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QW68 August 2026

Question: Select each option to validate with explanations

Clinical Case Scenario

A 58-year-old woman presented with persistent nausea, vomiting, constipation, progressive weight loss, dehydration, and altered sensorium worsening over the preceding 48 hours.

Β On examination, she was drowsy but arousable with features of severe dehydration. Her blood pressure was 100/60 mmHg, heart rate - 110 beats/min and she was afebrile.

Initial laboratory investigations revealed:

  • Corrected serum calcium: 8 mg/dL
  • Serum phosphate: 8 mg/dL
  • Serum creatinine: 2 mg/dL
  • Intact parathyroid hormone (PTH): 2400 pg/mL

ECG demonstrated a short QT interval.

Neck ultrasonography identified a parathyroid adenoma,

PET-CT confirmed a metabolically active parathyroid tumour with associated brown tumour, suggesting long-standing severe primary hyperparathyroidism with extensive skeletal involvement.

The patient was diagnosed with hypercalcaemic crisis secondary to primary hyperparathyroidism. Following aggressive intravenous hydration and optimisation of metabolic abnormalities, she underwent successful parathyroidectomy.

The immediate postoperative period was uneventful. However, on postoperative day 3, she developed perioral numbness, carpopedal spasm, and a positive Trousseau sign, suggestive of symptomatic hypocalcaemia.

Repeat investigations demonstrated:

  • Serum calcium: 6.2 mg/dL
  • Serum phosphate: 2.0 mg/dL
  • Serum magnesium: 1.4 mg/dL
  • Intact PTH: 45 pg/mL (within normal range)

Question: The presence of profound hypocalcaemia with normal postoperative PTH. What is the most likely explanation for the hypocalcemia?
😭

Wrong Answer: ❌ A. Accidental removal of all parathyroid tissue causing permanent hypoparathyroidism

😭

Wrong Answer: ❌ B. Transient postoperative suppression of remaining parathyroid glands

πŸ˜‰

Right Answer: βœ… C. Rapid skeletal uptake of calcium, phosphate, and magnesium following correction of chronic hyperparathyroidism

Hungry Bone Syndrome (HBS) : Hungry bone syndrome is a profound, prolonged hypocalcaemia that occurs after surgical treatment of hyperparathyroidism, most commonly following parathyroidectomy for severe primary or secondary hyperparathyroidism.

Pathophysiology

In chronic hyperparathyroidism, high PTH levels cause:
  • Increased bone resorption
  • High bone turnover
  • Loss of calcium and phosphate from bone
After successful parathyroidectomy:
  • PTH levels fall abruptly
  • Bone resorption decreases
  • Previously demineralized bone rapidly takes up calcium, phosphate, and magnesium ("hungry" bone)
  • This results in significant hypocalcaemia

Risk Factors

  • Severe hyperparathyroidism
  • Very high preoperative PTH levels
  • Elevated alkaline phosphatase
  • Large parathyroid adenoma
  • Significant bone disease (osteitis fibrosa cystica)
  • Secondary hyperparathyroidism due to chronic kidney disease
  • Vitamin D deficiency

Clinical Features

Usually develops within 2–4 days after surgery. Symptoms of hypocalcaemia:
  • Perioral numbness
  • Paresthesias
  • Muscle cramps
  • Tetany
  • Carpopedal spasm
  • Positive Chvostek and Trousseau signs
  • Seizures (severe cases)
  • QT prolongation and arrhythmias

Laboratory Findings

  • ↓ Serum calcium
  • ↓ Ionized calcium
  • ↓ Phosphate (typically in primary hyperparathyroidism)
  • ↓ Magnesium
  • Low or appropriately reduced PTH after surgery
  • Elevated alkaline phosphatase may persist

Diagnosis

Persistent hypocalcaemia after parathyroidectomy lasting >4 days, associated with:
  • Normal or low PTH
  • Increased skeletal uptake of calcium

Treatment

Mild to Moderate

  • Oral calcium carbonate or calcium citrate
  • Calcitriol (0.25–2 ΞΌg/day)
  • Correct magnesium deficiency

Severe/Symptomatic

  • Intravenous calcium gluconate infusion
  • Continuous ECG monitoring
  • Transition to high-dose oral calcium and calcitriol once stable
 

Prevention

  • Correct vitamin D deficiency before surgery
  • Identify high-risk patients
  • Early postoperative calcium and calcitriol supplementation
  • Always correct hypomagnesaemia first, as hypocalcaemia may not respond until magnesium is restored.
  • In CKD, native vitamin D alone is often insufficient; active vitamin D analogues (calcitriol or alfacalcidol) are usually required.
😭

Wrong Answer: ❌ D. Calcitonin-mediated suppression of bone turnover

😭

Wrong Answer: ❌ E. Acute vitamin D toxicity

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