pairs with leucocytes, and by a karyokinesis of local tissue cells-(we call this new tissue embryonic tissue); and this embryonic tissue terminates in cicatrical tissue which interferes with the nutrition to the distal -end of the appendix; therefore, an appendix once inflamed is more apt to become inflamed again.

I am of the opinion that careful blood examinations will aid us in -differentiating between functional conditions and typical inflammations, because it has been demonstrated to us that where we have an infection that nature can take care of, if we make an examination of the blood, we find a leucocytosis of the poly morpho nucleor neutrophiles. But when dealing with an infection that is virulent, nature sends out another force of cells known as eosinophilic leucocytes which possess greater bacteriolytic powers. I think in this way we are able to differentiate to a degree at least between functional disorders and typical cases of inflammation.

DR. SAMUEL: I enjoyed the paper extremely myself; I have nothing to add. I do not remember exactly the three propositions of Dr. Marshall, but one point in his paper makes me feel that it is possible for the appendix to be removed when it is not inflamed. As to the honesty of the surgeon no one can say. I believe that the most honest surgeon might make a mistake.

To the first proposition I can answer yes, that we do have functional troubles in the abdominal cavity. I believe that in the majority of cases appendicitis can be diagnosed from other abdominal lesions and extraabdominal lesions such as of the kidney. I believe the symptom-complex is so well marked clinically speaking that we can make a diagnosis. Gall stones may remain for years without giving any symptoms, but as soon as infection occurs then clinical symptoms begin. Appendicitis is not to be regarded in any sense as a medical lesion; it is a surgical lesion. The question hangs on the differential diagnosis.

I believe I have operated for appendicitis as many times as any surgeon here and have examined the appendix many times while operating for other conditions, and have found adhesions where the patient never gave any history of having had appendicitis. Unless the infection begins in the lumen of the appendix I do not believe that the condition would be recognized except where the contiguous tissues were broken down and we would have gangrene of the appendix there just as we have .by contact. The appendix being twisted does not mean that there is going to be trouble at all. It is when infection gets into the appendix that it gives trouble. I do not know what Dr. Marshall means by catarrhal inflammation. When infection occurs on a mucous surface

we speak of it as a catarrhal inflammation; when it occurs in the abdo; when it occurs in a joint we have an effusion, that is I believe that appendicitis is an infection; it is often

men...

all that it means.

the result of mechanical irritation from impacted fecal matter or an enterolith.

I agree in the main with the proposition of one of the previous speakers that, in strangulated hernia and intestinal obstruction, an operation should be done. I do not know that any one symptom could be given as a diagnostic means to differentiate either.

Dr. Allen has gone fully into the pathology of appendicitis. The third proposition would be hard to answer. In fact I am not quite clear as to what your meaning was in making that proposition.

DR. WILLMOTH: I would like to say a few words as the discussion has taken up the subject from the standpoint of the physician and the surgeon. It strikes me that all cases fall in one of three classes: First, where we get a history of the patient eating something as ice cream or some other substance. Second, where we are safe in saying that there is some inflammatory condition present, and then the third class where there is a question in the mind of the surgeon as to what the condition is. It strikes me that in this age and time there is but one thing to do. in this third class. With perfect asepsis we know that a two-inch incision in the belly only means putting the patient to bed for a few days, and in myself, if the practitioner said he did not know and the surgeon said he did not know, I should want an operation performed. If a functional trouble, no harm would be done, and if a surgical trouble, I would be benefited by it.

DR. MARSHALL (closing): If the society will bear with me I will read these three propositions again :

First-Do we have functional derangements simulating inflammatory lesions so closely that at times it is impossible to differentiate betweenthem?

Second-Without a reasonable assurance of inflammatory involvment should we advise abdominal section?

Third-Is there any one single condition sufficient to decide this subject?

I stated that an organ consisting of mucous membrane, covered by peritoneum, differed only as to degree in inflammation. If this organ became inflamed it would simply differ in degree. I restricted it to the appendix. Could we not have a functional trouble going on for a certain time break down with peritoneal involvment?

ALBUMINURIA:

ITS SIGNIFICANCE AND ITS DETECTION.

BY WILLIAM A. JENKINS, LOUISVILLE, KY.

FIRST-ITS SIGNIFICANCE.

INCE the classic observations of the celebrated English physician, Dr. Richard Bright, the significance of albumin in the urine has always been a pertinent and an important question, both from the standpoint of the physician and the physiologist. To present and to understand this subject thoroughly then, it will be necessary for us to take cognizance of all possible ways by means of which albumin may gain entrance into the urine; to ascertain the degree and extent to which albuminuria is pathologic; to discuss and decide whether the presence of albumin in the urine is ever without pathological significance. (The so-called physiological or functional albuminuria of the older writers.)

It will not

Physiologists tell us that the four proteid substances which are normally found in the blood, viz: Serum-albumin, serum-globulin, fibrin, and haemoglobin, are under certain conditions found in the urine. Of the above group, the chief interest of the general practitioner centers around serum-albumin. Serum-albumin then may be defined as a proteid substance, non-crystallizable, or colloid in character. under ordinary circumstances pass through an animal membrane. According then, to the modern physiological conception, certain alterations departures from the normal conditions are necessary before this substance can penetrate the basement membrane of the kidney tubules and make its appearance in the urine.

or

The first type of albuminuria to which I call attention is albuminuria due to structural change in the kidney, inflammatory, followed by degenerative changes with shedding of the specialized epithelium lining the uriniferous tubules. This is probably the type that would come into our minds first. And it is certain that, clinically speaking, it is the commonest and most serious form. We know that it is not possible in all cases to judge accurately the amount, character, or gravity of the changes taking place in the kidney by the amount of albumin in the

urine.

