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REASONING GP · Clinical algorithm · Quick reference
Hypercalcaemia in adults — triage and diagnostic approachTwo causes account for about 90% of cases — primary hyperparathyroidism and malignancy — and the PTH separates them in one test. Correct for albumin, then act on the adjusted value.
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| Trigger / red flag | Leading concern · destination | Do now · do not delay |
|---|---|---|
| Adjusted Ca²⁺ above 3.40 mmol/L, or above 3.00 with drowsiness, confusion, vomiting, dehydration or reduced urine output; reduced GCS or seizure. | Hypercalcaemic crisis · needs IV saline and an IV bisphosphonate Emergency admission now |
This is a self-amplifying problem: hypercalcaemia causes polyuria, the dehydration reduces calcium excretion, and the level climbs further — so the patient deteriorates while waiting. Oral rehydration at home is not treatment above 3.40. Stop calcium and vitamin D supplements, thiazides and lithium now, and say what was stopped. Send the adjusted calcium with albumin, U&E and the previous values. |
| Cardiac or drug risk: bradycardia, shortened QT, arrhythmia, or the patient takes digoxin. | Arrhythmia · digoxin toxicity precipitated by hypercalcaemia Emergency admission; ECG now |
Hypercalcaemia potentiates digoxin and can precipitate toxicity at a previously stable dose. ECG before or alongside transfer. Do not continue digoxin unreviewed, and do not wait for a repeat calcium to act. |
| Hypercalcaemia with acute kidney injury: creatinine rising, eGFR falling, oliguria, or a patient unable to maintain oral intake because of vomiting. | Hypercalcaemic AKI Emergency admission now |
Dehydration and AKI make the hypercalcaemia worse and vice versa; this needs IV volume replacement with monitoring, not oral fluids and a repeat next week. Hold ACE inhibitors, ARBs, NSAIDs, diuretics and metformin as appropriate and record what was held (NG148). |
| Adjusted Ca²⁺ 3.00–3.40 mmol/L in a patient who is alert, hydrated and without AKI. | Moderate-to-severe hypercalcaemia needing assessment today Same-day clinical assessment and bloods |
Assess hydration, GCS and orientation face to face; this cannot be judged on the telephone. Send PTH with a paired calcium, U&E, phosphate, magnesium, ALP, vitamin D, FBC, ESR or CRP, LFTs and TSH the same day. Stop calcium and vitamin D supplements, thiazides and lithium. Encourage oral fluids and repeat within 24–48 hours — with a named person to look at the result. |
| Known or suspected malignancy with a raised calcium — breast, lung, myeloma, renal, prostate, head and neck, lymphoma — or a rapid rise on serial results with a suppressed PTH. | Malignant hypercalcaemia · bone metastases · PTHrP-secreting tumour Same-day oncology or acute assessment |
Malignant hypercalcaemia rises quickly and carries a poor prognosis untreated; it is an oncological emergency, not a metabolic finding to monitor. Contact the patient's oncology team directly rather than arranging routine review. In a patient already on the palliative pathway, the treatment decision belongs with the specialist team and the patient's wishes. |
| Suppressed PTH with no obvious cause, or hypercalcaemia with high-dose vitamin D, calcium carbonate, lithium, a thiazide, teriparatide, excess vitamin A, or antacid or milk excess. | Non-parathyroid hypercalcaemia · drug or supplement cause Same-day review of the drug; urgent investigation of the cause |
Ask directly about over-the-counter supplements and high-dose vitamin D — these will not be on the repeat prescription and the patient may not volunteer them. Stop the culprit, and recheck at 1–2 weeks. A suppressed PTH that does not resolve on stopping supplements still needs the malignancy and granulomatous workup below. |
| Granulomatous or endocrine features: breathlessness with bilateral hilar changes, erythema nodosum or uveitis; tremor, weight loss and heat intolerance; recent immobility or a long bed-bound period; postural hypotension with fatigue. | Sarcoidosis · tuberculosis · thyrotoxicosis · immobilisation · adrenal insufficiency Same-day or urgent investigation depending on severity |
Send TSH, ACE, chest X-ray and vitamin D metabolites as indicated. These causes also present with a suppressed PTH, so they are on the same limb of the algorithm as malignancy and must not be assumed until cancer has been addressed. |
