Hypercalcaemia Algorithm

Safety

Screen for life-threatening hypercalcaemia & can't-miss diagnoses

Done

Hypercalcaemia can be asymptomatic or life-threatening. Use the laboratory-reported albumin-adjusted calcium, interpreted alongside symptoms, albumin, renal function and previous values. Act on the level and the clinical state — severity is not read off a number alone.

Adults only. Hypercalcaemia in children and young people needs paediatric/endocrine advice — do not apply adult thresholds without specialist input. Pregnancy: suspected or confirmed PHPT in pregnancy requires endocrine/obstetric specialist (MDT) advice; do not start cinacalcet or bisphosphonates in pregnancy; consider specialist surgical management where clinically indicated, and offer parathyroid surgery to women with PHPT who are considering pregnancy (NG132).

Adjusted Ca²⁺ >3.5 mmol/L Urgent correction is needed because of the risk of dysrhythmia and coma — emergency hospital assessment regardless of apparent wellness (Society for Endocrinology). Clinical condition and rate of rise override numerical thresholds

Adjusted Ca²⁺ 3.0–3.5 mmol/L May be tolerated if the rise has been gradual, but treatment is often required → urgent same-day clinical assessment or specialist discussion. Hospital assessment if symptomatic, rapidly rising, dehydrated, AKI, malignancy, abnormal ECG, vomiting or unable to maintain oral intake; emergency transfer if confusion, reduced GCS or arrhythmia

Severe symptoms at any calcium level Confusion, coma, seizure, serious arrhythmia, severe dehydration, AKI, persistent vomiting or inability to maintain intake → emergency assessment. A modest number with a sick patient is still an emergency

Substantial rise on previous results A substantial increase compared with previous results, particularly over days to weeks, should prompt urgent clinical review. Escalate to emergency care if accompanied by symptoms, AKI, dehydration, arrhythmia, known malignancy or inability to maintain oral intake

On digoxin Hypercalcaemia potentiates digoxin toxicity → emergency assessment if arrhythmia or any concern about toxicity

AKI or falling urine output Oliguria, rising creatinine, severe dehydration → emergency assessment at any calcium level, as in the core rule; hypercalcaemia with AKI needs monitored IV fluids in hospital

Features suggesting malignancy Weight loss, night sweats, bone pain, lymphadenopathy, known cancer. Investigate urgently and in parallel; use the NG12 cancer route when its symptom, examination or test criteria are met — not solely because PTH is suppressed

Suspected adrenal insufficiency Postural hypotension, weakness, hyponatraemia with hypercalcaemia → same-day assessment; emergency if shocked or unwell

Drug contributors Thiazide, calcium or vitamin D supplements, activated vitamin D analogues (alfacalcidol, calcitriol), lithium, high-dose vitamin A or vitamin A-containing retinoids, calcium-containing antacids or phosphate binders; dehydration and reduced renal function aggravate. Review and stop the contributor where appropriate — but never stop lithium unilaterally: contact the prescriber or psychiatry team, and arrange endocrine assessment if hypercalcaemia persists

Immobility Prolonged bed rest, spinal cord injury, Paget's, high bone turnover — a contributor rather than a destination; urgency follows the calcium level and clinical state

Adjusted calcium >3.5 mmol/L needs urgent correction because of the risk of dysrhythmia and coma (Society for Endocrinology). Below 3.0 is often asymptomatic and usually needs no urgent correction; 3.0–3.5 may be tolerated if the rise has been gradual, but frequently needs treatment depending on symptoms and context — which is why the same number can mean two different destinations. Malignancy is the most common cause in hospitalised patients and primary hyperparathyroidism the most common in outpatients. The key distinction is PTH-mediated (PHPT, tertiary, FHH, lithium-associated) versus non-PTH-mediated (malignancy, granulomatous disease, vitamin D excess, drugs). Use the laboratory's albumin-adjusted calcium rather than a remembered correction formula — methods differ between laboratories — and do not measure ionised calcium routinely when testing for PHPT (NG132).

