Surgical diagnosis

Front matter

SURGICAL DIAGNOSIS

BY

EDWAED MAKTIN, M.D.

Preface

The simplicity and safety of surgical intervention are, as a rule, proportionate to timeliness in diagnosis. This, in turn, is usually dependent upon the judgment of the general practitioner, who is, as a rule, the first to see the patient and should, therefore, be qualified to determine at the earliest moment when surgical treatment is required. The practitioner cannot be expected, however, to acquire such a knowledge of the probabilities deducible from general symptoms and of the variations from type as is necessary to establish the final diagnosis. This can be gained only by a conscious or subconscious grouping of the clinical features of many similar cases.

The proof of the advantage of early diagnosis is afforded by the lessened mortality which is found to result from such diagnosis in every department of modern operative surgery. This is in part due to more perfected technique and more rational after treatment, but mainly to the simplicity of earlier operation. To this element is also due, almost entirely, the larger percentage of radical cures.

Partly from custom^ but mainly because of examination requirements, it is the habit of teaching institutions to impress upon the minds of their students the symptom-complex of the completely developed disease. Such clear mental pictures are highly desirable from many points of view, but since action is often deferred until the picture is complete, they may work to the detriment of the patient. It too often happens that when the disease is so fully developed that the diagnosis can be made beyond doubt, the time for surgical intervention is past. If, for instance, a cancer of the breast is not recognized as possibly or probably such until the dense induration, skin adhesion, nodular lymphatic glands, and cachexia prove its nature, the only possible result accruing to the patient is the knowledge that she will have but little time to live and that she will suffer much. There are many affections, the neoplasms constituting the most conspicuous examples among these, in which an assured diagnosis other than by operative means is impossible at the time it is likely to be serviceable. It seems reasonable to hope that death or crippling or disfiguring deformity from surface or orificial malignant neoplasm may become even more rare than are now those monstrous growths which illustrate the text-books and frequent the clinics. This end will have been attained in part when it becomes generally recognized that the diagnosis of malignancy should be formulated by wide removal and microscopic examination of any persistent outgrowth, infiltration, or ulceration which is not certainly benign. The vi PREFACE

gross deformity of Pott's disease, the crippling ankylosis of coxalgia, the life-long pain and disability following bone and joint traumata too often represent sequelae which could have been averted but for a too faithful adherence to the rule of formulating the diagnosis and directing the treatment only upon the basis of a complete symptomatology.

It is, therefore, in the interest of early diagnosis in its relation to helpful and curative surgery that this book is written. Consequently, stress is laid mainly upon symptoms of major and deciding moment; or, when such are absent, upon the operative and laboratory means by which a conjecture may be transformed into a probability or a certainty.

In the section devoted to Laboratory Diagnosis, Dr. Warfield T. Longcope has presented, with a moderation highly creditable, a statement of the help that may be given the surgeon by those who work with the microscope, culture media, and test-tube.

Dr. Henry K. Pancoast has shown in his chapter on the X-rays in Surgical Diagnosis both the value and the limitations of a method which, because of its efficiency, is now as essential to the surgeon in his examination of patients as is the anesthetic in his operations upon them. Dr. Pancoast's outline drawings of negatives in his possession constitute the most complete series of x-raj fracture pictures yet published.

In the chapter devoted to Gynecological Diagnosis, Dr. Brooke M. Anspach has admirably described in detail the methods found most serviceable in his hospital and private practice.

Dr. Theodore H. Weisenburg has based his chapter on the Diagnosis of Nervous Affections upon a wide experience with those diseases of the nervous system in which surgical intervention must be considered.

Such merit and accuracy of statement as may be found in the section devoted to the Eye are due to the criticisms and suggestions of Dr. George E. de Schweinitz.

E. M.

Philadelphia, 1909.

Index 739

SURGICAL DIAGNOSIS

Chapter I. Laboratory Diagnosis

By WARFIELD T. LONGCOPE, M.D.

