Medicine – Hypercalcaemia

Hypercalcaemia means an abnormally increased concentration of calcium in the blood. The two most important causes are:

Primary hyperparathyroidism

and

Malignancy.

Together, these account for the great majority of clinically important cases. Primary hyperparathyroidism is particularly important in ambulatory patients, whereas malignancy is a major cause of more severe hypercalcaemia in hospitalised patients.

Hypercalcaemia can affect the kidneys, gastrointestinal tract, nervous system, muscles, bones and cardiovascular system. Severe or rapidly developing hypercalcaemia can become a medical emergency.

1. Definition of Hypercalcaemia

Hypercalcaemia is diagnosed when serum calcium exceeds the laboratory reference range.

Interpretation should take into account:

Albumin concentration

because a substantial proportion of circulating calcium is bound to albumin.

When the result is uncertain or the patient is critically ill, measurement of:

Ionised calcium

can provide a more direct assessment of biologically active calcium.

2. Regulation of Serum Calcium

Calcium balance is controlled primarily by:

Parathyroid hormone – PTH.

Vitamin D.

Kidneys.

Bone.

Gastrointestinal tract.

When serum calcium falls, PTH normally increases.

When calcium rises, PTH should become:

Suppressed.

This physiological relationship is extremely useful when investigating hypercalcaemia.

3. First Step in Finding the Cause

After confirming genuine hypercalcaemia, one of the most useful initial investigations is:

PTH.

Hypercalcaemia can then be broadly divided into:

PTH-dependent hypercalcaemia

and

PTH-independent hypercalcaemia.

4. PTH-Dependent Hypercalcaemia

If calcium is high but PTH is:

Elevated

or

Inappropriately normal,

PTH is contributing to the hypercalcaemia.

Important causes include:

Primary hyperparathyroidism.

Tertiary hyperparathyroidism.

Lithium-associated hyperparathyroidism/hypercalcaemia.

Familial hypocalciuric hypercalcaemia – FHH, an important differential diagnosis.

5. PTH-Independent Hypercalcaemia

If calcium is high and PTH is appropriately:

Suppressed,

consider non-parathyroid causes.

Important examples include:

Malignancy.

Vitamin D excess.

Sarcoidosis and other granulomatous disease.

Hyperthyroidism.

Milk-alkali/calcium-alkali syndrome.

Some medication-related causes also occur.

6. Primary Hyperparathyroidism

The original notes correctly identify:

Primary hyperparathyroidism

as one of the most common causes of hypercalcaemia.

The most common underlying lesion is:

A solitary parathyroid adenoma.

A single adenoma accounts for approximately:

80–85% of sporadic primary hyperparathyroidism.

7. Mechanism of Primary Hyperparathyroidism

Excessive PTH causes:

↑ Renal calcium reabsorption.

↑ Calcitriol production.

↑ Intestinal calcium absorption indirectly.

↑ Bone turnover.

At the same time:

↑ Renal phosphate excretion.

Therefore the characteristic biochemical pattern is:

Ca²⁺ ↑

PTH ↑ or inappropriately normal

Phosphate ↓ or low-normal

ALP normal or ↑.

8. Primary Hyperparathyroidism and Urinary Calcium

Urinary calcium is often:

Increased

because hypercalcaemia increases the filtered calcium load.

However, urinary calcium is variable and is not required to be elevated in every patient.

Urinary calcium is particularly useful for distinguishing primary hyperparathyroidism from:

Familial hypocalciuric hypercalcaemia – FHH.

9. Malignancy

The original notes correctly identify:

Malignancy

as another major cause of hypercalcaemia.

Hypercalcaemia of malignancy is often:

More rapid in onset and more severe

than the hypercalcaemia associated with uncomplicated primary hyperparathyroidism.

Several different mechanisms are possible.

10. PTH-Related Peptide

An important mechanism is tumour production of:

PTH-related peptide – PTHrP.

