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.
- Restore extracellular volume with 0.9% sodium chloride using repeated cardiorespiratory and urine-output assessment; frailty, heart failure and kidney impairment require slower individualised delivery.
- Loop diuretics do not directly treat the high calcium and are reserved for clinically important fluid overload after adequate resuscitation, not routine forced diuresis.
- Intravenous bisphosphonate effect is delayed for several days, so record renal function, product, dose and time and do not redose prematurely because the calcium has not fallen the next morning.
- Calcitriol-mediated lymphoma may respond to glucocorticoid treatment, while refractory disease may need specialist calcitonin, denosumab, dialysis or tumour-directed intervention.
- The episode often signals advanced cancer; combine biochemical treatment with prognosis, symptom control, treatment goals and palliative-care support where appropriate.
Key red flags
Thirst, polyuria, dry mucosa, tachycardia, postural hypotension and reduced urine output reflect nephrogenic water loss and worsening renal calcium clearance.
Fatigue, poor concentration, depression, confusion, delirium, seizure or coma can represent calcium toxicity and should not be assigned automatically to malignancy progression.
Shortened QT, bradyarrhythmia or other conduction disturbance with acute kidney injury or oliguria marks high-risk disease requiring monitored correction.
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.
- Escalate shock, oliguria, severe neurological change, arrhythmia or inability to rehydrate safely to critical care, renal and endocrine teams while treating the precipitating illness.