THE UNCOMPENSATED loss of fluids from the gastrointestinal tract or the immobilization of significant amounts of extracellular fluid into body tissues or cavities produces a diminution of physiologically effective extracellular volume that may be characterized by concentration of the formed elements of the blood1; decrease in the circulating blood volume, the major portion of which is diminution of plasma volume2; increased blood viscosity,3 and depletion of total body electrolyte, quantitatively, qualitatively, or both, according to the mechanism of loss.4 If such a loss is permitted to progress in a relatively rapid manner, with concomitant inadequate replacement, the resultant oligemia may produce all variants of peripheral vascular insufficiency that, in important manifestations, resemble peripheral vascular insufficiency produced by hemorrhage or trauma, but differ as regards initiation, as regards certain clinical and laboratory findings, and, particularly, as regards definitive therapy. The first documentations of this concept were made
BERRY REL. CLINICAL ASPECTS OF ACUTE PERIPHERAL OLIGEMIA FROM PLASMA WATER AND SODIUM SALT LOSS. AMA Arch Surg. 1953;67(3):408–425. doi:10.1001/archsurg.1953.01260040415013
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