PTHrP acts on PTH receptors and produces effects resembling PTH, particularly:

Increased bone resorption

and

Increased renal calcium reabsorption.

This produces:

Humoral hypercalcaemia of malignancy.

11. PTHrP and PTH

Although PTHrP behaves similarly to PTH at the receptor:

The patient’s own PTH is suppressed.

Therefore:

Hypercalcaemia + low PTH + elevated PTHrP

supports:

Humoral hypercalcaemia of malignancy.

This distinction is important because most cancers do not produce actual PTH.

12. Squamous Cell Carcinoma

PTHrP production is classically associated with:

Squamous cell carcinomas.

Examples include squamous malignancies arising in sites such as:

Lung.

Head and neck.

Oesophagus.

Other malignancies can also produce PTHrP.

For examination purposes:

SQUAMOUS CELL CARCINOMA + HYPERCALCAEMIA → THINK PTHrP.

13. Osteolytic Bone Disease

The second major malignant mechanism is:

Local destruction of bone.

Tumour involvement of bone stimulates osteoclast-mediated:

Bone resorption.

Calcium is then released from bone into the circulation.

Therefore:

OSTEOLYTIC BONE DISEASE → BONE RESORPTION → Ca²⁺ RELEASE → HYPERCALCAEMIA.

14. Breast Cancer

The original notes correctly include:

Breast carcinoma.

Breast cancer can cause hypercalcaemia through:

Skeletal metastases with increased bone resorption

and, in some cases, humoral mechanisms.

Therefore a patient with advanced breast cancer and hypercalcaemia should be evaluated for:

Malignancy-associated hypercalcaemia.

15. Multiple Myeloma – Important Additional Cause

An important malignant cause not listed in the original notes is:

Multiple myeloma.

Myeloma stimulates osteoclast activity and produces:

Lytic bone lesions.

This can cause:

Bone pain.

Pathological fractures.

Hypercalcaemia.

The classic association is often remembered as part of:

CRAB:

C – HyperCalcaemia

R – Renal impairment

A – Anaemia

B – Bone lesions.

16. Renal Cell Carcinoma

The original notes include:

Kidney carcinoma.

More specifically:

Renal cell carcinoma – RCC

can cause hypercalcaemia as a:

Paraneoplastic manifestation.

PTHrP is one possible mechanism.

Therefore hypercalcaemia can occasionally occur even without extensive skeletal metastases.

17. Thyroid Carcinoma

The original notes include:

Thyroid carcinoma.

Hypercalcaemia can occur in advanced malignancy with skeletal involvement, but thyroid carcinoma is not among the most characteristic common causes of malignant hypercalcaemia compared with squamous cell carcinoma, breast cancer, renal cell carcinoma and multiple myeloma.

Therefore it should be considered a possible association rather than a classic leading cause.

18. Other Malignant Mechanisms

Some lymphomas can cause hypercalcaemia through increased production of:

1,25-dihydroxyvitamin D – calcitriol.

Therefore malignancy-associated hypercalcaemia is not explained solely by:

PTHrP or bone metastases.

The major mechanisms are:

PTHrP production.

Osteolytic bone resorption.

Excess calcitriol production in selected lymphomas.

Rarely, ectopic true PTH production.

19. Calcium Intake and Calcium-Alkali Syndrome

The original notes refer to:

Calcium intake and milk-alkali syndrome.

The modern term commonly used is:

Calcium-alkali syndrome.

It occurs after excessive intake of:

Calcium

together with absorbable:

Alkali, often calcium carbonate preparations.

20. Calcium-Alkali Syndrome

The characteristic combination is:

Hypercalcaemia.

Metabolic alkalosis.

Acute kidney injury or renal impairment.

Therefore:

HIGH Ca²⁺ + METABOLIC ALKALOSIS + AKI

should raise consideration of:

Calcium-alkali syndrome.

Ordinary dietary calcium intake alone rarely produces major hypercalcaemia when normal regulatory mechanisms and renal function are intact.

