HYPOCALCAEMIA
Hpocalcaemia
is less common than hypercalcaemia. Sympoccurs when serum calcium is <1.9 mmol/L, or at higher values if there is
a rapid drop in calcium. The most common cause of hypocalcaemi ostsurgical hypoparathyroidism
following thyroidectomy.
Causes
Post-surgical hypoparathyroidism
Post-thyroidectomy hypocalcaemia is
often temporary, but can be permanent because of damage to or inadvertent
removal of the parathyroid glands. Long-term follow-up is needed to assess
recovery of parathyroid function.
Non-surgical hypoparathyroidism
A low serum calcium with low PTH
presenting in adulthood suggests idiopathic or autoimmune hypoparathyroidism.
This can accompany polyglandular autoimmune syndrome. In children, congenital
hypoparathyroidism should be considered; for example, Di George’s syndrome is a
rare condition associated with hypoparathyroidism, immunodeficiency and cardiac
defects resulting from developmental failure of the third and fourth branchial
arches.
Vitamin D deficiency
Severe vitamin D deficiency causes
hypocalcaemia and should be considered in high-risk groups. In the neonate,
severe vitamin D deficiency can present with seizures and tetany caused by
hypocalcaemia. Typically, phosphate is low in vitamin D deficiency because of
elevated PTH levels, unlike hypoparathyroidism where phosphate is high.
Hypomagnesaemia
Hypomagnesaemia causes functional
hypoparathyroidism, with normal or low PTH levels. Common causes of low
magnesium include gastrointestinal loss, alcohol and drugs, particularly proton
pump inhibitors.
Hyperphosphataemia
High phosphate levels lead to
hypocalcaemia by increased binding of free calcium. Causes include chronic
kidney disease and phosphate administration.
Miscellaneous causes
Other causes of hypocalcaemia
include cytotoxic drugs, pancreatitis, rhabdomyolysis and large volume drug
transfusions (Figure 17.1).
Clinical features
Symptoms
Acute severe hypocalcaemia causes
laryngospasm, prolonged QT interval and seizures, and is a medical emergency
(Chapter 41). However, hypocalcaemia usually presents less acutely with muscle
cramps, carpopedal spasm, peri-oral and peripheral paraesthesia, and
neuropsychiatric symptoms.
Signs
Patients may have a positive
Chvostek’s sign (facial spasm when the cheek is tapped gently with the finger)
or Trousseau’s sign (carpopedal
spasm induced after inflation of a sphygmomanometer).
Investigation
Renal function, phosphate, vitamin
D and PTH should be measured when the cause of hypocalcaemia is not clear
(Figure 17.1). Hypocalcaemia associated with high phosphate and low PTH
suggests hypoparathyroidism. Hypocalcaemia associated with low phosphate and
high PTH is in keeping with vitamin D deficiency and secondary
hyperparathyroidism (Figure 17.1). Demonstration of low vitamin D levels
confirms a suspected diagnosis of severe deficiency. Magnesium deficiency
should be excluded in refractory or unexplained hypocalcaemia. Parathyroid
antibody levels should be checked in non-surgical hypoparathyroidism to exclude
an autoimmune cause. In chronic hypoparathyroidism, brain imaging can reveal
basal ganglia calcification, caused by high phosphate binding to calcium within
tissues.
Treatment
Calcium replacement is the mainstay
of therapy. It is important to consider and reverse the underlying cause. Acute
hypocalcaemia can be life-threatening and requires urgent treatment with
intravenous calcium.
Vitamin D deficiency
Patients with severe vitamin D
deficiency should be given a loading dose of cholecalciferol. A dose of 20,000
IU/week is given for 7 weeks followed by a maintenance dose of 1000–2000
IU/week.
Hypoparathyroidism
Hypoparathyroidism is treated with
alfa-hydroxylated derivates of vitamin D (e.g. 1-alfacalcidol or calcitriol).
These have a shorter half-life than cholecalciferol and should not be used in
simple vitamin D deficiency. The typical starting dose is 0.25 µg/ day
1-alfacalcidol, with dose titration according to clinical and biochemical
responses. Oral calcium supplements (e.g. Sandocal and Adcal D3) are given in
combination with alfacalcidol. The aim of treatment is to keep calcium levels
at the lower end of the reference range to reduce the risk of nephrocalcinosis.
Magnesium deficiency
In the acute situation,
precipitating drugs should be stopped and IV magnesium replacement started.
This is usually given as MgSO4 24 mmol/24 hours. If chronic
gastrointestinal loss or alcohol ingestion is the cause, appropriate specialist
input is indicated to prevent recurrent symptoms.
Pseudo-hypoparathyroidism
This rare condition is caused by a
mutation in the GS alpha subunit (GNAS1) which is coupled to the PTH
receptor and leads to PTH resistance. It is characterised by hypocalcaemia and
a high phosphate level, which would normally suggest hypoparathyroidism, but
high PTH and normal vitamin D levels suggests PTH resistance rather than
deficiency, hence the term pseudo-hypoparathyroidsm. Patients have a syndromic
appearance with short stature, round face and short 4th and 5th ripheral
resistance to TSH and gonadotrophins an also be seen in this rare condition.
