History: A 33-year-old indigenous man presents with general malaise. Below is his ABG shortly after arrival:
|pH 6.95||Na 128 mmol/L|
|pCO2 21 mmHg||K 4.7 mmol/L|
|HCO3 4 mmol/L||Cl 97 mmol/L|
|Lactate 0.9 mmol/L||Glucose 5.9 mmol/L|
What’s the pH?
6.95 = severe acidaemia
What’s the primary process?
HCO3 4 = primary metabolic acidosis
Is there any compensation?
Expected pCO2 = 1.5 x HCO3 + 8
= 1.5 x 4 + 8
= 14 mmHg
Actual pCO2 is higher, suggesting incomplete compensation or co-existing respiratory acidosis.
Are there any other clues?
Anion gap = Na – (Cl + HCO3)
= 128 – (97 + 4)
Therefore the anion gap is markedly elevate.
Delta Gap = (Anion gap – 12) ÷ (24 – HCO3)
= (27 – 12) ÷ (24 – 4)
Consistent with a co-existing anion and non-anion gap acidoses.
Sodium is low, chloride is borderline low. Potassium, glucose and lactate are all within normal limits.
What’s the differential diagnosis?
Description: This arterial blood gas shows a severe acidaemia due to primary mixed high anion gap and non-anion gap acidoses. There is either incomplete respiratory compensation, or a coexisting primary respiratory acidosis. The sodium is low. The chloride is borderline low, which is normally associated with a metabolic alkalosis. The potassium, glucose and lactate are all within normal limits.
Interpretation: This is a potentially life threatening acidaemia. The markedly high anion gap limits the diagnostic possibilities in this clinical context to diabetic ketoacidosis, however the patient has a normal serum blood glucose which essentially excludes this possibility, alcoholic ketoacidosis, toxic alcohol ingestion and possibly uraemia. The severity of the acidosis suggests a sub-acute development consistent with this differential diagnosis. Renal tubular acidosis or Addison’s disease in the context of sepsis (although the lactate is low) should also be considered.
Additional information: Acute on chronic renal failure secondary to sepsis. Urea 63.1 mmol/L, creatinine 2880 μmol/L (previously 441).