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Case report of an infant with severe vitamin D deficiency rickets manifested as hypocalcemic seizures
Insights
Severe vitamin D deficiency caused hypocalcemic seizures in an infant. Prompt calcium gluconate treatment resolved seizures and stabilized the infant, highlighting vitamin D
Area of Science:
- Pediatric Neurology
- Endocrinology
- Nutritional Science
Background:
- Hypocalcemic seizures are rare in infants after the neonatal period.
- Vitamin D deficiency is a critical factor in pediatric hypocalcemia.
- Rickets presents with characteristic clinical and radiological signs.
Observation:
- A five-month-old infant presented with refractory seizures.
- Clinical examination revealed signs of rickets.
- Laboratory tests confirmed severe hypocalcemia and vitamin D deficiency.
Findings:
- Intravenous calcium gluconate immediately terminated seizures.
- Oral vitamin D3 and calcium supplementation normalized calcium levels and improved rickets.
- Biochemical markers (low 25(OH)D, high PTH, elevated alkaline phosphatase) indicated severe deficiency.
Implications:
- Severe vitamin D deficiency can manifest as hypocalcemic seizures in infants.
- Early diagnosis and treatment are crucial for stabilizing calcium homeostasis.
- This case underscores the importance of screening for vitamin D deficiency in infants with seizures.
Introduction:
Hypocalcemic seizures are uncommon in the post-neonatal period. We report an infant with hypocalcemic seizures caused by severe deficiency of vitamin D.
Case Outline:
A five-month-old male infant was admitted to hospital in March 2013 with recurrent generalized afebrile seizures resistant to clonazepam therapy. At the clinical examination, the infant showed characteristic rachitic signs, so that after a blood sample was taken for laboratory testing, the infant was given infusion of 2 ml/kg of 10% of calcium gluconate at a rate of 0.5 ml/min.The treatment resulted in immediate termination of seizures and normalization of the consciousness of the infant. Blood sample analysis showed extremely low levels of free and total calcium (0.36/1.24 mmol/) and 25(OH)D (<3 ng/ml), elevated alkaline phosphatase (878 U/) and parathyroid hormone (283 pg/ml), and low calcium/creatinine ratio (mg/mg) in a portion of urine (0.03), while the levels of serum phosphorus, pH, total protein, albumin and creatinine were within the reference range. Wrist X-ray showed typical signs of rickets. In order to fully stabilize calcium homeostasis, along with 2,000 IU of vitamin D3 daily and standard cow's milk formula, calcium gluconate (80 mg/kg daily) was given orally over a period of two weeks.The treatment resulted in complete stabilization of the infant's condition and rapid improvement in laboratory, radiological and clinical findings of rickets.
Conclusion:
Generalized convulsions in the afebrile infant represent a serious and etiopathogenically very heterogeneous problem. Extremely rare, as in the case of our patient, it may be due to severe hypocalcemia caused by a deficiency of vitamin D.
