Serum Calcium

Normal Values

ParameterNormal Range
Serum calcium (total)8.6–10.2 mg/dL
Ionized calcium4.6–5.3 mg/dL (1.15–1.33 mmol/L)

Note: The majority of body calcium is stored in bones. Only ~1% circulates in the bloodstream. About half of serum calcium is bound to albumin; the other half is ionized (physiologically active). In hypoalbuminemia, total calcium appears falsely low — ionized calcium is the more reliable measure.

Pathophysiology

Calcium is regulated by parathyroid hormone (PTH) and vitamin D:

  • PTH (released when Ca²⁺ is low) → reabsorbs Ca²⁺ from kidneys and intestines; releases Ca²⁺ from bones
  • Vitamin D → enhances intestinal calcium absorption
  • Phosphorus is inversely related to calcium: hyperphosphatemia (e.g., renal failure) → hypocalcemia

Calcium is critical for:

  • Neuromuscular excitability — low Ca²⁺ increases nerve/muscle excitability → tetany
  • Cardiac conduction — Ca²⁺ affects QT interval
  • Bone and teeth structure
  • Clotting cascade (Factor IV)
  • Persistent low calcium states weaken bone strength and can increase fracture risk when paired with vitamin D deficiency or poor intake.

Hypocalcemia (Ca < 8.6 mg/dL)

Causes

  • Hypoparathyroidism (post-thyroid/parathyroid surgery)
  • Vitamin D deficiency
  • Chronic kidney disease / renal failure (hyperphosphatemia)
  • Hypomagnesemia (impairs PTH secretion)
  • Massive blood transfusions (citrate binds calcium)
  • Pancreatitis (calcium deposits in pancreatic fat necrosis)

Clinical Manifestations

  • Chvostek’s sign — facial muscle twitching when tapping facial nerve (CN VII) just anterior to the ear
  • Trousseau’s sign — carpal spasm when a blood pressure cuff inflated above systolic pressure is held for 3 minutes
  • Muscle cramps and tetany
  • Paresthesia (tingling around lips, fingers, toes)
  • Seizures (severe cases)
  • Prolonged QT interval on ECG → risk for torsades de pointes

Treatment / Nursing Interventions

  • IV calcium gluconate (for symptomatic or severe hypocalcemia) — infuse slowly; extravasation causes tissue necrosis
  • Oral calcium supplements + vitamin D for mild/chronic cases
  • Seizure precautions; fall precautions
  • Cardiac monitoring (QT interval)
  • Treat underlying cause (hypomagnesemia, vitamin D deficiency)

Hypercalcemia (Ca > 10.2 mg/dL)

Causes

  • Hyperparathyroidism (primary — excess PTH)
  • Malignancy (most common hospital cause) — bone metastases or PTHrP secretion
  • Prolonged immobilization (bone calcium mobilization)
  • Excess vitamin D or calcium supplementation
  • Thiazide diuretics (decrease renal calcium excretion)

Clinical Manifestations

Mnemonic: “Bones, Groans, Moans, and Stones”

  • Bones — bone pain, pathologic fractures (malignancy)
  • Groans — GI symptoms: nausea, vomiting, constipation, anorexia
  • Moans — neurological: depression, confusion, lethargy, weakness
  • Stones — renal: kidney stones (nephrolithiasis), polyuria, polydipsia

Shortened QT interval on ECG.

Treatment / Nursing Interventions

  • IV saline hydration (promotes renal calcium excretion) — primary acute treatment
  • Loop diuretics (furosemide) after adequate hydration — increase calciuresis
  • Bisphosphonates (pamidronate, zoledronic acid) — for malignancy-associated hypercalcemia
  • Calcitonin — rapid-acting but short-term effect
  • Encourage weight-bearing activity and ambulation
  • Encourage fluid intake
  • Dietary calcium restriction
  • Treat underlying cause (e.g., surgical parathyroidectomy for primary hyperparathyroidism)

Self-Check

  1. What are Chvostek’s and Trousseau’s signs, and what electrolyte imbalance do they indicate?
  2. What is the most common cause of hypercalcemia in hospitalized patients?
  3. Why does hyperphosphatemia from renal failure cause hypocalcemia?