Acute severe hypocalcaemia most often occurs following extensive neck surgery e.g. for thyroid cancer. This emergency guide outlines a strategy to prevent this complication and to treat it and other causes of severe hypocalcaemia.


Baseline investigations - all patients

Bone profile

The clinical suspicious of hypcalcaemia must be confirmed biochemically. Phosphate and alkaline phosphatase levels may give useful clues to its aetiology.

HPTH is usually associated with hypocalcaemia and hyperphosphataemia. Alkaline phosphatas levels may vary.

Full blood count  

Useful indicator of general health, nutrition and underlying disease.

Urea and electrolytes

Glucocorticoid deficiency may be associated with autoimmune HPTH or with metastatic destruction, and might be indicted by hyponatraemia and hyperkalaemia. 

Liver function test

Useful indication of general health, nutrition and underlying disease. 

Parathyroid hormone  

PTH is low with HPTH of any cause, with very high levels indicating vitamin D deficiency, or pseudohypoparathryoidism. 

Vitamin D  

Vitamin D deficiency is common, may cause hypocalcaemia and requires treatment in its own right.

Vitamin D deficiency should be sought and treated prior to planned neck surgery to reduce the risk of post operative hypocalcaemia and the hungry bone syndrome.


Hypomagnesaemia is a common cause of HPTH in adults, particularly with the widespread use of proton pump inhibitors. This requires treatment in its own right before the hypocalcaemia will correct with conventional treatment. 


ECG should be performed with patients presenting acutely unwell or with severe hypocalcaemia to exclude conduction disturbances.

The changes of severe hypocalcaemia may mimic those of an acute myocardial infarction.

Further investigations - selected patients only

CT brain

CT scan is necessary to rule out other causes of fitting but may reveal reveal basal ganglia calcification particularly in patients with congenital HPTH.