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BOSTON MEDICA

WASHINGTON
MEDICALERANNALS

*

AN ATTEMPT TO EXPLAIN THE PERITONEAL ADHESIONS THAT SO FREQUENTLY PRECEDE TYPHLITIS AND APPENDICITIS.

By A. F. A. KING, A. M., M. D.,

Washington, D. C.

Something more than a year ago (November 30, 1904) I read before this society a paper on the Etiology of Appendicitis in which it was maintained that the disease began in many cases by the breaking up, stretching or other traumatism of adhesions between the appendix, caecum and neighboring surfaces of peritoneum; and further that the injury of these adhesions was due to violent action of the psoas muscle, etc., from the use of the bicycle. In the discussion, no one agreed with me; adverse criticism was universal. This was not unexpected, nor was it altogether undeserved, for, while I am convinced that the future will prove that I was in the main correct, I am willing to admit that my charge against the bicycle was somewhat too severe, or overdrawn—perhaps I should say too exclusive, for the reason that other forms of exercise-baseball, football, polo, rowing, the strains incident to stepping on and off cars, etc.-which began to become popularized coincidently with the bicycle, may also have contributed to injure the peritoneal adhesions, much in the same manner as bicycling. I do not wish (as the lawyers say) to nolle pros. my indictment against the bicycle by any means, but I am willing to ameliorate it by extending the charge to its etiological confederates.

However, it is not the purpose of the present paper to reopen this discussion, though a direct reference to it will be unavoidable.

My purpose now is to enquire why so large a proportion of modern men and women should have the morbid peritoneal ad

hesions to which reference has been made. Without these adhesions, the action of the bicycle and similar forms of strain would have no application at all to appendicitis.

In my former paper I quoted the statements of Dr. With (London Medical Record, 1880, Vol. VIII, page 213), that the appendix was found diseased in 110 out of 300 autopsies, and of Dr. R. H. Fitz (Trans. Association of American Physicians, Vol. I, 1886, page 118), that there is evidence of disease of the appendix in more than one out of every three autopsies; and of Dr. Robinson, who found peritoneal adhesions between the psoas muscle and whatever came in contact with it, in 72 per cent. of 128 mixed autopsies.

He

Dr. Howard Kelly, in his recent elaborate treatise on appendicitis (page 249), says that fibrous adhesions were found in 325 out of 3,770 autopsies (8.62 per cent.) in the Boston City and Johns Hopkins Hospitals, but adds that "this percentage is undoubtedly too low, and it is probable that adhesions were present in some cases not mentioned." further says: Hartley quotes Hektoen as finding adhesions 42 times in 280 cases (15 per cent.); Maurin 16 times in 112 cases (14.3 per cent.); McBurney in 230 autopsies found evidences of chronic inflammation (adhesions) in 70 per cent.; Boody in 528 autopsies found adhesions in 126 (24 per cent.).”

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Finally I may quote Dr. Kelly once more as follows: "No doubt adhesions about the appendix are so common as to indicate that many people, at some time during their lives, have had an inflammatory process involving the appendix, which has not however caused any serious consequences." In most cases he says there is no evidence of ill health or discomfort," etc.

Admitting, then—as I think we must-that these latent peritoneal adhesions around the appendix and caecum really are of common occurrence, how do we account for them? Hitherto they have been universally ascribed to inflammation. In fact the existence of peritoneal adhesions has been taken as prima facie evidence of peritonitis. But is this really true? I venture to think it is not. Of course all depends upon our definition of inflammation, and the term has a great many different definitions. Nowadays inflammation is held to imply a coexistent or preexistent septic infection. Such a process as an aseptic inflammation does not seem at all admissible with our present way

of thinking. Yet that what we recognize as morbid adhesions-differing in no respect from inflammatory adhesions—can occur without either infection or inflammation, is easily demonstrable. Note, for example, the adhesions that invariably occur in a joint that has been kept for some time immovable during the treatment of a fractured bone. The joint itself may not be implicated in the fracture, there may have been no external wound through which infection could occur, and yet we find adhesions, which, if we examined them post mortem, would be found indistinguishable from the adhesions of inflammation. Any joint kept at rest, with or without fracture, will in time develop such adhesions. Can we say they are always of inflammatory origin? They have been perfectly latent, without any discomfort or ill health; and with no redness, pain, heat or swelling; no fever and no septic infection.

May we not rather regard such adhesions as processes of evolution of adaption of structure to function-of readjustment of organs, to readjusted or modified use? Under such circumstances, if the adhesions are to be considered of inflammatory origin, we should have to look upon the inflammation as a physiological process rather than as an abnormal one. The reconstructed organs fastened by adhesions, will of course have suffered some degradation of functional activity. Instead of remaining, as they originally were, endowed with normal motility, they will, from continued disuse of this endowment, cease to possess it, and become as it were disfranchised of that more exalted plane of functional activity, which would, under circumstances of natural use, have been continued indefinitely without interruption.

Nature is frugal. Perhaps the cheapest tissue in the body is the connective or fibrous tissue out of which these adhesions are constructed. Everywhere throughout the body, and in all organs, liver, kidneys, lungs, as well as peritoneum and joints, where the normal functionating tissues atrophy, the almost functionless fibrous tissue takes their place. We call it fibrosis, sclerosis, cirrhosis and areolar hyperplasia. When a moving organ, from disuse ceases to move in conformity with the design of its original construction, it becomes fixed by adhesions. Nature will not support the more elaborate and more costly tissues of a moving structure when a cheaper fixed and immovable one is sufficient to meet the functional requirements of the individual under the environing conditions in which he lives.

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