21. Vitamin D Excess

The original notes correctly include:

Excess vitamin D.

Vitamin D increases gastrointestinal absorption of:

Calcium

and

Phosphate.

Therefore excessive vitamin D activity can produce:

Hypercalcaemia

and often:

Hyperphosphataemia.

22. Vitamin D Toxicity

In vitamin D toxicity:

Calcium ↑

Phosphate may ↑

PTH ↓

because the hypercalcaemia suppresses normal parathyroid secretion.

Excessive vitamin D supplementation is one possible cause.

23. Tertiary Hyperparathyroidism

The original notes correctly include:

Tertiary hyperparathyroidism.

This usually develops after prolonged:

Secondary hyperparathyroidism, particularly in advanced CKD.

Persistent stimulation causes progressive parathyroid:

Hyperplasia.

Eventually the glands may become:

Autonomous.

24. Tertiary Hyperparathyroidism Pattern

Once autonomy develops:

PTH remains excessively elevated

despite:

Hypercalcaemia.

Therefore:

PTH ↑↑

Ca²⁺ ↑

and, in advanced CKD:

Phosphate is often ↑.

This distinguishes tertiary disease from ordinary CKD-related secondary hyperparathyroidism, in which calcium is usually:

Low or normal.

25. Hyperthyroidism

The original notes correctly include:

Hyperthyroidism.

Excess thyroid hormone increases:

Bone turnover.

When bone resorption becomes sufficiently increased:

Calcium is released from bone.

Therefore some patients with thyrotoxicosis develop:

Mild hypercalcaemia.

PTH should normally be:

Suppressed.

26. Sarcoidosis

The original notes correctly identify:

Sarcoidosis.

Sarcoid granulomas contain activated:

Macrophages.

These macrophages can express:

1α-hydroxylase.

This enzyme converts vitamin D to:

1,25-dihydroxyvitamin D – calcitriol.

27. Mechanism of Hypercalcaemia in Sarcoidosis

Increased extrarenal calcitriol production causes:

↑ Intestinal calcium absorption

↓

Hypercalcaemia

and sometimes:

Hypercalciuria.

Therefore:

SARCOIDOSIS → MACROPHAGE 1α-HYDROXYLASE → ↑ CALCITRIOL → ↑ Ca²⁺ ABSORPTION.

28. Other Granulomatous Diseases

This mechanism is not exclusive to sarcoidosis.

Other granulomatous disorders can occasionally increase extrarenal calcitriol production, including:

Tuberculosis

and some:

Fungal infections.

Therefore granulomatous disease should be considered when hypercalcaemia occurs with:

Suppressed PTH and elevated/inappropriately high calcitriol.

29. Thiazide Diuretics

The original notes correctly include:

Thiazide diuretics.

Thiazides increase calcium reabsorption in the:

Distal nephron.

Therefore:

↓ Urinary calcium excretion

and occasionally:

↑ Serum calcium.

30. Thiazides and Primary Hyperparathyroidism

Thiazide-associated hypercalcaemia is often relatively:

Mild.

Importantly, thiazides can sometimes uncover previously unrecognised:

Primary hyperparathyroidism.

Therefore persistent hypercalcaemia should not automatically be attributed entirely to the medication.

31. Lithium

The original notes correctly include:

Lithium.

Lithium can alter the relationship between serum calcium and the:

Calcium-sensing receptor – CaSR.

The parathyroid glands may require a higher calcium concentration before PTH secretion is suppressed.

Therefore lithium can cause:

Hyperparathyroidism

and:

Hypercalcaemia.

32. Immobilisation – Important Additional Cause

Prolonged immobilisation can increase:

Bone resorption.

This can cause hypercalcaemia, particularly in patients with:

High baseline bone turnover, such as some young people or patients with certain skeletal disorders.

Therefore:

Prolonged immobilisation → increased bone resorption → hypercalcaemia.

