The following data are from the arterial blood gas analysis of a 71-year-old male with necrotising fasciitis:
|Parameter||Patient Value||Normal Adult Range|
|Barometric pressure||760 mmHg (100 kPa)||.|
|pH||7.43||7.35 – 7.45|
|PCO2||23 mmHg (3.1 kPa)*||35 – 45 (4.6 – 5.9)|
|PO2||107 mmHg (14.3 kPa)||.|
|Bicarbonate||15 mmol/L*||22 – 26|
|Standard Base Excess||-8.6 mmol/L*||-2.0 – +2.0|
|Lactate||23.0 mmol/L*||0.2 – 2.5|
|Sodium||147 mmol/L*||137 – 145|
|Potassium||6.7 mmol/L*||3.2 – 4.5|
|Chloride||95 mmol/L*||100 – 110|
List the acid-base abnormalities. (30% marks)
Anion gap elevation (37 mEq/L)
This is a triple disorder.
Let us dissect these results systematically.
- The A-a gradient is high; ~78mmHg
- There is neither alkalaemia nor acidaemia
- The PaCO2 is low, which is a move in the appropriate direction given the metabolic acidosis
- The SBE is -8.6, suggesting a metabolic acidosis
- The respiratory compensation is excessive - the expected PaCO2 (15 × 1.5) + 8 = 30.5mmHg, and so there is also a respiratory alkalosis according to the Boston rules.
According to the Copenhagen rules, the the expected PaCO2 = (40 - SBE) = 31.4mmHg.
So, in this case there is no Trans-Atlantic disagreement.
- The anion gap is (147) - (95 + 15) = 37, or 43.7 when calculated with potassium.
- The delta ratio (assuming an albumin of 40) would therefore be (37 - 12) / (24 - 15) = 2.77 thus there is a high anion gap metabolic acidosis which co-exists with a metabolic alkalosis.
Note that without taking this step, the candidates would still have guessed that there is an underlying metabolic alkalosis. How else would you have a normal pH with a lactate of 23?