Hypercalcaemia Nursing Guide

Definition & Severity

Hypercalcaemia = corrected serum calcium > 2.6 mmol/L. Normal: 2.1–2.6 mmol/L. Always check corrected calcium (adjusts for albumin):

Corrected Ca²⁺ = Measured Ca²⁺ + 0.02 × (40 − serum albumin g/L)
Example: Measured Ca 2.4, Albumin 25 g/L: Corrected = 2.4 + 0.02 × (40−25) = 2.4 + 0.3 = 2.7 mmol/L (hypercalcaemia)

Severity	Corrected Ca²⁺	Clinical Significance
Mild	2.6–3.0 mmol/L	Often asymptomatic; may have fatigue, thirst
Moderate	3.0–3.5 mmol/L	Symptomatic; nausea, confusion, constipation
Severe	> 3.5 mmol/L	Crisis — severe confusion, coma, arrhythmias, renal failure

Clinical Features — "Bones, Stones, Moans, Groans, Psychic Overtones"

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BONES

Bone pain, fractures, osteitis fibrosa cystica (hyperPTH), "salt and pepper" skull XR

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STONES

Renal stones (calcium oxalate/phosphate), nephrocalcinosis, polyuria, polydipsia

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MOANS

Muscle weakness, hyporeflexia, fatigue, nausea, vomiting, anorexia

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GROANS & OVERTONES

Constipation (GI), abdominal pain, pancreatitis, peptic ulcers; Confusion, depression, psychosis

ECG Changes

Shortened QT interval (Ca²⁺ shortens cardiac action potential)
Wide T waves, ST elevation-like changes (malignant hypercalcaemia)
Bradycardia, AV block in severe cases

Causes of Hypercalcaemia

80% of hypercalcaemia = primary hyperparathyroidism OR malignancy.
Outpatients: Primary hyperPTH more common. Inpatients: Malignancy more common.

Cause	PTH	PTHrP	Notes
Primary hyperparathyroidism	↑ HIGH	Normal	Usually solitary adenoma; chronic mild hypercalcaemia; most common outpatient cause
Malignancy	↓ suppressed	↑ (solid tumours) or normal (haematological)	Most common inpatient cause; breast, lung, renal, myeloma, lymphoma
Sarcoidosis / granulomatous	↓	Normal	Macrophages produce 1,25-OH vitamin D; sarcoidosis, TB, histoplasmosis
Vitamin D excess	↓	Normal	Iatrogenic over-supplementation (common in GCC vitamin D replacement)
Tertiary hyperparathyroidism	↑↑	Normal	Post-renal transplant or chronic renal failure; autonomous PTH secretion
Immobilisation	↓	Normal	Bone resorption without formation; seen in prolonged bed rest
Milk-alkali syndrome	↓	Normal	Excessive calcium carbonate antacid use; increasingly rare
Thiazide diuretics	↑ slightly	Normal	Reduces renal calcium excretion

Management of Hypercalcaemia

Step 1 — IV Fluid Rehydration (FIRST and MOST IMPORTANT)

IV 0.9% NaCl 2–3 litres over 3–4 hours (then 200–300 mL/hr to target UO 100–150 mL/hr)
Rationale: volume expansion → increased GFR → increased renal calcium excretion
Furosemide is NOT routinely added (no evidence; risks dehydration and hypovolaemia)
Monitor fluid balance, daily U&E, fluid overload risk in elderly/cardiac patients

Step 2 — Bisphosphonates (Definitive Calcium Lowering)

Zoledronic acid 4mg IV over 15–30 minutes — inhibits osteoclast-mediated bone resorption. Most potent bisphosphonate. Onset: 1–3 days; peak effect 4–7 days.
Pamidronate 60–90mg IV over 2–4 hours — slower, older alternative.
Check eGFR before: reduce/avoid if eGFR <30 mL/min. Monitor Ca²⁺ daily. Risk of osteonecrosis of the jaw with long-term use.

