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,
Fine J, Palmerio C, Rutenburg S. New Developments in Therapy of Refractory Traumatic Shock. Arch Surg. 1968;96(2):163–175. doi:10.1001/archsurg.1968.01330200001001
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