No

the left side which was the side affected. herpes present; tongue very red, dry and not coated; eyes bright and an anxious look. Respiratory excursion was less marked upon the left than upon the right side. No rash on chest or abdomen; the abdomen was not distended. Palpation showed no marked increase of vocal fremitus over the painful area. I did not think it was increased over the rest of the chest, except at the apices, however, the patient's voice was a little weak. A friction rub was palpable over an area of two square inches; the center being at the section of the post axillary line and eighth rib, left side. Percussion over this area gave a slightly dull note and was painful. There was no relaxation (Skoda's resonance) above this area. Auscultation over this area showed breath sounds to be somewhat harsh and a little nearer the ear; also some fine crackling rales at the end of inspiration. There was no discrepancy in the breath sounds over the rest of the lung, or over the other lung, except at the apices which were dull on percussion and breath tones had a bronchial character and were prolonged, but gave no rales. Pulse was rather weak, but regular and 95 per minute. Respiration was painful, shallow and 30 per minute. Temperature 102.4. Patient was given enema, glycerine 3i; sulph. magnesia 3ii; water 3iii; and mustard plaster placed over the painful area. Liquid diet was given every four hours, and diuretic mixture, in glass of water, every six hours. Aspirin gr. 5 every six hours was prescribed, unless pulse grew weaker; temperature bath was given every four hours, if temperature was 103 de grees or above. The following is the clinical record: November 23, 6 p.m., temp. 105.1; pulse 79; resp. 35, had been wet, but had not had sufficient stool. Mag. sulph. ounces onehalf.

November 24, 6 a.m., temp., 102.1; pulse 82; resp. 28; feeling much better. 6 p.m., temp. 103.2; pulse 93; resp. 38.

November 25, 2 a. m., temp 99.2; pulse 85; resp. 26. 10 a. m., temp. 101.4; pulse 77; resp. 25. 6 p.m., temp. 102.9; pulse 70; resp. 29; good bowel movement and wet the bed.

November 26, 6 a.m., temp. 101.5; pulse 77; resp. 25. 10 a.m.. temp. 98.8; pulse 83; resp. 24. 10 p.m., temp. 102.3; pulse 90; resp. 26.

November 27, 10 a. m., temp. 97; pulse 73; resp. 32. He was somewhat cyanotic. Aspirin was discontinued; strychnia gr. 1-40 every six hours was given.

November 28, 6 a.m., temp. 102; pulse 86; resp. 26. 6 p. m., temp. 104.4; pulse 70; resp. 29.

November 29, 6 a. m., temp. 99; pulse 86;

resp. 26. 6. p.m., temp. 103; pulse 84; resp. 26.

November 30, 6 a. m., temp. 101.9; pulse 88; resp. 27. 6 p.m., temp. 103.9; pulse 77; resp. 28.

December 1, 6 a. m., temp. 102.1; pulse 81; resp. 26. 6 p.m., temp. 104.4; pulse 80; resp. 30; friction rub over same area; no change, except being less painful, some extension of the congestion for past three days; lung does not seem to be hepatized. Aspirin gr. 5 two times in twenty-four hours was prescribed; also egg-nog-spirits ounces one-half, two times a day. Did not retain egg-nog and it was stopped. Perspiration marked.

December 2, 6 a. m., temp. 102.8; pulse 84; resp. 35. 10 a.m., temp. 99.3; pulse 72; resp. 30; pulse weak.

December 3, 6 a.m., temp. 102.9; pulse 88; resp. 28. 6 p.m., temp. 104.3; pulse 85; resp. 35; patient filthy, feet cold, perspiring freely. Hot water-bag to feet, strychnia increased to gr. 1-30 every four hours. coughing, but no expectoration; has been none since illness began. Palatol was prescribed, drachm 1, every two hours.

Some

December 4, 6 a.m., temp. 102.2; pulse 89; resp. 30. 10 a.m., temp. 101.4; pulse 80; resp. 37; slight expectoration, glairy mucous tinged with blood, which was examined; no tubercular bacilli found.

December 5, 6 a. m., temp. 103.2; pulse 89; resp. 36. 10 a.m, temp. 100.4; pulse 82; resp. 39. 6 p.m., temp. 104.4; pulse 92; resp. 56; bowels moved several times and there was a wandering delirium. There developed a pericardial friction sound heard loudest over an area the size of a dollar, two inches above the apex of the heart, louder with inspiration, but plainly heard when the breath was held both at inspiration and expiration.