EXAMINATION OF THE BLOOD.

At the present time our knowledge of the chemistry of the blood and blood serum is not sufficiently advanced to offer much aid in the practical study of a patient. In certain conditions a spectroscopic examination of the blood may reveal the presence of an abnormal substance, such as carbon monoxide hemoglobin. Until more knowledge has been accumulated, too, regarding the variations in the reactions of the blood, estimations of the alkalinity cannot prove of much value.

On the other hand, a determination of the coagulation time of the blood may be of great importance. To a surgeon who is about to operate, a knowledge of the fact that the formation of a blood clot is delayed twenty or thirty minutes may obviate an unpleasant experience. To estimate the coagulation time of the blood, Wright's tubes may be used, but the new instrument devised by Boggs is much simpler in application and probably more accurate. The most common condition in which the time of coagulation shows the greatest diminution is jaundice, especially when incident to chronic pancreatitis; in severe cases the blood may remain fluid after withdrawal for fifteen to twenty-five minutes. It must be remembered that in hemophilia, a disease which offers great dangers to the surgeon, the coagulation time of the blood may not be decreased.

The estimation of the hemoglobin, a procedure which may be done with the greatest ease, will decide quickly whether or not the patient has an anemia, and combined with an enumeration of the red blood corpuscles may give much information. In many of the acute infections, in chronic suppurative conditions, in cachexias due to malignant growths, in cirrhosis of the liver, and in Bright's disease, there is always more or less secondary anemia, with a greater loss proportionately in the amount of hemoglobin than in the numbers of red blood cells. Immediately after an acute hemorrhage the blood picture may be very nearly normal, for the absorption of fluid from the blood is so great that the loss of the formed elements is not obvious. Later, a loss in hemoglobin, relative to the size of the hemorrhage, and a less marked reduction in the red cells 2 become evident. When small but frequent hemorrhages take place the diminution of hemoglobin and loss of red blood corpuscles progress slowly, but finally the blood picture may reach that of an extreme grade of anemia. The anemia in the above condition is due either to an actual loss of red blood cells through hemorrhage or to a destruction of red blood cells in the circulation through the action of some toxic or poisonous substances. Smears from the blood show that the red blood cells are small and pale (Plate I). There may be some irregularity in size and shape of the cells, but this is not usually marked. Except in the severest secondary anemias, nucleated red blood cells are not numerous, and almost always when present they are of the normoblastic type.

Progressive pernicious anemia is to be sharply differentiated from the great group of secondary anemias. The exact cause of pernicious anemia is not known, but its mode of origin is different from that of the secondary anemias, inasmuch as the anemia is not alone due to a destruction of red cells in the circulating blood, but to an injury of the vital tissue which forms the red blood cells for the body — the bone marrow. The red corpuscles in this disease fall relatively lower than the hemoglobin, so that the hemoglobin index is above 1. The leukocytes are decreased. Microscopically the red blood corpuscles show great irregularity in size and shape (Plate II). Many of them are much larger than normal. Nucleated red blood corpuscles are found, sometimes in great numbers, and the megaloblasts are often more plentiful than the normoblasts. The blood picture serves to distinguish cases of pernicious anemia from severe secondary anemia, which may accompany hidden carcinoma of the internal organs, or follow repeated losses of small amounts of blood.

Great importance has been attached, within recent years, to estimations of the white cells or leukocytes of the blood. In dealing with this subject it must be remembered that the leukocytes play a very definite part in the economy of the body, and, so far as we know at present, are principally concerned in protecting the organism against injurious agents, among which are certain pathogenic bacteria.

