Rickets And Vitamin D Deficiency

Nutritional rickets is defective mineralization of the growing skeleton, most commonly from vitamin D deficiency, inadequate calcium intake, or both. Vitamin D deficiency reduces intestinal calcium and phosphate absorption, producing secondary hyperparathyroidism, phosphate loss and failure of mineralization at the growth plate.

• Widened wrists and ankles
• Bow legs or knock knees
• Rachitic rosary
• Frontal bossing
• Delayed fontanelle closure
• Delayed dentition
• Bone pain
• Proximal muscle weakness
• Delayed motor milestones

Severe hypocalcaemia can cause tetany, seizures, stridor or cardiomyopathy.

Typical biochemical pattern:

• Low or normal calcium
• Low phosphate
• Elevated alkaline phosphatase
• Elevated parathyroid hormone
• Reduced 25 hydroxyvitamin D

Radiographs of wrist or knee show metaphyseal widening, cupping and fraying.

For nutritional vitamin D deficiency:

• Vitamin D3 2,000 IU PO daily for at least 3 months in infants younger than 12 months.

• Vitamin D3 3,000 to 6,000 IU PO daily for at least 3 months in older children, depending on age and severity.

Provide elemental calcium at least 500 mg/day during treatment.

Symptomatic hypocalcaemia requires IV calcium. Give 10% calcium gluconate 0.5 mL/kg IV slowly over 5 to 10 minutes, with cardiac monitoring, then correct the underlying deficiency.

Repeat calcium, phosphate and alkaline phosphatase to document biochemical recovery.