Salicylate is a potent pharmacologic agent, and the rational therapy of salicylate intoxication must be based on an understanding of its pharmacologic actions and consequent pathophysiologic effects.l Because it acts to uncouple oxidative phosphorylation in a manner analogous to that of 2,4-dinitrophenol, salicylate is, first of all, a general metabolic stimulant.2 Oxygen consumption, carbon dioxide formation, and heat production are increased by its action; consequently, oxygen requirement, blood CO2 concentration, and the need to eliminate heat are also increased. Respiration, heart rate, and cardiac output must increase to satisfy the demands imposed by the acceleration of metabolic processes.

Second, saiicylate interferes in a complex manner with the normal metabolism of carbohydrate.3 Many factors seem to be involved, some tending to decrease and others to increase the blood glucose concentralion, and, clinically, either hyperglycemia or hypoglycemia may be observed. Hyperglycemia may be partially explained by the release of epinephrmne due to activation of hypothalamic sympathetic centers. However, large doses of salicyiate also decrease aerobic metabolism and increase glucose-6-phosphatase activity, effects which tend to increase the blood glucose level. Hypoglycemia, on the other hand, may be caused by an increased utilization of glucose by peripheral tissues or by interference with gluconeogenesis by salicylates. Recent studies suggest that brain glucose concentration may be decreased despite minimal alterations in blood glucose level.4

As a result of these salicylate-mnduced alterations in carbohydrate metabolism, organic acids, particularly lactic, pyruvic, and acetoacetic, accumuiate.5 Infants appear to be particularly susceptible to the toxic effects of salicylate on carbohydrate metabolism and are more likely to have disturbances in blood glucose concentration and metabolic acidosis than are older children.

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