The knowledge that the numbers of these cells in the circulating blood may vary greatly from normal, in many acute diseases, and even in some chronic affections, has been of much assistance in the diagnosis of certain conditions. Under normal circumstances the variation in the numbers of the leukocytes is not very great, and we can consider 7000 to 10,000 leukocytes per c.mm. within the normal limits. When the leukocytes are increased, perhaps to 15,000, to 20,000, or to 50,000 per c.mm., we speak of the condition as leukocytosis; and when they fall below the normal limit, the condition is known as leukopenia.

Several varieties of leukocytes go to make up the total number of these white cells, and of all the leukocytes, the polymorphonuclear neutrophilic leukocytes are the most numerous. They form 70 per cent, to 72 per cent, of the cells. Next in numbers are the small lymphocytes, which make up 22 per cent, to 25 per cent, of the cells. The large lymphocytes and

0»AlVfi BY J.N1 CnASi

PLATE I

BLOOD.

(Elu-licli triple stain.) (Prepared by Dr. I. P. Lvox.)

Fig. I. TYPES OF LEUCOCYTES.

a. Polymopphonueleap Neutpophile. b. Polymorphonuclear Eosinophile. c. Myelocyte (Neutrophilic), d. Eosinophilic Myelocyte, e. Large Lymphocyte (large Mononuclear). /. Small Lymphocyte (small Mononuclear).

Fig. IL NORMAL BLOOD.

Field contains one neutrophile. Reds are normal.

Fig. IIL ANEMIA, POST-OPERATIVE (secondary).

The reds are fewer than normal, and are deficient in haemoglobin and somewhat irregular in form. One normoblast is seen in the field, and two neutrophiles and one small lymphocyte, showing a marked post-haemorrhagic anaemia, with leucocytosis.

Fig. IV. LEUCOCYTOSIS, INFLAMMATORY.

The reds are normal. A marked leucocytosis is shown, with five neutrophiles and one small lymphocyte. This illustration may also serve the purpose of showing tha leucocytosis of malignant tumor

Fig. V. TRICHINOSIS.

A marked leucocytosis is shown, consisting of an eosinophilia.

Fig. VI. LYMPHATIC LEUKEMIA.

Slight anaemia. A large relative and absolute increase of the lymphocytes Cchiefly the small lymphocytes) is shown.

Fig. VII. SPLENO-MYELOGENOUS LEUKEMIA.

The reds show a secondary anaemia. Two normoblasts are shown. The leucocytosis is massive. Twenty leucocytes are shown, consisting of nine neutrophiles, seven myelocytes, two small lymphocytes, one eosinophile (polymorphonuclear) and one eosinophilic myelocyte. Note the polymorphous condition of the leucocytes, i.e., their variations from the typical in size and form.

Fig. VIII. VARIETIES OF RED CORPUSCLES.

a. Normal Red Corpuscle (normocyte), b, c. Anaemic Red Corpuscles, d-g'. Poikilocytes. h. Microcyte. i. Megalocyte. j-n. Nucleated Red Corpuscles., j;, fc. Normoblasts. I. Microblast. m,n. Megaloblasts.

Pernicious Anaemia.

The field shows marked anisocytosis and poikilocytosis: .V, young megaloblast (early generation); yP -I/'* .1/'', later generations of the megaloblast series; <S S S, " stippled" red ceils; R, ring body (nuclear remnant ?); T., lymphnr-yte.

FIG. 2

Pernicious Anaemia. (Actual Field.)

Field showing less poikilocytosis than Fig. 1: .l/i, young megaloblast; ,1/2, megaloblast of later generation; T T T, etc., transitional erythroblasts, not typical either of the megaloblastic or of the normoblastic series; .S, " stippled" erythrocyte; P. polynuclear neutrophile; L. large lymphocyte.

BXAMINATION OF THE BLOOD 19

transitional cells form 3 per cent, to 5 per cent., the eosinophilic leukocytes 2 per cent, to 4 per cent., and the basophiles 0.5 per cent.

