Clinical scenario: Vomiting | Dizziness | Rapid breathing | Tablets intake
A 16-year-old girl is brought to the emergency department with nausea, vomiting, ringing in her ears, dizziness, and increasing rapid breathing. Her mother says she developed these symptoms several hours after taking an unknown quantity of tablets kept at home for headaches. She is febrile at 38.2°C, tachypneic, and mildly confused. Chest examination is normal. Investigations show serum sodium 140 mmol/L, chloride 102 mmol/L, bicarbonate 14 mmol/L, and glucose 98 mg/dL. Arterial blood gas on room air shows pH 7.46, PaCO₂ 20 mmHg, and HCO₃⁻ 14 mmol/L.
Which of the following is the most appropriate interpretation of her acid–base disturbance?
A. Primary respiratory alkalosis with secondary metabolic compensation
B. Primary high-anion-gap metabolic acidosis with secondary respiratory compensation
C. Mixed respiratory alkalosis and high-anion-gap metabolic acidosis
D. Mixed respiratory alkalosis and normal-anion-gap metabolic acidosis
E. Primary metabolic alkalosis with secondary respiratory compensation
Correct answer & Explanation:
Correct Answer:
C. Mixed respiratory alkalosis and high-anion-gap metabolic acidosis
Detailed Explanation: Salicylate poisoning
The history provides important clues toward salicylate poisoning:
- Headache tablets of unknown quantity
- Nausea and vomiting
- Tinnitus
- Tachypnea
- Fever
- Altered mental status
Tinnitus is particularly useful as a clinical clue to salicylate toxicity.
The characteristic acid–base abnormality is:
Respiratory alkalosis + high-anion-gap metabolic acidosis
Step 1: Calculate the anion gap
Anion gap = Na − (Cl + HCO₃⁻)
= 140 − (102 + 14)
= 24 mmol/L
Therefore, there is a high-anion-gap metabolic acidosis.
Step 2: Determine whether the low PaCO₂ is simply compensation
For metabolic acidosis, use Winter’s formula:
Expected PaCO₂ = 1.5 × HCO₃⁻ + 8 ± 2
= 1.5 × 14 + 8 ± 2
= 29 ± 2 mmHg
Expected PaCO₂ = 27–31 mmHg
Actual PaCO₂ = 20 mmHg
The PaCO₂ is substantially lower than expected.
Therefore, the respiratory response is greater than would be expected from compensation alone.
This confirms an additional primary respiratory alkalosis.
Why salicylate poisoning produces this pattern
Salicylates stimulate the respiratory center in the brainstem:
↑ Ventilation → ↓ PaCO₂ → respiratory alkalosis
They also cause metabolic abnormalities with accumulation of organic acids:
Organic acid accumulation → high-anion-gap metabolic acidosis
Thus, significant salicylate poisoning classically produces:
Respiratory alkalosis + high-anion-gap metabolic acidosis
Why the other options are incorrect
A. Primary respiratory alkalosis with secondary metabolic compensation
Incorrect. Although respiratory alkalosis is present, the elevated anion gap demonstrates a concurrent primary metabolic acidosis.
B. Primary high-anion-gap metabolic acidosis with secondary respiratory compensation
Incorrect. The expected PaCO₂ for HCO₃⁻ of 14 mmol/L is 27–31 mmHg. A PaCO₂ of 20 mmHg is much lower, indicating an additional respiratory alkalosis.
C. Mixed respiratory alkalosis and high-anion-gap metabolic acidosis
Correct.
D. Mixed respiratory alkalosis and normal-anion-gap metabolic acidosis
Incorrect. The calculated anion gap is 24 mmol/L, demonstrating a high-anion-gap process.
E. Primary metabolic alkalosis with secondary respiratory compensation
Incorrect. The bicarbonate is markedly reduced rather than elevated.
CPSP Pearls
- Tinnitus + vomiting + tachypnea + altered mental status should raise suspicion of salicylate poisoning.
- The classic significant salicylate poisoning pattern is mixed respiratory alkalosis and high-anion-gap metabolic acidosis.
- Do not interpret the low PaCO₂ as compensation without calculating the expected value.
- A relatively normal pH can be misleading because two opposing primary disorders may partially offset each other.
- In a patient with suspected salicylate poisoning, rising PaCO₂ is particularly concerning, as it may indicate respiratory fatigue and worsening toxicity.
