Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.
Rickets and vitamin-D deficiency
Paediatrics and child health · UK scope · Sources checked 27 Aug 2026 · Clinical review pending
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Hypocalcaemic seizure, stridor or cardiomyopathy
Severe calcium deficiency can cause convulsion, laryngospasm, arrhythmia and cardiac failure before rickets is visibly obvious.
Action: Use ABCDE, check bedside glucose, obtain ionised calcium, magnesium, phosphate, ECG and secure IV access. Give 10% calcium gluconate slowly under the current paediatric emergency protocol, commonly 0.5 ml/kg with continuous cardiac monitoring, while correcting magnesium and arranging specialist treatment of vitamin-D and calcium deficiency.
Overview
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 occurs only before growth-plate closure and reflects failure to mineralise newly formed cartilage and osteoid. Osteomalacia is the corresponding defective mineralisation of bone matrix and can coexist in adolescents. Calcium and phosphate must both be available at the growth plate. Vitamin D supports intestinal absorption, but low dietary calcium can also cause calcipenic rickets, while renal phosphate wasting creates phosphopenic rickets through a different pathway.
Ask about infant feeding, maternal vitamin D, formula volume, supplementation product and actual drops given, diet, calcium sources, sunlight exposure, skin pigmentation, clothing, mobility, gastrointestinal symptoms, renal or liver disease and anticonvulsants. Clarify product concentration because drop preparations vary enormously. Assess family bone disease, short stature, dental abscesses and bowed legs, which may suggest inherited phosphate regulation rather than simple deficiency.
Aetiology
01
Nutritional vitamin-D deficiency
Low intake and limited skin synthesis reduce calcium absorption, especially during rapid growth without recommended supplementation.
02
Low calcium availability
Very low dietary calcium can sustain secondary hyperparathyroidism and rickets even when measured vitamin-D status is not profoundly deficient.
03
Malabsorption or organ disease
Coeliac, inflammatory bowel, cholestatic liver and chronic kidney disease impair vitamin absorption, activation or mineral homeostasis.
04
Inherited phosphate or vitamin metabolism
FGF23-mediated phosphate wasting and rare vitamin-D activation or receptor defects produce rickets despite ordinary preventive intake.
Pathophysiology
1
Reduced intestinal calcium absorption
Vitamin-D deficiency lowers calcium uptake, stimulating PTH to preserve serum calcium through bone and renal adaptations.
2
Secondary phosphate wasting
Raised PTH increases urinary phosphate loss, reducing the calcium-phosphate product available to mineralise growing growth-plate cartilage.
3
Growth-plate disorganisation
Unmineralised hypertrophic cartilage progressively accumulates, widening and deforming metaphyses under repeated weight-bearing and surrounding muscle forces.
4
Neuromuscular hypocalcaemia
Low ionised calcium increases neuronal and muscle excitability and impairs myocardial function, causing tetany, seizure or cardiomyopathy.
Clinical features and red flags
Infant calcipenic pattern
Craniotabes, widened fontanelle, rib beading, hypotonia, delayed milestones and poor growth develop during rapid skeletal demand.
Weight-bearing deformity
Widened wrists and ankles, bowed legs or knock knees appear after standing and walking begin.
Biochemical rickets
Raised alkaline phosphatase and PTH with low phosphate and deficient 25-hydroxyvitamin D supports nutritional calcipenic disease.
Phosphate-wasting phenotype
Short stature, leg deformity, dental abscesses and persistent low phosphate despite adequate vitamin D suggests inherited renal wasting.
Tachypnoea, feeding failure, hepatomegaly, prolonged QT or poor perfusion can indicate calcium-related myocardial dysfunction.
Red flags requiring action
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.
Investigations
01First-line mineral profileFirst stepFirst line
Why
Measure adjusted or ionised calcium, phosphate, alkaline phosphatase, PTH, magnesium and 25-hydroxyvitamin D.
Interpretation and limitations
Use age-specific ranges and the combined pattern to distinguish calcium deficiency, phosphate wasting and treatment urgency.
02Renal, liver and acid-base studies
Why
Identify organ dysfunction, renal tubular acidosis or impaired vitamin-D activation and absorption.
Interpretation and limitations
Abnormal creatinine, bicarbonate or liver tests argues against treating as uncomplicated nutritional deficiency alone.
