Mechanism of action:

• Prostaglandins, prostacyclins, and thomboxane cause direct gastric mucosal injury
• Stimulation of chemoreceptor trigger zone in the medulla causes nausea/vomiting
• Activation of the respiratory center in the medulla causes hyperventilation and respiratory alkalosis
• Interference with cellular metabolism (Krebs cycle and oxidative phosphorylation) causes metabolic acidosis

Clinical features

• Tinnitus
• Vertigo
• Nausea and vomiting
• Diarrhea
• Hyperpnea (tachypnea and hyperventilation)
• Hyperthermia (due to disturbances with oxidative phosphorylation)
• Lethargy and confusion

Diagnostic tests

• Serum ASA level < 30 = therapeutic; > 40 = toxic; > 100 = absolute indication for HD regardless of symptoms
• Check K (goal is to prevent both hypo AND hyperkalemia), Cr (renal failure may indicate a need for HD), lactate (can increase due to direct cell injury), and PT (ASA can cause coagulopathy)

Treatment goals

• Keep salicyclate (which is a weak acid) in it’s charged and deprotonated form to prevent it from crossing into the blood brain barrier by maintaining alkalemia

Management

• ABCs – only intubate if evidence of HYPOventilation
• Activated charcoal if patient awake and oriented
• Sodium bicarbonate to keep urine pH ~ 8 and serum pH alkalotic and pH < 7.6 (still give bicarb even if evidence of alkalosis as long as pH < 7.6)
• IVF
•  Prevent hypokalemia and HYPERkalemia because hyperkalemia can cause increase H secretion into the blood through the kidney H/K transporter which causes acidosis
• Glucose if altered mental status as neurohypoglycemia can be caused by ASA overdose despite a normal serum glucose level
• No acetazolamide because while that increases urine pH it causes increased H to be secreted into the blood causing acidosis which promotes the uncharged form of ASA which is toxic