying into the urine unusually large amounts of acid without disturbance of the acid-base equilibrium within the body.  The gross adjustment of an unusual acid production is an increase in production of ammonia.  The fine adjustment by means of which the reaction of the blood is maintained at the normal Ph is managed by excretion of phosphates in correct relative amounts.  Slight variations in acid production may be entirely compensated by variation in the relative amounts of the phosphates excreted, the ammonia factor remaining stationary.  The acidity of the urine on normal diets may for this reason vary widely, the hydrogen ion concentration being frequently as great as when acidosis is present.  It is therefore impossible to obtain from the hydrogen ion concentration of the urine a dependable indication of the presence of acidosis throughout the body.

    Acidosis may be recognized in various ways, by an increase in the ammonia co-efficient in the urine, decrease of carbon dioxid tension of alveolar air, the finding of abnormal acid in the blood and urine, increased alkali tolerance, and by diminished titratable alkalinity of the blood serum, by changes in the hemoglobin dissociation curve, and by actual determination of the hydrogen ion concentration of the blood.  A change in the hydrogen ion concentration of the blood indicates a failure of the protective mechanism, and the onset of acidosis.

    Let me call attention again to the ammonia factor of the body.  The body excretes nitrogen in the form of ammonia from the protein.  One gram of this ammonia will neutralize five times as much betaoxybutyric acid as one gram of sodium bicarbonate.  Howland (Bulletin Johns Hopkins Hospital, 1916, Vol. XXVII, Pg. 63) tells us that if it were not for these alkalies the body would produce an equivalent to several hundred cubic centimeters of concentrated hydrochloric acid in the course of a day.  This condition of the blood is impossible during life, and it throws a great responsibility upon the alkalies of the body for our daily existence.

    Whitney’s works on acidosis in relationship to the cause of death are important contributions to our literature.  Samples of blood were taken from the heart as soon as possible after life was extinct.  The Van Slyke method was used for determination.  Out of forty cases examined, dying of various diseases, all except three showed a more or less marked acidosis at the time of death.  In many of the cases this acidosis was so severe that it alone was sufficient to cause respiratory paralysis.  In other cases the acidosis was not sufficiently high to have been the immediate cause of death. Infection seemed to have a marked influence in causing acidosis.  However, a patient may have a marked infection and show no acidosis, providing his powers of elimination are active.  As causes of increased acid production in nephritis, the toxemia of the active parenchymatous form is itself operative; infection is an even more powerful factor.

Non-Protein Nitrogen on Blood (NPN)

    Non-protein nitrogen is a term applied to the nitrogen remaining after all the proteins have been precipitated out of the blood.  The N.P.N. substances in the blood are urea, uric acid, ammonia, creatin, creatinin, sugar, chlorides in the form of sodium chloride and cholesterol.  The normal N.P.N. is from 25-30 mg. per 200 cc blood.  Many figures have been given by various workers for its determinations, as well as upon the state of digestion at the time the blood is drawn for examination.  It has been clearly demonstrated that the N.P.N. of the blood rises and sinks like the tide, with reference to absorption from the digestive tract.  This rise is, of course, not a very great one, about 4 mg. per 100 cc of blood, but it is sufficient to necessitate a variable figure for the normal value of N.P.N.

    As the kidney is the great regulator of the composition of the blood, maintaining a practically constant level of the N.P.N., it is in disorder of this organ, especially, that most is to be expected from a study of the variations in non-protein nitrogen of the blood.  Numerous workers have shown that, in the majority of cases, the N.P.N. increases with an increasingly severe nephritis.  In cases tending toward uremia, or showing actual uremia, the values of N.P.N. are markedly increased, reaching in some cases as high as 350 mg. or over for 100 cc of blood.  This rarely is seen in conditions other than uremia, so that this factor assumes great importance in diagnosis.

    Further, the prognostic value of this examination is shown in that patients with high non-protein nitrogen do not, as a rule, survive for a very long period.  Another valuable point in the study of this factor, is that it furnishes a guide to the proper diet to be allowed nephritics, as cases of high retention require restriction of protein.  Also, surgical operations should be avoided when possible, in cases of high N.P.N.  Ordinarily, in nephritis, the less the phenosulphonephthalein output, the greater the amount of non-protein nitrogen in the blood.  However, in chronic passive congestion of the kidney, from cardiac insufficienty, the output of phenolsuphonephthalein my be markedly diminished without an increase of non-protein nitrogen being found in the blood.  Whenever the excretion of phenolsulphonephthalein is decreased, the amount of non-protein nitrogen in the blood should be ascertained, as this will indicate whether the fault lies with a damaged kidney, which is impermeable to the dye, or whether the fault lies with a damaged heart, which is inadequate to convey the blood to its point of exit from the system.

