Describe and interpret this arterial blood gas:
History: A 75-year-old man with end-stage renal failure on home dialysis and a history of a right-sided total hip replacement has a mechanical fall. He sustains a periprosthetic fracture of his chronically osteomyelitic right femur. He is hypotensive and requiring noradrenaline to maintain a mean arterial pressure ≥ 65 mmHg.
| pH 7.271 | Na 139 mmol/L |
| pCO2 28.5 mmHg | K 4.9 mmol/L |
| pO2 112 mmHg (FiO2 0.25) | Ca 1.18 mmol/L |
| HCO3 12.9 mmol/L | Cl 111 mmol/L |
| Albumin 26 g/L | Glucose 13.2 mmol/L |
| Hb 105 g/L | Lactate 2.5 mmol/L |
[expand title=”Interpretation”]
What is the pH?
7.271 = acidaemia
What is the primary process?
HCO3 12.9 = primary metabolic acidosis
Is there compensation?
Expected pCO2 = 1.5 x HCO3 + 8 (± 2)
= 1.5 x 12.9 + 8
= 27.4 (25.4 – 29.4)
Therefore there is maximal respiratory compensation.
Are there other clues to diagnosis?
Anion gap = Na – (HCO3 + Cl)
= 139 – (12.9 + 111)
= 15.1
Correct anion gap = calculated anion gap + (normal albumin – measured albumin)/4
= 15.1 + (40 – 26)/4
= 18.6
Therefore there is an elevated anion gap and thus a high anion gap metabolic acidosis.
Delta gap = (Anion gap – 12) ÷ (24 – HCO3)
= (18.6 – 12) ÷ (24 – 12.9)
= 0.59
This suggests a coexisting non-anion gap metabolic acidosis.
(= 0.38 if calculated using uncorrected anion gap, which is consistent with a pure NAGMA)
Corrected Na = Na + (glucose – 5)/3
= 139 + (13.2 – 5)/3
= 142
= normal range
Electrolyte clues:
Lactate is slightly elevated. Glucose is slightly elevated. Sodium, potassium, and calcium are within the normal range. Chloride is slightly elevated. Mild anaemia. Hypoalbuminaemia.
Formulation:
Description: This arterial blood gas shows a metabolic acidosis which, when the anion gap is corrected for hypoalbuminaemia, is likely a combination of a non-anion gap metabolic acidosis and a high anion gap metabolic acidosis. There is mild anaemia, hyperchloraemia, mild hyperglycaemia, and an elevated lactate.
Interpretation: In the clinical context, this arterial blood gas is consistent with septic shock (“a subset of sepsis in which particularly profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone”) resulting in a high anion gap metabolic acidosis and confirmed clinically by the requirement of a noradrenaline infusion to maintain a mean arterial pressure of ≥ 65 mm Hg and a serum lactate > 2 mmol/L. The coexisting non-anion gap metabolic acidosis is most likely the result of volume resuscitation with a 0.9% sodium chloride solution resulting in hyperchloraemia.
Albumin is the major unmeasured anion and contributes almost the whole of the value of the anion gap. A normally high anion gap metabolic acidosis in a patient with hypoalbuminaemia may appear as a non-anion gap metabolic acidosis; a lactic acidosis in a hypoalbuminaemic patient will often appear as a non-anion gap metabolic acidosis. [/expand]