THE RENAL RESPONSE TO ADMINISTRATION OF ACETAZOLAMIDE (DIAMOX®) DURING SALICYLATE INTOXICATION

Advanced salicylate intoxication in young children may produce severe acidosis due not only to the production and accumulation of organic acids in tissues, but also to the diminished content of buffer cation which is secondary to the loss of buffer cation during the excretion of organic acids. The excretion of an intensely acid urine all but prevents the excretion of free salicylate and thereby perpetuates the toxic effects of this ion. Despite severe deficit of buffer cation, the kidney responds to administration of a carbonic anhydrase inhibitor with excretion of alkaline urine. The magnitude of the loss of buffer cation is unpredictable both before and after enzyme inhibition. However, the systemic acidosis may be controlled by infusion of solutions of sodium bicarbonate, but frequent determinations of pH and content of carbon dioxide in the serum are mandatory. While the alterations in acid-base disturbance may be controlled during administration of acetazolamide, the occurrence of neurologic complications late in the course must be accepted as a serious additional hazard which may preclude the successful therapeutic value of this agent.