How should a 3‑month‑old infant with seizures due to hypocalcemia from vitamin D deficiency be treated?

Treatment of Hypocalcemic Hypovitaminosis D Seizures in a 3-Month-Old Infant

Immediately administer intravenous calcium gluconate 2 mL/kg of 10% solution at a rate of 0.5 mL/min to terminate seizure activity, followed by concurrent initiation of high-dose vitamin D supplementation (2,000 IU daily for 12 weeks) and oral calcium supplementation (80 mg/kg/day of elemental calcium) to restore calcium homeostasis. 1, 2

Acute Management: Immediate Seizure Control

The first priority is rapid correction of hypocalcemia to stop seizures:

• Administer IV calcium gluconate 10% solution at 2 mL/kg over 5-10 minutes (at a rate of 0.5 mL/min) under continuous cardiac monitoring to prevent bradycardia and arrhythmias. 3, 2
• Seizure activity typically terminates immediately following calcium administration. 4, 2
• Monitor for extravasation during IV administration, as calcium is highly irritating to tissues. 3
• If stable IV access cannot be maintained, continuous nasogastric calcium carbonate at 125 mg elemental calcium/kg/day is an effective alternative that avoids central line complications. 4

Critical pitfall: Do not delay calcium administration while awaiting laboratory confirmation if clinical suspicion is high—hypocalcemic seizures can be life-threatening and respond dramatically to calcium replacement. 2

Concurrent Vitamin D Repletion: Addressing the Root Cause

Begin high-dose vitamin D supplementation immediately after acute calcium administration:

• Administer 2,000 IU of cholecalciferol (vitamin D3) daily for 12 weeks as the standard loading dose regimen for severe deficiency in infants. 1, 5
• Cholecalciferol is preferred over ergocalciferol due to superior bioefficacy. 1, 5
• This dose is well within safety limits (upper tolerable limit for 0-6 months is 1,000 IU/day, but treatment doses up to 4,000 IU/day are used for severe deficiency). 1, 5

The rationale: Vitamin D deficiency causes hypocalcemia through impaired intestinal calcium absorption and secondary hyperparathyroidism. 2, 6 Without vitamin D repletion, calcium supplementation alone will not restore homeostasis. 2

Oral Calcium Supplementation: Bridging Therapy

Provide oral elemental calcium at 80 mg/kg/day in divided doses for 2 weeks:

• Use calcium gluconate or calcium carbonate preparations. 2
• Divide the daily dose into 3-4 administrations to optimize absorption. 2
• Continue oral calcium until vitamin D levels normalize and endogenous calcium absorption improves. 2

This bridging therapy is essential because vitamin D takes several days to weeks to restore normal calcium absorption, and the infant remains at risk for recurrent hypocalcemia during this period. 2

Monitoring Strategy

Check the following laboratory parameters to guide therapy:

• Ionized calcium levels every 4-6 hours initially until stable above 1.0 mmol/L, then daily. 3, 4
• Serum 25(OH)D, total calcium, phosphorus, alkaline phosphatase, and parathyroid hormone (PTH) at baseline. 1, 2
• Recheck 25(OH)D after 12 weeks of treatment to confirm normalization (target >20 ng/mL or 50 nmol/L). 1, 5
• Monitor for hypercalcemia during treatment by checking serum calcium weekly. 3

Radiographic assessment: Obtain wrist X-rays to evaluate for rickets (metaphyseal cupping, fraying, widening of growth plates). 2

Maintenance Phase After Acute Treatment

Once calcium homeostasis is restored (typically by 2 weeks):

• Transition to maintenance vitamin D dosing of 400 IU/day for infants 0-12 months. 1, 5
• Discontinue oral calcium supplementation once serum calcium and PTH normalize. 2
• Continue maintenance vitamin D indefinitely, as all infants require supplementation. 1, 5

Maternal Assessment and Prevention

Evaluate the mother for vitamin D deficiency:

• Maternal vitamin D deficiency is the primary cause of infantile hypovitaminosis D in exclusively breastfed infants. 6, 7
• Check maternal 25(OH)D levels and supplement if deficient. 6, 7
• Breast milk contains insufficient vitamin D (<25-78 IU/L), making supplementation mandatory for all breastfed infants. 1

Preventive counseling: Emphasize that all infants should receive 400 IU vitamin D daily starting shortly after birth, regardless of feeding method. 1, 5 This case represents a preventable condition resulting from lack of supplementation. 6

Special Considerations for This Age Group

At 3 months of age, this infant is at peak risk:

• Vitamin D stores from pregnancy are depleted by 8 weeks of age in exclusively breastfed infants without supplementation. 6
• Rickets typically presents clinically around 18 months, but biochemical deficiency and hypocalcemia can occur much earlier. 1
• Dark-skinned infants, those with limited sun exposure, and those born to vitamin D-deficient mothers are at highest risk. 8, 6

Common pitfall: Do not assume that formula-fed infants are protected—only those consuming ≥500 mL of fortified formula daily receive adequate vitamin D from formula alone. 1

Expected Clinical Course

With appropriate treatment:

• Seizures resolve immediately after IV calcium administration. 4, 2
• Biochemical parameters normalize within 2 weeks of combined calcium and vitamin D therapy. 2
• Radiographic signs of rickets improve over 2-3 months. 2
• Most infants can discontinue calcium supplementation by 2 weeks and transition to maintenance vitamin D by 8 weeks. 4, 2

Red flag: If seizures persist after calcium normalization, consider alternative etiologies or concurrent neurological pathology. 9