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SOCIETY NOTES

TRI-STATE (ALABAMA, GEORGIA, TENNESSEE) MEDICAL SOCIETY.-The eighteenth annnual meeting of the Tri-State Medical Society of Alabama, Georgia and Tennessee, will be held at Chattanooga, October 2-4, 1906. Reduced rates have been obtained from all points in Alabama, Georgia, Tennessee, Mississippi, Louisiana and Florida, and an unusually large attendance is assured. The preliminary program includes an excellent list of papers from leading medical men of the South. Strong pressure will be brought to bear to ultimately convert this organization into a branch of the Americal Medical Association-The Association of the Southeastern States, and recommendations will be made at this meeting. Physicians desiring to read papers should send their titles at once to the secretary, Dr. Raymond Wallace, Chattanooga, Tennessee.

MISSISSIPPI VALLEY MEDICAL ASSOCIATION. The next event of National interest. will be the annual meeting of this association, which will occur on November 6, 7 and 8, at Hot Springs, Ark., under the presidency of Dr. J. H. Carstens, of Detroit. A program of more than usual merit has been prepared by the efficient secretary, Dr. Tuley, including three orations, by President Carstens, and Drs. Frank P. Norbury and Florus F. Lawrence. Extensive preparations have been made by the profession of Hot Springs for the entertainment of members, their wives. and daughters, and a cordial welcome awaits. them. Reduced rates will be in effect on all lines of railway, the Missouri Pacific and Iron Mountain System offering special service and through trains for the occasion. For full particulars regarding rates, call at city ticket office, or write the editor of the FORT

NIGHTLY.

MEDICAL SOCIETY OF THE MISSOURI VALLEY.-The nineteenth annual meeting of this society was held at Council Bluffs, September 6 and 7, with an attendance of 125, Dr. Jno. E. Summers presiding. The program included twenty-five papers, and the discussions were most interesting and instructive. Among the guests at this meeting, who read papers, were Dr. Emil Reis, of Chicago; Dr. L. L. Uhls, superintendent of the State Hospital for Insane, Osawatomie, Kas.; Dr. Leo M. Crafts, Minneapolis; Dr. Alfred Schalek, Omaha; Dr. E. W. Clark, president of the Iowa State Medical Society, who responded to the address of welcome given by Congressman Smith of Council Bluffs. The society was royally entertained by the local members at the street carnival, and given a reception at

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O. B. CAMPBELL. M. D., St. Joseph, Mo. President-elect Medical Society of the Missouri Valley.

Bluffs, treasurer (re-elected); Dr. Chas. Wood Fassett, St. Joseph, secretary (reelected). The secretary's report showed the prosperous condition in which the society finds itself at the close of the year, having gained forty-four new members and losing but one. The annual Missouri Valley excursion to the A. M. A. was made a subject of special comment, and the secretary expressed the opinion that the next trip to Atlantic City would be even more enjoyable, if possible, than the last. Following is a list of members admitted at this meeting: Robert R. Hollister, F. W. Lake, L. B. Bushman, Alfred Schalek, S. Cole Little, and C. W. Pollard, of Omaha; J. H. Gassan, Albert V. Hennessy, T. B. Lacy, Jr., John F. Sprink, of Council Bluffs; Halsey M. Lyle, Kansas City; William H. Chapman, Ingleside, Neb.; William H. Anderson, Dunlap, Ia.; J. N. Medill, Persia, la.; J. R. Hollowbush, Rock Island, Ill. James W. Lehan, Dunlap, Ia.; C. V. Artz, Hastings, Neb.; H. P. Duffield, Marshalltown, Ia.; Charles L. Mullins, Broken Bow, Neb.; W. R. Young, Ausley, Neb.; H. D. Spencer, Oakland, Ia.; W. F. Pierce, Carson, Ia.; L. L. Uhls, Osawatomie, Kas. The papers and discussions will appear in the Medical Herald, the society's official journal.

REPORTS ON PROGRESS

Comprising the Regular Contributions of the Fortnightly Department Staff.

INTERNAL MEDICINE.