45.

December 6, 6 a.m., temp. 102.5; pulse 98; resp. 34. 6 p.m., temp. 104.5; pulse 90; resp. 10 p.m., temp. 100.3; pulse 92; resp. 40; bowels moved six times in twenty-four hours. Aspirin was stopped, ammonium carbonate, gr.5, every four hours prescribed, systolic blowing murmur over mitral area was heard, pulse fairly good quality.

December 7, 6 a. m., temp. 100.3; pulse 86; resp. 51. 6 p.m., temp. 103.9; pulse 94; resp. 52; quite restless, no cough, cyanosis, face flushed. Caffeine citrate, gr. 5, three times a day given, grew gradually weaker and died at 5 a. m. the following morning. The urine showed a small amount of albumen and a few hyaline casts, sp. gr. 1026 acid reaction, urea 3.9%.

To recapitulate here we have a patient with an old tubercular lesion, enjoying fairly good physical health who began to feel badly, los

ing his appetite, having malaise; developing a pleurisy, with a temperature which was of no regular onset or regular course, but with abrupt rises and falls; rapid respiration throughout; pulse rather weak, slow, no dicrotism; a pleuro-pneumonia without marked or typical findings; no rales except over the area of pleurisy; showing some increase in vesicular murmur all over the chest and back the patient looked very sick; face cyanotic, and no herpes. From this history with fever and slow pulse, we would think of typhoid fever with uarked pulmonary symptoms, but we have no history of a typhoid infection; no rose spots; no dicrotic pulse; no typical fever curve, and the pulmonary signs were too persistent. A blood count and Widal reaction test would have differentiated the diagnosis, but none were made. A broncho-pneumonia would have begun with a catarrh, cough and expectoration and more positve chest findings, such as rales. A lobar pneumonia would probably begin with a chill, cough with expectoration sooner or later, and would have shown positive consolidation in a patient as sick as was this one, especially considering the length of time. Again, low tension and lack of herpes also speak against it. It coincides more nearly with the picture of an acute miliary tuberculosis, caused by the entrance of the bacilli in large numbers into the blood stream, thereby being carried all over the body. This presupposes an old tubercular focus in the body. The most common location for such a focus is in the lungs, but in children it is often found in the lymph glands. The focus may be in the bones or kidneys. Cases of miliary tuberculosis may be divided into three classes: 1. Those showing symptoms of a general infection. 2. Those showing pulmonary involvement. 3. Those showing cerebral or cerebro-spinal symptoms. This case is of the pulmonary type, as is shown in cyanosis (which was not marked) and in resonance or hyper-resonance, especially over the chest (this is probably due to emphysema), fine crepitant rales, and very irregular fever rising at night to 103 or 104; feeble pulse which is often rapid. Unfortunately permission could not be had for a complete autopsy, so the lungs and heart only were removed. I will say that two drachms of pericardial fluid were obtained by a needle before the chest was opened, this was slightly turbid, of a yellowish green color, containing numerous leucocytes and many flat endothelial cells; many of them seemed to have double nuclei; others did not stain well; some contained fat droplets. Contrary to what I expected the pericardium was intact hroughout its inner surface, having normal

luster and perfectly smooth to the naked eye. As I have stated, there was a pericardial friction rub heard both during inspiration and expiration; and when the breath was held, this was due to the involvement of the portion of the external surface of the pericardium, which had become involved through contiguity with the lung (a pleuro-pericarditis. The incision was from the upper border of the sternum, extending two inches below the ensiform cartilage. The cartilages of the ribs were divided and the breast-plate elevated. Both lungs filled their respective pleural cavities and were studded with small millet seed-like bodies.

The left lung was adherent to the chest wall over the greater part of the lower lobe, especially around the area mentioned as the seat of the pleural friction rub. These adhesions were recent, as they were friable and easily broken. The adhesions at the apex were more dense and were with difficulty broken. The apex was hard and nodular. The lung was heavy, did not collapse, and crepitate upon being pressed, showing its emphysematous condition. The whole lung was covered with millet seed-like nodules. At a point opposite the apex of the heart there was a multiple cystic condition, the contents being a clear mucous fluid. The cut section shows an even dissemination of the tubercles throughout the whole lung; some of the larger nodules have become caseous and resulting in very small cavities. There was very little enlargement of the peribronchial glands; no thickening of the bronchial mucous membrane or peribronchial connective tissue. The mucous membrane of the bronchi was nearly normal, very slight catarrhal condition; consequently few bronchial symptoms, the whole lower lobe and most of the middle congested. The fissures between the lobes are agglutinated by the pleural inflammation. The cut surface is dryer than we would expect, notwithstanding the congestion. Some of the branches of the veins show coagulae of blood. Most of the air passages were patulous.

