plan of procedure, many who die in the primary attack will die without the aid of surgical relief which could have saved them. Now, if it is applied as Dr. Oschner applies it, only to those cases which are inoperable at the time, it is well and will save many lives undoubtedly; but it will make a wrong impression to teach that this is a curative process, and I do not understand that this is the case, but that it is to tide them over certain conditions. If it is intended to check a great deal of wild, reckless, and ill-advised surgery, I say amen. If it is intended to raise a doubt as to the efficacy of the office of the surgeon within appropriate limits, I say nay. Dr. Blailock is unquestionably right.

DR. HERZOG, Brazoria: I only want to say I think Dr. Morris is right. Thirty years ago we did not operate for every case of appendicitis. I think I cure just as many as other doctors, and I do not perform any operation. Now, the doctors when they find a case of appendicitis say “we must operate." They operate, and say it was a very successful operation-but the patient dies the third day.

DR. JOE WOOTEN, Austin: I would like to ask Dr. Morris how he would make a differential diagnosis between fecel impaction and involvement of the appendix where he was called in and found the patient suffering from tumefaction, dullness, and tenderness over the right iliac fossa, together with fever, nausea, and vomiting? Dr. Morris: The diagnosis would in that case be very difficult. Dr. Wooten: By the Oschner method, would you expect to relieve the fecel impaction and clear up your diagnosis without resorting to the use of salines and high rectal enemas? Dr. Morris: I would give high rectal enemas. The indiscriminate use of cathartics in those cases is unwarranted, because it aggravates the condition, and, if an operation later is necessary, it makes the mortality higher.

DR. MORRIS, closing: I appreciate the general discussion that has been elicited by my paper. I think perhaps I spoke indistinctly; that the gentlemen did not get everything I said in my paper-at least the criticisms lead me to think so. The paper is denominated the medical side of appendicitis. If the gentlemen had listened closely, they would have heard me say that ultimately most cases of appendicitis fall into the surgeon's hands. I also had the pleasure of hearing Dr. Oschner express his views on appendicitis, and I have read his little book entitled "Non-Operation Treatment of Appendicitis." One statement which he makes is that he had never seen in his experience an acute case of appendicitis die when food by mouth or purgatives had been prohibited from the very outset. The surgeons themselves are still discussing the question. A member of the medical profession recently propounded some queries to Dr. Wythe, Dr. Morris of New York, and Dr. Oschner pertaining to the treatment of appendicitis. Dr. Morris said operate in all cases, regardless of time and condition. Dr.

Wythe stated that, if he was called in the first twenty-four hours, if a mild case he would not operate, and some of the more conservative physicians are pursuing the same course. My own experience of course is too limited to entitle it to much weight. I have operated on a few and treated medicinally more, and from results I think it would be well for the profession to read carefully Dr. Oschner's book on appendicitis. I believe more die from indiscriminate purgation and indiscriminate diet than from any other reasons. I also stated that in many cases an operation was necessary, but that in acute cases they should be operated upon in the first forty-eight hours, otherwise the inflammation would be out of the appendix and we would have general peritonitis. I do not claim that appendicitis should be treated exclusively by medicine, but I believe the best interests of the patients will be subserved if more attention is paid to that side of the treatment.

THE SIGNS AND PATHOLOGY OF PLEURAL LESIONS.

A. E. THAYER, M. D., GALVESTON.

My purpose in the present paper is to correlate the symptoms, both subjective and objective, with the pathology of pleural lesions, by a brief discussion, by certain diagrams, and by a series of gross specimens. The best way to bring the subject before you is to pass the chief diseases in review, and for the time I must limit myself to inflammations.

Normally there is no pleural cavity, for the two layers are everywhere in contact. For the extension of inflammations, it is important that these two layers are everywhere in motion, except at the root of the lung. Only when some pathological product has separated the two layers do we have a pleural cavity; up to that time it is only potential.

The mechanism which keeps the layers in contact is the interpleural tension; this in health is always negative, varying from -6 to 8 mm. of mercury.

