- Defined as calcium >2.6 mmol/L
- Calcium >3.5 mmol/L is an emergency, always admit
- Corrected calcium used most in the UK, although correcting for albumin is controversial
- Consider admission if moderately high (3-3.5) – depending on how well tolerated, which is related to the rate of increase
- Milder hypercalacaemia can be managed in primary care or via SDEC
Clinical features
- Symptoms are rare if calcium <3
- If short history and severe symptoms – more likely malignancy
- If no symptoms, consider pseudohypercalcaemia (see below)
- ‘Bones, stones, groans, and psychic moans’
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- Bones – Aches and pains, fractures (osteomalacia / osteoporosis / osteitis fibrosa cystica – rare)
- Renal stones – nephrocalcinosis on xray, AVP resistance
- Groans – Abdominal pain, constipation, vomiting, anorexia, thirst, peptic ulcers, pancreatitis, pseudogout
- Moans – Depression, drowsiness, weakness, delirium
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- Additionally: Calcium band keratopathy, hypertension (if not hypovolaemic)
ECG changes
- Short QT interval
- J waves (just after R wave)
- Prolonged QRS interval
- Flat T waves
- AV-block
- VF, VT, PEA and asystole
Causes
- In 85% of cases, the cause is primary hyperparathyroidism or malignancy (but there are lots of others)
- Hyperparathyroidism
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- Primary
- Tertiary (very high PTH, occurs in advanced CKD)
- Don’t forget MEN1 and MEN2A
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- Malignancy
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- Especially associated with advanced disease and a poor prognostic sign (median survival 3-4 months)
- 80% PTH related peptide mediated especially in squamous cell carcinomas, lung, renal
- 20% humoral mediated osteoclast activity – especially breast and myeloma
- Also seen in bony metastases, parathyroid cancer, lymphoma
- Can be caused by activation of extra-renal vitamin D (lymphoma)
- Very rare in prostate cancer
- 65% of inpatient hypercalcaemia
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- Less common causes include
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- Granulomatous disease (especially sarcoid, TB, GPA)
- Immobility (high rate of bone turnover)
- Vitamin D toxicity
- Calcium supplementation and Milk-alkali syndrome
- Vitamin A toxicity
- Endocrine – hyperthyroidism, Addison’s, phaeochromocytoma
- Familial Hypocalciuric hypercalcaemia
- Ectopic PTH
- Drugs (lithium, thiazides, theophylline, all-trans retinoic acid, teriparatide)
- Rhabdomyolysis
- Renal failure
- HTLV1 infection
- CYP24A1 mutations (high serum Ca, high Ca in urine, renal stones)
- Pseudo-hypercalcaemia – corrected calcium high, ionised calcium normal. Occurs in myeloma, as the paraprotein binds calcium
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Investigations
- Always send phosphate, PTH level, TFTs, LFTs (alk phos), vitamin D, magnesium
- VBG (a metabolic acidosis or normal ionised calcium may be clues to the cause)
- Phosphate should be inversely proportional to PTH in absence of renal disease
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- So low phosphate suggests hyperparathyroidism, some malignancies (if PTH-related peptide hypercalcaemia), milk alkali syndrome
- High phosphate can occur in any of the other causes
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- ECG for all
- Parathyroid hormone level (PTH)
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- If elevated calcium, PTH should be low
- If PTH is normal/unsuppressed or high – this suggests hyperparathyroidism (but also exclude FHH, and consider tertiary hyperparathyroidism, parathyroid cancer, drugs like lithium)
- If PTH is suppressed with high calcium – generally a bad sign as this suggests malignancy (especially breast, thyroid and bone) but it could also be a rare cause
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- Other tests
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- Send magnesium as low levels can mask primary hyperparathyroidism
- If corrected calcium high but ionised calcium normal – do myeloma screen (pseudohypercalcaemia)
- Myeloma screen – ESR, serum protein electrophoresis, immunoglobulins, serum free light chains
- Consider serum ACE, cortisol
- 24 hr urinary calcium – this is typically high. Can be low in vitamin D deficiency and FHH
- Do a spot urine calcium and calculate the calcium:creatinine ratio to exclude FHH
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- Ensure vitamin D replete first
- Can be be falsely low in pregnancy, if on diuretics and in CKD
- This can exclude 98% of FHH and 66% of primary hyperparathyroidism
- In FHH the CCCR is < 0.02 (and if so, do a genetic test for known mutations)
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- Imaging to consider
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- CxR – sarcoid, TB, cancer
