In severe intoxication, patients can develop kidney and respiratory failure, cardiovascular collapse and coma. The common symptoms in all settings are nausea, vomiting, tachypnea, tinnitus, stupor, coma, and convulsions. Figure 2.Ĭlinical effects of salicylate intoxication. In chronic intoxication and in the elderly, symptoms will occur at lower levels. Most people will have some clinical effect of intoxication with serum levels > 40 mg/dL. The symptoms of salicylate intoxication differ according to the age of the patient and whether the intoxication is acute or chronic. Clinical and laboratory findings in salicylate intoxicationįigure 2 lists the most common findings in salicylate intoxication. ![]() Alkalinization of the urine increases the ionized form of salicylate which is then unable to diffuse out of the urine back into the tubular cell. The excretion of salicylate is pH dependent as well. The enzymatic metabolism of salicylic acid is saturable and at high levels, most of the removal is then due to excretion of salicylic acid in the urine. The metabolism and excretion of salicylic acid is also concentration dependent. This is very important clinically since salicylate causes its major toxicity once it is intracellular. Only the non-ionized form can penetrate the cell membrane and therefore when the systemic pH falls and more salicylate is in the form of salicylic acid, there is a greater distribution into the cells. The distribution of salicylic acid is also pH dependant. ![]() With overdoses, the protein binding is saturated and the V d increases to 0.4 L/kg or greater. At pharmacologic doses, binding to albumin is high, which keeps the compound extracellular and the V d low (0.2 L/kg). Salicylic acid is responsible for all of the toxic effects of ASA ingestion.
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