What is the recommended treatment for a patient with tetany, potentially due to hypoparathyroidism or vitamin D deficiency?

Tetany Management

Immediate intravenous calcium gluconate administration is the cornerstone of acute tetany treatment, followed by identification and correction of the underlying cause—most commonly hypoparathyroidism or severe vitamin D deficiency.

Acute Management of Tetany

Immediate Intervention

• Administer IV calcium gluconate 1-2 grams (10-20 mL of 10% solution) over 10-20 minutes with continuous cardiac monitoring for symptomatic hypocalcemia presenting with tetany, paresthesias, Chvostek's or Trousseau's signs, laryngospasm, bronchospasm, or seizures 1, 2.
• A 10-mL ampule of 10% calcium gluconate contains 90 mg of elemental calcium 1.
• For severe, refractory tetany, initiate continuous calcium gluconate infusion at 1-2 mg elemental calcium per kilogram body weight per hour, adjusting to maintain ionized calcium in the normal range (1.15-1.36 mmol/L or 4.6-5.4 mg/dL) 1.
• Measure ionized calcium levels every 4-6 hours initially, then twice daily until stable 1.

Critical Pitfall: Check Magnesium

• Measure serum magnesium immediately, as hypocalcemia is refractory to calcium replacement without adequate magnesium levels 3, 4.
• If hypomagnesemia is present, administer magnesium sulfate IV to correct the deficiency, as magnesium is required for PTH secretion and calcium homeostasis 5, 4, 2.

Diagnostic Workup During Stabilization

Essential Laboratory Tests

• Obtain serum calcium (corrected for albumin or ionized), phosphorus, intact PTH, 25-hydroxyvitamin D, magnesium, creatinine, and albumin 1, 6.
• Check serum chloride and CO2 to assess for alkalosis, which can precipitate tetany even with normal calcium 2.
• Obtain ECG to assess for prolonged QT interval, a potentially life-threatening complication of hypocalcemia 1.

Interpretation Algorithm

• If PTH is low or inappropriately normal with hypocalcemia: hypoparathyroidism (post-surgical, autoimmune, or genetic) 1, 7.
• If PTH is elevated with hypocalcemia and low vitamin D: secondary hyperparathyroidism due to vitamin D deficiency 1, 3.
• If PTH is normal with hypocalcemia and low vitamin D: consider pseudohypoparathyroidism (PTH resistance) 3.

Chronic Management Based on Etiology

Hypoparathyroidism (Low PTH)

• Start oral calcium supplementation at 1,000-2,000 mg elemental calcium daily in divided doses 1, 3, 8.
• Initiate calcitriol (active vitamin D) at 0.25 mcg daily in adults, increasing by 0.25 mcg at 2-4 week intervals based on response 1, 8.
• For pediatric patients ages 1-5 years with hypoparathyroidism, typical doses range from 0.25-0.75 mcg daily; for ages 6 years and older, 0.5-2 mcg daily 8.
• Target serum calcium in the low-normal range (8.0-8.5 mg/dL) to avoid hypercalciuria and nephrocalcinosis 7.
• Monitor serum calcium at least twice weekly during dose titration, then monthly once stable 8.
• Measure 24-hour urinary calcium to ensure it remains <300 mg/24hr to prevent renal complications 6, 3.

Vitamin D Deficiency (Elevated PTH)

• Supplement with ergocalciferol or cholecalciferol 800-4,000 IU daily depending on severity of deficiency (25-hydroxyvitamin D <30 ng/mL) 1, 3.
• Provide oral calcium supplementation 1,000-2,000 mg elemental calcium daily in divided doses 3.
• Do NOT give calcium and phosphate supplements simultaneously, as they precipitate in the gut and reduce absorption 3.
• Recheck 25-hydroxyvitamin D after 8-12 weeks to confirm repletion 3.
• If vitamin D deficiency fails to respond to ergocalciferol, particularly in patients with kidney failure, consider treatment with calcitriol 1.

Special Consideration: Malabsorption

• In patients with gastrointestinal malabsorption refractory to massive oral doses of calcium carbonate and vitamin D, consider oral calcium chloride solution (10% solution, 1.09 gm elemental calcium per 30 mL) 9.
• Alternatively, intramuscular vitamin D3 300,000 IU every 2-4 months may be effective in severe malabsorption cases 10.
• Monitor serum chloride and CO2 when using calcium chloride to avoid hyperchloremic acidosis 9.

Monitoring and Dose Adjustments

During Active Treatment

• Measure serum calcium and phosphorus at least twice weekly during initial dose titration 1, 8.
• Once stable, monitor calcium and phosphorus every 3 months 1, 3.
• Immediately discontinue calcitriol if serum calcium exceeds 10.2 mg/dL until normocalcemia returns 1, 8.
• When restarting after hypercalcemia, reduce calcitriol dose by 0.25 mcg/day from prior therapy 8.

Long-Term Surveillance

• Assess for symptoms of over-treatment: polyuria, polydipsia, nausea, constipation, or confusion suggesting hypercalcemia 6, 8.
• Maintain calcium-phosphorus product <55 mg²/dL² to prevent soft tissue calcification 1.
• Ensure total elemental calcium intake does not exceed 2,000 mg/day from all sources 1, 6.

High-Risk Situations Requiring Increased Monitoring

Hypocalcemia may arise or recur at any age despite apparent resolution, particularly during biological stress 1:

• Peri-operatively (any surgery) 1.
• Pregnancy and perinatally 1.
• During acute illness, infection, or injury 1.
• Fractures 1.

Targeted calcium monitoring should be performed during these vulnerable periods 1.

Critical Pitfalls to Avoid

• Never ignore normal PTH in the setting of hypocalcemia—this is inappropriate and warrants investigation for pseudohypoparathyroidism or PTH resistance 3.
• Do not supplement with vitamin D until hypercalcemia is resolved if treating a patient with concurrent hypercalcemia 6, 3.
• Avoid over-correction with calcitriol, which can result in iatrogenic hypercalcemia, renal calculi, and renal failure 1.
• Correct hypomagnesemia concurrently, as hypocalcemia is refractory to treatment without adequate magnesium 3.
• Avoid alcohol and cola drinks, which may worsen hypocalcemia 1.