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).

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