O. E. LADEMANN, M. D.

Blood Pressure and Pigmentation in Addison's Disease.-Short (The Lancet, Aug. 4, 1906) publishes a case of Addision's disease, on which many observations were made on the bood pressure. He summarizes his paper as follows: The symptoms of Addison's disease are due to vasomotor paralysis. This is due to absence of adrenalin, the normal excitant of the sympathetic nerve endings, from the blood. The pigmentation is due to vascular relaxation of the skin causing exaggerated functional activity of the pigment cells. The most promising line of treatment, on theoretic grounds, is the administration of vasoconstrictors of prolonged action; digitalin has given good results in one case.

A Case of Acute Rheumatism, Hypyrexia; Recovery. Smith (The Lancet, Aug. 4,1906) records a unique case of rheumatism with excessive pyrexia in a man 54 years old. On the eighth day of the illness the temperature by mouth registered 107.2 deg. F. with a pulse rate of 128 beats per minute. Just prior to using an ice pack the temperature in the rectum rose to 109.3 deg. A three-quarters of an hour application of the pack resulted in reducing the temperature to 107 deg. F. The author finds only two cases recorded in Birtish literature where a recovery followed so high a temperature in rheumatism, and in both of these cold baths had been employed.

Stokes-Adams Disease. Steiner (Buston Melical and Surgical Jour., Aug. 9, 1906) says that Stokes-Adams disease is an affection which presents clinically the following features: (1) A slow pulse, usually permanent, but sometimes paroxysmal, falling to 40, 20, or even to 6 beats per minute; (2) cerebral attacks which consists in vertigo of transient character, syncope, pseudoapoplectiform attacks or epileptiform seizures; and (3) visible auricular impulses in the veins of the neck, the beats varying greatly, as 2:1 or 3:1 rhythm being the most com. mon (Osler). During the last three years the author has seen three cases, which be details. The first patient, a man, aged 77, had recurrent syncopal attacks in the same month at intervals of a year or more, a slow pulse, venous pulsation in the neck, arterio-sclerosis and cardiac hypertrophy. There was a gradual improvement during the further course of the disease. The second patient, a

man 53 years old, had one epileptiform seizure and one attack of syncope apparently at the onset of the malady. The pulse was slow, venous pulsations in the neck were absent, slight arterio-sclerosis and hypertrophy of the heart. A brief sojourn at "Bad Nanheim" afforded no relief. The patient died two years after the apparent onset. During the course of the disease the pulse ranged from 37 to 19. The third patient, a woman, 51 years old, suffered from syncopal attacks, slow pulse, venous pulsations in the veins of the neck and cardiac hypertrophy. The pulse rate averaged 40 per minute.

The

Spontaneous Rupture of the Heart in a Case of Senile Dementia -Miller's (Boston Medical and Surgical Jour., Aug. 2, 1906) patient was a man 83 years old, who had a spontaneous rupture of the heart as a result of myomalacia cordis, the accident being determined by mental and physical excitement. rupture occurred at the site of an old infarct near the top of the left ventricle. The age of the patient, the condition of the arterial sysbly cited in cases of spontaneous heart ruptem, were favoring conditions almost invariature. The pre-existing myocardial disease, anemic necrosis, is regarded as a less frequent tive diseases of the myocardium. cause of heart rupture than other degenera

Id.-Palmer describes a remarkable case of spontaneous rupture of the heart in a man, 36 years of age. The rupture occurred in the pleural cavity and was probably determined by the obliteration of the pericardial cavity through the formation of adhesions which existed over the greater surface of both auricles and ventricles. The patient presented the physical signs and symptoms of aortic aneurism, accompanied by symptoms of pressure on the left recurrent laryngeal nerve. of the aortic arch present could not have posslight enlargement of the descending portion sibly been responsible for this clinical pic

ture.

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vanced stage of arteritis, while the systemic The coronary arteries were in an ad

vessels were normal.

