A 75-year-old female insulin-dependent diabetic presents to the Emergency Department semi-comatose. She has been unwell for several days and has a past medical history of left ventricular failure treated with digoxin and a thiazide diuretic.

The following data are from arterial blood gas analysis on admission:


Patient Value

Normal Adult Range





7.35 – 7.45


82.0 mmHg (10.8 kPa)


32.0 mmHg (4.2 kPa)*

35 – 45 (4.6 – 6.0)


19 mmol/L*

22 – 27


2.7 mmol/L*

3.5 – 5.0


67 mmol/L*

3.0 – 7.8

Anion Gap

34 mmol/L*

7 – 17

Interpret the acid-base disturbance and give your reasoning.

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College Answer

  • High AG implies severe metabolic acidosis
  • ∆ Ratio > 3 indicates pre-existing metabolic alkalosis
  • PCO2 slightly lower than expected for compensation (1.5 x [HCO3] + 8) implying mild respiratory alkalosis
  • History suggests DKA and K+ depletion secondary to diuretic use
  • Severe compensated metabolic acidosis 2° DKA with mild respiratory alkalosis and pre-existing metabolic alkalosis


Let us dissect these results systematically.

  1. The A-a gradient is high:
    PAO2 = (0.4 × 713) - (32 × 1.25) = 173.8
    Thus, A-a = 91.8 mmHg.
  2. There is a normal pH
  3. The PaCO2 is low, suggesting a respiratory alkalosis
  4. The SBE is not given but the bicarbonate is 19mmol/L, suggesting a metabolic acidosis
  5. The respiratory compensation is excessive - the expected PaCO2(19 × 1.5) + 8 = 36.5mmHg, confirming that there is also a respiratory alkalosis
  6. The anion gap is raised, and the college gave it to us (34)
    The delta ratio suggests that there is a pure high anion gap metabolic acidosis here, on the background of a metabolic alkalosis
    (34 - 12) / (24 - 19) = 4.4

So. What can account for such a massively raised anion gap?

Well. Firstly, the anion gap may be calculated incorrectly. One is not given a sodium value, and one wonders whether whoever calculated the anion gap corrected the sodium for hyperglycaemia. If one did this to only sodium and neglected all the other electrolytes, the anion gap would grow larger. In any case, there would be no point; the correction of sodium is really only a measure of dehydration, and a guard against unintelligent sodium replacement.

The extreme hyperglycaemia lends itself to the idea that a HONK state may be present. This is supported by the history - this patient is a diabetic who has been neglecting herself. However, she is an IDDM, which suggests that this is simply an extremely dehydrated DKA situation. The two conditions frequently overlap, after all. The low potassium supports this idea of severe dehydration; likely, while eschewing insulin, she continued to dutifully take her thiazides. The diuretics also explain the chronic metabolic alkalosis (if it were not the case, by this stage any self-respecting DKA patient would have a HCO3- level in the single digits).




Chiasson, Jean-Louis, et al. "Diagnosis and treatment of diabetic ketoacidosis and the hyperglycemic hyperosmolar state." Canadian Medical Association Journal 168.7 (2003): 859-866.

Lim, K. C., and C. H. Walsh. "Diabetic ketoalkalosis: a readily misdiagnosed entity." British medical journal 2.6026 (1976): 19.