Can hypocalcemia cause seizures in pediatric patients?

Hypocalcemia Can Cause Seizures in Pediatric Patients

Yes, hypocalcemia is a well-established and important cause of seizures in pediatric patients across all age groups, from neonates to adolescents, and should be routinely excluded in any child presenting with seizures. 1, 2

Clinical Evidence and Mechanisms

Seizures may be the first and presenting manifestation of hypocalcemia in children, particularly in those with underlying parathyroid dysfunction or genetic predisposition. 1, 2 This can occur even in patients without prior history of hypocalcemia or seizures. 1

Key Clinical Presentations:

• Neonatal seizures (day 5 of life and beyond) can result from hypocalcemia secondary to maternal vitamin D deficiency, excessive maternal calcium ingestion causing transient hypoparathyroidism, or genetic disorders. 3, 4
• Afebrile seizures in older children (beyond infancy) should prompt immediate measurement of serum calcium levels, as hypocalcemia from hypoparathyroidism can present this way. 2
• Infantile seizures are frequently caused by vitamin D deficiency-related hypocalcemia, with 90% of infants with hypocalcemic seizures having 25(OH)D levels <10 ng/mL. 4

Severity Thresholds and Risk Stratification

Severe hypocalcemia (corrected serum calcium <7.0 mg/dL or ionized calcium <0.75 mmol/L) causes seizures, tetany, laryngospasm, cardiac arrhythmias, and altered mental status requiring immediate intravenous calcium replacement. 1

Critical Cardiac Considerations:

• Prolonged QT interval on ECG is a hallmark finding that predisposes to ventricular arrhythmias and should be assessed in all hypocalcemic patients. 1, 5, 2
• Ionized calcium <0.8 mmol/L is linked to cardiac dysrhythmias and mandates immediate correction. 1

High-Risk Populations Requiring Vigilance

Genetic Syndromes:

• 22q11.2 deletion syndrome (DiGeorge syndrome) carries an 80% lifetime prevalence of hypocalcemia and is the most common cause of hypoparathyroidism in childhood. 1, 5, 2 Screen all patients with congenital heart disease (especially Tetralogy of Fallot) for this syndrome. 5

Neonatal Risk Factors:

• Early-onset hypocalcemia (first 24-48 hours) occurs from interrupted placental calcium transfer and delayed PTH surge, though usually asymptomatic. 6
• Late-onset hypocalcemia (after 72 hours) results from excessive phosphate intake, maternal vitamin D deficiency, or hypomagnesemia. 6
• Infants born to vitamin D deficient mothers have significantly higher risk—89% of infants with 25(OH)D <10 ng/mL were born to mothers with similar deficiency. 4

Diagnostic Approach

Measure pH-corrected ionized calcium (most accurate) rather than total calcium alone, as ionized calcium is the physiologically active fraction. 1, 6

Essential Initial Laboratory Tests:

• Ionized calcium (priority)
• Parathyroid hormone (PTH) levels
• Magnesium levels (critical—hypomagnesemia must be corrected first before calcium levels will normalize) 7, 6, 8
• Phosphate levels
• 25-hydroxyvitamin D levels
• Renal function (creatinine)
• Electrocardiogram for QT interval assessment 1, 2

Common Pitfall:

Calcium administration without magnesium correction is futile. 1 Magnesium deficiency impairs PTH secretion and creates PTH resistance; hypocalcemia will not resolve until magnesium is corrected. 6, 8

Acute Management of Hypocalcemic Seizures

Immediate Treatment:

• 10% calcium chloride (270 mg elemental calcium per 10 mL) is preferred for severe cases, given intravenously with cardiac rhythm monitoring due to arrhythmia risk. 1
• Alternative: Calcium gluconate 0.3 mL/kg of 10% solution over 30 minutes for total calcium <2 mmol/L. 7
• Correct hypomagnesemia first if present: 0.2 mL/kg of 50% MgSO4 over 30 minutes. 7

Seizure Management Algorithm:

Follow standard pediatric seizure protocols (lorazepam 0.1 mg/kg IV/IO), but prioritize calcium correction simultaneously as the underlying cause. 7

Maintenance and Prevention

Chronic Management:

• Daily calcium supplementation (total elemental calcium not exceeding 2,000 mg/day) with vitamin D is more effective than either agent alone. 1
• Calcitriol dosing for hypoparathyroidism: 20-30 ng/kg body weight daily or 0.5 μg daily in patients >12 months old. 1
• Correct vitamin D deficiency with cholecalciferol or ergocalciferol supplementation. 1

Monitoring Requirements:

• Measure serum calcium and phosphorus at least every 3 months during treatment. 1
• Monitor for hypercalciuria to prevent nephrocalcinosis. 1
• Targeted calcium monitoring during vulnerable periods: surgery, acute illness, puberty, pregnancy, or biological stress. 1, 5

Special Clinical Scenarios

Massive Transfusion:

Monitor ionized calcium closely, as citrate in blood products chelates calcium (each unit contains ~3 g citrate). Hypocalcemia <0.9 mmol/L predicts mortality better than fibrinogen, acidosis, or platelet count. 1

Prolonged Seizure Activity:

Rarely, prolonged seizures can cause cell lysis leading to severe hyperphosphatemia and secondary hypocalcemia, creating a bidirectional relationship. 9