Normally the two serous surfaces move over each other practically without friction. This is possible only so long as the integrity of the investing endothelial cells is preserved. In acute pleurisy without effusion, one of the first changes is swelling in the subendothelial fibrous tissue with increase in size of the endothelia, and granular degeneration of these, followed by desquamation. From the swelling the two roughened surfaces are pressed together more firmly than normal, and they stick and drag upon each other, since they can no longer glide smoothly. Hence the patient feels a quick pain in the side, which he describes as a stitch, that grows more severe upon movement and deep inspiration; partly because more of the tender surfaces glide over each other and they are more

firmly pressed together, and partly because the movement of the chest wall stretches the swollen area.

In a short time the serum of the blood in the dilated capillaries begins to ooze toward the surface of the pleura, and there it meets a fibrin ferment derived from the dead endothelia and coagulates. Now the raw surfaces are covered by a thin layer of fibrin, which is somewhat sticky, and hence the pull of one sore area upon the other is worse.

In consequence the patient limits his breathing as much as he can and bends toward the affected side to put the parts as nearly as possible in a state of physiological rest. This is a necessary condition for healing, but it brings with it the risk that the adhesions may become organized between the two layers and a permanent band of new connective tissue replace the temporary fibrin.

From the reflex along the intercostal nerves, spasm of the intercostal muscles, and diaphragmatic cramp, the whole side may be tender and painful. The intensity of these combined pains varies from trifling to extreme, and their site may be local or referred to distant points, as above the clavicle, the navel, or the inguinal fossa of the affected side. Yet another reflex is cough, dry and painful in character, and suppressed as nearly as possible. Owing to the pain, the respiration is also controlled, shallow or jerky, and more abdominal than thoracic.

Constitutional symptoms are usually slight. Fever may be absent in a mild case or run as high as 101 degrees F., but it depends in great measure upon the extent of the lesion and the cause. If the disease be bacterial, the particular kind present modifies the fever. When the pleurisy accompanies a lobar pneumonia which reaches the surface of the lung, we find the pneumococcus, and sometimes this is found without the pneumonic lesion. With bronchopneumonia the organism is commonly the streptococcus. Occasionally the staphylococcus, the bacillus coli, the bacillus of Friedlander and others cause the disease, and both as a primary and as a secondary lesion, the tubercle bacillus is responsible for a large number. As a general rule all the constitutional symptoms,

including nausea and vomiting, fever, depression, and in children, convulsions, are more distinct with the pus organisms and extensive lesions.

In a localized form the disease occurs at the apex with tuberculosis, or between the lobes of the lung, and may not be diagnosed, or over the cup shaped base of the lower lobe on the diaphragmatic pleura. In the latter case the pain and the diaphragmatic spasm may be the only local signs, together with abdominal breathing, and the resemblance to peritonitis is very close.

Physical Signs.-The affected side displays a diminished expansion, and this may be recognized in three ways: (a) By inspection from above and behind the patient. This is equivalent to examining a cross section of the chest, and is so valuable that it ought to be part of our unconscious routine in exery examination of the chest; (b) palpation of the two sides with the flat hand. The entire palm and fingers should be placed at exactly corresponding points on the two sides at the same time, while the patient takes as deep a breath as he can; (c) the cyrtometer. The expensive instruments are not necessary. Two flat pieces of lead joined by a piece of stout rubber tubing serve the purpose. With the rubber junction over the spine, the lead bands are brought round on a level and closely moulded to the chest, and the ends crossed in front. Upon the ends a mark is made where they meet in forced expiration and another in deep inspiration, and they are then removed. A tracing of the two on paper, with a rather soft pencil will give the outline of the two sides and the amount of expansion on each. The only thing it does not show is the local lagging when one part, usually over the lesion, expands slowly and irregularly, but this is noted by the eye and can be marked upon the diagram. Such a measurement will give accurate results, even when the chest is deformed.

As a rule there is no marked change in the percussion note, unless the area is large and the exudate thick, and usually this combination is found in the chronic pleurisies. The note would