- Renal USS – nephrocalcinosis, calculi
- CT CAP for malignancy
- DEXA scan
- Parathyroid imaging – only useful if parathyroid cancer suspected or planning surgery (so only if surgical candidate). Can do a Sestamibi scan and US neck
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Treatment
- Consider a cardiac monitor
- Management depends on symptoms as well as the calcium level
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- Patients with chronic hypercalcaemic can tolerate levels of 3-3.5, and don’t necessarily need emergency treatment
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- In peri-arrest situations where there is a risk of cardiac arrest treat hypercalcaemia with
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- IV fluids
- Furosemide 1 mg / kg
- Hydrocortisone 200-300 mg IV
- ICU review – consider dialysis
- and treat the underlying cause
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- Stop calcium supplements (plus vitamin D, vitamin A, and any other causative medications if possible) – this is often forgotten
- IV fluids is the mainstay of treatment
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- Aim to give 4-6L/24 hours if possible (for at least first 2 days) – aiming urine output 100-150ml/hour
- Patients will be dry initially. Once euvolaemic, you want urine output to match fluid input (or risk of overload)
- Normal saline fluid of choice (you need the Na for calcium excretion). Avoid Hartman’s. If the patient also has a high sodium, can give dextrose as well
- Keep going with fluids if you don’t know the diagnosis. They can take a while to work and calcium will continue to gradually fall. Aim is also to prevent an AKI
- Give even if history of HF (can use loop diuretics alongside fluid if clinically overloaded)
- Reduce IV fluid later once bisphosphonates are working
- Consider catheter and carefully monitor urine output
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- Frusemide 1mg/kg
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- Often used if the patient has HF (allows you to give more fluids, also mildly brings calcium down itself but not much)
- However, controversial, and some have suggested it might cause more harm than good
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- IV bisphosphonates
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- Arguably overused, but if calcium very high (>3.6) definitely give, and give if not responding to fluids
- Lower threshold to use if cancer causative
- Usually start once patient is rehydrated
- Can take a few days at least to have an impact
- Zolendronate (4mg IV over 15 minutes, or 60 minutes) is useful for malignancy-induced hypercalcaemia (do not give if diagnosis unclear because it can cause hypocalcaemia in hyperparathyroidism. Can drop magnesium and phosphate too). Reduce the dose in renal impairment
- Useful in pain of malignancy too
- Pamidronate (60-90mg) is an alternative – maybe a better choice in severe renal dysfunction (can divide doses), but less effective (though it is cheaper). Adjust dose if renal impairment (and might avoid if eGFR <30)
- Can repeat bisphosphonates but must wait 5 days at least
- They can cause bone pain, fever or flu-like symptoms, and can cause hypocalcaemia if vitamin D deficient or PTH suppressed
- Doesn’t fix the underlying cause of high calcium – so consider that whilst treating, or else hypercalcaemia can recur
- Avoid in milk alkali syndrome
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- Steroids
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- Generally used 2nd line
- Work though multiple pathways, including inhibiting calcium absorption and increasing urinary calcium excretion
- Prednisolone 20-60mg OD
- Only really works in myeloma, lymphoma, sarcoid and vitamin D excess
- Effective in 2-4 days
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- Calcitonin 200 IU TDS s/c injection
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- Used in cases of resistant hypercalcaemia (2-3 days post bisphosphonates). Often used for a few days only
- Risk of rebound hypocalcaemia, and poorly tolerated (nausea and vomiting is the main issue)
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- Denosumab (120mg s/c injection once)
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- In the latest US guidance, this is used in preference to bisphosphonates in hypercalcaemia of malignancy
- Also used in resistant cases, and those with severe renal failure
- Risk of hypocalcaemia (especially if vitamin D deficient)
- Works quite slowly (might take a week to reach full effect)
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- Dialysis if extremely resistant or anuric (especially if calcium > 4.5) or severe AKI
- Cinacalcet
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- Indicated in symptomatic primary and tertiary hyperparathyroidism if surgery inappropriate, or as bridge to surgery, or in parathyroid cancer
