Diagnosis and management of hypocalcaemiaBMJ 2008; 336 doi: http://dx.doi.org/10.1136/bmj.39582.589433.BE (Published 05 June 2008) Cite this as: BMJ 2008;336:1298
- Mark S Cooper, senior lecturer and consultant endocrinologist,
- Neil J L Gittoes, senior lecturer and consultant endocrinologist
- 1Division of Medical Sciences, University of Birmingham, Birmingham B15 2TH
- Correspondence to: N J L Gittoes, Department of Endocrinology, Queen Elizabeth Hospital, Birmingham B15 2TH
Hypocalcaemia is a potentially life threatening biochemical abnormality that carries risks for serious errors in diagnosis and treatment. Hypocalcaemia presents in primary and secondary care; it has a prevalence of 18% in all patients in hospital and 85% in the intensive care unit.1 2 The most common cause of hypocalcaemia in primary care is vitamin D deficiency, which—depending on population demographics—may have a prevalence as high as 50%.3 Hypocalcaemia may be an asymptomatic laboratory finding or a life threatening metabolic disturbance. Acute hypocalcaemia can result in severe symptoms that require rapid admission to hospital and correction. In contrast, when hypocalcaemia develops slowly patients can be surprisingly free of symptoms. This review will help clinicians to optimise the diagnosis and management of patients with hypocalcaemia. Because hypocalcaemia often presents as an emergency and symptoms are rapidly reversed by giving calcium, the evidence base for managing acute hypocalcaemia is mostly based on experience rather than controlled trials.
Sources and selection criteria
We searched PubMed for articles whose titles included the terms “hypocalcaemia”, “hypoparathyroidism”, or “osteomalacia” and restricted the search to articles published in English in the previous 10 years. We individually reviewed the titles of the resulting 578 articles to identify major themes. Additional searches were made of contemporary textbooks.
Who gets hypocalcaemia and why?
The concentration of calcium in the serum (normal range 2.10-2.60 mmol/l)is regulated by the action of parathyroid hormone and vitamin D on the kidneys, bones, and gastrointestinal tract (fig 1)⇓. Parathyroid hormone stimulates calcium resorption in the kidney and calcium release from bone. It also stimulates renal production of 1,25-dihydroxyvitamin D (calcitriol) from 25-hydroxyvitamin D. 1,25-Dihydroxyvitamin D is the most active form of vitamin D, and it acts on the gastrointestinal tract to increase calcium absorption. Vitamin D is obtained mainly through synthesis in the skin, with a small contribution from the …
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