The right lung was adherent also, but not densely, except at the apex; this lung was not so heavy and not so dry; it cut with resistance and was permeated with tubercles; the air passages were nearly normal to the naked eye. No peribroncihal thickening; the apex was hard and nodular. The pericardium was roughened on the other side over an area the size of a dollar corresponding to the area over which was heard the pericardial friction rub. The viscera pleural opposing it was also roughened. The sac contained about two drachms of yellowish green fluid, which was slightly turbid. The heart was of

about normal size, right heart collapsed and flabby. The right auricle contained a partially organized blood clot: the semi-lunar valves were normal; the right ventricle was dilated; the walls thin and dry, and the trabeculae were flattened. The tricuspid valves were normal. The left auricle contained a partially organized clot, which had its beginning in the ventricle, between the papillary muscles and extended upward through the mitral valve; it also extended behind the curtains of the valve, thereby making it impossible for the valve to properly open or close. This condition accounted for the blowing murmur which was heard the day before death of the patient. The aortic valves showed some thickening at their base, but they were still competent. The walls of the ventricle were hypertrophied. Now what was the source of infection. It could not have been through the lymphatics, as the current is from the periphery and the disease so general in the lungs. It must have found its way into the right ventricle, then carried into every portion of the lungs. This was evidenced by the general distribution of the tubercles; there must also have been a large number of bacilli, because of the similar size of the tubercles as they appeared in all parts of the lungs. This may have occurred by rupture of a caseous nodule into vein or the thoracic duct, then being carried to the right heart, thence to the lungs. It is to be regretted that a complete post-mortem examination could not be made, as it is possible there were other foci in the body (the liver and kidneys showed no infection upon their surfaces). There were no enlarged glands in the neck.

STAGNIN, STRYCHNINE.

A. L. BENEDICT, M. D.

BUFFALO.

STAGNIN is a splenic extract, discovered by Landau and Hirsch and named on account of its property of causing coagulation of blood in cases of capillary hemorrhage. Whether it is one of the physiologic precursors of fibrin or not, is not definitely known, but its styptic action has been definitely shown to be due to increased coagulability of the blood and not to constriction of arterioles, as in the case of adrenalin.

Its field of usefulness is, obviously, mainly limited to capillary hemorrhge or, at least, to hemorrhage from very minute vessels, as metrorrhagia. But a similar limitation applies to ergot, adrenalin and other substances

whose action is expended on the smooth mus. cle of the arterioles. Indeed it is exceedingly doubtful if any substance will ever be discovered which will have a sufficient influence on the blood or the vessels to control massive hemorrhage.

STRYCHNINE.-Within the last few years, several articles have appeared calling in question, the value of this old therapeutic friend. Dr. Richard C. Cabot, of Boston, has recently published in the Boston Medical and Surgical Journal, during and after, the administration of strychnine. This series includes 31 of typhoid, 4 of pneumonia and represesents over 5000 individual measure. ments of blood pressure in about eight months. months. The daily dosage was 8, occasionally 10 milligrams, given in some cases by the mouth, in others subcutaneously. While slight rises of pressure were noted in 16 cases, a fall was noted in 17 and in the whole series, either according to the "before and after' method, or by comparison with a series of similar cases not taking strychnine, the conclusion was forced upon him that strychnine has no effect at all on blood pressure.

It would be a mistake, however, to jump to the conclusion that strychnine is worthless as a drug, or even as a general stimulant. Indeed, Dr. Cabot's investigations simply corroborate in a technical way, the prevalent teaching with reference to strychnine. At first sight, one not used to the sphygmomanometer, might expect a rise of pressure following a cardiac stimulant. But, in the accumulated experience of years, whether by a therapeutic tests or by animal experiments, the indications for employing stroyhnine have been quite clearly formulated and they, by no means, imply an effort to raise blood pressure. For example, we do not think of employing strychnine to control hemorrhage by local constriction of artericles. Instead, we formerly used ergot and now adrenalin. Nor do we use strychnine in heart and kidney cases in which we wish, not only to sup. port the heart, but to raise blood pressure and produce diuresis. Nor do we use strychnine in cases of weak heart, organic or otherwise, in which we wish a slow, steady squeezing of the cardiac muscle and a toning up of the vascular muscle generally. In such cases we prefer digitalis or one of its congeners. For some time, it was taught that strophanthus was a digitalis with the vascular effect left out, in other words almost a pure cardiac tonic as distinguished from a cardiac-vascu lar tonic.