Diagnose

Confirm hypercalcaemia & classify severity

Done

Use the laboratory's albumin-adjusted calcium. Confirm before committing to a diagnosis — but never delay urgent assessment for repeat sampling.

Which calcium

Use the laboratory-reported albumin-adjusted calcium. Do not treat a single universal correction formula as interchangeable with the local laboratory method. Interpret with symptoms, albumin, renal function and previous values. Normal: 2.2–2.6 mmol/L

Ionised calcium

Do not request ionised calcium routinely for diagnosing PHPT (NG132). Discuss it with the laboratory or acute-care team only when total/albumin-adjusted calcium is unreliable — critical illness, major pH disturbance, severe hypoalbuminaemia

Under 3.0 mmol/L

Often asymptomatic Usually no urgent correction. Outpatient assessment if well — but symptomatic hypercalcaemia below 3.0 still warrants same-day assessment

3.0–3.5 mmol/L

Context-dependent May be tolerated if the rise has been gradual; treatment is often required depending on symptoms and context → urgent same-day clinical assessment or specialist discussion. Hospital assessment if symptomatic, rapidly rising, dehydrated, AKI, malignancy, abnormal ECG, vomiting or unable to maintain intake

>3.5 mmol/L

Emergency Urgent correction because of dysrhythmia and coma risk — emergency hospital assessment regardless of apparent wellness (Society for Endocrinology)

Repeat testing

Repeat the albumin-adjusted calcium at least once if ≥2.6 mmol/L, or ≥2.5 mmol/L with clinical features suggestive of PHPT (NG132). Timing follows the calcium level, the symptoms and the local laboratory pathway — not a fixed interval. Do not defer PTH for six months, and act on the first result if symptomatic or the level is high

When to measure PTH

Measure PTH when the threshold is confirmed (≥2.6 mmol/L on at least two occasions, or ≥2.5 mmol/L on two occasions with features suggestive of PHPT), unless urgent clinical circumstances require calcium and PTH in parallel. Interpret PTH against the calcium and the laboratory reference range; seek endocrine advice for a raised/inappropriately normal PTH, or a low PTH with calcium ≥2.6 mmol/L (NG132)

Albumin adjustment prevents under- and over-diagnosis, but adjustment methods differ between laboratories — which is why the laboratory's own adjusted value is the one to use, rather than a formula applied by hand. Ionised calcium is the physiologically active fraction, but NICE NG132 says not to measure it when testing for primary hyperparathyroidism; it is discussed with the laboratory or acute team only where adjustment is unreliable. A single elevated reading in an asymptomatic patient may reflect assay variation or a transient cause, so NG132 asks for at least one repeat at 2.6 mmol/L or above, with PTH measured once calcium is elevated on two occasions — unless urgency requires parallel testing. If the patient is symptomatic or the level is high, act on the first result.

Diagnose

Classify the aetiology — PTH-mediated vs non-PTH-mediated

Done

PTH is the critical branch point. Measure intact PTH and albumin-adjusted calcium concurrently using the local laboratory protocol — a routine random sample is appropriate; fasting is not required, and do not delay urgent assessment for repeat sampling.

How to read PTH

Interpret PTH as appropriate or inappropriate for the calcium level. A raised or non-suppressed PTH with hypercalcaemia suggests PTH-mediated hypercalcaemia and requires specialist interpretation — it does not by itself establish primary hyperparathyroidism. Seek specialist advice if PTH is above the midpoint of the reference range with suspected PHPT, or below the midpoint with calcium ≥2.6 mmol/L; if PTH is below the laboratory lower limit, look for alternative diagnoses including malignancy (NG132)

PTH-mediated causes

Primary hyperparathyroidism — the commonest outpatient cause · tertiary hyperparathyroidism, especially in longstanding CKD · FHH · lithium-associated hyperparathyroidism · assay and sampling issues. All need interpretation together, not a single label

Suppressed PTH

Non-PTH-mediated hypercalcaemia — needs urgent evaluation, but not automatically a cancer-pathway referral. Investigate in parallel for malignancy (guided by symptoms and examination), myeloma, vitamin D excess, granulomatous disease, thyrotoxicosis, immobilisation, milk-alkali syndrome and relevant medications