33. Clinical Features of Hypercalcaemia

The manifestations of hypercalcaemia depend on:

Severity.

Rate of rise.

Duration.

Underlying disease.

Mild chronic hypercalcaemia may be:

Asymptomatic.

Rapid or severe hypercalcaemia produces more pronounced symptoms.

34. Traditional Clinical Mnemonic

The classic manifestations can be remembered as:

“Stones, bones, abdominal groans and psychiatric overtones.”

A more complete version sometimes adds:

“Thrones”

to represent:

Polyuria.

This mnemonic captures renal, skeletal, gastrointestinal and neurological manifestations.

35. Lethargy and Malaise

The original notes correctly include:

Lethargy and malaise.

Patients may develop:

Fatigue.

Reduced concentration.

General weakness.

Low mood.

These manifestations become more prominent as calcium rises.

36. Neurological and Psychiatric Features

The original notes include:

Depression.

Confusion.

Psychosis.

Hypercalcaemia can cause a spectrum of neuropsychiatric abnormalities ranging from:

Fatigue and cognitive slowing

to:

Confusion, delirium and reduced consciousness in severe disease.

Severe hypercalcaemia can eventually cause:

Coma.

37. Muscle Weakness

The original notes correctly include:

Weakness.

Hypercalcaemia decreases neuromuscular excitability and may produce:

Generalised muscle weakness.

This contrasts with hypocalcaemia, which characteristically causes:

Increased neuromuscular excitability and tetany.

38. Polyuria and Polydipsia

The original notes correctly identify:

Polyuria and polydipsia.

Hypercalcaemia impairs the kidney’s ability to concentrate urine.

It can produce a form of:

Nephrogenic diabetes insipidus physiology.

Therefore:

Hypercalcaemia

↓

↓ Renal concentrating ability

↓

Polyuria

↓

Water loss

↓

Thirst and polydipsia.

39. Hypercalcaemia and Dehydration

Polyuria can lead to:

Volume depletion.

Dehydration then reduces renal calcium clearance and may worsen:

Hypercalcaemia.

This can create a vicious cycle:

Hypercalcaemia → polyuria → dehydration → ↓ renal calcium clearance → worse hypercalcaemia.

This is why fluid replacement is so important in severe symptomatic disease.

40. Constipation

The original notes correctly include:

Constipation.

Hypercalcaemia reduces gastrointestinal smooth-muscle activity.

Patients may develop:

Constipation.

Nausea.

Anorexia.

Abdominal discomfort.

Severe disease can occasionally produce:

Ileus.

41. Peptic Ulcer Disease

Older teaching commonly lists:

Peptic ulceration

as a feature of hypercalcaemia or hyperparathyroidism.

The association is much less diagnostically useful than the classic renal, neurological and gastrointestinal manifestations.

A particularly important association with peptic ulcer disease occurs when hyperparathyroidism is part of:

MEN1, because MEN1 can also include gastrin-producing neuroendocrine tumours causing Zollinger–Ellison syndrome.

Therefore peptic ulceration should not be regarded as a universal direct consequence of hypercalcaemia.

42. Renal Stones

The original notes correctly identify:

Renal stones.

Persistent hypercalcaemia and hypercalciuria can promote formation of:

Calcium-containing renal calculi.

This is particularly important in:

Primary hyperparathyroidism.

Patients may present with:

Renal colic

or:

Haematuria.

43. Nephrocalcinosis

The original notes correctly include:

Nephrocalcinosis.

This means deposition of calcium salts within:

Renal tissue.

Persistent abnormalities of calcium metabolism can contribute to:

Renal impairment.

Therefore chronic hypercalcaemia can damage the kidneys through both:

Stone formation

and

Nephrocalcinosis.

44. Pancreatitis

The original notes include:

Pancreatitis.

Hypercalcaemia, particularly in hyperparathyroidism, is a recognised but relatively uncommon association with:

Acute pancreatitis.

