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New Developments in Therapy of Refractory Traumatic Shock
Jacob Fine, MD;
Carlo Palmerio, MD;
Selma Rutenburg, MD
AMA Arch Surg. 1968;96(2):163-175.
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IN THIS paper I shall present new evidence in the support of the hypothesis that a bacterial factor is responsible for the refractory state of traumatic shock. This new evidence warrants reshaping the hypothesis as follows: the refractory state of shock is the result of ischemic damage to the reticuloendothelial system (RES) in liver and spleen, and this injury allows a neurotoxin of bacterial origin to produce fatal collapse of the peripheral circulation. The evidence will include data showing that perfusion of the arterial blood for less than one hour through a freshly excised donor spleen eliminates the toxin and thereby effects recovery from the state of shock.
Report of Cases
I shall begin with a recent clinical experience. A man of 70 left the hospital in good order a week after surgical repair of an obstructing duodenal ulcer. Five days later, when he returned for inspection of his wound,
. . . [Full Text PDF of this Article]
Author Affiliations
Boston
From Department of Surgery, Harvard Medical School; Surgical Research Department, Beth Israel Hospital; and Harvard Surgical Research Laboratories, Boston City Hospital, Boston.
Footnotes
Submitted for publication June 7, 1967.
Read before a meeting at the University Hospital, Stanford University Medical School, Jan 26, 1967.
Reprint request to Sears Laboratory of Surgical Research, Boston City Hospital, 818 Harrison Ave, Boston 02118 (Dr. Fine).
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