Question 30.2

A 27-year-old patient presents with the following laboratory results after a prolonged sub-acute illness.

Parameter

Patient Value

Adult Normal Range

Sodium

132 mmol/L*

135 – 150

Potassium

2.2 mmol/L*

3.5 – 5.5

Chloride

94 mmol/L*

100 – 110

Bicarbonate

28 mmol/L*

22 – 27

Urea

8.3 mmol/L*

3.0 – 8.0

Creatinine

236 μmol/L*

70 – 120

Total Calcium

5.04 mmol/L*

2.15 – 2.60

Ionised Calcium

2.6 mmol/L*

1.1 – 1.3

Magnesium

0.7 mmol/L

0.7 – 1.1

Phosphate

1.09 mmol/L

0.70 – 1.40

Albumin

37 g/L

35 – 47

Total Bilirubin

8 μmol/L

4 – 20

g-Glutamyl transferase

105 U/L*

0 – 50

Alkaline phosphatase

263 U/L*

40 – 110

Alanine transferase

76 U/L*

< 40

Aspartate transferase

48 U/L*

< 40

 
a) List the ECG changes associated with the most striking biochemical abnormalities. (1 mark)
b) List three differential diagnoses. (1.5 marks)
c) List three specific management strategies. (1.5 marks)

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College answer

Syllabus topic/section:

2.1.7    Renal Intensive Care / Acid-Base and Electrolyte Disorders. L1

Discussion:  

This is a core knowledge question which was generally answered well. This is an SAQ with simple lists of hypo and hypercalcaemia issues to complete. Candidates are reminded to only list the number of things asked for. If more than a stipulated number of responses is given (for example part b) asks for three differentials) the examiner will only mark the top three. It is not the responsibility of the examiner to pick the most appropriate of the answers given. This is a requirement of the candidate.

Several candidates omitted part/all of the question. Consider time management strategies to optimise the opportunity to address every question with enough time. We recommend practicing timed answers and practicing answering more than one SAQ consecutively during your preparation.

This is a deliberately timed examination designed to test recall and prioritisation as these are transferrable skills to senior, independent Intensive Care clinical practice. Every question is important for overall success. Candidates who have allocated enough time to address every question of the written paper have a statistically significant higher chance of successful participation and are more likely to be able to demonstrate the standard required on the journey to becoming a transitional fellow of the CICM
 

Discussion

The most "striking" abnormalities? Would those be the values which are the furthest from their normal values? In which case that would be the creatinine, which is about five times higher than what it should be, for a young person. But one must conceded that the intention of this stem is clearly to draw attention to the calcium. To be fair, it's more than just a bit high. The potassium is also far from normal. Moreover the creatinine would not cause ECG changes.

In short:

  • ECG changes of hypercalcemia:
    • Shortened QT interval
    • Osborn waves, notches in the end of the QRS complex (similar to those seen in hypothermia)
    • Weird-looking QRS complexes
    • VF 
  • ECG changes of hypokalemia

    • Ventricular tachycardia: classically, torsades de pointes

    • Atrial tachycardias
    • PR interval prolongation (>200 msec)
    • P wave amplitude increased (>2.5 mm in limb leads, >1.5 mm in chest leads)
    • P wave width increased (>120 msec)
    • u-waves
    • T-wave inversion
    • Ectopics (ventricular and atrial)

b) Differentials:

  • Primary hyperparathyroidism
  • Paraneoplastic (PTH-related protein)
  • Granulomatous disease (eg. sarcoid)
  • Drug-induced (eg. vit D, thiazides, lithium)
  • Immobilisation

c) Management of hypercalcemia:

  • Dilute serum calcium
    • Rehydration with IV fluids
  • Decrease calcium resportion from bone
    • Calcitonin
    • Bisphosphonates
    • Gallium nitrate
    • Mithramycin (for malignant disease)
  • Decrease calcium resportion from renal tubule
    • Loop diuretics (this has fallen out of favour)
    • Calcitonin
  • Decrease calcium absorption from the gut
    • Corticosteroids (also they decrease the 1,25-dihydroxyvitamin D production by monocytes within granulomae)
  • Forcibly remove excess calcium from the circulation
    • Haemodialysis
    • EDTA administration (as chelating agent)

References

Glover, P. "Hypokalaemia." Critical Care and Resuscitation 1999; 1: 239-251.

Gennari, F. John. "Hypokalemia." New England Journal of Medicine 339.7 (1998): 451-458.

Weiner, I. David, and Charles S. Wingo. "Hypokalemia--consequences, causes, and correction." Journal of the American Society of Nephrology 8.7 (1997): 1179-1188.

Shane, Elizabeth, and I. Dinaz. "Hypercalcemia: pathogenesis, clinical manifestations, differential diagnosis, and management." Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism, Favus MJ (ed.). Philadelphia: Lippincott, Williams &Wilkins (1999): 183-87.

Edelson, Gary W., and Michael Kleerekoper. "Hypercalcemic crisis." The Medical Clinics of North America 79.1 (1995): 79-92.

Carrol, Mary F., and David S. Schade. "A practical approach to hypercalcemia." Am Fam Physician 67 (2003): 1959-1966.