- More below
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- Parathyroidectomy – used for fractures, renal stones, keratopathy, pancreatitis (see PH section below)
- Consider bone protection long term
- Chemotherapy – can be useful in malignancy associated hypercalcaemia
- RANK-L inhibitors if refractory
Primary Hyperparathyroidism
- Rarely causes severe acute hypercalcaemia, but a common cause of chronic elevation in levels
- 45% of patients are symptomatic
- Correlates with an increased risk of CV disease, stroke, renal failure and stones, psychiatric disturbance, hypertension, fractures, cancer, diabetes, mortality
- Although might be more likely to be diagnosed in patients who are already sick with something else
- Usually due to
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- Solitary adenoma (85%)
- 2 gland adenomas
- Hyperplasia (10-15% – especially MEN1)
- Parathyroid cancer (<1%)
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- Familial in 1% – and may be associated with MEN1 or MEN 2A
- Complications
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- Osteopenia
- Rarely osteitis fibrosa cystica
- Renal stones (hypercalciuria is found in 60% of patients with renal stones)
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- MEN1
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- Parathyroid, pancreas, pituitary (need 2 glands involved to make diagnosis)
- Hyperparathyroidism is the most common finding (in 90%) and often recurrent
- Enteropancreatic tumours found in 70%
- 15-20% have pituitary tumours
- Patients should be under surveillance
- If suspected, check VIP, pancreatic polypeptide, gastrin, glucagon, somatostatin, chromogranin A and B, pituitary hormones
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- Investigations
-
- Usually either high PTH, or high calcium with unsuppressed PTH
- However… 15% have normal calcium and 15% have normal PTH
- Check vitamin D level
-
- Especially if calcium normal as elevated PTH is associated with vitamin D deficiency as well as primary hyperparathyroidism
- Concomitant Vitamin D deficiency can mask the diagnosis
-
- Check paired serum calcium and creatinine and urine calcium
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- Helps exclude FHH
- Calcium creatinine clearance ratio should be >0.02 in PH. FHH usually has a ratio of <0.01.
- If 0.01-0.02 might repeat test in 2 weeks
- Some have suggested that 24 hour collection is preferable to spot calcium testing – it’s more accurate, but also gives some information on the risk of stones
- 40% have increased urinary calcium
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- Do parathyroid USS and MIBI scan if patient is surgical candidate (not for diagnosis).
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- Imaging may not identify an adenoma if there’s an ectopic gland, less activity/less severe disease, germline genomic variants (multi-gland disease, needs MDT discussion)
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-
- Management
-
- Work up for complications (can be high yield)
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- DEXA (distal third of radius best)
- Renal US or CT (stones, nephrocalcinosis)
- Consider germline testing
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- If asymptomatic, usually surgery advised if
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- Calcium > 2.85 or >3 (depend on centre)
- Bone Mineral Density T score < 2.5 or fracture history
- eGFR <60
- 24 hour urinary calcium >10mmol
- Stones/nephrocalcinosis
- Patient aged <50
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- If asymptomatic, corrected calcium is < 3, no stones and bone mineral density is normal – do not need treatment (though you might treat a younger person)
- Surgery if fit
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- Remove a gland to remove the adenoma
- If calcium doesn’t normalise, remove all parathyroids
- Imaging can guide surgical options
- Can be done under local, but frail patients might not be suitable
- Expectation management – not all symptoms will necessarily melt away post-op, some, like low mood or energy may not have been related to the calcium. Stones can still form for a year or two post-op too
- Proven benefits include improved bone mineral density and quality of life, less risk of stones
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- Medical treatment if not fit for surgery, or surgery declined
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- Cinacalcet, 30-90mg BD
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- 73% respond well and normalise calcium within 2 weeks
- Can also be used short term pre-surgery to see if/which symptoms disappear with normalisation of calcium – this is off label use
- Also used in parathyroid cancer and secondary hyperparathyroidism.
