Nutritional Rickets

Nutritional rickets remains a significant clinical problem in the developing world.


It is due to the decreased nutritional intake of calcium or vitamin D.

The main cause of nutritional rickets is vitamin D deficiency. Vitamin D deficiency is due to inadequate intake; or unsuitable diets like prolonged breast milk intake, vegetarian diet or avoiding dairy products; or deficient exposure to sunlight.



Another rare cause is isolated calcium deficiency. It is due to inadequate intake or unsuitable diet like food with decreased calcium and high in phytate, oxalate or citrate content results in poor availability of calcium for absorption in the gut.



Sometimes, it is due to combined calcium deficiency and marginal vitamin D intake.

The peak age of presentation of nutritional rickets is between 3 and 18 months in children who have inadequate exposure to sunlight and no vitamin D supplementation in the diet.



Infants demonstrate generalized muscular weakness, lethargy, and irritability.

Craniotabes with softening of the occiput will present.

Sitting, standing, and walking are delayed.

The abdomen may appear protuberant.



Early bone manifestations –

Slight thickening of ankle, knee, and wrist

Beading of ribs – Enlargement of the costochondral junction

Harrison groove – Due to pulling of the diaphragm on ribs

Short stature

Pectus carinatum – Forward projection of sternum

Closure of fontanelle is delayed and sutures are thickened which results in hot cross buns appearance



As the child begins standing and walking, the softened long bones bow –

Bowleg or genu varum – Initial signs in the infancy and toddlers

Genu valgum and coxa vara – See in older children

Stress fractures of long bones

Later, kyphoscoliosis may develop

Serum calcium – Normal


Serum phosphate – Normal/ marginally decreased


Serum alkaline phosphatase – Increased


Parathyroid hormone assay – Increased


25(OH) vitamin D – Markedly decreased


1,25(OH)2 vitamin D – Decreased

Rickets is treated by the administration of vitamin D under the supervision of a pediatric specialist in metabolic bone disease.



The usual course of treatment is 6 to 10 weeks.



The residual deformity is rare after medical treatment of nutritional rickets, there is no specific orthopaedic treatment of nutritional rickets. However persistent residual deformities are treated with guided growth or corrective osteotomy.

Appropriately treated nutritional rickets will not result in the long term consequences.