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
- PTH is released in response to low serum 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
- if not overtly present, tapping the facial nerve over the parotid gland may illicit muscle spasm (Chvostek’s sign)
- 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
- may be elicited during application of a tourniquet/BP cuff in response to mild hypoxia (Trousseau’s sign)
- Can progress to tetany or seizures in severe cases
- muscle twitching, spasms,
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)
- If low/normal, check magnesium
- 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
- IV calcium gluconate
- 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