A 26-year-old man with a history of solvent abuse presents to the Emergency Department


Parameter Patient value     Normal range
FiO2 0.4  
pH                               6.94*                           7.35 – 7.45 
PO2                                        140 mmHg  
PCO2                                    17* mmHg               35 – 45 (4.6 – 6.0)          
HCO3                                   4* mmol/L                  22 – 27
Base excess               -28*                             -2.0 – +2.0
Sodium                      127* mmol/L 135 – 145          
Chloride           113* mmol/L              95 – 105
Urinary pH                 7.2                                         4.6 – 8.0               


a) Describe this acid-base picture

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

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College Answer



a) Normal anion gap severe metabolic acidosis with incomplete compensation



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






How did they reach these conclusions?

Let us approach this systematically.


  1. The A-a gradient is slightly raised:
    PAO2 = (0.4 × 713) - (17 × 1.25) = 263.95
    Thus, A-a = ( 263.95 - 140) = 143.95mmHg.
  2. There is severe acidaemia
  3. The PaCO2 is low, suggesting an attempt at compensation
  4. The SBE is -28, suggesting a severe metabolic acidosis
  5. The respiratory compensation is either complete, or there is a mild respiratory acidosis:
    Boston rules: the expected CO2 is (1.5 × 4) + 8 = 14mmHg (plus-minus 3)
    Copenhagen rules: the expected CO2 is (40-SBE) = 12
  6. The anion gap cannot be calculated in the conventional sense, but if you ignore the potassium it ends up being (127 – 113 – 4) = 10.


There is not enough information to calculate the osmolar gap.
This is a normal anion gap severe metabolic acidosis with incomplete compensation.


The solvent abuse mentioned in the question points to toluene.
Toluene toxicity alone would have caused a high anion gap metabolic acidosis (due to accumulation of hippuric acid). However, the hippurate anion is rapidly excreted via the kidneys, whereas the hydrogen ions remains. The RTA due to toluene is a type 1, which is a hyperchloremic hypokalemic acidosis due to a failure to acidify the urine in the distal tubule. Another characteristic feature is the extremely alkaline urinary pH which contrasts with the extremely acidic blood pH; such a situation tends to only occur in the case of a Type 1 (distal) RTA, whereas with the other RTAs the urinary acidification is at least somewhat preserved.




For a scenic overview of renal tubular acidosis, I turn to UpToDate.

An even better (free) resource is a beautiful article by Juan Rodríguez Sorianoentitled "Renal Tubular Acidosis: The Clinical Entity" which is available online.

Batlle DC, Sabatini S, Kurtzman NA. On the mechanism of toluene-induced renal tubular acidosis. Nephron. 1988;49(3):210-8.

Unwin RJ, Capasso G,The renal tubular acidoses J R Soc Med. 2001 May; 94(5): 221–225.

Chan JCM, Scheinman JI, Roth KS. Renal Tubular Acidosis Pediatrics in Review Vol.22 No.8 August 2001 2