History and exam

Key diagnostic factors

common

presence of risk factors

Key factors include inadequate exposure to sunlight, age <18 months, breastfeeding, inadequate calcium and phosphate intake, and positive family history.

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@5fe0ca5c

muscle weakness

May be due to hypocalcaemia or hypophosphataemia.[4]

uncommon

carpopedal spasm

May be seen associated with hypocalcaemia.

numbness or paresthesias

May be seen in association with hypocalcaemia.

tetany

May be seen associated with hypocalcaemia.

hypocalcaemic seizures

Can be a manifestation of rickets associated with hypocalcaemia.[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 aged 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 colecalciferol by the skin.[9][16] Increased sunscreen use has also been implicated.[14]

breastfeeding

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 mineralisation. 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 mineralisation. Phosphorus is abundant in most diets but may not be sufficient in rapidly growing low-birth-weight babies. Phosphate may be precipitated in the stomach by antacids.[3]​​

family history of rickets

A family history of short stature, orthopaedic 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 aluminium-containing antacids.​[4] Other medicines 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 colecalciferol.[3]​​

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