The Prompt Treatment of Salicylism with Sodium Bicarbonate

Abstract

The ingestion of toxic quantities of salicylate results in alterations of acid-base homeostasis which at times may be profound. The pathogenic mechanisms include hyperventilation secondary to respiratory stimulation, increase in metabolic rate, and disturbances in carbohydrate and lipid metabolism.^1-6 Further alterations frequently follow the vomiting and dehydration which are so often associated with ingestion of larger amounts of salicylate. There is no specific antidote for salicylism. Treatment is currently aimed at augmenting elimination of salicylate via the urine or, in severer cases, directly from the blood by hemodialysis or exchange transfusion. Ninety per cent of ingested salicylate is excreted by the kidney. It is eliminated in three forms: free salicylate, salicyluric acid, and salicylglucuronide. At an acid pH, free salicylate accounts for approximately 20% of the total excreted. However, as the urine pH rises above 7.0 both the relative percentage and the total amount of free salicylate increase progressively.