A 19-year-old male with a history of substance abuse presents to the Emergency Department with respiratory distress.

 Parameter Patient Value Normal Adult Range FiO2 0.4 pH 6.94* 7.35 – 7.45 PO2 140 mmHg (18.4 kPa) PCO2 17* mmHg (2.2 kPa) 35 – 45 (4.6 – 6.0) HCO3 4* mmol/L 22 – 27 Base Excess -28 mmol/L* -2.0 – +2.0 Sodium 127* mmol/L 135 – 145 Chloride 113* mmol/L 95 – 105 Potassium 3.9 mmol/L 3.5 – 5.0 Urine pH 7.2 4.6 – 8.0

a)Describe the acid-base disturbance.

b)What is the likely cause of the acid-base disturbance?

a) Normal anion gap severe metabolic acidosis with incomplete compensation.

b) Renal tubular acidosis Type 1 distal secondary to chronic toluene abuse.

## Discussion

Let us dissect these results systematically.

1. The A-a gradient is high; ~127mmHg
PAO2 = (0.4 × 713) - (17 × 1.25) = 266.95
Thus, A-a = (266.95 - 140) = 126.95mmHg.
2. There is acidaemia
3. The PaCO2 is compensatory
4. The SBE is -28, suggesting a severe metabolic acidosis
5. The respiratory compensation is slightly less than adequate - the expected PaCO2(4 × 1.5) + 8 = 14mmHg, and the measured 17mmHg is just outside the +/- 2mmHg error range for Winter's Rule.
6. The anion gap is essentially normal:
(127 + 3.9) - (113 + 4) = 13.9
The delta ratio suggests that there is a pure normal anion gap metabolic acidosis here.
(13.9 - 12) / (24 - 4) = 0.095
7. Urinary electrolytes are not available, but the pH is 7.2 - in fact its even more alkaline than the blood pH!

A result like this has you asking, what the hell are the kidneys doing? Why are they not acidifying the urine? The answer may lay in the history of this young man's substance abuse. One may eventually arrive at the conclusion that he is a connoisseur of volatile solvents.

The recreational enjoyment of toluene can lead to a nasty Type 1 (distal) renal tubular acidosis.

### References

References

Batlle, D. C., S. Sabatini, and N. A. Kurtzman. "On the mechanism of toluene-induced renal tubular acidosis." Nephron 49.3 (1988): 210-218.