03Wrist or knee radiograph
Why
Confirm active growth-plate disease and establish severity when clinical and biochemical findings suggest rickets.
Interpretation and limitations
Metaphyseal widening, cupping and fraying support rickets; imaging cannot identify the biochemical cause by itself.
04Urine calcium and phosphate
Why
Assess renal mineral loss and calculate tubular phosphate handling in persistent or atypical disease.
Interpretation and limitations
Inappropriate urinary phosphate loss during hypophosphataemia supports renal wasting and specialist FGF23 or genetic evaluation.
05
Differential diagnosis
01
Physiological leg variation
Infant bowing and preschool knock knees can be age-appropriate when symmetric, painless and unaccompanied by biochemical or radiographic rickets.
02
Skeletal dysplasia
Disproportion, characteristic radiographs, family history and abnormal segment ratios suggest intrinsic bone growth disorder rather than mineral deficiency.
03
Hypophosphataemic rickets
Persistent phosphate wasting, dental abscesses and family pattern with normal vitamin-D stores point toward FGF23-mediated disease.
04
Renal tubular acidosis
Growth failure, acidosis, urine abnormalities and mineral disturbance can cause rickets through chronic renal bicarbonate and phosphate loss.
05
Non-accidental or other fracture
Fractures require careful mechanism, bone-health and safeguarding assessment; vitamin-D deficiency neither proves nor excludes inflicted injury.
Management
01Suspected ricketsConfirm mineralisation failure and mechanismFirst stepBone deformity, pain, weakness, delayed development or hypocalcaemic symptoms occur with risk factors.+
1Assess growth, skeleton, gait, diet, supplementation, skin exposure, gastrointestinal, renal, liver and family features.
2Measure the full mineral, PTH and vitamin-D profile with renal and liver tests and radiograph a wrist or knee when indicated.
3Classify nutritional calcipenic disease versus phosphate-wasting or organ-related rickets before selecting long-term therapy.
02Acute hypocalcaemiaStabilise neuromuscular and cardiac functionSeizure, tetany, stridor, prolonged QT, arrhythmia or cardiomyopathy occurs with low calcium.+
1Use ABCDE, ECG monitoring and secure access and check glucose, ionised calcium, phosphate and magnesium urgently.
Complications
01
Hypocalcaemic seizure
Severe calcium deficiency produces marked neuromuscular excitability, laryngospasm, prolonged QT, convulsion and potentially fatal cardiac arrhythmia.
02
Dilated cardiomyopathy
Profound hypocalcaemia can reduce myocardial contractility, presenting with tachypnoea, hepatomegaly, feeding failure and circulatory shock in infancy.
03
Skeletal deformity and fracture
Soft undermineralised bone bends under load and fractures more easily, impairing gait, growth and later joint alignment.
04
Dental and growth impairment
Delayed dental eruption, enamel defects, recurrent abscesses and reduced linear height can accompany prolonged skeletal mineralisation failure.
05
Treatment hypercalcaemia
Incorrect high-concentration supplements or prolonged therapeutic dosing can cause vomiting, polyuria, nephrocalcinosis and significant acute renal injury.
Monitoring and follow-up
Repeat calcium, phosphate and magnesium early after starting treatment, especially after symptomatic hypocalcaemia or intravenous calcium.
Follow alkaline phosphatase and PTH over subsequent weeks as slower markers of biochemical and skeletal healing.
Measure 25-hydroxyvitamin D after the treatment course when response, adherence or continuing risk needs confirmation.
Plot growth, observe gait and leg alignment, ask about pain and motor progress and minimise repeat radiographs when recovery is clear.
For phosphate-wasting or active-vitamin-D therapy, monitor urine calcium, renal ultrasound and renal function under specialist care.
Check the actual bottle, concentration, dropper and daily amount at follow-up to prevent both underdosing and toxicity.
Move from therapeutic to preventive vitamin D and document who supplies it, including Healthy Start access and risk-group year-round use.
Special situations
Rickets is a pattern
No single vitamin-D result replaces calcium, phosphate, PTH, alkaline phosphatase, renal context and growth-plate evidence.
Calcium completes treatment
Vitamin D cannot mineralise bone when dietary calcium remains inadequate, so both substrates need explicit provision.
