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

[Click here to toggle visibility of the answers]

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

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.