This creates an interesting bidirectional relationship:

Hypercalcaemia can be associated with pancreatitis,

while:

Severe acute pancreatitis can itself cause hypocalcaemia.

45. Cardiac Effects

Hypercalcaemia affects cardiac electrophysiology.

The classic ECG change is:

Shortening of the QT interval.

This is the opposite of hypocalcaemia, which classically produces:

QT prolongation.

Severe hypercalcaemia can also contribute to:

Arrhythmias.

46. Severe Hypercalcaemia

Marked hypercalcaemia may produce:

Profound dehydration.

Acute kidney injury.

Severe weakness.

Confusion or delirium.

Cardiac rhythm abnormalities.

Reduced consciousness or coma.

Severe symptomatic hypercalcaemia therefore requires:

Urgent treatment.

47. Investigation

Once hypercalcaemia is confirmed, the most useful initial etiological test is usually:

PTH.

The basic diagnostic division is:

HIGH Ca + non-suppressed PTH → PTH-dependent cause.

HIGH Ca + suppressed PTH → PTH-independent cause.

48. High Calcium With High or Inappropriately Normal PTH

Think primarily about:

Primary hyperparathyroidism.

Also consider:

Tertiary hyperparathyroidism.

Lithium-associated disease.

Familial hypocalciuric hypercalcaemia.

The clinical context, renal function, phosphate and urinary calcium help distinguish them.

49. High Calcium With Suppressed PTH

Think about:

Malignancy.

Vitamin D toxicity.

Sarcoidosis/granulomatous disease.

Hyperthyroidism.

Calcium-alkali syndrome.

Immobilisation.

Additional tests are selected according to the suspected cause.

50. Malignancy Investigation

When malignancy-associated hypercalcaemia is suspected, investigations may include:

PTHrP when clinically appropriate.

Serum and urine monoclonal protein studies/free light chains when myeloma is suspected.

Imaging according to symptoms and clinical context.

Vitamin D metabolites in selected cases such as suspected lymphoma-associated calcitriol excess.

51. Treatment Principles

Treatment depends on:

Severity of hypercalcaemia.

Symptoms.

Rate of rise.

Renal and cardiac function.

Underlying cause.

Mild stable hypercalcaemia may require primarily treatment of the cause, whereas severe symptomatic disease requires urgent calcium-lowering therapy.

52. Intravenous Fluids

The original notes correctly identify:

Rehydration

as a central treatment.

For significant symptomatic hypercalcaemia with volume depletion, treatment commonly begins with:

Intravenous isotonic saline, adjusted to the patient’s cardiovascular and renal status.

Restoring intravascular volume improves:

Renal perfusion

and:

Urinary calcium excretion.

53. “Aggressive” Rehydration – Important Qualification

The older phrase:

“Aggressive rehydration”

should be interpreted cautiously.

Fluid replacement should be:

Adequate but individualised.

Excessive fluids can be dangerous in patients with:

Heart failure

or:

Significant renal impairment.

Therefore hydration is guided by the patient’s:

Volume status, urine output and cardiorenal function.

54. Intravenous Bisphosphonates

The original notes correctly include:

Bisphosphonates.

These inhibit:

Osteoclast-mediated bone resorption.

They are particularly important in:

Hypercalcaemia of malignancy.

Examples include:

Zoledronic acid

and:

Pamidronate.

55. Pamidronate

The original note specifically lists:

Intravenous pamidronate.

This remains an effective treatment.

However, modern practice also commonly uses:

Intravenous zoledronic acid, depending on the clinical situation and renal function.

Bisphosphonates do not act instantly; their calcium-lowering effect develops over:

Days rather than minutes.

56. Calcitonin

An important acute treatment not included in the original notes is:

Calcitonin.

Calcitonin can reduce serum calcium relatively:

Rapidly.

Its effect begins faster than that of bisphosphonates.

However, the effect is relatively modest and:

Tachyphylaxis develops, limiting prolonged use.