When to use NG12

Use the suspected cancer pathway when the relevant NG12 symptom, examination or test criteria are met — not solely because PTH is suppressed. Myeloma screening (protein electrophoresis and serum free light chains) where the picture fits

FHH

Familial hypocalciuric hypercalcaemia — usually benign. A calcium:creatinine clearance ratio below 0.01 is a screening clue, not a diagnosis: FHH and primary hyperparathyroidism overlap, and results are confounded by CKD, vitamin D deficiency, low calcium intake and thiazides. Do not conclude "no surgery" from a single low ratio — endocrine review, and genetic confirmation where appropriate, are needed. NICE NG132 accepts 24-hour urinary calcium, a random renal calcium:creatinine excretion ratio or the clearance ratio. Lithium also complicates interpretation; interpret urinary calcium after correcting vitamin D deficiency and reviewing thiazides where clinically safe. A low urinary calcium should not be used alone to exclude parathyroid surgery — discuss discordant or borderline results with endocrinology, and consider genetic testing where FHH is suspected (lifelong hypercalcaemia, family history, young age or an equivocal urinary result)

Drug contributors

Thiazides, lithium, calcium supplements, vitamin D excess, calcium-containing antacids (milk-alkali), high-dose vitamin A. Review rather than reflexively stop — and never stop lithium unilaterally

Granulomatous disease

Sarcoidosis, TB and others raise 1,25-dihydroxyvitamin D through macrophage production. If clinically suspected, arrange appropriate respiratory assessment, chest imaging and specialist-directed testing — ACE is not a routine diagnostic test (neither sensitive nor specific enough)

PTH read against the calcium drives the pathway — but it sorts hypercalcaemia into two groups, it does not name the diagnosis. A raised or inappropriately normal PTH means PTH-mediated hypercalcaemia, of which primary hyperparathyroidism is only the commonest member: tertiary hyperparathyroidism in longstanding CKD, FHH, lithium-associated hyperparathyroidism and assay artefact all sit in the same box, which is why specialist interpretation is needed before a label is applied. A suppressed PTH means the cause lies elsewhere and needs urgent evaluation — but the right response is parallel investigation (malignancy guided by symptoms and examination, myeloma screen, vitamin D status, granulomatous disease, thyrotoxicosis, immobilisation, milk-alkali, drugs), with the NG12 cancer route used when its own criteria are met. FHH matters because it mimics primary hyperparathyroidism and should not lead to surgery — but a single clearance ratio cannot settle it, since the two conditions overlap and CKD, vitamin D deficiency, low calcium intake and thiazides all confound the result.

Diagnose

Targeted examination — systemic & directed

Done

Physical examination directs urgency and guides the differential diagnosis. Pay particular attention to signs of malignancy and haemodynamic status.

Vital signs

HR, BP (postural drop → dehydration/Addison's), RR, O₂ sat, GCS. Tachycardia + hypotension = severe/emergency

Hydration status

Mucous membranes, skin turgor, JVP, UO — dehydration worsens hypercalcaemia (reduced renal Ca²⁺ excretion)

Lymphadenopathy

Cervical, axillary, inguinal — lymphoma, sarcoidosis, metastatic malignancy. Firm, fixed nodes = malignancy concern

Neck palpation

Thyroid mass (thyrotoxicosis), parathyroid lesion (rarely palpable — only if carcinoma, large adenoma)

Chest / lungs

Pleural effusion, consolidation — lung malignancy, sarcoidosis

Abdomen

Hepatomegaly, splenomegaly — lymphoma, malignancy. Nephrolithiasis tenderness (PHPT complication)

Skin / eyes

Band keratopathy (corneal calcium, a slit-lamp finding — refer), erythema nodosum (sarcoid), skin lesions (malignancy, sarcoid)

Neurological

Confusion, proximal weakness (hypercalcaemic myopathy), hyporeflexia — indicates severity, need for admission