- Commonly causes nausea
-
- Consider bisphosphonate to reduce fracture risk (but not to treat chronic hypercalcaemia)
- Consider HRT
- Advise calcium intake as per the general population (do not restrict) and replace vitamin D (do not let them run low in the hope of controlling calcium)
- Cinacalcet, 30-90mg BD
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- Work up for complications (can be high yield)
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Familial hypocalciuric hypercalcaemia (FHH)
- Benign condition
- Inherited AD (ask if family members have had high calcium or had unsuccessful parathyroid surgery)
- Prevalence 1:78,000
- Investigations
-
- Mild hypercalcaemia
- Normal PTH in 75% (slightly up in 25%)
- Slightly elevated magnesium (unlike hyperparathyroidism where magnesium is generally low)
- Calcium: creatinine clearance ratio <0.02, and often <0.01 (if so, follow up with a 24 hours urine collection)
- Consider genetic testing of patient and relatives
- Typically normal bone mineral density (unlike hyperparathyroidism)
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- Parathyroid can show mild hyperplasia and parathyroid surgery not curative
- If unwell/dehydrated patients can occasionally develop pancreatitis and chondrocalcinosis
Hypercalcaemia of malignancy
- Causes include
- Tumour secretion of parathyroid hormone-related peptide and vitamin D
- Cytokine release in osteolytic metastases
- Most commonly associated with malignancy of the breast, lung, kidneys, myeloma, lymphoma and head & neck cancers
- Standard measures
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- Stop thiazide diuretics, NSAIDs, vitamin D /calcium supplements
- IV fluids – aim for urine output > 2L/day
- Check for low magnesium
-
- Use bisphosphonates earlier in cancer than you might otherwise. Fluids unlikely to be sufficient in cancer.
-
- Usually give bisphosphonates after patient rehydrated. Might start at 24 hours
- Zoledronic acid 4mg if calcium > 3 and creatinine clearance >60 (reduce dose in renal impairment)
- If creatinine clearance <29 consider pamidronate instead, 90mg.
- They take a while to work – might take 4 days for the full effect. Do not repeat for at least 5 days (some say 7)
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- Other options
-
- Steroids – used sometimes in myeloma and lymphoma. Take 1-2 weeks to work.
- Calcitonin – acts fast but short lived. Give 100 IU TDS subcutaneously or IM. Increase to 400 IU max QDS
- Denosumab – monoclonal used for bone metastases. Standard dose is 120mg subcutaneously. Can repeat between days 8 and 15 (but only if calcium reduced after first dose)
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Less common causes
- Milk Alkali syndrome
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- Caused by calcium ingestion eg excessive antacids
- Triad of hypercalacaemia, AKI and metabolic alkalosis
- PTH suppressed and normal phosphate
- CKD is a risk factor
- Ask about ETOH use (this may be why excessive antacids used)
- Treat with IV fluids and stop calcium treatments
- Exclude other causes of hypercalcaemia
- Avoid giving bisphosphonates
-
- Vitamin D toxicity / hypervitaminosis D
-
- Can occur at intakes of >10,000 IU/day but patients may have taken much more
- Send vitamin D level
- Treat as usual with IV fluids and consider bisphosphonates and steroids
- Vitamin D is fat soluble so hypercalcaemia can take a long time to correct (weeks) and the patient will need regular monitoring after discharge
- Look for complications given likely chronic hypercalcaemia
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- CYP24A1 mutations
-
- High serum calcium, high calcium in the urine, renal stones
- Can check ratio of 25-OH-D3 to 24,25 (OH)2D3 – this distinguishes the mutation from hypervitaminosis D (ratio usually greater than 80)
- Treat with vitamin D restriction and sun protection
- Can also use ketoconazole, fluconazole and cinacalcet
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