    One hour after phenolsulphonephthalein has been injected intermuscularly, fifty per cent should be recovered in the urine, and eighty-five per cent at the end of two hours.  When only forty per cent is passed at the end of two hours, (Elliot. Jour. A.M.A. June 5, 1915, Pg. 1885) considers that not only are the kidneys defective, but also there is retention of waste nitrogen in the blood, and blood tests should be made.  A single determination of non-protein nitrogen of the blood is not conclusive unless a very large amount is found.  But gradual increase from day to day or week to week shows danger of uremia, and uremia is not a poison caused by one poison, but many.

    Tillestone & Comfort (Arch. Int. Med. Nov. 1914, Pg 620) give the following with reference to the amounts of non-protein nitrogen found in the blood:

    30 mg per 100 cc of Blood . . . . .Normal
    30-35 mg per 100 cc Blood. . . . .Slight increase
    35-50 mg per 100 cc Blood. . . . .Considerable increase
    50-100 mg per 100 cc Blood. . . .Great increase with serious prognosis

    While uremic patients practically always show nitrogen retention, it is interesting to note that this is not always the case in puerperal eclampsia, unless there has been a long previous nephritis.  Fehling says that 5% of pregnant cases, having an old nephritis, develop eclampsia.  In other words, puerperal eclampsia may not be a true uremia, as other retained intoxicants may cause convulsions besides those retained by kidney insufficiency.

    Gout and rheumatism are diseases on which the differential diagnosis, by blood chemistry, has thrown some light.  In gout we find a chronic disorder of metabolism, in which there is an undue accumulation of uric acid in the blood, whereas in rheumatism there is no such accumulation, the figure remaining around 1.3 mgs per 100 cc of blood.  Folin and Denis (Jour. Bio. Chem., 1913, Vol. XIV, p 82) showed that the amount of uric acid in the blood, under normal conditions, varied from 0.7-3.7 mg per 100 cc of blood.  However, we always find a hyperuricemia in gout and this condition is long continued while in other joint disorders the hyperuricemia is transitory.  In rheumatism we find a temporary increase in uric acid but it will not remain at this level or increase as it does in gout.  The obvious procedure, therefore, in suspected gout, is to follow one examination with others at interrupted intervals.  The fact that we get a diminution in the uric acid in the urine does not necessarily mean that we have a hyperuricemia.  For a positive diagnosis we must look to the blood.

    A retention of uric acid in the blood may be earlier evidence of renal impairment of an interstitial type than the classical tests of albuminuria and cylindruria.  In discussing the blood figure of chronic nephritis, interstitial and parenchymatous in variety, it will be necessary to refer to some of the other facts of the nitrogenous metabolism.

    In digestion, protein matter is broken down into amino-acids, some of which are retained and others are transformed into ammonia and eliminated.  The greater part of the nitrogen in the body comes from the food, exogenous, and its final elimination takes place in the form of urea by way of the kidneys.

    The source of creatinin is almost entirely endogenous.  Victor Myers (Jour. Of Amer. Med. Science, May 1919, P 674) gave a very complete article on creatinin determination.  The values he obtained are:

    1-2 mg per 100 cc blood. . . . . . . . . normal
    3 mg per 100 cc blood . . . . . . . . . . rather serious
    4 mg per 100 cc blood . . . . . . . . . . very serious
    5 mg per 100 cc blood . . . . . . . . . . fatal

    Theoretically, the increase in creatinin of the blood should be a better index of the decrease in the permeability of the kidney than the increase in urea, for the reason that the source of creatinin is entirely endogenous and very constant.  Urea, on the other hand, is largely exogenous, under normal conditions, and its formation subject to greater fluctuations.  For this reason it is evident that a lowered nitrogen intake may reduce the work of the kidney in eliminating urea but it will not affect the creatinin to any great extent.  It is only logical, therefore, for us to look to creatinin to furnish a satisfactory criterion as to the deficiency of the excretory power of the kidney and as a most reliable means of following the terminal course of the disease.  The prognostic value of 5 mg of creatinin, or more, in the blood is very definite.  It warns of the fatal termination of the disease invariably.

    By the examination of the urine alone, a great many conditions go unnoticed and a favorable prognosis is given when the patient’s chances for recovery may be very small.

    The normal amounts of the Non-Protein-Nitrogen constituents of the blood are:
    N.P.N. . . . . . . . . . . . . . . . . . . . .  25-30 mgs. per 100 cc.  blood
    Urea Nitrogen . . . . . . . . . . . . . . .  12-15 mgs. per 100 cc. blood
    Uric Acid . . . . . . . . . . . . . . . . . .   0.7-3.7 mgs. per 100 cc. blood
    Creatinin . . . . . . . . . . . . . . . . . . .  1-2.5 mgs. per 100 cc. blood
    Creatin . . . . . . . . . . . . . . . . . . . .   5-10 mgs. per 100 cc blood
    Sugar . . . . . . . . . . . . . . . . . . . . . .  0.08-0.12%
    Chloride as Sodium Chloride . . . .   0.65%
    Cholesterol . . . . . . . . . . . . . . . . .    0.15%