Management of Neurological Manifestations from Vitamin D Overdose
Immediately discontinue all vitamin D supplementation and initiate aggressive treatment of hypercalcemia, as neurological symptoms—including encephalopathy, confusion, apathy, and loss of developmental milestones—are direct consequences of severe hypercalcemia and require urgent correction to prevent permanent neurological damage. 1, 2
Initial Assessment and Diagnosis
When vitamin D intoxication is suspected with neurological manifestations, confirm the diagnosis by checking:
- Serum calcium levels (typically >14 mg/dL in symptomatic cases, with emergency intervention needed when >14 mg/dL due to adverse effects on cardiac, central nervous system, renal, and gastrointestinal functions) 1
- Serum 25(OH)D levels (>150 ng/ml confirms vitamin D intoxication; levels can reach 400-470 ng/ml in severe cases) 1, 3
- Serum phosphorus (normal or elevated) 1
- Parathyroid hormone (suppressed/low) 1
- Alkaline phosphatase (normal or low) 1
- Urine calcium/creatinine ratio (elevated) 1
The neurological manifestations correlate directly with serum calcium concentration and duration of hypercalcemia 1. Documented neurological presentations include subacute encephalopathy, loss of developmental milestones, floppiness, poor interaction, confusion, and apathy 2, 4.
Acute Management Protocol
Step 1: Discontinue Vitamin D Immediately
Stop all exogenous vitamin D sources and implement a low calcium and phosphorus diet 1. Critical caveat: Since vitamin D is fat-soluble and stored in adipose tissue, toxic effects may persist for months despite stopping the source 1.
Step 2: Aggressive Hypercalcemia Correction
For severe hypercalcemia (calcium >14 mg/dL with neurological symptoms):
- Intravenous hydration with normal saline at aggressive rates to promote calciuresis 1, 3
- Loop diuretics (furosemide) after adequate hydration to enhance calcium excretion 1, 3, 2
- Glucocorticoids (hydrocortisone or prednisolone) to reduce intestinal calcium absorption and increase renal calcium excretion 1, 3, 2
- Calcitonin for rapid but temporary calcium reduction 1, 3
- Bisphosphonates (pamidronate) for resistant cases—effective in achieving normocalcemia in approximately 6 days (mean 5.94±0.7 days with pamidronate) 5
Step 3: Intensive Monitoring
Monitor continuously during acute treatment:
- Serum calcium levels every 6-12 hours initially 3, 5
- Electrocardiography for arrhythmias 1, 2
- Volume status to avoid over-hydration 2
- Electrolytes (particularly potassium and magnesium) 2
- Blood pressure (persistent hypertension can complicate severe cases) 3
- Renal function and assess for nephrocalcinosis (present in approximately 40% of cases) 5
Expected Clinical Course
Normocalcemia typically requires 6-14 days to achieve, even with aggressive treatment 3, 5. Neurological recovery parallels calcium normalization—patients become alert, conscious, and begin achieving developmental milestones as calcium levels normalize 2. However, serum 25(OH)D levels remain elevated for extended periods (can still be 389 ng/mL at discharge despite clinical recovery) 3.
Critical Pitfalls to Avoid
- Do not underestimate duration of toxicity: Fat storage of vitamin D means prolonged treatment courses are necessary 1
- Do not delay bisphosphonates in resistant hypercalcemia: Pamidronate is effective and safe in pediatric VDI 5
- Do not assume neurological symptoms are unrelated: Encephalopathy, developmental regression, and altered mental status are direct manifestations of hypercalcemia from VDI 2, 4
- Always obtain detailed supplement history: Many cases result from dosing errors with imported supplements, improperly produced nutritional products, or confusion between drops and ampules 3, 5
Long-term Considerations
After acute management, continue monitoring for: