Aspirin (salicylate) toxicity can lead to a complex acid-base disorder due to its effects on multiple systems. Here’s how aspirin toxicity typically manifests in terms of acid-base balance:

Primary Effects:

1. Direct Respiratory Alkalosis:
   • Aspirin directly stimulates the respiratory center in the medulla, causing hyperventilation. This leads to a decrease in pCO2 (hypocapnia), which shifts the pH towards alkalosis.
   • Expected Findings:
     • Low pCO2
     • Elevated pH (above 7.45)
2. Metabolic Acidosis:
   • Aspirin uncouples oxidative phosphorylation, leading to increased production of lactic acid and ketoacids by interfering with cellular metabolism. This causes a decrease in HCO3- due to the accumulation of unmeasured anions.
   • Additionally, aspirin can cause direct renal tubular damage, impairing bicarbonate reabsorption.
   • Expected Findings:
     • Low HCO3-
     • Decreased pH (below 7.35) or normal if compensated

Acid-Base Picture:

• Mixed Acid-Base Disorder: Aspirin toxicity commonly results in a mixed respiratory alkalosis and metabolic acidosis. This is because:
  • Initially, you see respiratory alkalosis due to hyperventilation.
  • As toxicity progresses, metabolic acidosis develops, often leading to:
    • Normal pH if the two disorders balance each other out (compensated).
    • Acidemia if the metabolic acidosis predominates.
    • Alkalemia if the respiratory component is still dominant (less common in severe toxicity).

Diagnostic Clues:

• Anion Gap: The metabolic acidosis in aspirin toxicity is usually high anion gap due to the accumulation of organic acids. Calculate the anion gap with:
  • Anion Gap = Na+ – (Cl- + HCO3-). A gap significantly higher than 12-14 suggests increased unmeasured anions.
• Serum Salicylate Levels: Direct measurement of salicylate levels can confirm toxicity.
• Urinary pH: Salicylates can cause paradoxical aciduria (acidic urine) despite systemic alkalosis due to their effects on the kidneys.
• Osmolal Gap: Might be increased due to the osmotic effects of salicylates.

Treatment Considerations:

• Supportive Care: Correct fluid and electrolyte imbalances.
• Alkalinization: Sodium bicarbonate can be used to alkalinize urine to enhance salicylate excretion and to correct systemic acidosis. It also helps in reducing CNS toxicity by converting salicylates to their less toxic, ionized form.
• Activated Charcoal: If ingestion was recent, to bind salicylates in the GI tract.
• Dialysis: In severe cases with significant CNS symptoms, renal failure, or if alkalinization is ineffective.

Understanding the complex nature of acid-base disturbances in aspirin toxicity is crucial for proper diagnosis and management. Each patient might present differently based on the level of toxicity, time since ingestion, and their underlying health status.