In the commoner forms of leukocytosis these cells do not increase proportionately. One form predominates above all others, both relatively and in actual numbers, and this form is the polymorphonuclear leukocyte. The reason for this is not far to seek. If one injects a culture of some bacterium, such as Staphylococcus aureus, into the peritoneal cavity of a rabbit, the polymorphonuclear leukocytes pour from the bloodvessels of the mesentery into the peritoneal cavity to protect the body against the toxic action of the bacteria. So many leukocytes leave the blood stream that for a short time the numbers of white cells in the peripheral circulation are actually diminished. But the body soon feels the need of more leukocytes. Great quantities of these cells are required in the peritoneum, and they must reach the peritoneum from their point of origin through the blood stream. New leukocytes, therefore, are rapidly formed in the bone marrow and poured in great numbers into the circulation, whence they find their way to the peritoneum. This generous supply of cells circulating through the bloodvessels produces the leukocytosis.

If, now, a culture is chosen which is extremely virulent, and if this is inoculated into the animal in great quantity, the rabbit may die very soon and without the appearance of a leukocytosis. The explanation of this fact is found in the severity of the intoxication. The body cells, including those which form the leukocytes, are so badly injured by the bacterial toxins that leukocytes cannot be formed readily; not only is it impossible for the body to furnish leukocytes in excess of what is required, but it cannot even produce sufficient numbers to combat the infection.

It may readily be seen that leukocytoses cannot be considered by rule of thumb. When great quantities of leukocytes are required for some purpose in any part of the body, the body cells do their best to produce leukocytes in excess of what is actually needed, and the number of these cells increase in the blood.

Though it is impossible to draw definite conclusions from the grade of leukocytosis, still certain general principles may be followed in those infections where a leukocytosis usually occurs. If the patient is not very sick and the leukocytes are only slightly increased, we may assume that the infection is mild and great numbers of leukocytes are not required for protection. If the patient is very ill and the leukocytes are high, the body is probably reacting well against the infection, but if the patient is very ill and the leukocytes remain low, the reaction of the body is poor and the ultimate outlook is grave.

A leukocytosis may be physiological or pathological. Physiological leukocytoses occur after heavy meals, when the white cells may increase 30 per cent, to 40 per cent., and after excessive exercise and cold baths. During pregnancy the leukocytes increase 50 per cent, to 80 per cent., while in the newborn the leukocytes may be three to four times their normal number in the adult.

Pathological leukocytoses occur in a great variety of conditions, and certain diseases are almost always accompanied by a leukocytosis. Among these conditions may be mentioned pneumonia, rheumatic fever, epidemic meningitis, septicemia, erysipelas, scarlet fever, and tetanus. In practically all forms of pyogenic infections and purulent inflammations there is a leukocytosis of varying degree, and sometimes a leukocytosis which is quite high. In localized acute inflammations a leukocytosis is the rule, and it is sometimes surprising to find what a marked leukocytosis accompanies a comparatively mild infection. A small boil may give rise to a leukocytosis of 20,000 to 25,000 cells per c.mm. Purulent inflammations of the pleura, the pericardium, and the peritoneum are usually accompanied by a great increase in the leukocytes. In empyema it is not uncommon to find a leukocytosis of 20,000 to 50,000 cells per c.mm. The same is true of acute purulent inflammations of the gall-bladder and such internal organs as the liver, kidneys, and brain.

In appendicitis the leukocytes may vary considerably, depending upon the stage of the disease. With acute catarrhal conditions the leukocytes, if increased at all, are very slightly elevated; in the acute suppurative stages there may be a moderate leukocytosis (15,000 to 20,000 leukocytes per c.mm.), or as the process continues a very high grade of leukocytosis (30,000 to 40,000 leukocytes per c.mm.) may develop. As is true in all infections, the desperate fulminating cases may show but a slight rise in the leukocytes. When the process becomes chronic the leukocytes may be normal, and even though there is a localized abscess, provided it is walled off, the leukocytes may be scarcely above the normal limits. This, too, is true of all chronic localized inflammations. During the active stage of the infection, new leukocytes are constantly required at the seat of trouble and are constantly kept high in the circulating blood; but in an old walled-off abscess no leukocytes are required of the body, and there is, therefore, no increase of the cells in the blood.

