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New Developments in Therapy of Refractory Traumatic Shock

Jacob Fine, MD; Carlo Palmerio, MD; Selma Rutenburg, MD
Arch Surg. 1968;96(2):163-175. doi:10.1001/archsurg.1968.01330200001001.
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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,


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