# Question 29.4

The following results were obtained from a 32-year-old male:

 Parameter Patient Value Adult Normal Range Plasma Sodium 138 mmol/L 135 – 145 Potassium 3.4 mmol/L 3.4 – 5.0 Chloride 118 mmol/L* 100 – 110 Bicarbonate 15 mmol/L* 22 – 27 Arterial Blood Gas FiO2 0.3 pH 7.32* 7.35 – 7.45 PO2 125 mmHg (16.4 kPa) PCO2 30 mmHg (4.0 kPa)* 35 – 45 (4.6 – 6.0) Base Excess -10 mmol/L* -2 – +2 Urine pH 5.0 4.6 – 8.0 Sodium 40 mmol/L Potassium 10 mmol/L Chloride 80 mmol/L

a) Describe the abnormalities on the blood investigations.

a) What is the underlying mechanism for the primary abnormality?

(20% marks)

Not available.

## Discussion

This question is identical to Question 3.4 from the second paper of 2013.

Let us dissect these results systematically.

1. The A-a gradient is 51.4:
PAO2 = (0.3 × 713) - (30 × 1.25) = 176.4;
thus A-a = (176.4 - 125) = 51.4
2. There is acidaemia.
3. The PCO2 is a compensatory response.
4. The SBE is negative, suggesting that there is a metabolic acidosis
5. The respiratory compensation is adequate:
The expected CO2 is (15 × 1.5) + 8 = 30.5mmHg
6. The anion gap is normal:
(138) - (118 + 15) = 5, or 8.4 when calculated with potassium
7. The urinary anion gap is (40+10) - 80 = -30

A low urinary anion gap suggests that there is no RTA, and that GI losses are responsible for the NAGMA.

But of course one could come to this conclusion by looking at the urine pH (which is near-maximally acidic, suggesting that appropriate renal compensation is taking place).

Thus, the mechanism must be gastrointestinal. Or, somebody has infused this 32-year-old male with an absurd excess of normal saline.

## References

Batlle, Daniel C., et al. "The use of the urinary anion gap in the diagnosis of hyperchloremic metabolic acidosis." New England Journal of Medicine 318.10 (1988): 594-599.