Rickets is a disease of growing bones caused by inadequate mineralization due to vitamin D deficiency or disorders of calcium and phosphorus. It occurs in children before bone growth plate fusion. Common causes include nutritional deficiencies of vitamin D, calcium, or phosphorus. Clinical features include bone softening and deformities, muscle weakness, and hypocalcemic symptoms. Diagnosis is confirmed by blood tests and radiographic findings of widened growth plates. Treatment involves high dose vitamin D supplementation along with adequate calcium and phosphorus intake.

1. RICKETS
JENCYMARY ANTHONY PRAKASH
GROUP 3

2. RICKETS
 Disease of growing bones ,occurs in children only before the fusion
of epiphyses, and due to unmineralised matrix at the growth plates.
 Inadequate mineralization - Thick G.Plate
 Bones become soft.

3. Causes of Rickets
 VITAMIN D DISORDERS
 Nutritional Vitamin D deficiency
 Congenital Vitamin D deficiency
 Secondary Vitamin D deficiency
 Malabsorption
 Increased degradation
 Decreased Liver 25-hydroxylase
 Vitamin D dependent ricket Type 1
 Vitamin D dependent ricket Type 2
 Chronic Renal Failure
 PHOSPHORUS DEFICIENCY
 Inadequate intake
 Premature infants
 Aluminium containing antacids
 CALCIUM DEFICIENCY
 Low intake
 Diet
 Premature Infant
 Malabsorption
 Primary Disease
 Dietary inhibitors of calcium absorption

4. Causes of Rickets
 RENAL LOSSES
 X- linked hypophosphatemic ricket
 AD hypophosphatemic ricket
 Hereditary hypophosphatemic ricket with
hypercalcuria
 Overproduction of phosphatonin
 Tumors induced rickets
 Mccunealbright syndrome
 Epidermal nevus syndrome
 Neurofibromatosis
 Fanconi syndrome
 Dent Disease

6.  VITAMIN D DEFICIENCY is MC cause of Rickets Worldwide.
 Most commonly occur in infancy due to poor intake and inadequate
cutaneous synthesis
 Formula fed infants - receive adequate vit D even without cutaneous
synthesis
 Breast fed infants rely on cutaneous synthesis or vitamin D
supplements
 Cutaneous synthesis is limited due to:
 Ineffectiveness of winter sun
 Avoidance of sunlight
 Decreased cutaneous synthesis due to increased skin pigmentation

7. Clinical Features of Rickets
 GENERAL
 Failure To Thrive
 Listlessness
 Protruding Abdomen, UMBILICAL HERNIA due to hypotonia
of abdominal wall muscles
 Muscle Weakness (specially proximal)
 Fractures

8. HEAD
 CRANIOTABES: softening of cranial
bones
 Frontal Bossing
 Delayed Fontanelle Closure
 Delayed Dentition, early numerous
caries, enamel hypoplasia - mostly
deciduous teeth are concerned
 Craniosynostosis - early growing
together (or fusion) of two or more
bones of the skull.

9. CHEST
 RACHITICROSARY widening of
costochondral junction
 Harrison Groove pulling of softened ribs
by the diaphragm during inspiration,
 Pectus carinatum
 Thoracic asymmetry
 Widening of thoracic bone
 Respiratory Infections
 Atelectasis impairment of air movement

10. BACK
 Scoliosis
 Kyphosis
 Lordosis

11. EXTREMITIES
 Enlargement of wrists and ankles (Growth
plate widening)
 Valgus or varus deformities

12.  WINDSWEPT DEFORMITY
(combination of varus deformity of 1 leg with
valgus deformity of other leg Anterior
bowing of tibia and femur)
 Coxa Vara
 Leg pain

13. HYPOCALCEMIC SYMPTOMS
 Tetany
 Seizures
 Stridor due to laryngeal spasm

14. RADIOLOGY FINDINGS
 Changes are most easily visualized on PA view of wrist - although
characteristic racitic changes are seen at other growth plates
 Alterations of the epiphyseal regions of the long bones - most
characteristic
 Widening of the radiolucent space between end of bone shafts
(metaphyseal lines) and epiphysis

15.  The edge of the metaphysis loses its sharp border, which is described as
fraying.
 The edge of the metaphysis changes from a convex or flat surface to a more
concave surface. This change to a concave surface is termed cupping and is
most easily seen at the distal ends of the radius, ulna, and fibula.

16. LAB FINDINGS
 Serum calcium - N, ↓
 Phosphorus - ↓
 Alkaline phosphatase - ↑
 Parathyroid hormone(PTH) -↑
 25-hydroxyvitamin D - ↓
 1,25-dihydroxyvitamin D (1,25-D) - ↓, N, ↑
 Urine Ca – ↓
 Urine Pi - ↑

17. TREATMENT
 Children with should receive vitamin D and adequate nutritional intake of
calcium and phosphorus.
 With stoss therapy, 300,000-600,000 IU of vitamin D are administered
orally or intramuscularly as 2-4 doses over 1 day.
 The alternative is daily, high-dose vitamin D, with doses ranging from
2,000-5,000 IU/day over 4-6 wk.
 Either strategy should be followed by daily vitamin D intake of 400 IU/day if
<1 yr old or 600 IU/day if >1 yr old

18. MANGEMENT
 Infants  200 - 400 IU/D (Infants daily exposed to sunlight for 15-20
min.to prevent Rickets)
 Children  400 – 600 IU/D
 Breast feed infants must receive vit.D supplementations because breast
milk contains only 30-40 IU/L

19. CONGENITAL VITAMIN D DEFICIENCY
 Occur when there is severe maternal vitamin D
deficiency during pregnancy
 Risk factors
 Poor dietary intake of Vitamin D
 Lack of adequate sun exposure
 Clinical Features
 Symptomatic hypocalcemia
 IUGR
 Decreased bone ossification + classic rachitic
changes
 Treatment
 Vitamin D supplementation
 Adequate intake of calcium and
phosphorus
 Use of prenatal vitamin D