Therefore it can be useful as a short-term measure in:

Severe symptomatic hypercalcaemia.

57. Denosumab

Denosumab inhibits:

RANKL

and therefore reduces osteoclast formation and activity.

It has an important role in selected cases of:

Hypercalcaemia of malignancy, particularly when hypercalcaemia is refractory to bisphosphonate therapy or when bisphosphonates are unsuitable.

Treatment choice depends on the clinical context and kidney function.

58. Furosemide – Important Correction

The original notes list:

Furosemide.

Historically, loop diuretics were routinely used after saline administration because they increase urinary calcium excretion.

However:

Routine furosemide is no longer recommended solely to treat hypercalcaemia.

It can worsen:

Volume depletion

and electrolyte abnormalities.

59. When Furosemide May Be Used

A loop diuretic may still be useful when there is a specific indication, particularly:

Fluid overload after adequate rehydration.

Therefore the modern principle is:

REHYDRATE FIRST.

Then use a loop diuretic only when clinically required for:

Volume management, rather than routinely forcing calcium diuresis.

60. Corticosteroids

The original notes correctly include:

Steroids, but they are not useful for every cause of hypercalcaemia.

Glucocorticoids are particularly useful in hypercalcaemia driven by excessive:

Calcitriol activity.

Examples include:

Sarcoidosis.

Other granulomatous diseases.

Some lymphomas.

Selected vitamin D-mediated hypercalcaemia.

61. Why Steroids Work in Sarcoidosis

Glucocorticoids reduce abnormal macrophage-mediated production of:

Calcitriol.

Therefore:

↓ Calcitriol

↓

↓ Intestinal calcium absorption

↓

↓ Serum calcium.

Hence:

SARCOIDOSIS + HYPERCALCAEMIA → GLUCOCORTICOIDS CAN BE EFFECTIVE.

62. Treat the Underlying Cause

Definitive management depends on the cause.

For example:

Primary hyperparathyroidism → parathyroidectomy when indicated.

Malignancy → treat malignancy plus acute calcium control.

Vitamin D toxicity → stop excessive vitamin D and manage hypercalcaemia.

Calcium-alkali syndrome → stop calcium/alkali excess and restore volume appropriately.

Sarcoidosis → glucocorticoids in appropriate symptomatic hypercalcaemic disease.

Medication-associated hypercalcaemia → review/stop the responsible drug when appropriate.

63. Dialysis

In selected patients with severe hypercalcaemia, particularly when there is:

Severe kidney failure,

refractory hypercalcaemia,

or an inability to safely administer adequate intravenous fluids,

dialysis may be considered.

This is reserved for severe clinical circumstances rather than routine hypercalcaemia.

64. Causes of Hypercalcaemia – Note Form

PTH-DEPENDENT

Primary hyperparathyroidism – most commonly a solitary parathyroid adenoma.

Tertiary hyperparathyroidism.

Lithium-associated hyperparathyroidism.

Familial hypocalciuric hypercalcaemia.

MALIGNANCY

PTHrP production – particularly squamous cell carcinoma.

Osteolytic bone disease/metastases – including breast cancer.

Multiple myeloma.

Renal cell carcinoma – possible PTHrP/paraneoplastic mechanism.

Calcitriol production – selected lymphomas.

VITAMIN D/CALCITRIOL RELATED

Vitamin D toxicity.

Sarcoidosis.

Other granulomatous disease.

Selected lymphomas.

MEDICATIONS

Thiazide diuretics.

Lithium.

Excess calcium/vitamin D preparations.

OTHER

Calcium-alkali syndrome.

Hyperthyroidism.

Prolonged immobilisation.

65. Features of Hypercalcaemia – Note Form

GENERAL/NEUROMUSCULAR

Lethargy.

Malaise.

Fatigue.

Muscle weakness.

NEUROPSYCHIATRIC

Poor concentration.

Low mood.

Confusion.

Delirium.

Severe cases → reduced consciousness/coma.

