4th April 2024

Hypercalcaemia

Severe hypercalcaemia is defined as >3.5mmol/L. Patients may tolerate high calcium levels if there has been a slow increase, however more rapid rises, despite the overall level, often result in a patient being symptomatic. Malignancy-related hypercalcaemia often rises more rapidly, resulting in patients becoming highly symptomatic.

Rarely, patients with ESRF who develop hypercalcaemia, hyperphosphatemia or hyperparathyroidism may present with skin ischaemia and necrosis. This complication, known as calciphylaxis, is due to arteriolar calcification, resulting in microvascular occlusion.

Acute hypercalcaemia also directly shortens the QT interval. 

Causes

Hypercalcaemia is caused by either primary hyperparathyroidism or cancer in over 90% of cases. Malignancy-related hypercalcaemia occurs more commonly in patients with multiple myeloma, leukaemia, lung or breast cancers and may be due to PTHrP secretion or bony metastases. Other causes include:

• Excessive vitamin D or calcium supplementation 
• Thyrotoxicosis : due to rapid bone turnover
• Sarcoidosis: increased vitamin D activation by macrophages
• Hypercalcaemia of immobility: commonly in young patients who develop massive bone demineralisation following prolonged immobility 
• Familial hypocalciuric hypercalcaemia: autosomal dominant cause of mild hypercalcaemia and hypocalciuria

Management 

Emergency treatment is discussed above (see The Parathyroid Gland: Hyperparathyroidism).

If there is poor response to initial rehydration, intravenous bisphosphonates may be used, which inhibit osteoclastic bone resorption, but have a more delayed onset of action.

Glucocorticoids may be beneficial in the management of calcitriol-induced hypercalcaemia secondary to sarcoidosis, tuberculosis, and lymphomas. Cinacalcet increases the sensitivity of CaSRs on the parathyroid gland to calcium, thus are useful in patients with secondary hyperparathyroidism.