Though the presence of a leukocytosis may aid in the diagnosis of certain conditions, the discovery of a leukopenia may be equally helpful in clearing the diagnosis. Just as certain diseases are characterized by an increase in the leukocytes others may be recognized by a decrease. This is particularly true of typhoid fever, and the knowledge of this fact may serve to differentiate this disease from certain acute infections which it may so closely resemble. Another very important fact which must be borne in mind when one is dealing with typhoid fever is that secondary acute inflammations, such as pneumonia, subcutaneous abscesses, osteomyelitis, cholecystitis, and peritonitis, complicating typhoid, may give rise to only a slight leukocytosis, which is in no way comparable to the leukocytosis occurring in such acute infections alone. Whereas, the leukocytes in croupous pneumonia usually average 15,000 to 30,000 cells per c.mm., and may be much higher, in pneumonia complicating typhoid fever the leukocytes may number only 8000 to 12,000. If one takes into account the usual leukopenia of typhoid fever (3000 to 6000 leukocytes per c.mm.), this represents an increase in the leukocytes of the blood, but is insignificant as compared with the leukocytosis seen in croupous pneumonia itself.

EXAMINATION OF THE BLOOD .21

When a perforation of the bowel takes place in typhoid fever there may be a transient increase in the leukocytes, and in rare cases the leukocytosis is high. More commonly the white cells increase to 10,000 or 12,000, and then, particularly in unfavorable cases, their numbers fall rapidly. Often in quickly fatal cases it is impossible to detect any definite rise in the leukocytes, and the leukopenia becomes steadily more pronounced until death.

In tuberculosis a leukocytosis makes its appearance only when a secondary infection is engrafted upon the original process.

A few non-inflammatory conditions may give rise to a leukocytosis, and unless one is cognizant of this fact, confusion may arise. Acute hemorrhage is followed by a leukocytosis which is often very pronounced, and the leukocytes may reach as much as 20,000 per c.mm. Less marked leukocytoses are seen after intoxications by certain drugs, such as phenacetin and antipyrine, and after chloroform narcosis. Occasionally a leukocytosis develops during the course of such malignant tumors as carcinoma and sarcoma.

So far we have considered only the leukocytoses which are characterized by an increase in the polymorphonuclear neutrophilic cells, but it is also possible to have a leukocytosis due to an increase in the eosinophile leukocytes. Eosinophilia occurs in a number of conditions. It is most marked in trichinosis and in infections by certain intestinal parasites, particularly the ankylostoma duodenale. Eosinophilia may also appear during certain stages of bronchial asthma, and may be present in pemphigus and some varieties of skin diseases.

The study of the white cells of the blood in the diseases which we have mentioned so far, though it may suggest or aid a diagnosis, is not essential for the diagnosis. In a few diseases the diagnosis cannot be made without a blood examination.

The diagnosis in leukemia must rest entirely upon a study of the blood. There are two main forms of leukemia, lymphatic leukemia and myelogenous leukemia.

Lymphatic leukemia may again be divided into two types, the acute and the chronic. In acute lymphatic leukemia the clinical picture is usually that of an acute infection with fever and general prostration. The lymph glands are not enlarged, as a rule. The leukocytes are increased. They may number 50,000 to 200,000 or more. The stained smear shows an enormous preponderance of a form of large lymphocytes. The chronic variety is characterized by an enlargement of the lymph glands and spleen and by a leukocytosis in which the white cells may reach from 100,000 to 500,000 per c.mm. In smears the cell which forms from 80 per cent, to 95 per cent, of all the white corpuscles is the small lymphocyte. In both types the red blood corpuscle and hemoglobin may be decreased, but anemia is usually most marked in the acute leukemias.

