Salicylates

Salicylates is a topic covered in the Washington Manual of Medical Therapeutics.

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General Principles

  • Salicylate toxicity may result from acute or chronic ingestion of acetylsalicylic acid (ASA). Toxicity is usually mild after acute ingestions of <150 mg/kg, moderate after ingestions of 150–300 mg/kg, and generally severe with overdoses of 300–500 mg/kg.
  • Toxicity from chronic ingestion is typically due to intake of >100 mg/kg/d over a period of several days and usually occurs in elderly patients with chronic underlying illness. Diagnosis is often delayed in this group of patients, and mortality is approximately 25%. Significant toxicity due to chronic ingestion may occur with blood concentrations lower than those associated with acute ingestions.
  • Topical preparations containing methyl salicylate or oil of wintergreen can cause toxicity with excessive topical use or if ingested.

Pathophysiology

  • At toxic doses, salicylates disrupt aerobic respiration in the mitochondria. They uncouple oxidative phosphorylation from ATP production by disrupting the proton gradient in the intermembrane space.
  • The resultant impairment of aerobic respiration produces an elevated anion gap metabolic acidosis, impairs effective glucose utilization, and leads to widespread cellular metabolic failure.
    • The brain is particularly reliant on glucose as an energy source. Disruption of aerobic metabolism by salicylate poisoning leads to rapid depletion of central nervous system glucose through less effective anaerobic respiration.
  • In the early stages of poisoning, salicylates directly stimulate the medullary respiratory centers, producing the characteristic early tachypnea and primary respiratory alkalosis. As poisoning progresses, metabolic acidosis worsens and the tachypnea becomes compensatory.

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General Principles

  • Salicylate toxicity may result from acute or chronic ingestion of acetylsalicylic acid (ASA). Toxicity is usually mild after acute ingestions of <150 mg/kg, moderate after ingestions of 150–300 mg/kg, and generally severe with overdoses of 300–500 mg/kg.
  • Toxicity from chronic ingestion is typically due to intake of >100 mg/kg/d over a period of several days and usually occurs in elderly patients with chronic underlying illness. Diagnosis is often delayed in this group of patients, and mortality is approximately 25%. Significant toxicity due to chronic ingestion may occur with blood concentrations lower than those associated with acute ingestions.
  • Topical preparations containing methyl salicylate or oil of wintergreen can cause toxicity with excessive topical use or if ingested.

Pathophysiology

  • At toxic doses, salicylates disrupt aerobic respiration in the mitochondria. They uncouple oxidative phosphorylation from ATP production by disrupting the proton gradient in the intermembrane space.
  • The resultant impairment of aerobic respiration produces an elevated anion gap metabolic acidosis, impairs effective glucose utilization, and leads to widespread cellular metabolic failure.
    • The brain is particularly reliant on glucose as an energy source. Disruption of aerobic metabolism by salicylate poisoning leads to rapid depletion of central nervous system glucose through less effective anaerobic respiration.
  • In the early stages of poisoning, salicylates directly stimulate the medullary respiratory centers, producing the characteristic early tachypnea and primary respiratory alkalosis. As poisoning progresses, metabolic acidosis worsens and the tachypnea becomes compensatory.

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