Bone tenderness

Percussion over spine, long bones — metastatic disease, myeloma, osteitis fibrosa cystica (severe PHPT)

Examination findings in hypercalcaemia often provide the diagnosis before investigations return. Lymphadenopathy with suppressed PTH = lymphoma or sarcoidosis until proven otherwise. Dehydration significantly worsens hypercalcaemia by reducing urinary calcium clearance — spotting this drives immediate fluid management. Neurological signs (confusion, weakness) indicate severity and need for same-day admission regardless of the exact calcium level. Band keratopathy is a chronic sign indicating long-standing hypercalcaemia, typically PHPT.

Diagnose

Investigations — first-line, and what is specialist-directed

Done

First-line bloods establish the cause in most cases. Several tests commonly listed for hypercalcaemia are specialist-directed and should not be ordered routinely from primary care — they are set out below.

Tier 1 — Bloods

Albumin-adjusted Ca²⁺ + albumin Intact PTH (paired, random sample) U&E / creatinine / eGFR Phosphate Magnesium ALP LFTs FBC 25-hydroxyvitamin D TSH ESR / plasma viscosity if myeloma plausible

Interpret PTH + Ca²⁺

Raised or non-suppressed PTH with hypercalcaemia = PTH-mediated (specialist interpretation). Suppressed PTH = non-PTH-mediated — investigate causes in parallel. Interpret phosphate and ALP in context: low phosphate with non-suppressed PTH supports PTH-mediated disease, whereas raised phosphate, ALP, inflammatory markers or an abnormal blood count may suggest alternative pathology but are not diagnostic

Tier 1 — Urine

Calcium excretion assessment where FHH is being considered: NICE NG132 accepts 24-hour urinary calcium, a random renal calcium:creatinine excretion ratio, or the calcium:creatinine clearance ratio. A single result does not settle FHH — see step 3

Tier 1 — ECG

ECG for symptomatic, moderate or severe, or rapidly rising hypercalcaemia: look for QT shortening, bradyarrhythmia or other conduction abnormality. The ECG supports the severity assessment — it does not determine the diagnosis, and no fixed QTc cut-off should be used

Tier 1 — Imaging

CXR where malignancy or granulomatous disease is suspected — hilar lymphadenopathy, pulmonary lesion, primary lung tumour

Specialist-directed only

Not routine primary-care tests. PTHrP is specialist-directed and is not needed to establish that malignancy is possible. 1,25-dihydroxyvitamin D is selective — suspected granulomatous disease or lymphoma, usually after specialist discussion; 25-hydroxyvitamin D is the relevant initial vitamin D test. ACE is not a routine test for sarcoidosis

Myeloma screen

Serum protein electrophoresis + serum free light chains where the clinical picture fits — anaemia, bone pain, renal impairment, raised ESR/plasma viscosity

Bone and renal assessment

Once PHPT is confirmed, arrange or request specialist assessment including DXA of the lumbar spine, distal radius and hip and a renal tract ultrasound at diagnosis (NG132). Thereafter repeat renal imaging when a stone is suspected, with renal colic, or on specialist advice — do not book routine annual or 2–3-yearly renal ultrasounds without a clinical indication

Localisation imaging

Sestamibi and neck ultrasound localise an adenoma before surgery — ordered by endocrinology or the surgical team, not in primary care, and never used to make the diagnosis

Paired PTH and albumin-adjusted calcium answer most of the question, and NG132 asks only for a routine sample using the local laboratory's protocol — fasting and special handling are not general requirements. 25-hydroxyvitamin D is the initial vitamin D test and matters because deficiency can mask primary hyperparathyroidism by keeping calcium in range; correcting it can then unmask hypercalcaemia. Phosphate is typically low in PHPT because PTH promotes renal phosphate excretion, while a raised ALP or phosphate may suggest alternative pathology but is not diagnostic. The tests deliberately absent here matter as much as those present: ACE is neither sensitive nor specific enough to diagnose or exclude sarcoidosis and risks false reassurance; PTHrP is specialist-directed and is not needed to establish that malignancy is possible; 1,25-dihydroxyvitamin D is selective and usually follows specialist discussion. DXA at diagnosis is part of NICE NG132 assessment in confirmed PHPT, and renal ultrasound is for diagnosis or suspected stones rather than routine surveillance.