Children need child ranges
Growing children normally have higher alkaline phosphatase and age-varying phosphate, making adult reference intervals misleading.
A knee shape may be physiological
Symmetry, age, pain, growth and biochemistry distinguish normal bowing or knock knees from active rickets.
Drops are not interchangeable
Different products contain radically different units per drop, so inspecting the bottle prevents serious dosing error.
Common pitfalls
01
Diagnosing rickets from low vitamin D without assessing calcium, phosphate, PTH and alkaline phosphatase.
02
Using adult phosphate and alkaline-phosphatase reference ranges for a growing child.
03
Giving vitamin D without ensuring adequate calcium intake.
04
Treating a hypocalcaemic seizure with oral supplements alone.
05
Assuming every bowed leg is nutritional rickets or every fracture is explained by deficiency.
06
Repeating high-dose vitamin-D courses without checking adherence, product concentration or alternative disease.
07
Missing renal phosphate wasting when vitamin D is normal and dental or family features are present.
08
Operating on leg deformity before correcting active metabolic bone disease.
Practice
Two practice questions
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Question 1 of 2
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Paediatrics and child healthOriginal SBA
Treating nutritional rickets
A 3-year-old with bowed legs has low 25-hydroxyvitamin D, raised PTH and alkaline phosphatase and low phosphate, with normal renal function. Which treatment principle is most appropriate?
Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
Sources
Sources and review status
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.
NICE PH56 vitamin DUK prevention, supplementation access, risk groups and implementation for vitamin-D deficiency.
SACN vitamin D and healthUK evidence base and reference nutrient intake underpinning population supplementation advice.
NHS vitamin DCurrent age-based public supplementation advice, formula threshold and toxicity information.
BNF for ChildrenChild-specific colecalciferol, calcium and intravenous calcium preparations, doses and cautions.
Examine growth and gait, leg alignment, wrists, ankles, skull, ribs, spine, muscle power and teeth. Infants may have craniotabes, frontal bossing, widened fontanelle, rib beading and hypotonia. Older children develop genu varum or valgum, bone pain, delayed motor milestones or fractures. Hypocalcaemia can cause tetany, laryngospasm, seizure or cardiomyopathy before obvious skeletal deformity, especially during rapid infant growth.
Obtain adjusted calcium, phosphate, alkaline phosphatase, PTH, 25-hydroxyvitamin D, magnesium, renal and liver profiles. In nutritional vitamin-D deficiency, 25-hydroxyvitamin D is low, PTH rises, phosphate often falls through renal loss and alkaline phosphatase is high; calcium can be low or maintained until late. Age-specific phosphate and alkaline-phosphatase ranges are essential because children normally have different values from adults.
Radiograph the wrist or knee when clinical or biochemical rickets is suspected, showing widening, cupping and fraying of the metaphysis and reduced mineral density. Imaging helps establish active growth-plate disease and later healing, but a normal scan does not explain every biochemical deficiency and an abnormal leg shape can be orthopaedic without rickets. Avoid repeated radiographs when biochemical and clinical recovery is clear.
Classify calcipenic versus phosphopenic disease. A low 25-hydroxyvitamin D with raised PTH and appropriate history supports nutritional deficiency. Normal vitamin D with persistent low phosphate, dental abscesses, disproportionate short stature or family history suggests renal phosphate wasting such as X-linked hypophosphataemia. Check urine calcium and phosphate, tubular phosphate handling and acid-base status with paediatric renal or bone expertise. Chronic kidney disease changes vitamin-D activation and cannot be treated by routine colecalciferol alone.
For nutritional rickets, therapeutic oral colecalciferol is combined with adequate calcium for 8 to 12 weeks. Widely used child regimens are 3,000 IU daily below 6 months, 6,000 IU daily from 6 months to 12 years and 10,000 IU daily from 12 to 18 years, with the exact preparation checked in BNFC and specialist guidance. Supply at least around 500 mg elemental calcium daily by food or supplement. Avoid unsupervised repeated high-dose boluses because concentration errors and hypercalcaemia can harm.
A hypocalcaemic seizure, tetany, stridor, arrhythmia or cardiomyopathy requires ABCDE, ECG and slow intravenous calcium gluconate through secure access under paediatric emergency guidance, often 10% calcium gluconate 0.5 ml/kg with continuous monitoring, while magnesium and the underlying deficiency are corrected. Extravasation causes tissue injury and rapid administration can cause bradycardia. After stabilisation, continue oral calcium and vitamin D and monitor for rebound.
