Acute hypocalcaemia can be life threatening, necessitating urgent treatment. In severe cases, intravenous calcium forms the mainstay of initial therapy, but it is essential to ascertain the underlying cause and commence specific therapy as early as possible. This guideline aims to take the non-specialist through the initial phase of assessment and management.
Symptoms of hypocalcaemia typically develop when adjusted serum calcium levels fall below ~1.9 mmol/L. However, this threshold varies greatly and is dependent on the rate of fall.
Symptoms and signs of hypocalcaemia include:
Peri-oral and digital paraesthesiae
Positive Trousseau’s and Chvostek’s signs
Tetany and carpopedal spasm
ECG changes (prolonged QT interval) and arrhythmia
The most common cause of acute symptomatic hypocalcaemia in hospital practice is disruption of parathyroid gland function due to total thyroidectomy. Hypocalcaemia may be temporary or permanent.
Other causes include:
Following selective parathyroidectomy (hypocalcaemia is usually transient and mild)
Severe vitamin D deficiency
Mg2+ deficiency (consider PPI-associated hypomagnesaemia)
Cytotoxic drug-induced hypocalcaemia
Pancreatitis, rhabdomyolysis and large volume blood transfusions
Serum calcium (adjusted for albumin)
Parathyroid hormone (PTH)
Urea and electrolytes
‘Mild’ hypocalcaemia: asymptomatic; serum calcium >1.9 mmol/L.
Commence oral calcium supplements such as Sandocal 1000, 2 tablets BD (Alternatives include Adcal 3 tablets BD, Cacit 4 tablets BD, or Calcichew Forte 2 tablets BD).
If post-thyroidectomy and patient asymptomatic, repeat calcium 24 h later:
When adjusted calcium is >2.1 mmol/L, patient may be discharged and recheck calcium within 1 week.
If serum calcium remains between 1.9 and 2.1 mmol/L increase Sandocal 1000 to three BD
If patient remains in mild hypocalcaemic range beyond 72 h post-operatively despite calcium supplementation, start alfacalcidol 0.25 micrograms/day (calcitriol may also be used) with close monitoring (see ‘Long-term follow-up’ below)
If vitamin D deficiency is the cause, commence vitamin D supplementation: load with ~300,000 units of cole- or ergocalciferol over ~6–10 weeks
If hypomagnesaemia-related, stop any precipitating drug and administer i.v. Mg2+, 24 mmol/24 h, made up as 6 g of MgSO4 (30 mL of 20%, 800 mmol/L, MgSO4) in 500 mL Normal saline or 5% dextrose. Monitor serum Mg2+ and aim to achieve normal serum magnesium level
If other cause of hypocalcaemia, treat underlying condition.
Severe hypocalcaemia: serum calcium <1.9 mmol/L and/or symptomatic at any level below reference range.
This is a medical emergency
Administer i.v. calcium gluconate
Initially, give 10–20 mL 10% calcium gluconate in 50–100 mL of 5% dextrose i.v. over 10 min with ECG monitoring. This can be repeated until the patient is asymptomatic. It should be followed up with a calcium gluconate infusion as follows:
Dilute 100 mL of 10% calcium gluconate (10 vials) in 1 L of Normal saline or 5% dextrose and infuse at 50–100 mL/h. (Calcium chloride can be used as an alternative to calcium gluconate, but it is more irritant to veins and should only be given via a central line)
Titrate the rate of infusion to achieve normocalcaemia and continue until treatment of the underlying cause has taken effect
Treat the underlying cause; in post-operative hypocalcaemia and other cases of hypoparathyroidism, this consists of alfacalcidol or calcitriol therapy. Starting doses should be approximately 0.25–0.5 micrograms per day
1-alpha hydroxylated vitamin D metabolites are potent causes of hypercalcaemia. Frequent blood tests are required in stabilisation phase of treatment
alfacalcidol can be administered (at equivalent doses) intravenously if there are concerns about absorbtion or difficulties with oral drug administration
NB: Large volume calcium infusions should not be used in patients with end stage renal failure or who are on dialysis. Guidance on management of hypocalcaemia in these patients is available in the NKF KDOQI guidelines (http://www2.kidney.org/professionals/KDOQI/guidelines_bone/Guide14.htm)
Vitamin D deficiency or hypomagnesaemia should be treated as described above
Hazards of i.v. calcium administration
Uncommon, but include local thrombophlebitis, cardiotoxicity, hypotension, calcium taste, flushing, nausea, vomiting and sweating. Patients with cardiac arrhythmias or on digoxin therapy need continuous ECG monitoring during i.v. calcium replacement.
For patients commenced on alfacalcidol or calcitriol, monitoring of adjusted serum calcium levels should initially be performed approximately one week post discharge, then if satisfactory at one, three and then six months. Follow-up by a specialist with an interest in calcium disorders is recommended.
The document should be considered as a guideline only; it is not intended to determine an absolute standard of medical care. The doctors concerned must make the management plan for an individual patient.