Refer

Referral pathway — who, when, and how urgently

Done

The aetiology determines the specialty and the urgency follows the clinical state, not the number alone. Acute treatment is a hospital decision — primary care arranges transfer and hands over.

Emergency assessment

Emergency Adjusted Ca²⁺ >3.5 mmol/L regardless of apparent wellness · any level with confusion, coma, seizure, serious arrhythmia, severe dehydration, AKI, persistent vomiting or inability to maintain intake · substantial rise with symptoms, AKI, dehydration, arrhythmia, known malignancy or inability to maintain intake · digoxin with arrhythmia or toxicity concern. Arrange urgent transfer and give a clinical handover — calcium, renal function, medications, observations and time

Same-day acute assessment

Same-day Adjusted Ca²⁺ 3.0–3.5 mmol/L (same-day assessment or specialist discussion; hospital if symptomatic, rising, dehydrated, AKI, malignancy, abnormal ECG or vomiting) · symptomatic hypercalcaemia below 3.0 · suppressed PTH with concerning symptoms or malignancy features · (AKI, falling urine output or severe dehydration → Emergency, above)

Suspected cancer pathway

Suspected cancer · NICE NG12 Use the suspected cancer route when the relevant NG12 symptom, examination or test criteria are met — not solely because PTH is suppressed. A suppressed PTH means urgent evaluation with parallel investigation of malignancy, myeloma, vitamin D excess, granulomatous disease, thyrotoxicosis, immobilisation, milk-alkali and medications

Haematology

Urgent If hypercalcaemia is accompanied by persistent bone/back pain, unexplained fracture, anaemia, renal impairment, raised ESR/plasma viscosity or other features of myeloma, request FBC, calcium, renal function, ESR/plasma viscosity, serum protein electrophoresis and serum free light chains. Discuss abnormal results urgently with haematology or follow the local suspected-myeloma pathway — free light chains are interpreted with electrophoresis, immunoglobulins, renal function and the laboratory's renal-adjusted range. Suspected cancer pathway referral when tests suggest myeloma (NG12)

Parathyroid surgical referral

Refer to a surgeon with parathyroid expertise where confirmed PHPT is associated with (NG132): symptoms of hypercalcaemia · renal stones · fragility fracture or osteoporosis · albumin-adjusted calcium ≥2.85 mmol/L. NICE NG132 also says to consider surgical referral even when these features are absent. Specialist / shared-decision criteria Age under 50 appears in international criteria and is a matter for specialist discussion — it is not an NG132 primary indication

Endocrinology

Confirmed or suspected PHPT not meeting surgical criteria, uncertainty about FHH, tertiary or lithium-associated hyperparathyroidism, or any raised/non-suppressed PTH needing interpretation. Tertiary hyperparathyroidism in CKD is usually already on a renal pathway

Respiratory

Routine–urgent Suspected sarcoidosis or other granulomatous disease → respiratory assessment, chest imaging and specialist-directed testing. Glucocorticoids are a specialist decision, not a holding measure started in primary care

Drug-associated

Mild asymptomatic hypercalcaemia with a thiazide or supplements may be reviewed after stopping the contributor — but this is not always "primary care only": never stop lithium unilaterally (involve mental health/psychiatry) · persistent hypercalcaemia may be unmasked PHPT · renal impairment, symptoms or calcium ≥3.0 need more urgent assessment · calcium and vitamin D supplements may be clinically necessary in osteoporosis and should be reviewed rather than automatically stopped long-term

NICE NG132 sets four features that make parathyroid surgical referral appropriate in confirmed PHPT — symptoms of hypercalcaemia, renal stones, fragility fracture or osteoporosis, and an albumin-adjusted calcium of 2.85 mmol/L or above — while also saying to consider referral even when none is present, so the conversation is rarely closed by a threshold alone. Age under 50 comes from international criteria and belongs in the shared decision rather than in a list of NG132 indications. Much mild asymptomatic PHPT is managed conservatively with annual review. For non-PTH-mediated hypercalcaemia the discipline is parallel investigation rather than a reflex cancer referral: a suppressed PTH is a reason for urgent evaluation, but the NG12 route earns its place only when its own criteria are met — sending every suppressed PTH straight to a cancer pathway both over-refers and delays the patient whose cause is granulomatous, drug-related or myeloma.