Myelogenous leukemia is characterized by enlargement of the spleen, and sometimes of the lymph glands, with, again, a great increase in the numbers of white blood corpuscles. Anemia is also present, and the proportion of white and red cells may be 1 to 5 or 1 to 3, or even 1 to 1. The stained smear shows a variety of cells which are not normally found in the blood. Neutrophilic and eosinophilic myelocytes, cells which normally are seen only in the bone marrow, form a large percentage of the cells. Nucleated red blood corpuscles may also be seen in large numbers. A blood examination is imperative in every patient who has marked enlargement of the spleen and general marked enlargement of the lymph glands.

Besides the examination of the formed elements of the blood, one may obtain much information through other methods. It is known that when a culture of a given bacterium, for instance the typhoid bacillus, is injected in non-fatal doses into an animal, the serum of that animal gradually develops the property, when brought into contact with a suspension

Fig. 1

- .1

-^ffll.

Positive agglutination reaction.

of cultures of that specific organism, of causing the bacteria to clump together in great masses. This is known as agglutination, and the serum may develop such high agglutinative properties that it will be active when diluted 100, 1000, or even 10,000 times. During the course of typhoid fever the serum develops the power of agglutinating the typhoid bacillus, and this specific agglutinative reaction (the Widal reaction) is made use of for the diagnosis of this disease. In order to say certainly that the Widal reaction is positive, the blood serum of a patient, diluted at least fifty times and better one hundred times, must stop the motion of the typhoid bacilli and cause them to form well defined clumps within one hour (Fig. 1). The reaction is rarely present before the second week of the disease, and may be delayed until the end of the third or fourth week. Serum from patients suffering from certain other bacterial infec-

EXAMINATION OF THE URINE 23

tions, such as Malta fever or tuberculosis, may develop the power to agglutinate the infecting organisms, though the reaction which is of most practical importance is that occurring in typhoid fever.

Another very valuable serum reaction for diagnosis is the complement deviation method of Wasserman. By a technique which is complicated and much more elaborate than that of the Widal reaction, it is possible to obtain this deviation of the complement of the blood serum in a large percentage of syphilitics. The reaction usually fails when the patient has been treated for some time by antisyphilitic measures. The reaction depends upon the union of a specific antibody present in the serum of the syphilitics with a so-called antigen which is present in tissue richly infected with Spirocheta pallida. Recently, lecithin has been substituted for the syphilitic tissue. During the union of the antibody and antigen the thermolabile complement of serum is absorbed. The same method of diagnosis has been applied to the serum of typhoid and tuberculous patients, an extract of the typhoid bacillus and tuberculin being used as antigen.

More accurate information may be received in systemic bacterial infections from blood cultures. Small amounts of blood may be readily withdrawn by means of a syringe from the veins at the elbow, and cultures may be made from this blood on different media. This method is of great value for diagnosis in the early stages of typhoid fever, when typhoid bacilli may be obtained in 80 to 95 per cent, of the cases. Septicemia due to the pyogenic cocci or other bacteria may often be discovered by this means; or when the diagnosis is suspected it may be confirmed and the nature of the infecting organism accurately determined.

Finally, it is necessary to mention the aid which may be given by an examination of the blood for parasites. The discovery of the malarial Plasmodia may explain the presence of alarming chills, while it is not necessary to emphasize the importance of a search for the embryos of Filiaria sanguinis hominis in cases of lymph scrotum and chyluria, for Spirillum obermeieri when relapsing fever is suspected, and in rare instances for trypanosomes.

EXAMINATION OF THE URINE.

