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.
This question is identical to Question 3.4 from the second paper of 2013.
Let us dissect these results systematically.
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.
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.