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)

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College answer

Not available.

Discussion

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

Let us dissect these results systematically.

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

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