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.
Any neck surgery can lead to hypoparathyroidism, which is most commonly transient but can be permanent in up to 1% all neck surgeries.
This is most commonly seen following extensive surgery for thyroid cancer, or other head and neck malignancy, but can also complicate surgery for benign thyroid disease, hyperparathyroidism, laryngeal or oesophageal pathology.
Transient post-surgical HPTH usually recovers within 6-12 months, and can be predicted by PTH levels >18ng/l.
Surgery for hyperparathyroidism may also lead to the hungry bone syndrome. After chronic hypercalcaemia, the dramatic fall in PTH leads to marked skeletal calcium uptake and the patient may become hypocalcaemic requiring high dose calcium replacement for several days post operatively.
The index of suspicion for severe hypocalaceamia is significantly increased in patients known to have HPTH, a family history of HPTH or other complex condition e.g. Wilson's disease.
Perioral paraesthesia and cramps are the commonest symptoms of hypocalcaemia of any cause.
Muscle cramps and sometimes spontaneous contractions are common symptoms of hypocalcaemia of any cause.
Severe cramp or carpopedal spasm indicates more severe hypocalcaemia.
Laryngospasma nd bronchospasm are rare but can occur with severe hypocalceamia.
This usually occurs only in very severe untreated hypocalcaemia, and so usually precedes diagnosis of HPTH.
Cardiac conduction disturbance usually ony occurs with severe hypocalcaemia.
HPTH has also been associated with chemotherapeutic agents and antiretroviral drugs, but is most commonly seen with proton pump inhibitors through hypomagnesaemia.
Any cause of hypomagnesaemia may lead to reduced production of PTH and hence hypocalcaemia due to HPTH.
Hypomagnesaemia may also occur with renal tubular defects. Very rarely, hypomagnesaemia may occur due to HNF1 mutations which more commonly cause maturity onset diabetes of the young (MODY).
Transient HPTH may occur in offspring of mothers with hyperparathyroidism, in premature or very low birth wieght babies. Hypomagensaemia in diabetic mothers may also lead to transient neonatal HPTH.