Synopsis
Stabilise malignant hypercalcaemia, define its mechanism and severity, protect renal function and coordinate durable cancer-directed and supportive care.
- Confirm true hypercalcaemia using albumin-adjusted calcium or ionised calcium when albumin, pH, paraprotein or critical illness makes total calcium difficult to interpret.
- Malignancy usually raises calcium through PTH-related peptide, focal or diffuse osteolysis, tumour calcitriol production or, less commonly, ectopic PTH; more than one mechanism may coexist.
- An intact PTH that is appropriately suppressed supports a non-parathyroid cause, while a non-suppressed result should reopen the possibility of coincident primary hyperparathyroidism.
Key red flags
Thirst, polyuria, dry mucosa, tachycardia, postural hypotension and reduced urine output reflect nephrogenic water loss and worsening renal calcium clearance.
Investigation priorities
Confirm the abnormality, grade its trajectory and avoid albumin or paraprotein artefact.
Management branches
A patient with suspected or known malignancy has symptomatic, rapidly rising or severe hypercalcaemia.
- Use ABCDE, ECG and neurological assessment, repeat calcium with renal and companion electrolytes, establish accurate fluid balance and stop avoidable calcium-raising medicines or supplements.
- Begin 0.9% sodium chloride according to the Society and local acute-oncology schedule, reassessing lungs, pressure, perfusion and urine output after each stage.
Key medicines
Intravenous 0.9% sodium chlorideUse the staged volume and rate in the current Society for Endocrinology and local acute-oncology pathway, adjusting each prescription to deficit, urine output, age, heart failure and renal function rather than applying a universal daily volume.
Zoledronic acid for tumour-induced hypercalcaemiaThe current SmPC recommends a single 4 mg intravenous dose for adults with albumin-corrected calcium at least 3.0 mmol/L, infused over no less than 15 minutes by an experienced prescriber after hydration and renal assessment.