Question 18.2

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

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College Answer

a) Interpret these results

Metabolic alkalosis with partial respiratory compensation and severe hypokalaemia

b) List 2 likely diagnoses

Primary Hyperaldosteronism most likely secondary to an aldosterone producing adenoma (Conn’s syndrome – 50-60%) or adrenal hyperplasia (40-50%)
Licorice ingestion
Liddle’s syndrome
Excessive diuretic use

c) Give 2 drugs used to treat this condition

Aldosterone antagonist (spirinolactone or eplerenone)
Amiloride

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

Discussion

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.

Differential Diagnosis for the Causes of Metabolic Alkalosis
Chloride depletion Gastric losses by vomiting or drainage Diuretics: loop diuretics thiazides diarrhoea posthypercapneic state (chronic compensatory renal loss) dietary chloride deprivation gastrocystoplasty cystic fibrosis (loss due to high sweat chloride content) Bicarbonate excess (real or apparent) Iatrogenic alkalinisation Recovery from starvation Hypoalbuminemia	Potassium depletion Primary hyperaldosteronism Mineralocorticoid oversupplementation Licorice (glycyrrhizic acid) β-lactam antibiotics Liddle syndrome Severe hypertension Bartter and Gitelman syndromes Laxative abuse Clay ingestion Calcium excess Hypercalcemia of malignancy Milk-alkali syndrome

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.

References

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.

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Question 18.2

College Answer

Discussion

Chloride depletion

Bicarbonate excess (real or apparent)

Potassium depletion

Calcium excess

References