Treat

Treatment pathway — by severity and aetiology

Done

Acute hypercalcaemia is treated in hospital. This pathway sets out what primary care does — recognise, arrange transfer, hand over, and manage the mild chronic disease that stays in the community.

Acute or severe hypercalcaemia — what primary care does

Step 1Arrange urgent transfer and provide a clinical handover — the adjusted calcium and its trend, renal function, current medications (especially digoxin, thiazide, lithium, calcium and vitamin D), observations, oral intake and conscious level, and the suspected cause. This is the primary-care action

Step 2Hospital treatment usually begins with monitored IV isotonic saline. IV bisphosphonate, calcitonin, denosumab, glucocorticoids and dialysis are specialist decisions — the choice depends on the cause, renal function, malignancy, vitamin D status, fluid-overload and heart-failure risk, and the local acute or endocrine protocol. Doses and rates are deliberately not given here.

FluidsDo not start IV fluids in the community unless this is a trained ambulance or acute-care setting with monitoring and a local protocol. Fluid management in acute hypercalcaemia belongs in monitored secondary care — heart failure, CKD and frailty make unmonitored fluid loading unsafe.

DiureticsA loop diuretic is not a calcium-lowering treatment and may worsen dehydration. Loop diuretics are rarely used, and are generally reserved for fluid overload during monitored treatment (Society for Endocrinology). Loop diuretics are not routine treatment for hypercalcaemia and should not be used simply to lower calcium; in hospital they may be considered if fluid overload develops during monitored rehydration.

AntiresorptivesThe hospital, endocrine or oncology team selects and monitors antiresorptive treatment. NICE NG132 specifically advises against bisphosphonates for long-term calcium reduction in primary hyperparathyroidism; they may be considered for fracture-risk reduction. This does not prohibit specialist use of IV bisphosphonates in acute severe hypercalcaemia when clinically indicated. Cinacalcet, where used, is endocrinology-initiated under the current local shared-care protocol and SPC.

Mild PHPT not meeting surgical criteria — primary-care surveillance

Meets a NG132 referral feature

Refer to parathyroid surgery Via NG132

Symptoms of hypercalcaemia, renal stones, fragility fracture or osteoporosis, or adjusted calcium ≥2.85 mmol/L — and consider referral even where none is present. Localisation imaging is arranged by the specialist team, not before referral.

No surgical feature, stable, asymptomatic

Conservative surveillance Primary care

Annual albumin-adjusted calcium and eGFR/creatinine; DXA at diagnosis and every 2–3 years, and renal tract ultrasound at diagnosis (NG132). Review the surgical criteria at each annual review. Maintain adequate hydration within cardiac and renal limits.

Unsuitable for or declining surgery

Endocrinology decision Specialist-initiated

Cinacalcet may be considered when surgery is unsuccessful, unsuitable or declined and adjusted calcium is ≥2.85 mmol/L with symptoms or ≥3.0 mmol/L with or without symptoms (NG132); it does not improve bone density. Initiated and monitored by endocrinology under the current local shared-care protocol and SPC — do not rely on the 2017 local protocol without confirming it remains locally valid.