| Hypercalcaemia with a myeloma or cancer feature: unexplained bone pain (especially back pain), fractures on minimal trauma, anaemia, weight loss, fatigue, unexplained renal impairment, a raised ESR or plasma viscosity, or hypercalcaemia at 60 or over with no parathyroid explanation. | Myeloma · metastatic bone disease · other malignancy Very urgent FBC, calcium, plasma viscosity/ESR and protein electrophoresis with Bence Jones protein — within 48 hours; urgent suspected-cancer referral if positive · NICE NG12 |
NG12: in anyone 60 or over with hypercalcaemia or leucopenia and a presentation consistent with possible myeloma, arrange a very urgent FBC, calcium, plasma viscosity or ESR and serum protein electrophoresis with urinary Bence Jones protein — within 48 hours — and refer on the urgent suspected-cancer route if the results suggest myeloma. Hypercalcaemia with unexplained bone pain or renal impairment should not be investigated at a leisurely pace. Normal results with persisting symptoms still need review and a decision on referral. |
REASONING GP · Hypercalcaemia in adults — triage and diagnostic approach |
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| Primary hyperparathyroidism PTH raised or inappropriately normal | The commonest cause in the community, usually incidental in an asymptomatic older woman: mildly raised calcium, low-to-normal phosphate, raised or unsuppressed PTH. Assess the end-organ consequences — renal function, stones on imaging, DEXA — because these, not the calcium alone, decide whether surgery is offered (NG132). |
| Malignancy PTH suppressed | Must be excluded first when the PTH is low: PTHrP secretion (squamous lung, renal, breast, head and neck), osteolytic metastases (breast, lung, prostate, renal), and myeloma — hypercalcaemia with anaemia, renal impairment and bone pain. Typically higher, faster-rising, with a raised ALP. Investigate urgently; do not monitor. |
| Drugs, then the granulomatous and endocrine causes PTH usually suppressed | Drugs — the commonest reversible cause in primary care: high-dose vitamin D and calcium carbonate (including antacids), thiazides, lithium (raises PTH), teriparatide, excess vitamin A. Most often missing from the drug history because the patient buys it — ask directly. Then: sarcoidosis and tuberculosis (excess 1,25-dihydroxyvitamin D), thyrotoxicosis, adrenal insufficiency, phaeochromocytoma — all on the same suppressed-PTH limb as malignancy, so they do not remove the need to look for cancer. |
| FHH, tertiary, immobility and spurious | Familial hypocalciuric hypercalcaemia: lifelong mild hypercalcaemia, raised or normal PTH, low 24-hour urinary calcium, family history, no end-organ damage — needs no treatment and no surgery, and mistaking it for primary hyperparathyroidism leads to an unnecessary parathyroidectomy. Tertiary: long-standing CKD, raised PTH with a high phosphate. Immobilisation: especially in Paget's or prolonged bed rest. Spurious: a cuffed sample, dehydration or a high albumin — hence the adjusted value on a repeat. |
| Confirm on the adjusted value, and send the PTH | Repeat the calcium uncuffed with albumin and send a PTH with a paired calcium at the same time — not after another six months of watching the calcium. Add U&E, phosphate, ALP, vitamin D, FBC, ESR and, in the 60-and-overs, the NG12 48-hour myeloma panel. Without a PTH there is no diagnosis, only a number. |
| Stop the culprits | Stop calcium and vitamin D supplements (prescribed and bought), calcium-containing antacids and thiazides, switching antihypertensive class. Review lithium with mental-health input rather than stopping it unilaterally, and check the level. Review digoxin. Recheck at 1–2 weeks. Encourage 2–3 litres of fluid daily if cardiac and renal function allow, since dehydration raises the calcium further, and avoid prolonged immobility — but do not give a loop diuretic at home, which worsens the dehydration driving the level. |
| Assess the end-organ damage — it decides the referral | Arrange renal function, DEXA, and imaging for renal stones where indicated. These findings, not the calcium alone, determine whether parathyroid surgery is offered, so the letter is far more useful with them (NG132). Treat confirmed osteoporosis in parallel (NG146). |
| Monitor and the escalation rule — write it down | For mild asymptomatic disease: adjusted calcium, U&E and eGFR at least annually, DEXA periodically. Write the triggers down: adjusted Ca²⁺ above 3.40, or above 3.00 with drowsiness, confusion, vomiting or dehydration → emergency admission; 2.85 or above, or new symptoms, stones, fractures or falling eGFR → endocrine referral. |
| What not to do | Do not act on a total calcium. Do not monitor a suppressed PTH — that is the cancer limb. No loop diuretic at home. Do not restart the thiazide. Do not file a raised calcium as "borderline" with no PTH and no reviewer — that is how myeloma is missed for years. |