A 35-year-old female with a history of poorly controlled hypertension presents with paraesthesia and weakness. Her blood results are shown below:
Patient value |
Normal range |
|
Sodium |
145 mmol/L |
135 – 145 |
Potassium |
1.8 mmol/L |
3.5 – 5.0 |
Chloride |
85 mmol/L |
97 – 109 |
Bicarbonate |
40 mmol/L |
24 – 32 |
Urea |
3.4 mmol/L |
3.0 – 8.0 |
Creatinine |
80 µmol/L |
70 – 110 |
Arterial blood gases
Patient value |
Normal range |
|
pH |
7.56 |
7.35 – 7.45 |
pO2 |
85 mmHg (11.3 kPa) |
80 – 110 mmHg (10.5 – 14.5 kPa) |
pCO2 |
46 mmHg (6.1 kPa) |
35 – 45 mmHg (4.6 – 5.9 kPa) |
Bicarbonate |
40 mmol/L |
23 – 33 |
a) Interpret these results
b) List 2 likely diagnoses
c) Give 2 drugs used to treat this condition
d) List 3 other potential causes of these biochemical abnormalities
a) Interpret these results
Metabolic alkalosis with partial respiratory compensation and severe hypokalaemia
b) List 2 likely diagnoses
c) Give 2 drugs used to treat this condition
d) List 3 other potential causes of these biochemical abnormalities
1/ laxative abuse
2/vomiting
3/diarrhoea
3/cushings and ACTH tumors
5/ primary metabolic alkalosis
Let us dissect this ABG according to the classical rules.
With a bicarbonate level of 40, the PCO2 should be (0.7 × 40 + 20) - or about 48, ± 5mmHg.
The gas we get from the college gives us a PCO2 of 46 mmHg, which is within the range of error.
I could call that a compensated disorder, but - lets be fair - its 2mmHg lower than the predicted value, so the savage ABG purist would be forced to label this as "partial" compensation.
The only other (massive) abnormality is the almost-unsurvivable K+ level (1.8mmol/L).
What are the causes of metabolic alkalosis, then? Particularly with such hypokalemia?
Answers b) and d) essentially ask the candidate to spew forth a torrent of differentials. Its a game of "how many causes of metabolic alkalosis can you think of in under 3 minutes". Judging by the pass rate, a fair few of us are rather good at this.
Even though this list of differentials is discussed in another chapter (Causes of metabolic alkalosis), I reproduce it here in order to simplify revision.
Chloride depletion
Bicarbonate excess (real or apparent)
|
Potassium depletion
Calcium excess
|
Lastly, management is asked about. It requires little imagination to answer "block the aldosterone excess", and a receptor blocker such as spironolactone is a convenient and reasonably safe means of doing so.
Tripathy, Swagata. "Extreme metabolic alkalosis in intensive care." Indian journal of critical care medicine: peer-reviewed, official publication of Indian Society of Critical Care Medicine 13.4 (2009): 217.
Galla, John H. "Metabolic alkalosis." Journal of the American Society of Nephrology 11.2 (2000): 369-375.