Dr Ira Shah
M.D, DNB, DCH(Gold Medalist), FCPS

A 20 days old male child presented with multiple episodes of generalized tonic clonic convulsions since 3 days. He was a full term normal vertex vaginal delivery with birth weight of 3.75 kg and had no antenatal or post natal complications. He was exclusively breast fed child. On examination, he had marked beading, craniotabes and sutural separation. He was very jittery and deep tendon reflexes were brisk. His activity was good and other systemic examination was normal. A differential diagnosis of a metabolic disorder such as hypocalcaemia, hypoglycemia was considered. His S.calcium was low (7.4 mg/dl) and alkaline phosphatase was high (641 IU/L) with low ionic calcium (0.69 mmoL/L). His serum phosphorus was 4.9 mg/dl. His septic work up in form of CRP, CSF examination, hemogram and blood culture was negative. His random b lood sugar was 92 mg% with glycosylated hemoglobin of 4.7. X ray chest showed no evidence of rickets. His serum magnesium was normal (1.7 mg/dl) and serum parathyroid hormone was 186 pg/ml (normal = 1.1 – 12.95 pg/ml). In view of rickets biochemically in an exclusively breast fed infant, the mother’s serum calcium, phosphorus, alkaline phosphatase was done which were normal. The child was treated with IV calcium gluconate, 5,000 U of Vitamin D daily and oral calcium supplements. His serum calcium after 14 days was 9.2 mg/dl and alkaline phosphatase was 235 IU/L thus confirming nutritional Vitamin D deficiency in 20 days old child.

Significant aberrations of serum calcium concentrations are frequently observed in the neonatal period. The flow of calcium ions from mother to fetus during 3 rd trimester of gestation to associated with chronic fetal hypercalcemia. At birth, the umbilical serum calcium level is elevated (10 to11 mg/dl) and serum calcium declines in the term babies for first 24 to 48 hours; nadir is usually 7.5 to 8.5 mg/dl. Thereafter calcium concentrations progressively rise to mean values observed in older children and adults. Early onset hypocalcaemia (during 1 st 3 days of life) is seen in preterm babies, low birth weight infants, infants of diabetic mothers and birth asphyxia. Late onset hypocalcaemia usually presents at the end of 1 st week but onset ranges from first days to several weeks after birth. It is classically seen in term infants fed high phosphate diets. Other etiologies include hypoparathyroidism, Magnesium deficiency and vitamin D deficiency. Vitamin D deficiency may be secondary to maternal vitamin D deficiency, malabsorption, Maternal anticonvulsant therapy, renal insufficiency and hepatobiliary disease. Human milk has a total antirachitic sterol content of only 25 to 50 IU/L which may be just enough to maintain the normal 25 hydroxy vitamin D [25 (OH) D 3] levels in term infants. Laboratory evaluations of vitamin D deficiency in newborns may reveal a low to normal serum calcium levels and low to normal phosphorus levels. Serum alkaline phosphatase is elevated and may invariantly be correlated with the disease severity. Treatment of vitamin D deficiency in neonates consists of initial doses of oral vitamin D 2 upto 5000 units/day, though higher doses may be required. Once the deficiency resolves, weaning off slowly of vitamin D 2 is advised. Frequent assay of ser um calcium level is necessary to avoid rebound hypervitaminosis D. Defects in vitamin D metabolism are treated with vitamin D analogues such as dihydrotachysterol and calcitriol. Oral calcium supplements may be necessary during high dose vitamin D therapy since serum calcium levels may drop precipitously as bones mineralize rapidly