Aspirin/Salicylate Toxicity

Toxicokinetics

Toxicity:

– Single dose > 150 mg/kg

– Acute ingestion level  35-40 mg/dl = tx threshold

-Acute ingestion level > 90 mg/dl = bad

– Chronic ingestion level > 60 mg/dl

Peak plasma – often delayed d/t pylorospasm or bezoar formation

  • Consider frequent level rechecks and activated charcoal even if delayed presentation

Vd – Increases  w/ acidemia favoring un-ionized form of salicylic acid which crosses BBB more easily -> seizure

Presentation

-GI upset – NV or hemorrhagic gastritis

-Hyperpyrexia – d/t oxidative uncoupling

-Acid base – early primary resp alkalosis, developing superimposed metabolic acidosis, ultimately with metabolic and resp acidosis – can look like anything in b/t on the way

-AMS

-Hearing changes – tinnitus vs muffled vs “whooshing”

-ARDS – can be asymmetric

Chronic toxicity – Subacute presentations usually misdiagnoses in elderly pts as infection, delirium NOS

UA – often positive for ketones and blood w/o cells

Treatment

Activated Charcoal – Binds aspirin well, low threshold

  • Can repeat q4h if there’s ongoing absorption but needs bowel reg w/ this strategy

Alkalinization – Salicylate is a weak acid, alkalinization ion traps in urine and out of CNS compartment

  • Bicarb gtt – 3 amps NaHCO3 in 1 L D5W at 200 ml/hr
  • Goal urine pH ~ 8
  • Do Not Stop for Pulmonary Edema! – ARDS can develop d/t tox, stopping gtt will worsen toxicity and pulmonary edema

Replace K+ – Hypokalemia will cause renal H+/K+ exchange to recover K+ and cause concurrent acidification of urine preventing adequate treatment/ion trapping – goal K+ > 4

Therapeutic hyperglycemia – toxicity causes hypoglycorrachea (low CNS glucose) low threshold for empiric dextrose bolus and gtt w/ target to keep high peripheral glucose

Check VBG and chemistry – with every salicylate level check

Dialysis – for severe poisonings

Consider active cooling