Intermittent Peatosuria and Glycosuria.Kaplan (N. Y. Med. Jour., Aug. 4, 1906) divides pentosuria into: (1) Chronic pentosuria, occurring when the excretion of pentose in the urine is constant, and when glycosuria cannot be induced after the ingestion of one hundred grams of glucose. (2) Alimentary pentosuria occurring in individuals who cannot oxidize large amounts of pentosans introduced with the food, exerting a portion of the pentosan as pentose; when the articles containing these pentosans are excluded from the dietary the pentose disappears from the

urine. (3) Intermittent pentosuria, occurring when the excretion of pentose takes place at more or less regular intervals uninfluenced by external conditions and when one hundred grams of glucose will not give rise to a glycosuria. (4) Intermittent pentosuria and glycosuria. When this condition occurs pentose is present in appreciable quantities, and glucose appears in the urine, either independently or after the administration of one hundred grams of glucose.

The Influence of Excessive Meat Diet on Growth and Nutrition.- Watson's (Lancet, July 21, 1906) paper deals with the clinical results obtained by feeding rats on an exclusive meat diet. His experiments prove that the use of such an excessive meat diet is attended by a retarded growth, and sterility is induced if the diet is commenced in early life. The power of lactation is diminisheda permanent weakening of the resisting power of the animals is induced by the use of excessive flesh diet in early life, the animals succumbing to disease at an unusually early age, and there is a high death rate in the offspring of animals fed on excessive meat diet. Clinical experience leads Watson to think that there is also a close parallel in diseases of the human subject, and especially in that class of affections commonly included under the terms of gout and goutiness. He mentions that particular attention should be given to early dietetic history of patients as far as obtainable.

A Simple Test for Biliary Pigments in the Urine. Krokiewicz (Bulletin général de therapeutique, May 23, 1906) recommends a test consisting of aqueous solutions of sulphanilic acid (1 per cent) and sodium nitrite (1 per cent) as highly sensitive for bile pigments in the urine, and that its application, is not affected by the presence of other substances. The test is carried out as follows: Equal quantities of the sulphanilic acid and sodium nitrite solution (cc.) are placed in a test tube, to which an equivalent quantity of urine (1 cc.) is added. The mixture is shaken for ten or fifteen seconds, and if the urine contain bile pigment the solution will become a ruby red, which upon the addition of one or two drops of hydrochloric acid changes to a violet amethyst.

Microbic Cyanosis.-Gibson and Douglas (Lancet, July 1, 1906) relate an interesting case of a woman, 36 years of age, who had been subject to headaches, weakness, attacks of dizziness and faintness for some years The appearance of the skin was of a distinctly cyanotic tint. Gastric as well as enteric disturbances frequently evidenced them

selves, and for some time there had been a tendency to diarrhea. The hematologic examination presented the following: Red blood corpuscles less than 4,000,000; the hemaglobin amounted to 70 per cent; the leucocytes were above 10,000. The blood, save that of a slight secondary anemia, was otherwise normal. The physical examination was nega tive. A bacteriologic examination of the blood gave a pure culture of bacillus coil communis. The condition, therefore, belongs to the group of affections often termed false cyanosis.

Tuberculin in the Treatment of Tuberculo

sis.-Pogue (Med. Record, Aug. 4, 1906) deducts the following conclusions from a study of 167 cases: An early diagnosis is the most important step to the successful treatment of tuberculosis. Tuberculosis may be arrested by proper treatment, with a certainty of a permanent cure. Tuberculin is a valuable adjuvant in the treatment of tuberculosis, as is evidence by the recovery of twenty-eight out of thirty cases that were treated with practically nothing but tuberculin while they continued to follow their ordinary occupation during the treatment. Cases of tuberculosis treated with the addition of tuberculin show a much less tendency to recur than similar cases treated without tuberculin. Tuberculin in small doses (0.01 to 0.005) seems to have a more curative action than when given in large and increasing doses. No ill effects follow the administration of small doses of tuberculin. Purely incipient cases improve very rapidly under the use of small doses of tuberculin, both as to the arrest of the disease and the clearing up of the diseased area. Tuberculin should never be given to a patient who has a fever or who is suffering from mixed infection. Third stage cases, especially advanced cases, receive little or no benefit from the use of tuberculin.

