position is an endowment of the normal uterus. If it becomes displaced to a pathological degree from falls or concussions, it is because it has lost its power of normal recoil, that is to say, the organ, or its sustaining element, is in a diseased condition. The entire medico-legal field is a wide one and presents many obstacles to a free investigation. I claim to have opened up a portion only, and, dropping the metaphor, I surrender to others the right of evolution. DISCUSSION ON PNEUMONIA. QUESTIONS RELATING TO ACUTE LOBAR PNEU MONIA. By AUSTIN FLINT, M. D., of New York County. Read November 17, 1885. MR. PRESIDENT: It will not, I think, be questioned that acute lobar pneumonia offers points of inquiry which have much pathological interest and practical importance, and that this disease has been judiciously selected by the Committee of Arrangements for the scientific business of our Association as a subject for discussion. Acknowledging the honor of having been requested to open the discussion, I will not consume any time by introductory remarks, but proceed at once to consider briefly a series of questions embracing topics concerning which, at the present time, there are differences of opinion. These questions will be severally discussed by Fellows who have prepared brief papers, and it is hoped that others will be sufficiently interested. to engage in the discussion. I. Is acute lobar pneumonia a primary local inflammatory disease, or is it an essential fever, the pulmonary affection being secondary thereto and constituting its anatomical characteristic ? If the pneumonia be purely a local affection, the fever which accompanies it, and all the phenomena therewith associated, are symptoms of, or secondary to, and dependent upon, the local affection. If, on the other hand, the disease which we call pneumonia be an essential fever, the pneumonic affection is a local manifestation of the disease in the same sense as the characteristic intestinal affection is a local manifestation of typhoid fever. It is only within a few years that the latter of these two pathological views has been entertained. Indeed, heretofore, pneumonia has, by common consent, been regarded as typical of a purely local inflammatory affection, and measures of treatment as applied to this affection have been studied with reference to principles which should govern their application to all acute inflammations. In 1877 I read a paper at the Annual Meeting of the New York State Medical Society in support of the doctrine that acute lobar pneumonia is not a purely local affection, but an essential fever. At that time this doctrine had very few supporters in this country, and the same may be said of other countries. The most prominent of the advocates of the doctrine was Juergensen, author of the article on pneumonia in Ziemssen's "Cyclopædia." Since that date the doctrine has been steadily gaining ground, but it is doubtful if at the present time it has been adopted by the majority of those of our profession who undertake to grapple with pathological questions of this character. It is probably true that a large majority of the profession, as a whole, hold to the opinion that the affection is primarily and purely a local inflammation. I suppose it to be true that acute lobar pneumonia is an inflammatory affection-that the pneumonic exudation is the result of an inflammatory process. Some late writers, however, have come to the conclusion that the local affection is non-inflammatory.2 The doctrine that the pneumonic affection is the local manifestation of an essential fever is sustained by facts which distinguish this affection from primary acute inflammations, and which affiliate it with febrile diseases. The more prominent of these facts are embraced in the following enumeration: 1. Acute lobar pneumonia, is characterized by an enormous exudation into the pulmonary alveoli, and this exudation may be rapidly absorbed, leaving the tissues intact. This anatomical fact has no analogue in the history of acute primary inflammations. The deposit within the mesenteric glands in typhoid fever is analogous, except that the quantity is much less. 1 Vide “Transactions of the New York State Medical Society,” 1877. • Vide article by Dr. John Galt, in the "Louisville Medical News." Sir Andrew Clark regards the exudation as non-inflammatory. 2. Acute lobar pneumonia never persists and becomes a chronic affection. Is this true of any acute primary inflammatory affection? 3. Acute lobar pneumonia is never referable to any appreciable local condition, nor is it possible, by any form of traumatic injury, to produce this affection. 4. The ordinary causes of disease are not capable of producing acute lobar pneumonia. The traditional belief that the affection may be caused by cold has no solid foundation, and is now abandoned even by the Germans, who have been accustomed to reckon cold as the great etiological factor in many affections. 5. That a special or specific cause is involved in the causation of acute lobar pneumonia, is rendered probable by its occurrence especially at certain seasons of the year, by its relatively greater frequency in certain climates, by its infrequency in infancy, and by its prevalence at certain times and places as an endemic disease. 6. Acute lobar pneumonia differs from an acute primary local inflammation in the occurrence, as a rule, at the outset, of a pronounced chill comparable to that which announces a malarial paroxysm. This fact distinguishes it from an acute primary local inflammation. 7. In the course of the disease the temperature and associated febrile phenomena bear no constant relation to the local affection. In this respect the disease is in affiliation with a selflimited fever, and differs from an acute local primary inflammation. 8. Experience shows that acute lobar pneumonia is influenced therapeutically by measures addressed to the fever rather than to the local affection. II. What facts and rational grounds, with our present knowledge, can be cited in support of the doctrine that acute lobar pneumonia depends on the presence of a specific micro-organism? Changing the form of this question, it is, What proof have we, at the present time, of the truth of the assertion that acute lobar pneumonia is a parasitic disease? I shall not enter into any discussion of this question. The question will be answered by one fully competent to consider it. I may state, however, the essential requirements for accepting the parasitic doctrine as applied to any disease. First, a particular micro-organism must be uniformly present in cases of the disease. Second, it must be shown that this organism is not present in other diseases, nor in the healthy body. Third, pure cultures of the organism must be found capable of producing the disease when introduced into the bodies of healthy animals. It is claimed by Carl Friedländer and others that these requirements have been fulfilled as regards the disease under consideration. The facts on which this claim rests will be presented by my colleague Professor Janeway. III. What conditions or circumstances incident to acute lobar pneumonia tend to render the disease fatal? Some twenty or more years ago the late Dr. Hughes Bennett published a monograph in which he maintained that acute lobar pneumonia has no tendency per se to a fatal termination, death being in all instances due to complications. This conclusion was based on examinations after death in hospital cases. Co-existing lesions were invariably found to which a fatal result was attributable. As a general statement, I believe it to be true that this disease, disconnected from associated affections or lesions, and, I will add, exclusive of certain events which may be called accidents, intrinsically tends to recovery. If this be a true statement, it is obviously of much importance to consider what are the conditions or circumstances incident to, but not necessarily connected with, the disease, which tend to render it fatal. This question opens a field which I can only cursorily survey in this paper. Pneumonia is not infrequently secondary to diseases which are more or less grave, such as typhoid fever, rubeola, pertussis, valvular lesions of the heart, renal disease, etc. Under these circumstances it is not the pneumonia but the combination which kills. Again, the disease, in some instances, appears to act as an exciting cause of other disease. We all know how |