Synopsis
Recognise calcipenic rickets and hypocalcaemic emergencies, confirm the mineral and radiographic pattern, distinguish nutritional vitamin-D deficiency from renal, malabsorptive and phosphate-wasting disease and deliver age-specific treatment plus durable prevention.
- Rickets is defective mineralisation at the growing growth plate; vitamin-D deficiency is common but renal phosphate wasting, chronic kidney disease, liver disease and inherited metabolism can produce similar skeletal findings.
- Risk rises with dark skin, little ultraviolet-B exposure, concealing clothing, absent supplementation, maternal deficiency, exclusive breastfeeding without vitamin D, malabsorption, chronic liver or kidney disease and enzyme-inducing medicines.
- Features include bone pain, delayed walking, proximal weakness, widened wrists or ankles, bowed legs or knock knees, rachitic rosary, craniotabes, delayed dentition and poor growth.
- Hypocalcaemia may present first with jitteriness, carpopedal spasm, stridor, prolonged QT, seizure or dilated cardiomyopathy and requires emergency calcium and cardiac monitoring.
- First-line tests are adjusted calcium, phosphate, alkaline phosphatase, parathyroid hormone, 25-hydroxyvitamin D, renal and liver profiles and magnesium; interpret the pattern rather than vitamin D alone.
- Wrist or knee radiography supports active rickets through metaphyseal cupping, fraying and widening, but treatment of severe hypocalcaemia must not await imaging.
- For nutritional rickets, give age-specific therapeutic colecalciferol for 8 to 12 weeks plus adequate calcium; common daily regimens are 3,000 IU below 6 months, 6,000 IU from 6 months to 12 years and 10,000 IU from 12 to 18 years.
- Provide at least about 500 mg elemental calcium daily through diet or supplement during treatment unless the specialist plan differs; vitamin D without calcium may not heal calcipenic rickets.
- Escalate to paediatric bone, renal or metabolic expertise when phosphate remains low, renal indices are abnormal, 25-hydroxyvitamin D is not deficient, response is poor or family history suggests inherited rickets.
- Prevention uses 10 micrograms or 400 IU vitamin D daily in UK risk groups and age bands specified by government advice, with Healthy Start access and safe dosing explained to families.
Key red flags
Seizure, stridor, tetany, arrhythmia or heart failure with low calcium requires immediate monitored intravenous replacement.
Asymmetric deformity, focal bone pain, swelling or refusal to bear weight may indicate fracture, infection or tumour.
Poor growth with chronic diarrhoea, steatorrhoea or abdominal distension suggests malabsorption rather than simple intake deficiency.
Low phosphate that persists after vitamin-D and calcium correction requires renal tubular and inherited rickets assessment.
Renal impairment, acidosis or nephrocalcinosis changes vitamin-D therapy and needs paediatric renal expertise.
Multiple fractures or an inconsistent history requires a complete safeguarding assessment without assuming rickets explains every injury.
Vomiting, polyuria, confusion or renal dysfunction during supplementation can indicate vitamin-D or calcium toxicity.
Jitteriness, carpopedal spasm, stridor, tetany or seizure reflects dangerous ionised-calcium deficiency.
Investigation priorities
Measure adjusted or ionised calcium, phosphate, alkaline phosphatase, PTH, magnesium and 25-hydroxyvitamin D.
Management branches
Bone deformity, pain, weakness, delayed development or hypocalcaemic symptoms occur with risk factors.
- Assess growth, skeleton, gait, diet, supplementation, skin exposure, gastrointestinal, renal, liver and family features.
- Measure the full mineral, PTH and vitamin-D profile with renal and liver tests and radiograph a wrist or knee when indicated.
- Classify nutritional calcipenic disease versus phosphate-wasting or organ-related rickets before selecting long-term therapy.