The Loss of Patellar-Reflex in Pneumonia. Barnes (Birmingham Med. Review, April, 1906) like Hughlings Jackson, observed a loss of knee and other reflexes in cropuous pnenmonia, while in pulmonary consoildations due to tuberculosis and septic pneumonias the reflexes invariably persisted until death. He noted an absence of the patellar reflexes in thirty out of thirty-four cases of croupous pneumonia. A disappearance of the knee reflex on the first or second day generally indicates a severe attack with a bad termination. In those cases which ended fatally, the author was able to demonstrate changes in the third lumbar segment. Barnes believes that the absence or presence of the knee reflexes is not only a valuable differential sign, but also a guide to the prognosis.

DEPARTMENT OF LEGAL MEDICINE.

R. B. H. GRADWOHL, M. D.

from Electricity.- Kratter (Veirteljahrsschrift fuer Ger. Medizin, Band XXX Heft 2, Proceedings of the German Association of Legal Medicine) has contributed several monographs upon the subject of death from electricity. He opened the discussion of this subject anew at this convention by dividing the subject into three headings, viz. 1. What is death by electric ity? 2. How can the diagnosis of death from electricity be verified? 3. Which current can kill a man?

Knowledge can be gained of the fact that death is caused by the electric current by the many deaths of persons and animals by accident and the pathologic-anatomic changes found in them; secondly, by experimental researches upon animals with this current. Death occurs suddenly in some, sometimes with an outcry, sometimes without it, with only tetanic-like convulsion of the body, without leaving any visible traces upon the outside of the body. In other cases death does not occur immediately, there is loss of consciousness, a soporific effect of the current, death finally taking place with sterterous breathing and gradually increasing cyanosis. In experimental animals where naturally observation can be more acute, there is remarked a difficulty in breathing at first, followed by conclusion of the entire muscular system. The breathing difficulty is either permanent (death), or begins after a quarter, a half or an entire minute, and gradually is restored. Jellinke has observed other phenomena; at the moment of contact, there is a spasm of the entire circulatory system, with an mous increase in the blood pressure, this going far to explain the hemorrhaes which have been described in some cases of electric shock. This can be determined by the sphymographic tracings, which show that if the breathing stops for any long period of time, there is a sinking in the blood pressure, with almost impreceptible movement of the pulse and very slight palpable heart's action. This is the picture of an asphyxiation.

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The anatomic picture found in these cases does not differ either in man or in animals. The blood in the body is very fluid, or with very slight clots in the bodies of animals, of a dark color, over-filling of the lungs and heart and great vessels with blood, many ecchymoses visible to the naked eyes in places in the body, just as we find them in drowned bodies. In one case Kratter found ecchymoses under the endocardium of the left heart, as Dietrich has pointed out in cases of death from sun-stroke. The venous

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What changes take place in the central nervous system as to lead to death by asphyxia was the subject of an inquiry by Kratter; he made sections of the spinal cords of two subjects, one human and one experiwental animal, dying from the electric stream. He made out minute hemorrhages. Corrado found in the brains of dogs killed with the current decided changes in the ganglion cells of the cortex. These changes were in the shape of distortion of the nuclei and chromatin substance and vacuole formation. There was a condition of varicose atrophy. Kratter is unable to confirm Carrado's findings. Neither can Jellinek confirm the same, although he has made many sections of animals dying from the current.

1.

In short, Kratter inquires, "Can we accurately draw a picture of the pathologic anatomic findings in a case of electric death and make a diagnosis thereon? He replies, that we cannot and for the following reasons: The peculiar character of the current and lack of control over the same makes it impossible to reason on one case from all cases. It is a fact that much more severe changes than are found in cases of electric death are produced in the brains of men who rally survive. 2. Experiments and clinical cases of electric shock show us that reparable effects are sometimes produced by the current from which the animals recover.

It is a fact that while the anatomic diagnosis cannot be distinguished from that of "shock" in the ordinary expression of the term, as regards the effect upon the internal organs, yet fortunately the effects of the current upon the exterior of the body serves to make a competent diagnosis, i. e., the effects of burns either from lightning or from actual electric shocks from motors, etc. The burns produced in industrial accidents are characteristic; a long blister usually upon the index finger of the hand receiving the shock. Other means of diagnosis depend upon the point where the shock was received in the body, burning and tearing of the clothing, foot or head apparel, in lightning deaths burning and melting of metallic substances like watches, watch. chains, etc., on the body, and magnetization of iron substances on the body, such as knife blades, keys, etc.

