History and exam

Key diagnostic factors

common

history of breast-feeding

Breast milk is deficient in vitamin D. Without nutritional supplementation, rickets is possible.[3]​​

history of inadequate sunlight exposure

Living in latitudes above 40º north or south, or sociocultural factors (such as burka-wearing practices, an increase in sedentary lifestyles, less time spent outdoors) result in reduced synthesis of cholecalciferol by the skin.[9][16] Increased sunscreen use has also been implicated.[14]

history of calcium deficiency

Inadequate intake of calcium can lead to insufficient bone mineralization. Breast milk contains limited amounts of calcium, but cows' milk is a richer source.[4] In societies without a tradition of milk drinking, calcium intake is often <300 mg daily. The net absorption of calcium and other minerals is limited by other food substances, such as phytate, present in most cereals.[3]​​

history of phosphate deficiency

Inadequate intake of phosphorus can lead to insufficient bone mineralization. Phosphorus is abundant in most diets but may not be sufficient in rapidly growing low-birthweight babies. Phosphate may be precipitated in the stomach by antacids.

Other diagnostic factors

common

bone pain

May be associated with pseudofractures or insufficiency fractures.[3]​​

growth faltering

Faltering growth is a common presentation of rickets.[4]

delayed achievement of motor milestones

Consider rickets in children presenting with developmental delay.[4]

bony deformities

Such as bowlegs.[4][Figure caption and citation for the preceding image starts]: Malnutrition manifested as rickets. Note the bowed legs and kneesCDC [Citation ends].com.bmj.content.model.Caption@528706a2

muscle weakness

May be due to hypocalcemia or hypophosphatemia.[4]

carpopedal spasm

May be seen in association with hypocalcemia.

tetany

May be seen in association with hypocalcemia.

uncommon

numbness or paresthesias

May be seen in association with hypocalcemia.

hypocalcemic seizures

Can be a manifestation of rickets associated with hypocalcemia.[4]

Risk factors

strong

age 6 to 23 months

The peak incidence of rickets is between 6 and 23 months, with a further peak among adolescents ages 12 to 15 years.[11]

Onset of rickets can only occur while epiphyseal plates have not yet closed.[12]

inadequate sunlight exposure

Living in latitudes above 40º north or south, or sociocultural factors (such as burka-wearing practices, an increase in sedentary lifestyles, less time spent outdoors) result in reduced synthesis of cholecalciferol by the skin.[9]​[16]​​ Increased sunscreen use has also been implicated.[14]

breast-feeding

Breast milk is deficient in vitamin D. Without nutritional supplementation, rickets is possible.[3]​​

calcium deficiency

Inadequate intake of calcium can lead to insufficient bone mineralization. Breast milk contains limited amounts of calcium, but cows' milk is a richer source.[4] In societies without a tradition of milk-drinking, calcium intake is often <300 mg daily. The net absorption of calcium and other minerals is limited by other food substances, such as phytate, present in most cereals.​[3]

phosphate deficiency

Inadequate intake of phosphorus can lead to insufficient bone mineralization. Phosphorus is abundant in most diets but may not be sufficient in rapidly growing low-birthweight babies. Phosphate may be precipitated in the stomach by antacids.[3]​​

family history of rickets

A family history of short stature, orthopedic abnormalities, poor dentition, alopecia, and parental consanguinity may signify inherited rickets.[4]

antacids, loop diuretics, corticosteroids, or anticonvulsants

Phosphate may be precipitated in the stomach by aluminum-containing antacids.​[4] Other medications that can cause calcium and phosphorus deficiency include loop diuretics and corticosteroids, and phenytoin can cause target organ resistance to calcitriol.[4]

weak

darker skin complexion

Increased skin pigmentation may require increased exposure to sunlight to allow adequate conversion of 7-dehydrocholesterol to cholecalciferol.[3]​​

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