RENAL

Polyuria.

Polydipsia.

Dehydration.

Renal stones.

Nephrocalcinosis.

Renal impairment.

GASTROINTESTINAL

Constipation.

Nausea.

Abdominal discomfort.

Anorexia.

Occasionally pancreatitis.

CARDIAC

Short QT interval.

Arrhythmias in severe disease.

66. Treatment – Note Form

1. REHYDRATION

IV isotonic saline when clinically indicated.

Correct volume depletion while avoiding fluid overload.

2. ANTIRESORPTIVE THERAPY

IV bisphosphonate such as:

Zoledronic acid

or:

Pamidronate, particularly in malignancy-associated hypercalcaemia.

Denosumab in selected cases.

3. RAPID TEMPORARY CALCIUM LOWERING

Calcitonin for selected severe symptomatic cases.

4. GLUCOCORTICOIDS

Particularly useful for:

Sarcoidosis.

Other granulomatous disease.

Selected lymphoma/vitamin D-mediated hypercalcaemia.

5. LOOP DIURETICS

Not routinely used solely to lower calcium.

Consider only for a specific indication such as:

Fluid overload after adequate rehydration.

6. DEFINITIVE TREATMENT

Treat the underlying:

Parathyroid disease, malignancy, medication effect, vitamin D excess or granulomatous disorder.

67. Important Corrections to the Original Notes

The original:

“Some tumours secrete a PTH-related protein”

is correct.

Remember:

PTHrP ↑ but endogenous PTH ↓.

The tumour usually does not produce ordinary PTH.

The original:

“Bone metastases lead to destruction of bone and calcium release”

is also correct for:

Osteolytic skeletal disease.

However, an important additional malignant cause is:

Multiple myeloma.

The original list includes:

Thyroid carcinoma.

This can be associated with hypercalcaemia in advanced disease, but it is less characteristic than:

Squamous cell carcinoma + breast cancer + renal cell carcinoma + multiple myeloma.

The original:

“Milk-alkali syndrome”

is now commonly called:

CALCIUM-ALKALI SYNDROME.

Remember the triad:

HYPERCALCAEMIA + METABOLIC ALKALOSIS + RENAL IMPAIRMENT.

The original:

“Furosemide”

requires an important modern correction:

Do not routinely use furosemide simply to lower calcium.

It may worsen dehydration. Use it mainly when there is a specific need to manage:

Fluid overload after adequate rehydration.

The original:

“Steroids”

also requires qualification.

Steroids are particularly useful for:

CALCITRIOL-MEDIATED HYPERCALCAEMIA, such as sarcoidosis and selected lymphomas, rather than all forms of hypercalcaemia.

Key Clinical Pattern

The most important first diagnostic distinction is:

HYPERCALCAEMIA → CHECK PTH.

Ca ↑ + PTH ↑/INAPPROPRIATELY NORMAL

Think:

PRIMARY HYPERPARATHYROIDISM

first, while considering tertiary disease, lithium and FHH according to context.

Ca ↑ + PTH ↓

Think:

MALIGNANCY + VITAMIN D EXCESS + SARCOIDOSIS + HYPERTHYROIDISM + CALCIUM-ALKALI SYNDROME.

For malignancy:

SQUAMOUS CELL CARCINOMA → PTHrP.

BREAST CANCER/MYELOMA → OSTEOLYTIC BONE RESORPTION.

SOME LYMPHOMAS → ↑ CALCITRIOL.

For symptoms remember:

“STONES, BONES, ABDOMINAL GROANS, THRONES AND PSYCHIATRIC OVERTONES.”

Stones → renal calculi.

Bones → skeletal disease.

Groans → constipation/abdominal symptoms.

Thrones → polyuria.

Psychiatric overtones → lethargy, confusion and neuropsychiatric disturbance.

And the classic ECG distinction is:

HYPERCALCAEMIA → SHORT QT.

HYPOCALCAEMIA → LONG QT.