As to the third question, what kind of a current can kill, there arises an important question, theoretic as well as practical. It can be accepted as a fact that a current with a voltage of 500 is dangerous, and the danger increases as we go over the 500 mark. This rule varies with individuals as a rule. For instance, men have been killed by a current of 250 volts and others have survived a current of over several thousand volts. It is a well-known fact that currents of 20 milliamperes are used for medicinal purposes. A current of 100 M. A. is a dangerous. Moisture of the skin increases the effect of the current, as well as salt solutions and acid solutions upon the skin.

The idiosyncrasy of certain persons to the current must not be forgotten. Alcoholics, patients with heart disease and lymphatic trouble, as well as youthful people in general are quite susceptible to the current. Alternating currents are more dangerous than the direct.

GENITO-URINARY.

T. A. HOPKINS, M. D.

An Analytical Study of Uremia.-Dr. A. C. Croftan, Chicago (Jour. A. M. A.), criticises the current theories of uremia, showing that neither anuria nor the variations of excrementitious nitrogen output suffice to explain the phenomena. Only when we determine separately the various groups of ni. trogen bodies that occur in the blood and urine do we find abnormal conditions that may be deemed fairly characteristic. The two most important of these are: 1. A relative increase of the ammonia salts, both of the blood and urine as compared to normal average values and as compared to the circulating and excrementitious urea. 2. A relative decrease of the urea, both of blood and urine as compared to normal average values and to the total nitrogen of the circulating and excrementitious nitrogenous waste products. There may also be highly toxic albuminoid or alkaloid bodies in the blood or urine that might have an enormous effect without appreciably changing the amount or relative proportions of the nitrogen content. As regards the inorganic salts, the most delicate tests, Croftan states, give little evidence that uremia is due to salt retention. That there must be some poisons acting in the productions of uremia can not be denied. The decreased urea secretion, Croftan is inclined to think, is due rather to non-formation than to retention. It is not increased in the blood, as it should be if it were merely not eliminated, and the corresponding increase of ammonia is normally concerted into

urea.

Disturbances of the kidney and liver, Croftan states, often are seen to go hand in hand, and he believes this would be found much more frequently if the liver were examined as thoroughly as the kidneys in every case of Bright's disease that comes to autopsy, and if mild functional disorders of the liver were as easily recognizable as like disorders of the kidney. Even if the kidneys are primarily share the function of eliminating toxic matters and some of the most important of these must pass through the liver before being finally eliminated by the kidneys. Even if the kidneys are primarily diseased more work is thrown on the liver, not only in its disintoxicating function, but also in making up for the waste caused by a leaky kidney. The organ consequently becomes fatigued, its function of disintegration of albumins is impaired and less urea and more incompletely disassimilated intermediary products of albuminous metabolism are thrown into the circulation and intoxication results. Though this may thus follow or accompany renal disease, it is still due more to hepatic than to renal insufficiency. Hence the importance of recognizing early even mild degrees of hepatic insufficiency (particularly in renal cases and in pregnant women) and of safeguarding the patient against anything that may suddenly impose a strain on the fatigued liver. Instead, therefore, of stimulating the kidneys, the chief object of treatment should be to prevent development of uremia by attention to those organs that threaten to fail. Croftan advises first rest for the liver, even starvation for a few days, and in any case complete elimination from the diet of all substances irritating to the organ, and that every effort should be made to reduce intestinal putrefaction to a minimum. He would follow this by mild stimulation, the carefully guarded use of salicylates, of bile acids, possibly of calomel, and such dietetic and physical means as are available, all under careful supervision. For the acute uremic attack the most sensible procedure, he says, is blood letting, a lost art that should be revived in such cases as these. The injection of a saline to replace the lost fluid can do no harm, especially if some salt is injected that can stimulate the hepatic function, e.g., salicylate of soda in normal salt solution, or a solution of sodium citrate or phosphate in proper molecular concentration. Symptomatically, he has seen good results from the use of such infusions.

The Rational Treatment of Urethritis.— N. E. Aronstam M.D., Detroit, Mich. (Jour. A.M.A.), condemns the A.M.A.), condemns the so-called abortive plan of the treatment of acute urethritis and

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