Hypocalcaemia

Background and Epidemiology

  • Severe hypocalcaemia can be a medical emergency and can be life-threatening.  In contrast, mild hypocalcaemia is not uncommon and is often just treated supportively.
  • It is often associated with illness (correlates with severity)- up to 88% of patients in intensive care will have some degree of hypocalcaemia
  • It is uncommon and all patients should be referred/investigated further

Normal Calcium Homeostasis

  • Calcium concentrations in the serum (normally 2.1-2.6 mmol/l) is regulated by the action of PTH (parathyroid hormone) and vitamin D on the kidneys, bones and GI tract
    • PTH is released in response to low serum calcium.
      • It acts to stimulate calcium re-absorption in the kidney and calcium resorption from the bone
      • It also stimulates renal production of 1,25-dihydroxyvitamin D (active form)
        • Acts to increase GI absorption of calcium
  • NB Calcium homeostasis is linked with magnesium homeostasis.  As such, hypocalcaemia is often coupled with hypomagnesaemia.  IMPORTANT: if patient require calcium replacement, magnesium must also be replaced (if low).

625_Calcium_Homeostasis

Presentation

  • Mild/gradually progressive hypocalcaemia is often asymptomatic
    • Most common symptom/sign is confusion
  • More severe or rapidly deteriorating hypocalcaemia (typically <1.9mmol/l) can present with symptoms of muscular dysfunction e.g.
    • muscle twitching, spasms,
      • if not overtly present, tapping the facial nerve over the parotid gland may illicit muscle spasm (Chvostek’s sign)
        • NB this can be present in normal individuals and absent in hypocalcaemia
    • tingling, numbness (particularly around the mouth and peripheries
    • Carpopedal spasm (wrist flexion, fingers are drawn together)
      • may be elicited during application of a tourniquet/BP cuff in response to mild hypoxia (Trousseau’s sign)
        • More specific for hypocalcaemia (94% people with hypocalcaemia and 1% of normocalcaemic patients have it
    • Can progress to tetany or seizures in severe cases

Investigation/Evaluation

  • Check calcium levels
    • If <1.90, treatment should be initiated whether the patient is symptomatic or not
    • Check other U&Es (phosphate and magnesium are important), LFT (particularly alkaline phosphatase- if high this suggests osteomalacia as a result of vitamin D deficiency)
  • Check for obvious causes (see below)
  • PTH
    • If low/normal, check magnesium
      • If low- magnesium deficiency
      • If normal- hypoparathyroidism or calcium sensing defect (rare)
    • If high, check kidney function (urea, creatinine, eGFR)
      • If high (or low GFR)- kidney failure may cause hypocalcaemia (possibly a common cause in hospitalised patients)
      • If low/normal- check vitamin D
        • If low- vitamin D deficiency (most likely cause)
        • If normal- pseudohypoparathyroidism or calcium deficiency (both are relatively rare)
  • ECG

Other causes

  • Hyperventilation
  • Drugs e.g. bisphosphonates; antiepileptics
  • Acute pancreatitis
  • Acute rhabdomyolysis (usually after crush injury)
  • Malignancy

Management

  • Acute hypocalcaemia (or severe hypocalcaemia- Corrected Ca <1.9mmol/l- of unknown cause)
    • IV calcium gluconate
      • Rule of 10- 10ml of 10% solution over 10 minutes (diluted in 50ml of 5% dextrose)
      • NB Often this provides only temporary improvement and so a continuous infusion is required
        • 100ml of 10% calcium gluconate in 1l of 5% dextrose or 0.9% saline at 50ml/hour
    • Monitor ECG on treatment as it can cause dysrhythmias
  • In non-urgent cases
    • Treat the underlying cause e.g. magnesium deficiency
    • Oral calcium
    • Vit D deficient and normal PTH
      • Treat with vit D3 or D2 e.g. cholecalciferol or ergocalciferol (respectively)
    • In patients with low PTH
      • Vit D e.g. calcitriol or alfacalcidol

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