Under normal conditions an adult passes from 1500 to 2000 c.c. of urine in twenty-four hours. This quantity varies slightly in health, according to the amount of fluid taken into the body or the amount of fluid lost through sweating, etc. Under pathological conditions the amount of urine may vary enormously. It is increased in diabetes mellitus and diabetes insipidus, in certain forms of chronic nephritis, and in certain nervous disorders, while the amount is decreased principally in acute nephritis and certain forms of chronic nephritis.

In recurring occlusion of the ureters through any cause, or in certain forms of hydronephrosis, the quantity of urine may vary from time to time. The periods in which the ureters are partially blocked are characterized by decreased urinary secretion, while relief of the block is followed by marked and often sudden polyuria.

The specific gravity of the mixed twenty-four-hour urine from healthy persons usually lies between 1015 and 1020. After the drinking of much water or beer the specific gravity may fall to 1002, or after excessive sweating rise to 1035. As a general rule, in diseased states the specific gravity of the urine varies with the quantity of urine excreted. A concentrated urine has a high specific gravity, while in polyuria the specific gravity is low. There is one glaring exception. In the marked polyuria of diabetes mellitus the specific gravity is greatly increased, and may be 1040 to 1050.

The urine from a normal person is quite transparent and varies in color from a pale yellow to a dark amber. On standing, a flocculent cloud forms, which is composed of mucus enclosing a few cells. A precipitate of urates or phosphates or a growth of bacteria may cloud the urine diffusely. Certain characteristic changes in the color are seen in disease. In febrile states the urine becomes dark yellow or reddish; blood, of course, imparts a red, smoky appearance, while bile produces a yellow or greenish tinge, particularly noticeable in the foam. Besides these commoner causes, certain drugs give rise to colored urine. Injection of carbolic acid, hydrochinone, and salol produce a dark brown or olive-green urine; rhubarb and senna give a yellow color, due to chrysophanic acid ; santonin gives either yellow or green ; while methylene blue produces a deep blue or green coloration.

The reaction of freshly voided normal urine is slightly acid, due to the presence of several acid salts, the most important of which is diacid sodium phosphate. The acidity varies in health according to the type of diet, becomes more marked when there is increased consumption of proteid, less marked on a vegetable diet, and during different periods of the day. Immediately after meals the acidity is lowest. The acidity is diminished or the urine becomes alkaline under a variety of circumstances, but most noticeably in the condition known as phosphaturia, or when it is mixed with blood or alkaline secretions, or when alkaline fermentation takes place anywhere in the urinary tract. The alkaline reaction, if it is due to ammonia, is caused by a growth of certain forms of bacteria. On standing, urine from normal individuals tends to become alkaline through bacterial fermentation.

Increase in the acidity is rare, though it may occur probably as the result of a neurosis, and cause symptoms of cystitis. Cryoscopy, or the determination of the freezing point of the urine, may give information concerning the activity of the kidneys. A freezing point above 0.9° indicates low molecular concentration, and shows that the functional activity of the kidneys is interfered with. The value of this method for determining the relative activities of the two kidneys from an examination of the urine obtained by ureteral catheterization is not unquestionable.

The presence of albumin in the urine is spoken of as albuminuria, and the commonest and most important form of albumin found is serum albumin. The finding of albumin in the urine may denote that the

EXAMINATION OF THE URINE 25

kidneys have failed, at least partially, in their function as filters, thus allowing the passage of albumin from the blood (renal albumin), or it may point to the presence of blood or piis in the bladder or kidneys or an admixture of seminal or prostatic fluids with the urine (accidental albuminuria).

If the albumin is renal in origin, it is safe at least to suspect disease of the kidneys. There is, however, a group of very interesting cases in which albuminuria may occur in persons enjoying apparently perfect health. This physiological albuminuria may occur under a great variety of circumstances. Albuminuria may be present in the urine of healthy pregnant women, in men after severe exertion, as in bicycle riders or football players, after mental exertion, cold baths, and certain other conditions. It is still dubious as to whether the cyclical and orthostatic albuminurias are truly functional, and appear in persons who have healthy kidneys.