Check the patient is not in a dysrhythmia.If your patient require resuscitative measure for seizures, coma, hypotension or pulmonary oedema this is a time critical situation and indicates a high risk of mortality.Alkalisation promotes the salicylate to its ionised state and therefore cannot be reabsorbed across the renal tubular epithelium This can be used to our advantage by alkalinising the urine. Salicylate will move into the extravascular spaces in acidaemia (e.g.Hepatic metabolism with first order kinetics except in overdose it changes to zero order as the metabolic pathway becomes saturated.Absorption can be delayed with enteric coated compounds but also erratic if large doses or consumed due to the formation of a bezoar.Highly protein bound (although in overdose this is saturated and free salicylate levels increase).This process can actually cause a fever (slightly ironic). This results in in a build up of lactic acidosis and a resultant metabolic acidosis. Its other effect is uncoupling of the oxidative phosphorylation which in simple terms means it halts the electron transport chain in the mitochondria. It stimulates the respiratory centres causing hyperpnoea (one of the first signs of toxicity, although rarely seen in children), noted as a respiratory alkalosis on a gas sample. Salicylates irreversible block the COX-1 pathway and modify the COX-2 pathway resulting in a decrease in inflammation (reduced prostaglandin synthesis) and platelet aggregation. The chronic toxicity is under recognised due to its vague presentation (patient might just be confused) and therefore an increased mortality, particularly in the elderly. Management is largely urinary alkalisation and haemodialysis.
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