But it is asking a good deal of a drug not only to act only on the smooth mus cle of the circulatory apparatus, but even to select the modification of thistissue found

in the heart alone. Such a demand is almost as unreasonable as the homeopathic claim that drugs are right and left-handed, so that certain are better for the right lung, others for the left. Thus, in general, if a drug has a definite action upon smooth muscle in one part of the body, it is to be expected that it will have a similar influence in other parts. There are some apparent exceptions, as that digitalis acts more on the heart, ergot on the arterioles and uterus, but possibly the explanation is that ergot causes a still more clonic contraction than digitalis. Strophanthus, at any rate, is no longer regarded as a pure cardiac tonic.

It will be noted that we have no objection to raise to the statements of Dr. Cabot and others regarding the negative action of strychnine on blood pressure. But we wish to guard against the inference drawn by some reviewers and expressed in independent articles, that the use of strcyhnine is based on a fallacy.

Of

What may be termed cardio-vascular well being, does not depend in great measure upon elevation of blood pressure, nor does blood pressure beyond a certain point depend to any great degree upon cardiac action. course, without cardiac action, blood pressure is nil, and up to a certain normal maximum, it increases pretty directly as the force of the ventricular contraction. Beyond this point, an increase of tension depends quite directly upon the tonus of the arterioles, or possibly upon a fibroid contraction of the smaller vessels. Conversely, in most cases of shock, as has been long known and as has been corroborated by Crile's and Turck's experiments, the essential element is depression of the vasomotor control, especially of the splachnic or portal area.

One reason why the elevation of cardiac impulse does not, in and of itself, produce a conspicuous rise of blood pressure is the simple but often forgotten truism that every onward propulsion of blood implies an equal suction through the great centripetal veins. Of course, at any one contraction, we can suppose that the ventricle sends more blood into the pulmonary artery or aorta, respectively, than it receives from the auricle during the next ventricular diastole. But, in the long run, or even for a comparatively short series of cardiac cycles-say ten minutes as a maximum-just as much blood must flow through any one chamber of the heart, as through each of the others. No matter how great the muscular power of the heart, it cannot produce a marked rise of blood pressure immediately ahead of the semilunar valves unless a large mass of blood is actually there to be pumped out.

Any great rise or fall in blood tension in the arterial system usually depends upon twofactors, the volume of blood and the tone of the arterioles. The total volume of blood is diminished immediately after hemorrhage and by prolonged deprivation of liquids. It is somewhat doubtful whether there is a genuine volumetric plethora. But, both physiologically and pathologically, the amount of blood in active circulation depends largely upon the state of the splanchnic area and, as can be shown by experimental ligation of the portal vein. or as is really shown in every case of fatal shock, in man or animals, it is possible to bleed to death into one's own abdominal vessels. Variations in the capacity: of the pulmonary vessels are said to be almost nil, congestion and ischemia depending upon the bronchial branches of the aorta.

A

An essentially weak heart obviously is associated with low blood pressure. A heart whose action is increased within physiologic limits. does not necessarily produce a correspondingly marked increase of blood tension. heart whose action is increased pathologically by hypertrophy usually accompanies a statə of increased blood pressure. When such a condition occurs in interstitial fibrosis of the kidneys, with corresponding changes in the vessels, it is obvious that, in spite of the high tension, the circulation may be inefficient, on account of the difficulty of forcing, blood through the arterioles into the capillaries, where, alone, its essential function of nutrition and removal of waste, is accomplished.

The therapeutics of strychnine must depend upon the exact condition to be met. Obviously, as strychnine does not produce strictly tonic spasm even in toxic dose, it would not be of great service when the essential condition is relaxation of arterioles, as in shock, except as indicated for concomitant essential cardiac weakness. In such cases, the proper treatment is atropine in m.g. dose, adrenalin, say ten drops of the 1:1000 solution, and rectal or subcutaneous. injections of 6:1000 salt solution. But, while strychnine is not an ideal remedy in such conditions, it is plainly not directly contraindicated, as are nitroglycerine and alcohol, both of which are frequently employed. would require too much space to enter into the differentiation between cardiac and vascular failure and, indeed, the diagnosis depends largely upon individual judgment. As a rule, when there is no great renal complication and no special indication for, or a contraindication of, digitalis, strychnine is to be chosen.