Drug-associated hypercalcaemia

Thiazide diuretics

Review and stop where clinically appropriate, then recheck the adjusted calcium. Persistent hypercalcaemia may represent unmasked PHPT — investigate rather than assume the drug was the whole answer

Lithium

Do not stop lithium unilaterally. Discuss with mental health/psychiatry — the psychiatric risk of stopping may outweigh the hypercalcaemia. Contact the prescriber or psychiatry team, and arrange endocrine assessment if hypercalcaemia persists — lithium-associated hyperparathyroidism needs endocrine interpretation

Vitamin D excess

Stop the supplement and recheck. Glucocorticoids are not a routine primary-care response to vitamin D toxicity — they have a place in granulomatous disease and some lymphoma-related or vitamin-D-mediated hypercalcaemia, but only with endocrine or acute-care guidance. Severe or symptomatic hypercalcaemia goes to acute assessment

Calcium supplements

Review rather than automatically stop — they may be clinically necessary in osteoporosis. Check dietary intake and calcium-containing antacids (milk-alkali)

Next steps: see Malignant hypercalcaemia · Haematological cancers · Osteoporosis · Chronic kidney disease

Monitored intravenous fluid is the cornerstone of acute treatment, but it is a hospital intervention: the rate and volume depend on heart failure and fluid-overload risk, renal function and the cause, and it requires monitoring of urine output and electrolytes that primary care cannot provide. The same applies to bisphosphonates, denosumab, calcitonin, glucocorticoids and dialysis — each depends on the cause, renal function, malignancy, vitamin D status and dental risk, which is why this pathway names them without dosing them. Loop diuretics are a specific trap: they increase calcium excretion but worsen dehydration, which raises calcium further, and Society for Endocrinology guidance describes them as rarely used and generally reserved for fluid overload during monitored treatment. Cinacalcet lowers calcium without improving bone density or preventing stones, unlike parathyroidectomy, and NICE NG132 advises against bisphosphonates for long-term calcium reduction in PHPT.

Lifestyle

Non-pharmacological measures — for stable, mild hypercalcaemia

Done

These measures support management of stable, mild hypercalcaemia. They are not a substitute for assessment, and fluid management in acute hypercalcaemia belongs in monitored secondary care.

Hydration — adequate, not prescriptive For stable mild disease, encourage normal adequate hydration if cardiac and renal function allow. A fixed 2–3 L/day is not safe as a universal instruction in heart failure, CKD, frailty or older age, or anyone at risk of fluid overload. Dehydration is a common precipitant of deterioration — the message is to avoid it, individualised to the patient

Avoid immobility Prolonged bed rest increases bone resorption and worsens hypercalcaemia. Encourage regular activity as tolerated, and pay particular attention during acute illness or after injury

Dietary calcium — do not restrict Counter-intuitive but important: a low-calcium diet increases PTH secretion and can worsen PHPT. Aim for a normal dietary calcium intake — not a high intake, and not indiscriminate supplementation. Review supplements rather than stopping necessary osteoporosis treatment outright

Review diuretics Thiazides reduce renal calcium excretion and may need review with the prescribing indication in mind. A loop diuretic is not a substitute and is not calcium-lowering treatment — it is reserved for fluid overload during monitored treatment

Vitamin D supplements Review against the 25-hydroxyvitamin D level and the clinical indication. In granulomatous disease, vitamin D handling is abnormal — supplementation decisions there are specialist-guided. In PHPT, correct vitamin D deficiency cautiously with monitoring of calcium and renal function, particularly where calcium is substantially raised or urinary calcium is high — do not withhold treatment automatically, but seek specialist advice in marked hypercalcaemia (NG132)

Alcohol Avoid excess, which worsens dehydration

Medication review Calcium supplements, calcium-containing antacids, lithium, thiazides, high-dose vitamin A, vitamin D. Review and document — and never stop lithium unilaterally

Stone prevention if a stone-former Adequate fluid intake within cardiac and renal limits, reduced dietary sodium, moderate animal protein. Refer to urology for recurrent stones — stones are also a NG132 surgical referral feature

Bone health Weight-bearing exercise supports bone density in PHPT managed conservatively. DXA at diagnosis and every 2–3 years (NG132)

Avoiding dehydration genuinely matters — reduced urinary calcium clearance is one of the main ways mild hypercalcaemia becomes severe — but a blanket 2–3 L/day instruction is unsafe in heart failure, CKD, frailty and older age, which is why the advice here is adequate hydration within the patient's cardiac and renal limits. The instruction not to restrict dietary calcium is frequently misunderstood by patients who intuitively cut out dairy: a low-calcium diet raises PTH and can worsen PHPT. Sun protection is not a general hypercalcaemia measure — avoiding excessive vitamin D exposure may be relevant in sarcoidosis or other granulomatous disease, but that is specialist advice for a specific condition, not lifestyle advice for everyone with a raised calcium. NG132 supports conservative management, including these measures, for asymptomatic PHPT not meeting surgical criteria.