Prevention is different from treatment. UK advice generally provides 10 micrograms or 400 IU daily from birth for breastfed infants and for formula-fed infants taking less than 500 ml formula daily, with year-round supplementation from 1 to 4 years. Older children and adults take 10 micrograms during autumn and winter, and higher-risk groups throughout the year. Use Healthy Start vitamins where eligible and verify that families understand micrograms, units and drops.
Review symptoms, calcium and phosphate promptly, and alkaline phosphatase and PTH over weeks because skeletal healing lags. Poor response should trigger adherence and product check, calcium intake review, malabsorption or liver and renal assessment and reconsideration of inherited disease. Orthopaedic deformity may improve with growth after biochemical healing; refer persistent severe angulation after the metabolic problem is controlled rather than operating on active rickets.
Key points
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.
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.
Malabsorption and dietary assessment
Why
Quantify calcium and vitamin-D intake and test for coeliac or other gastrointestinal disease when indicated.
Interpretation and limitations
Poor response despite reliable treatment is often explained by inadequate calcium, wrong product use or ongoing malabsorption.
06ECG and echocardiography
Why
Assess prolonged QT, arrhythmia and ventricular function in symptomatic or profound hypocalcaemia.
Interpretation and limitations
Cardiac dysfunction increases replacement urgency and requires intensive monitoring until calcium and contractility recover.
2
Give slow 10% calcium gluconate under paediatric emergency dosing with line and rhythm observation and correct magnesium deficiency.
3Begin sustained calcium and vitamin-D treatment once stable and monitor closely for rebound low calcium or treatment excess.
03Nutritional treatmentRestore vitamin D and calcium togetherBiochemistry and clinical context support nutritional vitamin-D or calcium-deficiency rickets without an organ-specific mechanism.+
1Give age-banded daily colecalciferol for 8 to 12 weeks using a verified preparation and provide at least around 500 mg elemental calcium daily.
2Teach exact units, micrograms and drops, address food and Healthy Start access and remove continuing risk factors.
3Recheck calcium and phosphate early and PTH, alkaline phosphatase and clinical healing later, then move to preventive dosing.
04Atypical or resistant ricketsInvestigate phosphate and organ pathwaysVitamin D is not low, phosphate wasting persists, renal disease exists or appropriate therapy produces poor healing.+
1Verify adherence, product concentration and calcium intake and calculate renal phosphate handling with acid-base assessment.
2Refer to paediatric bone, renal or metabolic specialists for FGF23, genetic and active vitamin-D evaluation.
3Use cause-specific phosphate, active vitamin D or targeted therapy with renal, urinary calcium and nephrocalcinosis monitoring.
Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
Replenishes vitamin D to restore intestinal mineral absorption and permit growth-plate and bone-matrix healing.
Colecalciferol treatment
For nutritional rickets give orally each day for 8 to 12 weeks: 3,000 IU below 6 months, 6,000 IU from 6 months to 12 years and 10,000 IU from 12 to 18 years, using a verified child preparation.
Check product concentration and units carefully, avoid repeated unmonitored loading doses and reassess if renal, liver or malabsorptive disease alters handling.
Supplies mineral substrate and suppresses secondary hyperparathyroidism so vitamin-D treatment can heal calcipenic rickets.
Elemental calcium
Provide at least about 500 mg elemental calcium daily through food or oral supplement during nutritional-rickets treatment, unless age, intake, hypocalcaemia severity or specialist advice requires a different amount.
State elemental rather than salt weight, divide larger doses when needed, separate interacting medicines and monitor urine or serum calcium when prolonged.
Raises ionised calcium rapidly to treat seizure, laryngospasm, prolonged QT, arrhythmia or myocardial dysfunction.
Calcium gluconate 10%
For symptomatic severe hypocalcaemia, give slowly intravenously under paediatric resuscitation guidance, commonly 0.5 ml/kg of 10% solution, through a secure line with continuous ECG and repeated ionised-calcium assessment.
Rapid administration can cause bradycardia, extravasation causes necrosis and persistent hypocalcaemia will recur unless magnesium, vitamin D and calcium deficit are corrected.
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.