It.

Probably the majority of cases in which strychnine is to be used as a circulatory

tonic may be grouped as (1) chronic weak hearts, functionally or organically involved, and (2) emergency cases of sudden heart fail. ure, or those in which it is desired to tide the heart over a strain like an operation.

Aside from its action on the cardio-vascular apparatus, strychnine seems to be a vaiuable tonic to the muscles generally, apparently to the nervous system itself, and, almost certainly, to the various glands. Quite in analogy to its action on the cardio-vascular apparatus, strychnine is an excellent uterine stimulant in the early stages of labor, when intermittent contractions are wanted, while it is worthless to secure the permanent contraction desired after the expulsion of the placenta. Vice versa, ergot should not be used until the uterus is empty, or until just before the time at which the expulsion of the placenta can be confidently expected.

It seems rather too much to ask the profession to set aside the empiric observation of restoration of cardiac tone from the use of strcyhnine. The writer recalls, in addition to the ordinary run of cases of acute and chronic heart failure, one of delirium tremens with extreme hepatic and renal degeneration. When practically immediate death seemed inevitable, morphine was used to secure euthanasia. Then a consultant, not appreciating the state of the liver and kidneys and the failure of hopeful therapeutics, denounced the morphine as tending to lock the excretions and ordered strychnine. The heart had stopped for a appreciable interval, perhaps half an minute, but immediately responded for a few minutes. Similar experiments have, of course, been employed on the lower animals, even on the separated heart, and they establish the direct efficacy of stroyhnine as an essential cardiac stimulant.

To abort a cold, Dr. Potter gives 7 grains of sodium salicylate in one-half dram each of syrup of orange and aromatic spirits of ammonia every four hours.

PRUSCHINSKY, of Warsaw, Russia, saved the lives of two persons who had poisoned them selves with opium and morphine respectively, by the intravenous injection of solution adrenalin chloride. He reported the cases to the local medical society, with the result that every physician in Warsaw received a notification from the society to the effect that similar poisoning cases should be immediately sent to the hospital of Dr. Pruschinsky. Pruschinsky thinks ardenalin should be tried in cases of strychnine poisoning. -Therap. Notes.

IF a general practitioner is treating infectious patients at the time he is called to attend a woman in labor, he should take a full bath and make a complete change of clothing.

GLUTTONY AS A CAUSE OF SYMPTOMATIC EPILEPTIC CONVULSIONS.-W. P. Spratling describes a type of epilepsy due to errors of diet which is fairly common and is generally amenable to treatment. The patients are usually middle-aged men of plethoric phy. sique, leading inactive lives, and eating and drinking to excess. The primary cause of the convulsive attacks in these cases seems to lie, first in a weak stomach, and second in some obscure disorder of metabolism. The type of convulsion induced is usually of the grand mal variety, though petit mal seizures are also observed. The treatment is that of the toxic state induced by the faulty metabolism and is mainly dietetic and hygienic.Medical Record.

THE REMEDY FOR QUACKERY.-We must reform our ways. We must cultivate the highest ethical and that means moral standard, so that we shall be looked upon as the first refuge in the hurricane of greedy selfishness that is overwhelming society since the era of the Captain of Industry began. Be pure and clean; think, feel. act and speak, only from the most disinterested motives; and the time will not be long when the world will recognize your worth and trust you as you deserve. Nothing is so urgently needed today as men who are worthy of confidence. We must improve our methods of treatment. We must use better remedies, and apply them more intelligently. We must study our cases better, must learn to recognize the pathologic conditions, rather than to name the diseases. We must learn to know our remedies, and to see the precise indications for the use of precise remedial agents; and to recognize the effect of these so that we use neither too little nor too much, but just enough to accomplish our definite, well-considered purposes. Guesswork and chance must be eliminated from our practice. We must be prepared to use that most impressive branch of our art, prognosis, so as tu teach our patients our mastery of the case in a way no quack can possibly do. These are the things that make for better doctors, and we can not afford to be turned aside from anything that tends in that direction, by the sneers of self-interest or arguments addressed to prejudices, that do not touch the merits of the question. And if there be any other or better methods of opposing quackery the writer knows of them not.-W.F. Waugh, in The Alkaloidal Clinic.