Other Agents

Drug	Use	Mechanism
Calcitonin 4–8 units/kg SC/IM 12-hourly	Rapid effect (within hours); short-term only (tachyphylaxis develops)	Inhibits bone resorption + increases renal Ca²⁺ excretion
Denosumab 120mg SC	Malignancy-associated; when bisphosphonates contraindicated (renal failure)	RANKL inhibitor — blocks osteoclast activation
Corticosteroids (prednisolone 40mg OD)	Sarcoidosis, vitamin D toxicity, lymphoma	Reduces intestinal calcium absorption and granuloma production of vitamin D
Haemodialysis	Severe hypercalcaemia with renal failure	Removes calcium rapidly

Treat Underlying Cause

Primary hyperPTH → parathyroidectomy
Malignancy → chemotherapy, radiotherapy to bony metastases
Vitamin D excess → stop supplementation

GCC-Specific Hypercalcaemia Context

Vitamin D supplementation over-correction: GCC governments and healthcare providers widely promote vitamin D supplementation given high rates of deficiency (paradoxically despite abundant sunshine — indoor lifestyle, sun avoidance, covered clothing). Over-zealous supplementation without monitoring can cause vitamin D toxicity and hypercalcaemia. Regular serum 25-OH vitamin D and calcium monitoring during supplementation is recommended.
Sarcoidosis in GCC: Sarcoidosis is less common but reported across GCC countries. Granulomatous disease from TB (highly prevalent in expat populations) can also cause hypercalcaemia through activated macrophage 1,25-vitamin D production. Consider TB as cause of granulomatous hypercalcaemia in GCC.
Multiple myeloma: Myeloma is among the most common causes of inpatient malignant hypercalcaemia. In GCC, myeloma can present with hypercalcaemia, bone pain, and renal failure — the classic "CRAB" criteria.
Dehydration amplification: GCC summer heat increases fluid losses, worsening hypercalcaemia (volume depletion reduces renal calcium clearance). Aggressive IV fluid hydration in GCC summer hypercalcaemia patients is particularly important.

MCQ Practice — Hypercalcaemia

Q1. What is the FIRST line treatment for severe symptomatic hypercalcaemia (corrected Ca²⁺ 3.8 mmol/L)?

A) IV zoledronic acid 4mg immediately

B) Aggressive IV 0.9% NaCl rehydration

C) IV furosemide 80mg to force calcium excretion

D) IM calcitonin 8 units/kg

✅ B — IV fluid rehydration is the first and most important step. Volume expansion increases GFR and calcium excretion. Bisphosphonates take 1–3 days to work (given after rehydration). IV furosemide is NOT routinely recommended — risks worsening dehydration without proven benefit.

Q2. A 65-year-old patient with known metastatic breast cancer has corrected calcium of 3.4 mmol/L and is confused. After initial IV fluids, which is the next most appropriate treatment?

A) Oral calcium restriction only

B) IV zoledronic acid 4mg (after confirming adequate renal function)

C) IV calcitonin as definitive long-term treatment

D) Prednisolone 40mg — effective for malignancy-related hypercalcaemia

✅ B — IV bisphosphonate (zoledronic acid) is the definitive treatment for malignancy-associated hypercalcaemia after initial rehydration. Calcitonin has rapid onset but tachyphylaxis limits it to short-term bridging only. Corticosteroids work for sarcoidosis/lymphoma, not solid tumour hypercalcaemia.

Q3. An outpatient has mild hypercalcaemia (corrected Ca 2.9 mmol/L), elevated PTH, and normal PTHrP. No kidney stones or bone disease. What is the most likely diagnosis?

A) Malignancy — refer urgently for CT staging

B) Primary hyperparathyroidism — refer for parathyroid assessment

C) Vitamin D toxicity — check supplementation history

D) Sarcoidosis — check ACE level and CXR

✅ B — High PTH + high calcium = primary hyperparathyroidism (usually solitary adenoma). Malignancy suppresses PTH. Primary hyperPTH is the most common cause of outpatient hypercalcaemia. Treatment is parathyroidectomy (recommended if symptomatic, young <50, or Ca >2.85).

Q4. ECG changes characteristic of hypercalcaemia include:

A) Prolonged QT interval

B) Peaked T waves

C) Shortened QT interval

D) Widened QRS with delta waves

✅ C — Hypercalcaemia shortens the QT interval (calcium shortens cardiac action potential plateau). Contrast: hypocalcaemia PROLONGS QT; hypokalaemia shows prominent U waves; hyperkalaemia shows peaked T waves → broad QRS → sine wave.

Hypercalcaemia — Nursing Guide