In the early inflammatory stage of acute Bright's disease (acute parenchymatous nephritis) the amount of albumin does furnish a fairly reliable estimate of the gravity of the pathologic changes going on. The same thing is true of the inflammatory stages of chronic parenchymatous nephritis. This is particularly true of that subdivision of this class

known as the large white kidney. On the other hand, the small mottled or cirrhotic kidney, which in a large majority of cases safely passes the acute inflammatory stage, and enters upon a stage, the changes of which resemble the kidney of chronic interstitial nephritis; in this last case,

the

amount of albumin present is not a trustworthy indication of the * Read before the Academy of Medicine, of Louisville, Feb. 1st, 1905.

amount of damage going on. Finally, in chronic interstitial nephritis, the patient may go for weeks at a time without albumin being present at all; and yet he may have badly damaged kidneys. His urine is increased in amount; of less specific gravity; light color; decrease of urea and all solids, and it may contain an occasional cast. Marked and grave cardio-vascular changes may be present, e. g., great hypertrophy of the left ventricle apexbeat looking downward and outward from the normal point, reduplication of the first sound (gallop rythm of Musser); second sound accentuated, general arteriosclerosis present, well marked uremic attacks possible at any time. Certainly in this class of cases the quantitative albumin test is practically nil.

Second.-Albuminuria due to changes in the constitution of the blood, said changes so altering the diffusibility of the albumin as to permit it to pass into the tubules and appear in the urine without any ascertainable kidney lesion, at least at first. If the condition be long continued, cell integrity is finally overcome. We notice this type of albuminuria in chronic anaemias. If the disorders of malnutrition, e. g., scurvy, struma, in the cachexias, in the so-called hydraemic states of enfeebled individuals, fevers and the infectious states with their micro-organisms. These micro-organisms in all probability act not only by producing changes in the composition of the blood, but also by affecting the integrity of the cells along the uriniferous tubules.

Semmola is a warm adherent of this explanation of albuminuria. He believes that even in Bright's disease the primary change is in the blood, and the organic kidney changes are secondary to, and dependent upon the blood changes.

Third. Albuminuria due to changes in blood pressure. These changes must, to meet the conditions of the problem, affect the bloodvessels of the kidney and also the general circulation. Generally speaking, they must accelerate the arterial current or retard the venous current. Instances of this type of albuminuria are furnished by prolonged fatigue, excessive muscular exercise, e. g., soldiers on forced march (Leube found it in sixteen per cent. of cases under above circumstances), prolonged application of cold to the surface, and nervous derangements which interfere with vascomotor control, e. g., after epileptiform seizures. And lastly, carefully conducted experiments on lower animals have conclusively proven that blood-pressure changes will produce albuminuria.

We now come to that part of our subject which has heretofore proven a serious stumbling block, viz: A type of transient or intermittent albuminuria. Pavy calls it the albuminuria of adolescence. Others speak of it as physiological or functional albuminuria. It may show without any apparent cause or after exercise, fatigue, or after the ingestion of large quantities of albumins. It is generally intermittent in character. The quantity is usually small. As a rule there is absence of casts, blood

and degenerative elements; slight or no change in specific gravity; no -evidence of cardiac or blood vascular changes. The causes of this type are practically those given above, only they are acting in milder degrees. And if the observer use due diligence and care, he is sure to find the cause. Consequently then, we affirm that all cases of renal albuminuria are tracable to three great causes, acting singly or jointly, viz: 1st, changes in the renal structures. 2nd, qualitative alterations in the blood. 3rd, alterations in blood-pressure. Finally we venture the assertion that whatever changes of blood-pressure or blood composition are present, they must act upon and alter in a certain degree (not always beyond repair) the integrity of the cells lining the uriniferous tubules, before it is possible for albumin to pass the barrier and gain entrance into the urine.

Thus we see that albuminuria is a symptom of varying clinical value. We are convinced, however, that is always of local or general pathological import; that the patient invariably presents some departure from the normal standard of perfect physical health. The gravity of the process must be determined by a careful investigation and weighing of the accompanying clinical symptoms and physical signs. The presence of albumin can only be accepted as positive evidence of kidney lesion when cellular elements and debris characteristic of the kidney are shown by the microscope.

Up to this point, we have considered only that form of albuminuria which has as its source the kidneys, or renal albuminuria. We now call attention to extra-renal albuminuria: Adventitious, false or accidental albuminuria. In this type of cases, the urine on leaving the kidneys is normal, but it meets with the products of inflammation in the lower urinary passages, e. g., ureters, bladder and urethra. The source of the albumin in these cases is to be determined by the following considerations: Ist, local examination of the urethra and bladder with the endoscope and cystoscope. 2nd, the clinical symptoms and physical signs; 3rd, a thorough urinalysis, both chemical and microscopical.

SECOND-ITS DETECTION.

First. The urine must be perfectly clear (if possible) before the tests are applied. If it is not clear, steps must be taken to render it clear. The procedure necessary will depend upon the nature of the substance producing the turbidity or cloudiness. Filtration through a good filter paper (you having previously placed a pledget of clean absorbent cotton in the bottom of the filter cone) will remove practically everything except excess of earthy amorphous phosphates, urates and micro-organisms, e. g., micrococcus ureae (an alkaline urine). If your specimen is clear after above method of filtration, you may proceed with your tests for albumin. If it is not clear, it is due to one or a combination of the above mentioned causes. If the turbidity is due to urates, the application of heat to a small quantity in a test-tube will immediately clear it