April 10, 1926


Author Affiliations

From the Albert Kuppenheimer Fund of the Michael Reese Hospital, the Nelson Morris Memorial Institute for Medical Research, and the Hull Physiological Laboratory of the University of Chicago.

JAMA. 1926;86(15):1112-1113. doi:10.1001/jama.1926.02670410008004

In this paper I present a brief preliminary report of a group of experiments, the object of which was, if possible, to obtain more information concerning the causes and the nature of the violent toxemia occurring in acute hemorrhagic pancreatitis. Ultimately, it was hoped, a more rational and effective treatment of the disease might be evolved than is now generally employed.

No attempt will be made here to discuss the literature on acute pancreatitis, or to describe the clinical manifestations of the disease. For this information the reader is referred to the recent very inclusive paper by Moynihan.1 Suffice it to say that almost every conceivable method by which the pancreas could be seriously injured has been utilized to reproduce in animals the clinical picture of acute pancreatitis; all that is necessary is that a sufficient amount of pancreatic tissue be suddenly so devitalized that an extensive necrosis and

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