Safety

Follow-up, monitoring & safety-netting

Done

Monitoring follows the aetiology. For confirmed PHPT managed without surgery, NICE NG132 specifies annual albumin-adjusted calcium and eGFR/creatinine, DXA at diagnosis and every 2–3 years, and renal tract ultrasound at diagnosis and when a stone is suspected — routine annual 24-hour urine calcium and routine renal ultrasound every 2–3 years are not NICE NG132 requirements.

Post-acute discharge

Review shortly after discharge — adjusted calcium, U&E and eGFR, oral intake maintained, medications reconciled, and specialist follow-up confirmed as arranged

Drug contributor stopped

Recheck the adjusted calcium after stopping or reducing the contributor. If it does not normalise, investigate for underlying PHPT rather than attributing it to the drug. Lithium changes are made with mental-health input, not unilaterally

PHPT without surgery — NICE NG132

Annual albumin-adjusted calcium and eGFR/creatinine. DXA at diagnosis and every 2–3 years. Renal tract ultrasound at diagnosis, and again if a renal stone is suspected or renal colic occurs. Specialist monitoring if taking cinacalcet. Review the surgical referral features at each annual review (NG132)

Not NICE NG132 requirements

Routine annual 24-hour urine calcium and routine renal ultrasound every 2–3 years are not stated NICE NG132 requirements and should not be booked as automatic recalls

Post-parathyroidectomy

Specialist-led early monitoring for post-operative hypocalcaemia ("hungry bone"), then calcium and renal function per the surgical team's protocol. Confirm the plan is in the record before taking over monitoring

Malignancy-associated

Oncology-led. Calcium monitoring and any antiresorptive treatment follow the oncology regimen; dental assessment before antiresorptive treatment is arranged by the initiating team

Granulomatous disease

Respiratory or specialist-led, including any glucocorticoid treatment and its monitoring. Primary care monitors calcium and renal function as directed by that plan

When to escalate urgently

Calcium rising despite treatment · new or worsening renal impairment · new or worsening confusion · unable to maintain oral fluids · bone pain with new neurological deficit

Safety-net — 999

999 Confusion, drowsiness, coma or collapse · seizure · cardiac arrhythmia or chest pain · persistent vomiting unable to keep fluids down · back pain with leg weakness (possible cord compression)

Safety-net — same-day

Same-day Significant worsening weakness or lethargy · unable to eat or drink for more than a day · severe bone pain · markedly reduced urine output · an adjusted calcium of 3.0 mmol/L or above returning on routine monitoring, or a symptomatic result below that

Annual review

Confirm specialist appointments attended, reconcile calcium and vitamin D supplements, reinforce individualised hydration, and make the explicit decision to continue surveillance or refer for surgery

Asymptomatic PHPT often remains stable for years, which is why NG132 supports conservative management with annual albumin-adjusted calcium and eGFR/creatinine, DXA at diagnosis and every 2–3 years, and renal imaging at diagnosis and when a stone is suspected — a schedule designed to detect the patients who cross a surgical referral threshold without subjecting everyone to annual urine collections and repeated scanning. Post-parathyroidectomy hypocalcaemia ("hungry bone") is the serious early complication: the suppressed skeleton rapidly takes up calcium, and monitoring in that window is specialist-led. Safety-netting matters particularly in hypercalcaemia because patients adapt to a chronically raised calcium and may not recognise gradual deterioration — so the trigger for review is the symptom set, not only the number.